Foundations of Respiratory Care, 2E (2012) (PDF) (UnitedVRG) PDF

Foundations of
Respiratory Care
This page intentionally left blank
Foundations of
Respiratory Care
Second Edition
Kenneth A. Wyka, MS, RRT, AE-C, FAARC

Center Manager and Respiratory Care Patient Coordinator
Anthem Health Services
Queensbury, New York and Healthcare Consultant
Lake George, New York
Paul J. Mathews, PhD, RRT, FCCM, FCCP, FAARC

Associate Professor
School of Allied Health
Department of Respiratory Care Education
University of Kansas Medical Center
Kansas City, Kansas
Honorary Professor University of Costa Rica,
San Jose Costa Rica
Honorary Professor National University of Medicine and Pharmacy,
Ho Chi Minh City Peoples Republic of Vietnam
John A. Rutkowski, MPA, MBA, FACHE, RRT

Director Cardiorespiratory Services
Bergen Regional Medical Center
Paramus, New Jersey
Adjunct Assistant Professor
University of Dentistry and Medicine of New Jersey
School of Health Related Professions
Newark, New Jersey
Australia • Brazil • Japan • Korea • Mexico • Singapore • Spain • United Kingdom • United States
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Printed in the United States of America

1 2 3 4 5 6 7 14 13 12 11
Dedication
To my wife, Kathy, in sincere gratitude for her continued

encouragement, support, and love.
KAW
To my parents, Paul J. and Ruth Irene (O’Malley) Mathews.

May they rest united and in peace. To the next generation
Logan Elizabeth and Sydney Marie Rush - Grand kids
extraordinare.
PJM
To my wife, Joanne, thank you for your unwavering patience,

understanding, and most of all love.
JAR
BRIEF CONTENTS
Preface xvii 15. Clinical Laboratory Studies 387

16. Arterial Blood Gases and Noninvasive
Section I: Scope of Practice 1 Monitoring of Oxygen and
Carbon Dioxide 408
1. The History and Scope of
Respiratory Care 3 17. Pulmonary Function Testing 455
2. Legal, Professional, and Ethical 18. Polysomnography and Other Tests
Practice 23 for Sleep Disorders 482
19. Cardiac and Hemodynamic Monitoring 504
Section II: The Applied Sciences 51
3. Applied Physics 53 Section IV: Essential Therapeutics 555
4. Applied Chemistry 82 20. Oxygen and Medical Gas Therapy 557
5. Applied Microbiology 101 21. Humidity and Aerosol Therapy 597
6. Cardiopulmonary Anatomy 22. Hyperinflation Therapy 626
and Physiology 116 23. Pulmonary Hygiene and Chest
7. Cardiopulmonary Pharmacology 171 Physical Therapy 640
8. Pulmonary Infections 201 24. Airway Management 661
9. Airflow Limitation Diseases 227 25. Physiological Effects of Mechanical
Ventilation 687
10. Diffuse Parenchymal Lung
Diseases 251 26. Initiation, Monitoring, and
Discontinuing Mechanical Ventilation 698
11. Atelectasis, Pleural Disorders,
and Lung Cancer 266 27. Mechanics and Modes of Mechanical
Ventilation 728
12. Diseases That Affect the Pulmonary
Vasculature 284 28. Noninvasive Mechanical Ventilation 766
Section III: Essential Diagnostics 299 Section V: Levels of Care Delivery 795
13. Comprehensive History, Assessment, 29. Neonatal and Pediatric
and Documentation 301 Respiratory Care 797
14. Radiology for the Respiratory Therapist 343 30. Geriatric Applications 835
vii
viii Brief Contents
31. Emergency Respiratory Care 853 Appendix A: The Respiratory Therapist

in Nontraditional Roles 1137
32. Managing Disasters: Respiratory Care
in Mass Critical Care 891 Appendix B: Abbreviations 1142
33. Adult Critical Care 918
Appendix C: Routes for Entry-Level
34. Subacute and Long-Term Care 937 (CRT) Practice and
35. Respiratory Home Care 952 Registry-Level (RRT)
Practice 1148
36. Pulmonary Rehabilitation 984
Appendix D: Selected Diagnostic
37. Patient Transport in Respiratory Care 1025
Studies 1151
Appendix E: Arterial Blood Gases:

Section VI: Miscellaneous Normal Values 1155
Applications 1035
Appendix F: Characteristics of
38. Protecting the Patient and
Adventitious Breath
the Health Care Provider 1037
Sounds 1156
39. Health Promotion 1068
Glossary 1157
40. Fundamentals of Patient Education 1098
Index 1185
41. Management of Respiratory
Care Services 1115
EXTENDED CONTENTS
Preface xvii
Contributors xxi
About the Authors xxiii
How to Use This Text xxiv
Section I Scope of Practice 1
CHAPTER 1 THE HISTORY AND SCOPE OF RESPIRATORY CARE 3

Scope of a Profession 4 / Respiratory Care as a Profession 5 /
History 6 / The Organizing of the Profession 10 / Formal Education
System 11 / Certified Inhalation Therapy Technicians 13 / Effects of
Governmental Programs 15 / The 1990s: A Maturing Profession 16 /
Respiratory Care in the Twenty-First Century 16 / Professional
Recognition 19 / Summary 20
CHAPTER 2 LEGAL, PROFESSIONAL, AND ETHICAL PRACTICE 23

Defining a Profession 24 / Professional Obligations 26 / Legal Aspects of
Respiratory Care Practice 27 / The Foundations of U.S. Law 27 / The Civil
Lawsuit 32 / The Duty of Ethical Practice 33 / Basic Principles of Health
Care Ethics 34 / Basic Decision-Making Models 38 / The Decision-Making
Process 45 / Some Practical Advice 45 / Summary 45
Section II The Applied Sciences 51
CHAPTER 3 APPLIED PHYSICS 53

Scientific Discovery and Belief 54 / Measurements and Nomenclature 55 /
Mathematical Operations 57 / Physics 59 / States of Matter 64 /
Mass, Weight, and Density 66 / Basic Electrical Theory 67 / Light Waves 69 /
Fluid Physics 70 / Gas Laws 72 / Surface Tension 78 /
Thermodynamics 78 / Summary 80
ix
x Extended Contents
CHAPTER 4 APPLIED CHEMISTRY 82

Review of Atoms and Molecules 83 / Acids, Bases, and Buffers 86 /
How Acids, Bases, and Buffers Affect Respiration 91 / Disturbance of the
Acid–Base Balance 92 / Summary 98
CHAPTER 5 APPLIED MICROBIOLOGY 101

Classification of Microorganisms 102 / Staining Methods 102 / Specimen
Collection 104 / Culturing 104 / Human-Microbe Interactions 105 /
Human Defense Mechanisms 105 / Control of Microbial Growth 108 /
Sterilization and Disinfection 108 / Antimicrobials 110 / Microbial
Pathogenicity 112 / Epidemiology 113 / Important Respiratory
Pathogens 113 / Predisposition 114 / Summary 114
CHAPTER 6 CARDIOPULMONARY ANATOMY AND PHYSIOLOGY 116

Upper Airway: The Nose, Oral Cavity, and Pharynx 118 / Lower
Airways 120 / Bronchial Cross-Sectional Area and Bronchial Blood
Supply 127 / The Lungs 131 / Ventilation 136 / Pulmonary Function
Measurements 142 / Diffusion of Pulmonary Gases 144 / Cardiovascular
System 146 / Hemodynamic Measurements 153 / Oxygen Transport 153 /
Pulmonary Shunting and Venous Admixture 156 / Tissue Hypoxia 157 /
Cyanosis and Polycythemia 157 / Carbon Dioxide 158 / Acid–Base
Balance 158 / The Renal System and Its Effects on the Cardiopulmonary
System 160 / Ventilation/Perfusion Relationships 161 / Control of
Ventilation 162 / Cardiopulmonary Physiology of the Fetus and the
Newborn 164 / Effects of Aging on the Cardiopulmonary System 167 /
Effects of Exercise and of High-Altitude and High-Pressure Environments
on the Cardiopulmonary System 168 / Summary 169
CHAPTER 7 CARDIOPULMONARY PHARMACOLOGY 171

Principles of Pharmacology 172 / Drug Actions and Interactions 174 /
Drug Calculations 174 / Bronchodilators 176 / Anti-Asthmatic and
Anti-Inflammatory Drugs 181 / Drugs Used in the Management of
COPD 184 / Wetting Agents and Mucolytics 184 / Aerosol Antimicrobial
Therapy 186 / Surface Active Aerosols 188 / Assessing the Effectiveness
of Aerosol Medications 190 / Conscious Sedation 190 / Anesthesia
Drugs 191 / Advanced Cardiac Life Support Pharmacology 191 /
Summary 195
CHAPTER 8 PULMONARY INFECTIONS 201

Pulmonary Infections 202 / Community-Acquired Bacterial and Viral
Infections 202 / Classifications of Pneumonia 204 / Community-Acquired
Pneumonia 205 / Hospital-Acquired Pneumonia 211 / Mycobacterium
Infections 214 / Nontuberculous Mycobacterium Infections 218 / Fungal
Pulmonary Infections 221 / Summary 222
CHAPTER 9 AIRF LOW LIMITATION DISEASES 227

Asthma 228 / Chronic Bronchitis (COPD) and Emphysema 238 /
Bronchiectasis 246 / Summary 247
Extended Contents xi
CHAPTER 10 DIFFUSE PARENCHYMAL LUNG DISEASES 251

Diffuse Parenchymal Lung Diseases 253 / Summary 262
CHAPTER 11 ATELECTASIS, PLEURAL DISORDERS, AND LUNG CANCER 266

Atelectasis 267 / Pleural Disorders 269 / Lung Cancer 273 /
Summary 280
CHAPTER 12 DISEASES THAT AFFECT THE PULMONARY VASCULATURE 284

Hemodynamic Pulmonary Edema 285 / Pulmonary Heart Disease 289 /
Noncardiogenic Pulmonary Edema: Acute Lung Injury 294 / Summary 296
Section III Essential Diagnostics 299
CHAPTER 13 COMPREHENSIVE HISTORY, ASSESSMENT,

AND DOCUMENTATION 301
Patient History: The Interview 302 / Assessment 312 / Documentation
and the Medical Record 332 / Summary 339
CHAPTER 14 RADIOLOGY FOR THE RESPIRATORY THERAPIST 343

Why Should a Respiratory Therapist Learn Radiology? 344 /
How Can This Knowledge Be Gained? 345 / Body Planes and
Directional Terminology 345 / Types of Radiological
Studies 347 / Radiographic Studies Using Contrast
Materials 350 / Radiation Safety 358 / How to Interpret
Studies 358 / Example Cases 361 / Device Positioning 377 /
Chest Trauma 382 / Summary 384
CHAPTER 15 CLINICAL LABORATORY STUDIES 387

Body Fluids and Electrolytes 388 / Laboratory Methods for Determining
Electrolytes 394 / Laboratory Methods for Determining Arterial Blood pH,
Carbon Dioxide Pressure, and Oxygen Pressure 395 / Laboratory Methods
for Analyzing Carbon Dioxide and Chloride 396 / Laboratory Findings in
Acid-Base Disturbance 397 / Statistical Quality Control 399 / Summary 403
CHAPTER 16 ARTERIAL BLOOD GASES AND NONINVASIVE MONITORING

OF OXYGEN AND CARBON DIOXIDE 408
Blood Gases 410 / Acid-Base Balance 411 / Measurement of ABG and
Acid-Base Results 412 / Oxygen Saturation 413 / Nomenclature 414 /
Homeostasis 415 / Arterial Blood Gas 415 / Indwelling Blood Gas
Analyzer Electrodes 421 / Noninvasive Methods Used to Measure
Oxygenation Status 422 / Normal Values 424 / Deviations from
Normal 426 / Analysis Techniques 435 / Role of Hemoglobin and Its
Variants in ABG Analysis 440 / Other Factors That Affect ABG Results 442 /
Quality Control, Quality Assurance, and Performance Improvement 445 /
Interpreting Blood Gas Analysis Results 449 / New and Emerging
Technologies 450 / Summary 451
xii Extended Contents
CHAPTER 17 PULMONARY FUNCTION TESTING 455

Indications for Pulmonary Function Testing 456 / Normal or Predicted
Values 457 / Lung Volumes 458 / Spirometry 458 / Additional Laboratory
Assessment 464 / Spirometers 477 / Body Plethysmograph 478 /
Calibration 478 / Quality Assurance 478 / Infection Control 479 /
Age-Related Considerations 479 / Summary 479
CHAPTER 18 POLYSOMNOGRAPHY AND OTHER TESTS

FOR SLEEP DISORDERS 482
Normal Sleep 483 / Sleep Disorders 486 / The Polysomnogram 488 /
The Polysomnographic Recording 490 / Recording and Monitoring
During the Night 491 / Nasal Continuous Positive Pressure Therapy 497 /
Measuring Daytime Sleepiness 500 / Summary 501
CHAPTER 19 CARDIAC AND HEMODYNAMIC MONITORING 504

The Cardiac Cycle 505 / Cardiac Leads 507 / Continuous ECG
Monitoring 511 / Special Diagnostic Monitoring 511 / The ECG: Waveforms
and Intervals 512 / Determination of Heart Rate 516 / Steps in Dysrhythmia
Recognition 517 / Causes of Cardiac Dysrhythmias 517 / Types of Cardiac
Dysrhythmia 518 / Pulseless Electrical Activity 538 / Hemodynamic
Evaluation 538 / Summary 551
Section IV Essential Therapeutics 555
CHAPTER 20 OXYGEN AND MEDICAL GAS THERAPY 557

Physical Characteristics of Medical Gases 558 / Production and Regulation
of Medical Gases 559 / Storage and Distribution of Medical Gases 561 /
Therapeutic and Diagnostic Uses of Oxygen 571 / Therapeutic Use of Gas
Mixtures 592 / Summary 594
CHAPTER 21 HUMIDITY AND AEROSOL THERAPY 597

Concepts of Humidity 598 / Physiological Mechanisms of Airway
Humidification 600 / Concepts of Aerosols 602 / Therapeutic Use of
Humidifying Devices 603 / General Principles of Humidifying Devices 606 /
Therapeutic Use of Aerosol-Generating Devices 613 / General Principles of
Aerosol-Generating Devices 614 / Summary 622
CHAPTER 22 HYPERINFLATION THERAPY 626

Key Definitions, Concepts, and Professional Standards 627 / Historical
Perspectives 628 / Hyperinflation Therapy 629 / Deep Breathing
Techniques 629 / Glossopharyngeal Breathing 631 / Sustained Maximal
Inflation (Incentive Spirometry) 631 / Positive Airway Pressure 632 /
Intermittent Positive Pressure Breathing 635 / Outcomes Assessment 636 /
Summary 637
Extended Contents xiii
CHAPTER 23 PULMONARY HYGIENE AND CHEST PHYSICAL THERAPY 640

Key Definitions, Concepts, and Professional Standards 641 / Goals and
Objectives of Pulmonary Hygiene and Chest Physical Therapy 641 /
Normal Mucociliary Clearance 641 / Diseases and Conditions Associated
with Abnormal Mucous Clearance 644 / Assessment of Pulmonary
Hygiene 644 / Improving Pulmonary Hygiene 644 / Chest Physical
Therapy 645 / Summary 658
CHAPTER 24 AIRWAY MANAGEMENT 661

Airway Management 662 / Summary 683
CHAPTER 25 PHYSIOLOGICAL EFFECTS OF MECHANICAL VENTILATION 687

Pulmonary and Thoracic Pressure Gradients 688 / Modalities of
Ventilation 690 / Pulmonary Dynamics 691 / Complications from
Mechanical Ventilation 693 / Summary 696
CHAPTER 26 INITIATION, MONITORING, AND DISCONTINUING

MECHANICAL VENTILATION 698
Indications for Mechanical Ventilation 699 / Initiation of Mechanical
Ventilation 700 / Patient Monitoring 707 / Ventilator Management 715 /
Ventilator Discontinuance 719 / Summary 722
CHAPTER 27 MECHANICS AND MODES OF MECHANICAL VENTILATION 728

Waveforms 729 / Interaction of Pressure, Volume, and Flow over Time 729 /
Types of Ventilation 732 / Ventilator Modes 733 / Interpretation of
Ventilator Graphics 734 / Loops 757 / Summary 764
CHAPTER 28 NONINVASIVE MECHANICAL VENTILATION 766

Noninvasive Positive Pressure Ventilation 767 / Long-Term Use 784 /
Negative Pressure Ventilation 787 / Summary 790
Section V Levels of Care Delivery 795
CHAPTER 29 NEONATAL AND PEDIATRIC RESPIRATORY CARE 797

The Practice of Neonatal and Pediatric Respiratory Care 798 /
Epidemiology 799 / Common Neonatal Respiratory Diseases and
Conditions 800 / Common Pediatric Respiratory Diseases and
Conditions 814 / Respiratory Assessment in the Neonatal and Pediatric
Patient 819 / Technology of Pediatric and Neonatal Respiratory
Therapy 821 / Summary 829
CHAPTER 30 GERIATRIC APPLICATIONS 835

Demographic Changes in the United States 836 / Health Care
Venues 837 / The Cost of Health Care 837 / Assessment of the Older
Patient 838 / Communicating with Older Patients 849 / Summary 850
xiv Extended Contents
CHAPTER 31 EMERGENCY RESPIRATORY CARE 853

Basic Life Support 854 / Advanced Cardiovascular Life Support 859 /
Pediatric Advanced Life Support 874 / Neonatal Resuscitation
Program 881 / Emergency Airway Adjuncts 887 / Summary 888
CHAPTER 32 MANAGING DISASTERS: RESPIRATORY CARE

IN MASS CRITICAL CARE 891
National Incident Management System 893 / Incident Command
System 893 / Hospital Disaster Preparation 894 / The Respiratory Therapist
in Response to Multiple Casualty Incidents 894 / Natural Disasters 894 /
Man-Made Disasters 899 / Disease 911 / Summary 913
CHAPTER 33 ADULT CRITICAL CARE 918

Entry of the Patient into the Critical Care System 919 / Intensive Care Unit
Design and Function 924 / Tools for Success in the Intensive Care Unit 927 /
Management of the ICU Patient 932 / Summary 934
CHAPTER 34 SUBACUTE AND LONG-TERM CARE 937

Definition of Subacute Care 938 / Core Elements of an Ideal Subacute Care
Program 938 / Accreditation and Regulation of Facilities 940 /
Respiratory Care Acuity Levels and Modalities 941 / Weaning 944 /
Discharge Planning 944 / Reimbursement 945 / Current Practices in View
of PPS 948 / Long-Term Care 948 / Reimbursement 949 / Summary 949
CHAPTER 35 RESPIRATORY HOME CARE 952

History and Evolution 953 / Oxygen Therapy 956 / Basic Respiratory
Equipment 962 / Sleep Apnea Therapy 964 / Home Polysomnography 965 /
Home Mechanical Ventilation 965 / Pediatric Home Care 971 / Clinical
Respiratory Services 973 / Assessment 973 / Patient Education 974 /
Disease Management 975 / Care Planning 975 / Reimbursement 976 /
Regulatory Bodies, Accreditation, and Licensure 978 / Summary 981
CHAPTER 36 PULMONARY REHABILITATION 984

Scope and Changing Definitions 985 / Rationale for Pulmonary
Rehabilitation 987 / Goals and Objectives of Pulmonary Rehabilitation 988 /
Basis for Patient Selection 988 / Program Formats 994 / Program
Components 997 / Program Content 999 / Outcomes Assessment 1010 /
Reimbursement for Pulmonary Rehabilitation 1014 / Summary 1020
CHAPTER 37 PATIENT TRANSPORT IN RESPIRATORY CARE 1025

General Considerations for Patient Transport 1026 / External Patient
Transport 1030 / Air Transportation 1031 / Summary 1033
Extended Contents xv
Section VI Miscellaneous Applications 1035
CHAPTER 38 PROTECTING THE PATIENT AND THE

HEALTH CARE PROVIDER 1037
Chain of Infection 1038 / Health Care Setting 1043 / Hand Hygiene 1044 /
Standard Precautions 1046 / Preventing Needlestick Injuries 1056 / Special
Issues in Infection Control 1060 / Summary 1065
CHAPTER 39 HEALTH PROMOTION 1068

General Principles and Concepts of Health 1070 / Models of Health 1073 /
Dimensions of Health 1074 / Philosophy of Holistic Health 1076 /
Factors Affecting Health Care in the United States in the Twentieth
Century 1080 / Leading Causes of Death 1082 / Behavioral Causes
of Death 1083 / Determinants of Health Status 1083 / Continuums 1086 /
Health Promotion Process 1086 / Role of the Federal Government 1089 /
Role of Respiratory Therapist in Health Promotion 1092 / Summary 1094
CHAPTER 40 FUNDAMENTALS OF PATIENT EDUCATION 1098

The Educational Process 1099 / The Respiratory Therapist
as the Educator 1108 / Summary 1112
CHAPTER 41 MANAGEMENT OF RESPIRATORY CARE SERVICES 1115

Key Definitions, Concepts, and Professional Standards 1116 / History,
Professional, and Community Involvement in Respiratory Care 1117 /
Departmental Structure 1118 / Diversity of Respiratory Care Services 1119 /
Operational Issues 1120 / Fiscal Issues 1122 / Reimbursement 1126 /
Human Resource Management 1128 / Manager Accountability 1130 /
Computer Applications 1133 / Summary 1134
APPENDIX A: THE RESPIRATORY THERAPIST IN

NONTRADITIONAL ROLES 1137
APPENDIX B: ABBREVIATIONS 1142
APPENDIX C: ROUTES FOR ENTRY-LEVEL (CRT) PRACTICE AND
REGISTRY-LEVEL (RRT) PRACTICE 1148
APPENDIX D: SELECTED DIAGNOSTIC STUDIES 1151
APPENDIX E: ARTERIAL BLOOD GASES: NORMAL VALUES 1155
APPENDIX F: CHARACTERISTICS OF ADVENTITIOUS BREATH SOUNDS 1156
Glossary 1157
Index 1185
P R E FAC E
The field of respiratory care is continually growing and processes. Radiology and lab studies, including blood
changing as new research, therapies, and theories about gases and noninvasive monitoring, are discussed in
the causes and treatments of respiratory alterations detail. Pulmonary function testing, polysomnography,
emerge. Foundations of Respiratory Care, Second Edition and cardiac and hemodynamic monitoring round out
provides a clear presentation of the concepts and issues this section.
in the field. Practitioners will find the book helpful as Section IV outlines current therapies and approaches
a review of interventions and therapeutics and as a tool to managing patients with respiratory alterations.
to update their knowledge. Oxygen and medical gas therapy, humidity and aerosol
therapy, and hyperinflation therapy are all thoroughly
Conceptual Approach discussed. Specifics on pulmonary hygiene and chest
physical therapy, as well as techniques of airway man-
The concept underlying Foundations of Respiratory Care, agement, are included. The chapters on invasive and
Second Edition was born of the need for a straightfor- noninvasive mechanical ventilation offer readers the
ward text that could be easily read and assimilated. most up-to-date information on these therapies.
Empowering readers as educated decision makers, Section V covers levels of delivery. Age-related
helping them develop skills of analysis and critical considerations for neonatal, pediatric, and geriatric
thinking, and providing guidance for excellent clini- patients are discussed. Variations in approaches based
cal and patient care skills were all goals in writing this on care setting are also covered; emergency medicine,
text. Chapters cover all the technical aspects of anat- critical care, subacute care, home care, and rehabilita-
omy, physiology, and intervention while highlighting tion settings are each discussed in a separate chapter.
clinically relevant information. The text offers users a Section VI helps the reader assimilate and synthe-
friendly approach that delivers a wealth of information size the wealth of information presented in the text.
in a consistent, easy-to-follow format with recurring Specific guidelines and reminders for protecting the
pedagogical features. This text was written by respira- patient and health care provider are outlined. Health
tory therapists for respiratory therapists. promotion and patient education receive thorough
coverage. A final chapter on management of respira-
Organization tory care services speaks to the administrative aspects of
managing a service unit.
Foundations of Respiratory Care, Second Edition
comprises 41 chapters organized into six sections.
Section I lays the foundation for understanding the Chapter Format and Features
respiratory care profession by outlining its history and
Innovative features in Foundations of Respiratory Care,
scope of practice and discussing related legal and ethi-
Second Edition stimulate critical thinking and technical
cal principles.
competence and encourage readers to synthesize and
Section II presents the applied sciences that under-
apply information presented in the text:
lie sound respiratory practice. Applied physics, chem-
istry, and microbiology are covered as they relate to • Objectives open each chapter and introduce the
respiratory care. Chapters on cardiopulmonary anat- main areas targeted for mastery in each chapter,
omy, physiology, pathology, and pharmacology give providing a checkpoint for study and a tie-in to
the reader the information needed to understand the crucial skills.
chapters that follow. • Chapter Outlines prepare the reader for study
Section III opens with a description of the compre- by indicating the content and order of material
hensive patient history, assessment, and documentation to be covered in each chapter.
xvii
xviii Preface
• Key Terms are listed so the reader can become CHAPTER 3

familiar with terms to be used and can research • Additional examples to demonstrate principles
those that are unfamiliar. Key terms are bold- and formulas
faced in text the first time they are used and are
included in the end-of-text glossary. CHAPTER 4
• Case Studies present realistic scenarios, offering • New illustrations to demonstrate the concepts
an opportunity for the reader to apply the chap- discussed in the chapter
ter material, thereby encouraging analysis and
critical thinking. Case studies include a sample CHAPTER 5
patient or equipment troubleshooting scenario • Improved description of the immune system as a
followed by several critical thinking questions defense mechanism for fending off disease
requiring understanding and decision making
on the part of the reader. CHAPTER 7
• Spotlight On . . . boxes describe new or upcom- • Chapter 8 in the first edition
ing approaches involving new therapies, new • Definitions of drug actions and interactions
equipment, or technological innovations. • Addition of drugs used to manage COPD
• Best Practice helps the reader to apply basic
knowledge to real-life situations and offer hints CHAPTER 8
and shortcuts useful to both new and experi- • New stand-alone chapter (Topics formerly
enced practitioners. covered in Chapter 7 have been placed in their
• Age-Specific Competencies outline skills that own chapter with more well-rounded discus-
have variations based on the age of the patient sions: pneumonia, tuberculosis, nontuberculous
or highlight considerations the reader should be Mycobacterium infections, and fungal pulmonary
sensitive to when managing the care of patients infections.)
of different ages.
• A Summary concludes each chapter, offering a CHAPTER 9
conceptual framework for chapter review and • New stand-alone chapter (Topics formerly
highlighting the main content points. covered in Chapter 7 have been placed in their
• Study Questions offer readers an opportunity own chapter with more well-rounded discussion:
to assess their understanding of the content asthma, chronic bronchitis (COPD) and emphy-
and to define areas needing additional study. sema, and bronchiectasis.)
Questions are included in three formats (review
questions, multiple choice questions, and critical CHAPTER 10
thinking questions) to challenge the reader and • New stand-alone chapter (Topics formerly cov-
to develop recall, analysis, and critical thinking ered in Chapter 7 have been placed in their own
skills. chapter with more well-rounded discussions:
• References and Suggested Readings at the end diffuse parenchymal lung diseases.)
of the chapter document the theoretical basis of
each chapter and provide additional resources CHAPTER 11
for continued study. • New stand-alone chapter (Topics formerly cov-
• A Glossary at the end of the book defines all key ered in Chapter 7 have been placed in their own
terms used in the text and serves as a compre- chapter with more well-rounded discussions:
hensive resource for study and review. atelectasis, pleural disorders, and lung cancer.)
• The Index facilitates access to material
and includes special entries for tables and CHAPTER 12
illustrations. • New chapter with coverage of hemodynamic
pulmonary edema, pulmonary heart disease, and
New to this Edition noncardiogenic pulmonary edema
CHAPTER 2 CHAPTER 14
• Discussion of HIPAA • Fully updated with extensive images
• Discussion of the ethical decision making model
CHAPTER 15
of Divine Command
• Content on indirect ion-specific electrodes
Preface xix
• Discussion and explanation of calculations and • All new chapter on the physiological effects of
the significance of anion gap variations mechanical ventilation
• The differentiation of SaO2, SpO2, and O2
content CHAPTER 26
• All new chapter on ventilator graphics, focusing
CHAPTER 17 on the interpretation of wave forms
• Updated content and clarified procedural steps
CHAPTER 27
CHAPTER 18 • Comprehensively revised and updated, focusing
• Added discussions on insomnia, multiple sleep on the initiation and maintenance of invasive
latency test, and maintenance of wakefulness test mechanical ventilation and including a discus-
• Updated and expanded discussions related to sion of a variety of modes of ventilation
new manual for scoring sleep, sleep stages across • Discussion of the work of breathing
the life span, and obstructed sleep apnea
CHAPTER 28
CHAPTER 19 • Updated information on newer forms of EPAP,
• Added discussion of combined disorders of CPAP, and BiPAP
automaticity and conductivity, nonparoxysmal
junctional tachycardia, second degree/advanced CHAPTER 29
heart block • Completely new chapter covering neonatal and
• Updated discussion of atrial tachycardia and pediatric respiratory care
atrial fibrillation and hemodynamic monitoring
CHAPTER 30
CHAPTER 20 • Thoroughly updated
• Added discussion of oxygen-conserving devices • Added discussion of increased costs of health
• Discussion of new low-flow oxygen delivery care for the elderly
devices the Oxy-Arm and the Oxy-View • Added discussion of improving communication
• Updated uses of carbogen with the elderly
• Updated discussion of humidification devices • Updated content on standards of care for
• Added discussion of heated humidification by BLS and ALS in both the adult and pediatric
nasal cannula populations
• Added discussion of breath-actuated devices
CHAPTER 32
CHAPTER 22 • Completely new chapter covering the timely
• Discussion of glossopharyngeal breathing topics of emergency preparedness
• Added discussion of the functions of airway • Updated discussion of the design and function
mucous of the intensive care unit
• Added discussion of combined mechanical and • Provides upgraded explanation of evidence-
acoustical vibration based scientific research
• Added discussion of ventilator-associated pneu-
CHAPTER 24 monia under the quality improvement section
• Added discussion of use of stylet, elastic gum
bougie, and lighted stylet CHAPTER 34
• Added discussion of fiberoptic intubation and • Discussion of long-term care
blind nasotracheal intubation
• Added discussion of the management of the dif- CHAPTER 36
ficult airway • Addresses new evidence-based guidelines by the
• Added discussion of patient safety and use of American College of Chest Physicians (ACCP)
artificial airways and the AACVPR recommending pulmonary
rehabilitation for patients with COPD
xx Preface
• Discussion of HR 6331 (Medicare Improvements the NBRC exams. The instructor can create and admin-
for Patients and Providers Act) ister online tests that automatically correct and return
the grades to the instructor via e-mail. Online testing
CHAPTER 37 allows exams to be administered online via a school
• New chapter on the transport of the respiratory network or stand-alone PC. Site license is included.
care patient
IMAGE LIBRARY
CHAPTER 38 The Image Library is a software tool that includes an
• Expanded discussion on health care settings organized digital library of more than 700 illustrations
where the risk of hospital-acquired infection is and photographs from the text. With the Image Library
increased you can:
• Discussion of respiratory hygiene and cough
• Create additional libraries.
etiquette
• Set up electronic pointers to actual image files or
• Discussion of bioterrorism and pandemic influenza
collections.
CHAPTER 39 • Sort art by desired categories.
• Print selected pieces.
• Updated statistics throughout
The Image Library works in combination with
CHAPTER 40 standard presentation packages such as Microsoft
• Updated as relevant throughout PowerPoint for Windows.
• Discussion of how to assess effectiveness of
preprepared patient education materials WORKBOOK AND LAB MANUAL
Order 1-4354-6987-9
The workbook/lab manual provides a review of
Ancillary Materials each chapter and additional exercises and activities
The complete supplements package was developed to to study and apply knowledge. Additional activities
assist instructors in planning and implementing their include short answer questions, multiple choice
programs for the most efficient use of time and other questions, lab exercises, just to name a few.
resources. Components of this package include the
following:
WebTutor on WebCT and
INSTRUCTOR’S MANUAL Blackboard
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Order 1-4354-6989-5 for Blackboard
The Instructor’s Manual is designed to assist instruc-
Order 1-4354-6988-7 for WebCT
tors in preparing for class lectures and examinations.
This resource is an online workbook that contains
Sections include objectives, introduction, outline, sum-
a variety of additional exercises and questions for
mary, activities, and answers to text review questions,
study and review, flashcards, Web links, and discussion
multiple choice questions, and case study questions.
questions.
INSTRUCTOR RESOURCE CD-ROM
Order 1-4354-6986-0 Acknowledgments
This invaluable instructor tool consists of several
We gratefully acknowledge all of the reviewers for
components, an electronic version of the Instructor’s
their hard work and all of our contributing authors for
Manual, a computerized test bank, and an electronic
understanding our deadlines and insistence on quality.
image library.
We also thank the following individuals for their help
COMPUTERIZED TESTBANK with this book.
The electronic testbank contains more than 1000
multiple choice questions. The format follows that of
CONTRIBUTORS
Dianne A. Adams, AS, BS, MA, RRT, NPS Raymond Edge, EdD, RRT
Associate Professor and Program Director, County Former Dean, Maryville University
College of Morris Randolph, New Jersey St. Louis, Missouri
G. William Atkinson, MD, FACP, FCCP Anthony Everidge, BA, RRT-NPS

Senior Associate Dean for Clinical Affairs Respiratory Therapy Program Director, Prima
Professor, Pulmonary and Critical Care Medicine, Medical Institute
School of Medicine Las Vegas, Nevada
Medical Director, Respiratory Care Education
School of Allied Health, University of Kansas
Medical Center Robert R. Fluck Jr, MS, RRT, FAARC
Kansas City, Kansas Associate Professor Emeritus, Upstate
Medical University
Syracuse, New York
Patricia Carroll, RRT, RN, BC,
CEN, MS George W. Gaebler, MSEd, RRT, FAARC
Adjunct Professor, School of Health Sciences,
Director, Respiratory Care, Upstate Medical University
Excelsior College
and Golisano Children’s Hospital
Albany, New York
Syracuse, New York
Owner, Education Notebook, LLC
Meriden, Connecticut
William F. Galvin, MSEd, RRT, CPFT,
William F. Clark, PhD, RRT AE-C, FAARC
Dean of Health, Wellness and Sports Technology Assistant Professor, School of Allied Health Professions
(Retired), Hillsborough Community College Program Director, Respiratory Care Program
Hillsborough, Florida Administrative and Teaching Faculty, TIPS Program
Gwynedd Mercy College
Gwynedd Valley, Pennsylvania
Glendon G. Cox, MD, MBA, MHSA, FCCP
Professor and Chair, Department of Health Policy
and Management Melaine (Tudy) Head Giordano, MS,
Professor of Radiology, School of Medicine RN, CPFT, RCP
University of Kansas Medical Center Geriatric Consulting
Kansas City, Kansas Carrollton, Texas
Robert DiBlasi RRT-NPS David A. Gourley, RRT, MHA, FAARC

Respiratory Research Coordinator, Seattle Children’s Executive Director of Regulatory Affairs,
Hospital, Research Foundation Chilton Hospital
Seattle, Washington Pompton Plains, New Jersey
xxi
xxii Contributors
Jodi B. Green, BS, RRT Adjunct Assistant Professor, Respiratory Care

Education, School of Allied Health
Patient Care Coordinator, Home Therapy Equipment
Nurse Preceptor, School of Nursing,
Glens Falls, New York
University of Kansas Medical Center
Kansas City, Kansas
Bethene Gregg, PhD, RRT
Associate Professor, Respiratory Care Education, Doug McIntyre, MS, RRT, FAARC
School of Allied Health, University of Kansas
President, Durable Medical Supply
Medical Center
Destrehan, Louisiana
Kansas City, Kansas
Joy Hargett, BS, RRT, RCP Chad Pezzano, MA, RRT-NPS

Pediatric Clinical Instructor, Albany Medical Center
Manager, Patient Care Services, Respiratory Care,
Albany, New York
St. Luke’s Episcopal Hospital
Houston, Texas
John Salyer RRT-NPS, MBA, FAARC
Ken Hargett, MHA, RRT, RCP, FAARC Director Respiratory Therapy, Seattle Children’s
Hospital, Research Foundation
Director, Respiratory Care Services, Pulmonary
Seattle, Washington
Diagnostic Laboratory, The Methodist Hospital
Houston, Texas
Helen M. Sorenson, MA, RRT, FAARC
Al Heuer, PhD, MBA, RRT, RPFT Associate Professor, Department of Respiratory Care,
University of Texas Health Science Center
Associate Professor, University of Medicine and
San Antonio, Texas
Dentistry, School of Health Professions
Newark, New Jersey
Gail Varcelotti, BS, RRT, FAARC
Thomas J. Johnson, MS, RRT, EMT-B, RT Vice President, Ganésco, Inc.
Venetia, Pennsylvania
Program Director and Assistant Professor of
Respiratory Care, Division of Respiratory Care,
School of Health Professions, Long Island Tina Wellman, BA, RRT, CPFT
University, Brooklyn Campus Senior Sales Consultant, Carefusion
New York City, New York Yorba Linda, California
Ingo S. Kampa, PhD Robert Whitman, PhD, D.ABSM,

Director, Medical Multi-Specialty Associates, P.A.
Fair Lawn, New Jersey
RRT, RPFT
Director, Sleep Disorders Center
Director, Pulmonary Diagnostics Services,
Barbara Ludwig, MA, RRT Cardiopulmonary Rehab and Neorophychology
Assistant Professor and Chair, Respiratory Care Adjunct Assistant Professor, Pulmonary Medicine
Education, School of Allied Health, University University of Kansas Medical Center
of Kansas Medical Center Kansas City, Kansas
Kansas City, Kansas
Kathleen S. Wyka, AAS, CRT, AE-C
L. Micky Mathews, BA, RN, CEN Respiratory Clinical Specialist
Emergency Nurse Clinician, Menorah Medical Center Anthem Health Services
Overland Park, Kansas Queensbury, New York
A B O U T T H E AU T H O R S
Kenneth A. Wyka, MS, RRT of the AARC, and, in 1990, he was selected for AARC
Life Membership. He is also a Fellow of the American
Kenneth A. Wyka has been in the field of respira-
College of Critical Care Medicine and of the American
tory care since 1970. He obtained his bachelor’s and
College of Chest Physicians. Currently, he is a member
master’s degrees from Fairleigh Dickinson University in
of the New York Academy of Sciences and is listed in
Teaneck, New Jersey, and formal training in respiratory
Who’s Who in America and Who’s Who in the World.
care from the Lenox Hill Hospital School for Respira-
tory Therapy in New York City. In 1972, he founded
the respiratory therapy program at Passaic County
Community College in Paterson, New Jersey. Since John Rutkowski, MPA, MBA, RRT
then, he managed the respiratory care department at John Rutkowski is the director of Cardiopulmonary
Valley Hospital in Ridgewood, New Jersey, was the Services at Bergen Regional Medical Center in Paramus,
director of respiratory clinical education at the Uni- New Jersey. He is also an adjunct assistant professor
versity of Medicine & Dentistry of New Jersey, started at the University of Medicine and Dentistry in New-
several pulmonary rehabilitation programs, worked ark, New Jersey. His career in respiratory care includes
in home care, and began a health care/respiratory care over 40 years of clinical, managerial, and community
consulting practice. He is the author of Respiratory outreach experience. He received his formal respira-
Care in Alternate Sites and coauthor of Oakes’ Respira- tory therapy training and certificate from St. Joseph
tory Home Care: An On-Site Reference Guide. In addi- Hospital School of Respiratory Therapy in Lancaster,
tion, he has been the president of both the New Jersey Pennsylvania, along with an associate of science degree
and New York Societies for Respiratory Care and has from York College of Pennsylvania. He has also earned
been actively involved in several voluntary health and an undergraduate degree in chemistry from Jersey City
professional organizations. Currently, Ken is the Center State College, a master of business administration from
Manager and Respiratory Care Patient Coordinator for Fairleigh Dickinson University, and a master of public
Anthem Health Services in Queensbury, New York. administration from Seton Hall University. In addi-
tion to his work as a respiratory therapist, he remains
active in the American Association for Respiratory Care
Paul J. Mathews, PhD, RRT and its New Jersey affiliate. He has served as a board
Paul J. Mathews is associate professor of respiratory member and on many committees for the New Jersey
care, School of Allied Health; associate professor in Society for Respiratory Care, including president, and
physical therapy; and adjunct associate professor at as the New Jersey representative to the AARC House of
the Center on Aging, University of Kansas. He received Delegates. He is a member of the American College of
his respiratory therapy training at Yale–New Haven Healthcare Executives and its New Jersey affiliate, the
Medical Center in New Haven, Connecticut. He holds Association of Healthcare Executives of New Jersey,
his undergraduate degree from Quinnipiac College, and has earned the Fellow of the American College of
Hamden, Connecticut; a master of public administra- Healthcare Executives (FACHE) credential. Throughout
tion degree from the University of Hartford in Con- his career, he has been active in the American Lung
necticut; and EdS and PhD degrees from the University Association. He is a member of the ALA’s Nationwide
of Missouri in Kansas City, Missouri. He has published Assembly, board member, and past chair of the Ameri-
more than 160 articles in various national journals, can Lung Association in the Mid-Atlantic, advisory
has authored several books, serves on six editorial board member and past chair of the American Lung
boards, and has lectured at many national and interna- Association in New Jersey, and a member of the
tional meetings. In 1989, Dr. Mathews was president Pediatric/Adult Asthma Coalition of New Jersey.
xxiii
HOW TO USE THIS TEXT
The following suggests how you can use the features of this text to gain
competence and confidence in your respiratory care skills.
OBJECTIVES
Objectives
Upon completion of this chapter, the reader should be able to: Read this list before starting the chapter so
• List the characteristics used to classify microorganisms.
that you are prepared for the material that
• Describe disinfection and sterilization methods.
• Identify the beneficial roles of endogenous microflora. will be presented. Ask yourself which goals
• Describe the factors influencing bacterial growth. you are already familiar with and which will
• Identify human defenses against infectious diseases.
• Discuss infectious diseases of the respiratory system. require more investment on your part to
master.
CHAPTER OUTLINE
Chapter Outlines
Scope of a Profession The Organizing of the Profession These outlines serve as your reference guide
Self-Regulation
Union Status
A National Professional Association
The Late 1950s and the 1960s: Organizational
to reviewing material.
Discrete Body of Knowledge and Clinical Maturation
Patient Status Formal Education System
Educational Requirements Joint Review Committee for Inhalation
Therapy Education
Historical Agreement on Professional Status
American Registry for Inhalation Therapy
Respiratory Care as a Profession
Certified Inhalation Therapy Technicians
History
The 1970s: Growth and Unrest
Early Foundations
The 1980s: Change in Many Areas
Twentieth-Century Developments
KEY TERMS
Key Terms
acute respiratory distress high-order explosion (HE) Pirfenidone Glance over this list and identify the terms
syndrome (ARDS) hospital emergency incident primary blast injury
anthrax command system (HEICS) quaternary blast injury you need to look up in the Glossary. Keep a
blast lung injury (BLI) incident command system (ICS) racemic epinephrine
blast overpressure injuries interferon ribavirin running list of terms and check them off as
bronchopleural fistula interleuken-6, 7, 8 secondary blast injury
cidofovir lewisite self-contained breathing
you master their meaning.
coccidioidomycosis live attenuated vaccine (LAV) apparatus (SCBA)
cytokine storm low-order explosion (LE) self-evacuation
Diplopia mass casualty incident (MCI) spalling
disseminated intravascular MetHb staphylococcal enterotoxin B
coagulopathy (DIC) multidrug-resistant tuberculosis (SEB)
dumbbells (MDRTB) systemic inflammatory response
d h l l f l d ( )
CASE STUDY 13-1

Case Studies
William Smith is a 35-year-old male who has
Brief scenarios in selected chapters encour-
come to the clinic and who has been waiting for
over 2 hours. Mr. Smith is finally called into a
age you to approach situations with a criti-
treatment room, and the practitioner enters to cal eye and to assimilate the information
start the history and physical. As the practitioner
enters the room, she observes an anxious Cauca- presented in text. Use the related questions
sian male sitting on a chair. The patient looks up
as the practitioner approaches. (Note: Mr. Smith to apply the information you have learned
will be the patient throughout most of the
chapter. For simplicity and clarity, the patient in the chapter to actual clinical cases. Con-
FIGURE 13-1 The patient interview.
in the text will be assumed to be male, the
practitioner female.)
sider alternative solutions to the questions
Questions by discussing the cases with your classmates
1. How far away should the practitioner be and colleagues.
when she makes her initial introduction?
final area, intimate space (less than 11/2 feet), is where
the actual physical examination is performed.2 The 2. When can the practitioner move into the
patient’s privacy should be honored at all times. room and enter the personal space?
In addition to space, other environmental factors 3. What should the practitioner do to make the
influence the interview. Room lighting, noise, and environment more comfortable for the
temperature can be controlled to provide the best patient?
xxiv
How to Use This Text xxv
Spotlight On Spotlight
On
Pause when you come across one of these
The Logistics Service Branch of the ICS
boxes and take time to research the innova- • Communication Unit. Prepares and implements incident. The Unit orders, receives, stores,
tion or therapy discussed. Search the Inter- the Incident Communication Plan (ICS-205),
distributes and maintains communications
and distributes supplies, and services
nonexpendable equipment. All resource
net, visit the library, or ask your instructor equipment, supervises the Incident
Communications Center, and establishes
orders are placed through the Supply Unit.
The unit maintains inventory and
for more information. adequate communications over the incident. accountability of supplies and equipment.
• Medical Unit. Develops the Medical Plan • Facilities Unit. Sets up and maintains
(ICS-206), provides first aid and light required facilities to support the incident.
medical treatment for personnel assigned Provides managers for the incident base and
to the incident, and prepares procedures for camps. Also responsible for facility security
a major medical emergency. and facility maintenance services: sanitation,
Best Practices Best Practice

court) have a jury. Once the jury has been impaneled,
the trial begins with the attorneys’ opening statements,
with the plaintiff’s attorney leading. The opening
In any profession, many helpful hints can In the Event of a Suit … statements outline the facts that the attorneys hope to
help you perform more efficiently. The During dispositions and court testimony, do not
establish in the trial process. The plaintiff has the
burden of proving the case to the jury. The defendant
answer:
wide variety of hints, tips, and strategies • Questions you do not understand.
does not have a burden of proof, has to prove nothing,
and could, technically, remain silent. After each side
presented here help you as you work toward • Compound questions. has presented its case and cross-examined the wit-
• Questions with double negatives in them. nesses, each is allowed time for a closing argument.
professional advancement. Study, share, and For each of these, ask the lawyer to simplify
After the closing argument, the judge instructs the jury
of any applicable law and any presumptions the jury
discuss them with your colleagues. and restate the question.
Do not answer questions that were not asked.
should consider in their deliberations. Then the jury is
dismissed to deliberate. The trial usually ends with the
Answer only the question that was asked; do not
verdict.
expand on the answer. If the question can be
Age-Specific Competencies Age-Specific Competency

After reading these boxes, ask yourself what Preventing Injury and Death
other considerations would be appropri- Even more than for adults, for children, the key to • Because drowning is a major cause of death
minimizing injury and death is prevention. in the younger population of children, adults
ate when managing the care of patients at • Because motor vehicle trauma causes
should supervise these children closely when
they are near water. Children should know
different ages. Make a list of approaches you nearly half of all pediatric injuries and
deaths each year, it behooves adults to use
how to swim and what to do in an emergency
around water. Even such a seemingly innocu-
could use when working with children or appropriate restraints when children are in
ous “body” of water as a 2-gallon bucket can
the car. Children should be buckled into
elderly people. an age-specific car seat that is properly
be fatal to the unsupervised child.
• Adults have the responsibility to minimize
fastened to the car. (Proper fastening of
the danger from house fires, which result in
a child or infant seat may include a strap
the overwhelming majority of burns. Having
that fastens to the car floor.) They should
k d t t h fl f th h
I. vibration
Summary Summary
II. noise
III. motion
When transporting critically ill patients, safety is IV. temperature variations
Read the summary. Then go back to the paramount. However, many patients are transported a. I and II
within or between health-care facilities because they b. I, II, III, and IV
objectives and consider how well you have are critically ill and need special services or procedures. c. I and IV
d. I, II, and III
assimilated and understood the information The additional stress that may be imposed on such
patients can be clinically challenging. However, 4. It is recommended that all of the following equip-
in the chapter. Use the summary as a brief through proper planning and execution and follow-up,
these risks can be minimized. By following the proce-
ment accompany all critically ill patients on
transport, except which?
review when you study and prepare for an dures outlined in this chapter, including maintaining a a. oxygen source with sufficient duration of flow
state of readiness, properly prescreening patients, b. cardiac defibrillator
examination. selecting the most appropriate means of transportation, c. manual resuscitator bag and mask
and ensuring the proper personnel and equipment in d. cardiac pacemaker
Study Questions Study Questions c. retributive justice.

d. beneficence.
REVIEW QUESTIONS
After reading a chapter, read the study ques- 4. Informed consent flows mainly from the basic
ethical principle of:
1. List three major criticisms to the use of utilitarian-
tions and identify areas in which you need ism in making ethical decisions. a. autonomy.
b. beneficence.
2. List four legal requirements for breaking patient
to work on your understanding. Go back confidentiality.
c. justice.
d. role duty.
and reread those sections of the chapter; 3. List three forms of intentional torts that a respira-
5. In its best sense, paternalism is a contest between
tory therapist might be involved with.
then answer the questions again until you 4. List three major criticisms to the use of Kantian
which of the following principles?
a. autonomy and beneficence
are comfortable that you have grasped the ethics in making ethical decisions.
5. List and define the basic principles of health-
b. justice and role duty
c. veracity and nonmaleficence.
material. care ethics. d. role duty and autonomy
6. List three major criticisms to the use of the 6. Which of the following ethical decision-making
divine command theory in making ethical formats is focused on the moral agent rather than
decisions. on the decision?
7. Define the basic function of normative ele- a. utilitarianism
b d t i t d th i
xxvi How to Use This Text
HOW TO USE STUDYWARE™ TO ACCOMPANY wrong and helps you learn quickly by explaining
FOUNDATIONS OF RESPIRATORY CARE, why an answer was correct or incorrect. Use quiz
SECOND EDITION mode when you are ready to test yourself and
The StudyWARE™ software helps you learn terms and keep a record of your scores. In quiz mode, you
concepts in Foundations of Respiratory Care, Second have one try to get the answers right, but you can
Edition. As you study each chapter in the text, be sure take each quiz as many times as you want.
to explore the activities in the corresponding chapter
in the software. Use StudyWARE™ as your own private
tutor to help you learn the material in the textbook.
Getting started is easy. Install the software by
downloading it to your computer’s CD-ROM drive
and following the on-screen instructions. To access the
software, go to Cengagebrain.com, and log into your
CengageBrain account. Search for the book by title,
author, or ISBN. Click on the access now button for
additional resources that accompany the book. When
you open the software, enter your first and last name
so that the software can store your quiz results. Then
choose a chapter from the menu to take a quiz or
explore one of the activities.
• Menus. You can access the menus from wherever
you are in the program. The menus include quiz-
zes and other activities.
• Quizzes. Quizzes include multiple choice, true/

false, word building, fill-in-the-blank, and case
study questions. You can take the quizzes in
practice or quiz mode. Use practice mode to
improve your mastery of the material. You have
multiple tries to get the answers correct. Instant
feedback tells you whether you are right or
How to Use This Text xxvii
• Scores. You can view your last scores for each • Activities. Activities include hangman, con-
quiz and print your results to hand in to your centration, and championship game. Have fun
instructor. while increasing your knowledge!
SECTION I
Scope of Practice
CHAPTER 1
The History and Scope of Respiratory Care

Raymond S. Edge and Paul J. Mathews
OBJECTIVES
Upon completion of this chapter, the reader should be able to:
• List the general criteria for a profession.
• Describe the contributions to the study of respiration made by the early foundational figures.
• Provide a synopsis of the pre–twentieth-century scientific foundations for respiratory care.
• Outline the contributions to the development of respiratory care provided by Thomas Beddoes, Joseph
Priestley, and Robert Boyle.
• Provide a short, historical synopsis for the organizational development of the specialty, with attention to the
AARC, CoARC, and NBRC.
• Identify and describe three of the “Allied” Professional Organizations who are aiding in advancing our
professional status.
• Provide an analysis of the strengths of the allied health specialty and the challenges it will face in the
twenty-first century.
CHAPTER OUTLINE
Scope of a Profession The Organizing of the Profession
Self-Regulation A National Professional Association
Union Status The Late 1950s and the 1960s: Organizational
Discrete Body of Knowledge and Clinical Maturation
Patient Status Formal Education System
Educational Requirements Joint Review Committee for Inhalation
Historical Agreement on Professional Status Therapy Education
American Registry for Inhalation Therapy
Registered Respiratory Therapists
History
Certified Inhalation Therapy Technicians
Early Foundations
The 1970s: Growth and Unrest
Twentieth-Century Developments
The 1980s: Change in Many Areas
(continues)
3
4 SECTION I ■ Scope of Practice
(continued)
Effects of Governmental Programs Respiratory Care in the Twenty-First Century

Cost Containment Education
Changing Acuity Levels Licensure
The 1990s: A Maturing Profession Scope of Practice
Managed Care Specialty Practice and Credentials
Crisis in Care Professional Recognition
KEY TERMS
American Association for fiduciary relationship Pneumatic Institute
Respiratory Care (AARC) health care protocols process-oriented essentials
Committee on Accreditation of managed care product-oriented essentials
Respiratory Care Programs Medicaid prospective payment system
(CoARC) Medicare (PPS)
diagnosis-related group (DRG) National Board for Respiratory respiratory care practitioner
fee-for-service Care (NBRC) respiratory therapist
FAARC outcome-oriented essentials scope of practice
fellowship phlogiston theory Sugarloaf Conference
T
his chapter addresses respiratory care’s status lawyers, educators, and the clergy. (Of course, physicians,
as a profession and explores its development, lawyers, educators, and the clergy are not the only profes-
history, and related organizations. Anyone sionals, but they are the four whose professional nature
launching a career as a respiratory therapist enjoys a high level of agreement.) Other careers are not
or respiratory care practitioner will find it helpful to thought of as professions, such as sales, carpentry, cosme-
understand the history of the profession. Knowing its tology, and taxi driving. This distinction does not mean
historical foundations and place among the medical that some occupations are better than others or even that
professions enables the entrant to better appreciate one group acts more professionally than another. Rather, it
why training and certain skill sets are required to means only that there is a generally recognized difference
become a respiratory care practitioner. between professions and occupations.
The question is, What distinguishes some specialties
from occupations in general? Is there a way to examine
Scope of a Profession occupations, such as nurse, respiratory care practitio-
Any working person can function professionally. For ner, or pharmacist, to determine whether they may be
example, we might comment that, “Our hair stylist is a real considered professions? What separates professions
professional” or “The salesperson was very professional.” from other occupations? One answer is based on an
Using the term “professional” in this sense is a reference to examination of the common attributes of professions.
a person’s work attributes, such as being knowledgeable
and competent, showing up on time, providing fair prices,
honoring one’s word, providing good service, and having SELF-REGULATION
appropriate attitudes or exceptional skills. No one needs to Professional groups regulate their members in accordance
be a member of a profession to function as a professional. with criteria for ethical behavior and standards of practice.
The term “professional,” used in this generic sense, These groups thus often play an important gatekeeping
describes an individual’s personal work attributes and is function; that is, they determine who may enter the
very value laden. specialty and practice within it. Self-regulation is consid-
However, the terms “profession” and “professional” ered a major attribute of a profession and a special
are also used more discriminately to describe certain obligation of its practitioners. Most professions hold their
occupations and those who work in them. The individuals members to a code of ethical conduct. Typically, the
in many careers are considered professionals—physicians, relationship of professionals with their clients is based on
CHAPTER 1 ■ The History and Scope of Respiratory Care 5
trust, and they are held to a higher standard of behavior situation, individuals come to the professional for
than in those who work in nonprofessional fields. information that they do not possess or for skills and
services they cannot provide for themselves. Of course
though, the professional does not circumvent the
UNION STATUS autonomy of the individual. (In simple terms, autonomy
Unions serve their individual members whereas profes- [or self-determination] means that the individual has a
sional organizations serve the profession as a whole. right to make his or her own decisions.) However, the
Professional organizations concern themselves with patient or client is not always right; the concept just
such issues as standards of practice, the education of does not suit the relationship. Instead, professionals
their members, service to the community, the mainte- are thought to be in a fiduciary relationship with
nance and expansion of the body of knowledge, those they serve. A fiduciary is a trustee, one who holds
communication with government and other profes- something in trust. The central feature of a fiduciary
sional groups, and the mentoring of new practitioners. relationship is some form of duty. Once the health care
They generally do not take on the personal bread-and- provider establishes a relationship with the patient, the
butter concerns, such as working conditions and wages. provider has a duty to offer a proper standard of care.
However, in recent years, some professional groups, In fact, the provider can be held liable for failure to
such as teachers and physicians, have begun to organize provide service in accordance with the established
into true unions. So it is difficult to know whether standards of practice.
neutrality on working conditions and wages will remain
a distinctive feature of professional groups in the future.
EDUCATIONAL REQUIREMENTS
Since professional work is predominately intellectual
DISCRETE BODY OF KNOWLEDGE and varied in character—as opposed to routine mental,
Medicine, education, law, and theology have discrete manual, mechanical, or physical labor—professionals
bodies of knowledge that other specialists or the lay public often have to undergo extended periods of specialty
generally do not possess. Professionals often use terms and education. The prolonged course of intellectual study
language—jargon—not commonly used by those outside usually takes place in a specialized institution of higher
the profession that may be confusing to the general public. education or hospital, as distinguished from a general
Students of respiratory therapy learn not only the science academic institution or apprenticeship. This can be
and art of respiratory care but also its specialized language, seen especially clearly in law, medicine, and theology.
most of which (but not all) is shared with fellow health
care professionals. Advanced higher education and years of
internships are often required to master the subject area. HISTORICAL AGREEMENT ON
In addition to a common language, colleagues in PROFESSIONAL STATUS
other health care professions also share much of the same What qualifies occupations as professions is somewhat
knowledge base and skills sets. Even though the depth dependent on societal agreement. In other words, to some
and breadth of these shared attributes vary, all health care extent, some occupations are professions because people
practitioners have much in common. The variations in believe they are. For instance, nursing is often thought of
learning and experience are valuable to the overall quality as a profession, even though it may not have all the
of patient care because the different perspectives provide attributes commonly associated with professional groups.
an enriched inventory of knowledge to draw on. Yet, given the historical context and the social climate at
An interesting feature of a profession’s body of the time of the American Civil War, most ordinary citizens
knowledge is that it is directed toward doing away with would not have considered nursing a profession in 1865.
the need for the practice. The practice of medicine is Over the last 140 years, however, nursing has come to be
directed toward ending disease, the practice of law is held in much higher esteem by everyday people and is
directed toward ending injustice, and the practice of theol- now often regarded as a profession.
ogy is presumably directed toward creating an ethical
society. At the moment, no profession has managed to
achieve its chief aim of ending society’s need for its
services, and none is likely to do so in the foreseeable Can as much be said of respiratory care and its practi-
future. Yet, that remains the goal of most professions. tioners? Clearly, respiratory care practitioners act
professionally, but are they members of a profession?
The history and development of respiratory care
PATIENT STATUS furnish evidence that the field fulfills most of the
Those who work in sales and commerce often say, “The criteria for being a profession. Respiratory care has a
customer is always right.” In a client- or patient-focused distinguished history and a professional organization;
it is self-regulating; and practitioners have a profes- TABLE 1-1 Early foundational figures
sional relationship with the people they serve. How-
ever, in the areas of a discrete body of knowledge, Early Figure Area of Origin
advanced education, and societal acceptance, the field Huang Ti (reigned from 2697 BCE) China
needs further development to meet all the basic criteria Hippocrates (460–377 BCE) Greece
for a profession.
Aristotle (384–322 BCE) Greece
In large measure, the issue of professionalism lies
more in perception than it does in classical definitions. Galen (131–201 CE) Rome
The professionalism of respiratory therapists is deter- Maimonides (1135–1204) Arabia
mined by how their colleagues “see” them, how their Leonardo da Vinci (1452–1519) Rome
patients perceive them, and, most importantly, how they
William Harvey (1578–1657) England
view themselves individually and collectively. To be
“seen” as professionals, they must act as professionals. Robert Boyle (1627–1691) England
Joseph Priestley (1733–1804) England
History Antoine Lavoisier (1743–1794) France

Thomas Beddoes (1760–1808) England
Some professions are based on a singular event such as
the development of a certain technology. Most profes- John Dalton (1766–1844) England
sions, however, have an historical context and roots. Most
people think of respiratory care as a modern profession
with roots that extend back only to the 1940s, but it has
one of four elemental substances; the others were
foundations that extend back much further in time.
earth, water, and fire. He recorded some of the first
studies showing the effects of oxygen deprivation on
EARLY FOUNDATIONS animals. Like most of his contemporaries, Aristotle
misunderstood the nature of respiration, believing that
“And the Lord God formed man from the dust of the
it served the purpose of cooling the system. When he
ground, and breathed into his nostrils the breath of
placed animals in airtight chambers and observed their
life; and man became a living soul…” (Genesis 2:7).
deaths, he concluded that they had lost the ability to
The Bible contains a vivid description of mouth-to- control body temperature because they could not
mouth resuscitation. In II Kings 4:34, breathe. This conclusion is somewhat understandable
given that persons who are ill and die often have a
Elisha breathes life into his son: “And he [Elisha]
fever as part of the process.
went up, and lay upon the child, and put his mouth
Perhaps the most influential successor to the
upon his mouth, his eyes upon his eyes, and his
Hippocratic framework of medical thinking was Galen
hands upon his hands and he stretched himself upon
(131–201 CE). He was a Greek physician who synthe-
the child, and the flesh of the child waxed warm.”
sized a system of medicine that dominated Western
This and other early references are evidence of thinking for the next thousand years. Galen did founda-
respiratory therapy having its origin thousands of years tional work in cardiac physiology and taught that blood
ago (as early as 2697 BCE). Table 1-1 lists some leaving the right ventricle passed through the lungs and,
important early figures in the development of the in doing so, mixed with air, which formed a necessary
practice of respiratory therapy. “Vital Spirit.” Unfortunately, the early Greek idea regard-
Hippocrates (460–377 BCE) and Aristotle (384– ing respiration as essentially a mechanism for cooling the
322 BCE) are credited with adding to the early founda- blood continued in his writings. Galen’s observations
tion of the understanding of respiratory physiology and and writings cover every aspect of medicine, and much of
the therapeutic use of oxygen. Hippocrates is rightly his thinking went unchallenged until the Renaissance.2
recorded as the father of Western medicine because he His work essentially framed the discussion of medicine
rejected much of the mysticism surrounding the in the West for over a thousand years.
medical thinking of his time and emphasized the Huang Ti, the Yellow Emperor of China who began
importance of clinical observation. In his treatise “On his reign about 2697 BCE, had a similar impact on
Air, Minerals, Waters, and Places,” Aristotle influenced Eastern medical thought. In the classic work Nei Ching
the early thinking regarding the therapeutic use of the (The Yellow Emperor’s Book of Internal Medicine), Huang
so-called vital spirit (air).1 In this period, before the age Ti outlined the tenets of traditional Chinese medicine.
of science, most people recognized that air was an The text provides a coherent system of health care,
important vital spirit, but no one understood its diagnostic methods, and therapeutic regimes, and it
physical properties. Aristotle concluded that air was extensively covers pulmonary diseases such as asthma.
The thinking regarding preventive care in this that air was inert and that it did not take part in
manual of health care bears a striking similarity to combustion. Most scientists of the day accepted an
modern Western thought. The text calls for the physi- erroneous assumption, which held that burning
cian to maintain the patient’s health rather than to cure materials released an invisible gas known as phlogiston,
disease, on the premise that waiting for an illness to which was associated with heating and was known as
occur is like forging weapons after the battle has begun the phlogiston theory.
or like digging the well after you are already thirsty. As Joseph Priestley (1733–1804), an English cleric,
Galen’s work did in the West, the Yellow Emperor’s Book discovered that plants consumed a gas that was harm-
of Internal Medicine tended to freeze the discussion of ful to animals and gave off another that rendered the
medicine in the East, and it is still influential in the air capable of supporting animal life. In 1774, by
current practice of traditional Chinese medicine.3 concentrating the sun’s rays through a magnifying
In the West, advancement in medical thinking glass, Priestley heated red mercuric oxide and produced
during the Dark Ages often came from non-Western oxygen. As a follower of phlogiston theory, which held
physicians such as Maimonides (1135–1204), who that during combustion phlogiston (a gas) was given
brought new thinking from the Arabic culture. Mai- off, Priestley called his new gas “dephlogisticated air.”
monides, a Jewish physician and philosopher, was After a clinical trial with mice, he emptied a container
appointed physician to the court of the Egyptian of oxygen, breathed it, and noted the following effects:
sultan. His writings, particularly Regimen Sanitatis and
My reader will not wonder that, having ascertained
Medical Aphorisms, exerted great influence on European
the superior goodness of dephlogisticated air by
medicine.4 The drawings and writings of Leonardo da
mice living in it, and the other tests above men-
Vinci (1452–1519) clearly indicate that, by the late
tioned, I should have the curiosity to taste it
1400s, he had come to understand the true nature and
myself. . . . I have gratified that curiosity by breath-
function of respiration. However, perhaps as a matter
ing it, drawing it through a glass siphon, and by
of pragmatism, he chose not to resist the dogma of
this means I reduced a large jar full of it to the
the time.5
standard of common air. The feeling of it to my
A rebirth, or Renaissance, of medical science was
lungs was not sensibly different from that of
soon to come. By the early 1500s, the task of finally
common air, but I fancied that my breath felt
dispelling the ancient dogma regarding human anat-
peculiarly light and easy for some time afterwards.
omy waited for Vesalius and Michael Servetus. They not
Who can tell but that in time this pure air may
only came to know the truth by their dissections and
become a fashionable article of luxury? Hitherto,
studies, but also taught it. Unfortunately, Servetus paid
only two mice and myself have had the privilege of
a heavy price for his heretical beliefs; he was burned at
breathing it.9
the stake on orders of John Calvin. Vesalius published
his De Fabrica Humani Corporis in 1543, which put to French chemist Antoine Lavoisier (1743–1794)
rest many of the false dogmas regarding human body duplicated Priestley’s early experiments and thought
structure.6 that he had isolated pure air. Lavoisier later concluded
The Galenic system of medicine, along with the that he had separated only a component of air but that
view that respiration was a means of cooling the blood, it came into existence when air was heated. He named
was finally put to rest by William Harvey (1578–1657). the gas oxygen, meaning “acid-maker.” Lavoisier
In his De Motu Cordis (1628), Harvey demonstrated correctly described the basic physiology of respiration
blood circulation through the heart and provided the and demonstrated that the lungs absorb oxygen and
first estimations for the volume of blood pumped that water and carbon dioxide are given off during
through the vascular system. The book was influential exhalation.10
in founding the modern principles of physiology.7 At approximately the same time as the work of
In 1660, the work of scientist Robert Boyle Priestley and Lavoisier, Swedish scientist Carl Scheele
(1627–1691) added to the understanding of air and (1742–1786 AD) had also been working on oxygen,
the process of respiration. Boyle built a primitive isolating it from saltpeter. Although he had completed
barometer for the prediction of weather and speculated his studies earlier than Priestley or Lavoisier, he
that the processes of combustion and respiration are published his results in the treatise Air and Fire
due to a substance in air. During this time, he created (1781)—after they had published their results—and
what is now called Boyle’s law, which states that the has been given very little credit for his discoveries,
volume of a gas decreases as pressure increases.8 proving once again that publication in science, like
The discovery of oxygen offers an interesting timing in investments, is everything.
problem of credit. In the middle of the eighteenth Who should be given the credit for the discovery of
century, despite Boyle’s speculations, scientists still held oxygen? Priestley isolated oxygen but did not know
what he had; Lavoisier understood that oxygen was a TWENTIETH-CENTURY DEVELOPMENTS

component of air and gave it its name, but he did not The development of the knowledge and technical base
quite understand its nature. Scheele may have been first for respiratory therapy in the twentieth century can be
to isolate the gas but published his works only after divided roughly into halves. The first half is filled with
others had received the credit. Maybe the credit belongs scientists whose names all practitioners memorize as
to none of them because oxygen could not truly be part of the principles and equations that are fundamental
understood using the science of the day. to our practices: Sir William Arbuthnot-Lane
In this light, perhaps the credit should go to the British (1856–1943), Jack Emerson (1906–1997), Donald
chemist and physicist John Dalton (1766–1844 AD), Dexter (1881–1973), Sir George Gabriel Stokes
who, in his formulation of the atomic theory of matter, (1819–1903), and John Scott Haldane (1860–1936),
placed the final piece into the oxygen puzzle. to name a few. An important development of the
Thomas Beddoes (1760–1808), who established period was that of Karl Von Linde (1842–1934), whose
the Pneumatic Institute of Bristol, England, is cred- 1901 large-scale, commercial application of fractional
ited with the first therapeutic use of oxygen. In the distillation made compressed oxygen available in
Institute, Beddoes and his colleagues used primitive amounts suitable for large-scale use. Table 1-2 provides
oxygen masks made of oiled silk rags to treat heart a chronology of other important clinical and research
disease, leprosy, asthma, opium addiction, venereal developments during the twentieth century.
disease, and dyspnea. Although oxygen has no thera-
peutic effect on many of the diseases on which it was The Early 1900s. The first half of the twentieth century
tried at the Institute, Beddoes is often referred to as the is a fascinating period in which scientist-clinicians
father of respiratory therapy because he was the first to made the first serious attempts at mechanical ventila-
use oxygen therapeutically.11 tion. Heinrich Drager’s portable pulmotor device
During the 1800s, several clinical attempts were allowed for resuscitation, and the 1909 Emerson
made to use oxygen under ambient and positive pressure ventilator showed the efficacy of positive
pressure to effect some health benefit. In 1878, M. J. pressure in reducing pulmonary edema in rabbits.13
Oertel, using air compressed by 1/50 of an atmosphere This same period saw a number of attempts to use
to 775.2 mm Hg, was the first to try using positive oxygen therapeutically. Oxygen rooms and even hotels
pressure to treat asthma. In 1897, N. R. Norton were established that had greater-than-ambient pres-
attempted to treat acute pulmonary edema caused by sure. These rooms were very difficult to control, and,
carbolic acid poisoning with oxygen under positive given the potential for fire, they were quickly replaced
pressure. Although these attempts were innovative and by smaller tents. There is a story about the eminent
advanced for the time, truly therapeutic uses of oxygen scientist Haldane, who entered an oxygen room after
required the technological advances of the 1900s.10 putting the pipe he was smoking into his pocket. The
TABLE 1-2 Twentieth-century chronology

Lane (1907) Advised the use of oxygen via nasal catheter
Emerson (1909) Demonstrated that artificial ventilation could successfully treat pulmonary edema
in rabbits
Stokes (1917) Reintroduced the idea that oxygen could be administered by nasal catheter
Haldane (1917) Developed an oxygen mask for the treatment of pulmonary edema
Hill (1920) Developed the first oxygen tent
Barcroft (1920) Built the first oxygen chamber (in England) and created the oxygen deficiency
classifications anoxic, anemic, and stagnant
Van Slyke (1931) Added to the three Barcroft classifications a fourth type, histotoxic
Barach (1926) Improved the oxygen tent by controlling heat and moisture buildup
Drinker and Shaw Developed the first iron lung device, in which the patient’s head extended from
(1929) the ventilator
Boothby, Lovelace, and Developed the BLB mask; Boothby established the use of oxygen postoperatively
Bullbullion (1938) for bronchopneumonia
increased oxygen concentration and pressure restored quickly made the transition to a postwar economy
his tobacco to a flame, and, as one can imagine, he and made these devices available for treatment and
quickly left the chamber.14 Other early attempts at the research. There had also been much war-related
use of therapeutic oxygen were Lane’s 1907 advocacy research into the measurement and recording of
for the administration of ambient oxygen through the venous and arterial saturation and pressures and of
nasal catheter and its introduction into the United pulmonary function through the use of spirometry.
States in 1931 by Waters and Wineland.10 This knowledge quickly found its way into clinical
Lawrence Joseph Henderson did preliminary work practice.
on blood gas analysis and delineated the basic relation- One singularly important clinical practice that
ships used in the acid-base studies used today.14 developed in the postwar period was intermittent
Although World War I interrupted much of the research positive pressure breathing (IPPB). After World War II,
on pulmonary physiology, the war effort itself was a a simple valve that had been designed at the University
stimulus for developing additional modes of oxygen of Southern California was redesigned as a device that
therapy to handle patients injured in poison gas allowed for the provision of positive pressure during
attacks. During this period, tracheal intubation was inspiration and expiration to the atmosphere.
begun, and masks to treat pulmonary edema were This valve, which took the name of its engineer
developed. There is little indication that any effective designer (V. Ray Bennett), became the basic equipment
efforts were made toward positive pressure ventilation for providing intermittent positive pressure breathing
during World War I. treatments. Shortly after the commercial arrival of the
After the war, experiments in animal ventilation Bennett IPPB device, Forrest M. Bird, MD, PhD, ScD
continued in American and British laboratories, with a (1921–) developed a series of devices (Bird Machines)
great sharing of ideas and theories. Sir John Barcroft in that allowed for intermittent positive pressure breath-
England and Leonard Hill in the United States devel- ing as well as for ventilation during anesthesia.10
oped oxygen tents to treat edema, but these early tents The increased usage of oxygen and other types of
had serious problems. Without a system for the control modified atmosphere, as well as the rapid advances in
of humidity and temperature, they were incredibly new technologies and therapeutics, quickly went
uncomfortable.14 beyond the basic training of the nurse. Before long, a
The first half of the twentieth century was a time of new technician was working at the bedside. At first, the
seminal scientific and clinical research. During this new technicians were orderlies dispatched from central
period, masks, catheters, tents, and basic ventilators— supply or maintenance to deliver the heavy oxygen
albeit crude—were first developed. However, to become cylinders to the patients’ rooms and to put ice in the
a modern field of study, respiratory therapy needed to tent chambers. Often these orderlies were responsible
wait for the technological and therapeutic advances for diverse tasks, such as oxygen therapy and orthope-
that followed World War II. dic traction. Because their work was most closely
associated with the delivery of oxygen, however, they
The 1940s and 1950s: Early Clinical and Organiza- became known as oxygen orderlies.
tional Growth. One of the important pioneers of the The physicians and nurses using the services of the
profession was Dr. Alvin Barach. His work in devising oxygen orderlies were not particularly knowledgeable
low-flow oxygen devices, nonrebreathing masks, and a about the equipment. As a result, the on-the-job-
postoperative device known as the Cof-a-lator, which trained orderlies who delivered, took down, cleaned,
simulated deep breathing and a cough, turned many and repaired the equipment soon became the experts.
of the early ideas of the first half of the twentieth They were assisted in becoming the experts by the
century into practical therapeutic realities. In 1944, commercial companies, such as Linde and Bennett,
Barach authored the first textbook for what was then that would often provide classes, seminars, films, and
known as inhalation therapy.12 Other pioneers whose handbooks on the use of the equipment. The new
clinical work extended into the second half of the technicians began to see themselves as unique and
century were Drinker and Shaw, who in 1929 modified separate from the other hospital orderlies and began to
the oxygen chamber into what was to become the iron meet with other local technicians to share information
lung. These devices were later to become the standard about new practices.
for treating polio patients during the epidemics of the The reliance of physicians on the technicians’
1940s and 1950s.10 understanding of the equipment formed strong
World War II brought several important techno- professional bonds between the two groups. Many
logical advances that were rapidly applied to medicine physicians gave of their time and knowledge to further
in the postwar period. Manufacturers that had devel- the education of this new group of specialists. This
oped oxygen systems and masks for the war effort generosity actually enlightened self-interest because
the time spent by the physicians in educating the In 1947, the Inhalational Therapy Association
technicians translated into better care and improved (ITA) was established as an incorporated entity in
bedside therapeutics for their patients. the state of Illinois, with 59 members. George A.
Kneeland, from the University of Chicago Hospitals,
served as chair for the new organization, and
The Organizing of the Profession Drs. Levine, Andrews, and Sadove served as medical
The close bond between physicians and technicians has advisers. The charter of the ITA clearly established
been a hallmark of the field of respiratory therapy. it as a professional organization. Its goals were
Since its beginnings, the profession has had the far-reaching and ambitious. It called on its
recognition and support from the American Society of members to:
Anesthesiologists (ASA), the American Thoracic Society
• Promote high standards in methods and the
(ATS), and the American College of Chest Physicians
professional advancement of association
(ACCP). Over time, these close associations proved to
members.
be a great strength for the developing allied health
• Create mutual understanding and cooperation
profession.
among the technician, the physician, and all
The growth of the early technician groups was
others who were employed in the interest of
uneven. There were small groups throughout the
individual and public health through the
United States, with significant growth throughout
Tri-State Hospital Assembly.
California and in Chicago, Miami, Washington, D.C.,
• Advance the knowledge of inhalation therapy
and New York City. In Chicago, three exceptional
through institutes, lectures, and other means
physicians—Drs. Edwin Levine, Max Sadove, and Al
given under the sponsorship of doctors of the
Andrews—supported the technician groups. Recogniz-
American Society of Anesthesiologists and to
ing that the orderly status of the technicians was not in
grant certificates of qualification to individuals
keeping with the clinical requirements of their role,
who successfully complete the prescribed
these physicians began to meet regularly with the
requirements.12
Chicago technician group and to elevate their educa-
tion from the bedside to the classroom. The fledgling ITA continued to plan local seminars and
In the mid-1940s, the technicians’ groups in the institutes for the technician group. In 1948 the organi-
various centers began to form organizations. The zation changed its name to the Inhalation Therapy
Miami group formed the Florida Inhalation Therapy Association, and George Kneeland was elected its
Association. The Washington, D.C., group formed the president.
American Society of Inhalation Therapy. However,
the Chicago group formed the organization that
was to evolve into the American Association for A NATIONAL PROFESSIONAL ASSOCIATION
Respiratory Care (AARC) (Figure 1-1).12
In 1950, the Inhalation Therapy Association sponsored
its first annual convention and began to publish its first
newsletter, known as Bulletin. In 1953 the association
again changed its name, this time to the American
Association of Inhalation Therapy (AAIT). In 1955
the organization, which had by this time grown to
177 members, established a national office and
NBRC
employed Albert Carriere as its first executive director.
Carriere provided dynamic managerial leadership
AARC CoARC
to the organization, assisting in the establishment
FAARC
of local chapters across the nation.
© Delmar/Cengage Learning
In 1955, the Bulletin was revised in format and

ICRC style and was published as the AAIT Bulletin, a name
that continued in use until 1977, when the associa-
tion began publication of the AARC Times.10 The first
editor of the AAIT Bulletin was James Whitacre, a
FIGURE 1-1 The AARC and its related organizations. Green distinguished early educator.12 By 1956, the associa-
entities are subsidiary organizations. Red entities are tion had two publications. In addition to the AAIT
independent organizations that are closely related to the Bulletin, a new scientific journal, known as Inhalation
AARC and provide professional credentialing (NBRC) or Therapy, was the forerunner to the current Journal of
program accreditation. Respiratory Care.
Over time, the demand for services across the Formal Education System
country was broadened to include such services as
the administration of aerosolized medications, In recognition of these problems, Emma and Collins
oxygen, carbon dioxide–oxygen mixtures, helium- began to work toward the development of legitimate
oxygen mixtures, iron lungs, and intermittent positive schools of inhalation therapy. In April 1956,
pressure breathing and Cof-a-lator treatments. In “Essentials of an Acceptable School of Inhalation
1953, Drs. Motley and Smart published an article Therapy Technicians” was published in the New York
describing a series of cases in which patients were State Journal of Medicine and later reprinted in the
treated with intermittent positive pressure breathing August 1956 edition of the AAIT Journal. The so-called
(IPPB). IPPB treatments, with or without bronchodi- essentials were offered in the form of a recommenda-
lators (medications that increase the size of narrowed tion to hospitals wishing to start training programs.5
airways in the lungs), were given to asthma patients, In 1963, representatives from the American
patients suffering with chronic obstructive pulmo- Medical Association (AMA), Council on Medical
nary disease (COPD), and preoperative and postop- Education (CME), the American College of Chest
erative patients.14 The demand for these services Physicians (ACCP), the American Registry for Inhala-
became such that specialty departments were estab- tion Therapy (ARIT), and the American Society of
lished to facilitate the delivery of the services, and the Anesthesiologists (ASA) came together in the Chicago
oxygen orderlies became generally known as inhala- headquarters of the AMA to create a Board of Schools
tion therapists. Although the overuse of IPPB was for the new field. The board was to function under the
eventually to become an embarrassment to the AMA Council on Medical Education. In 1964, the
profession, IPPB devices could be seen throughout Board of Schools, which later was renamed the Joint
most hospitals in the United States in the late 1950s Review Committee for Inhalation Therapy Education
and 1960s. (JRCITE), began its first site visits to evaluate inhalation
therapy educational programs. The establishment of
the AMA-sponsored accreditation process was an
important step in the creation of the profession. Not
THE LATE 1950s AND THE 1960s:
only did it elevate the programmatic requirements and
ORGANIZATIONAL AND CLINICAL MATURATION
thus weed out the poor and exploitative programs, but
Respiratory therapy started coming together as a it also legitimized the field with AMA’s recognition of
discrete profession in the late 1950s. In 1957, the inhalation therapy as a true allied health occupation.
American Society of Anesthesiologists (ASA) began its
official sponsorship of the AAIT. The ASA medical
advisers to the AAIT were Drs. Vincent Collins, Edwin JOINT REVIEW COMMITTEE FOR INHALATION
Emma, and Meyer Saklad. By 1958, the AAIT had THERAPY EDUCATION
grown to 600 members. It had two professional The Joint Review Committee for Inhalation Therapy
publications, it held a national convention, and it Education played an important part in the develop-
was sponsored and supported by physician groups. ment of the profession. Each approved program had to
Inhalation therapy was becoming an important comply with the essentials, which were the general lists
revenue center in hospitals and clinics. Perhaps most of processes and inputs that had been deemed neces-
importantly, the AAIT’s growing membership was sary for the education of clinicians. Only graduates of
young, hard-driving, creative, and eager to improve approved programs could gain access to the specialty
their education. credentialing system (see “American Registry for
It was apparent early on that the training could not Inhalation Therapy”).
remain at the on-the-job level. The therapists were As the field developed, the essentials evolved, and
being called on to perform tasks well above their the programs were moved from hospitals to academic
training level. Often the least trained technicians could institutions. The early essentials were process oriented,
be found on the evening and weekend shifts, when and programs were approved on the basis of such
there was also the least supervision. Most of the things as the types of equipment available, the books
training programs were hospital based. Although some available, the level of medical support, and the types
were doing an excellent job in preparing practitioners, and numbers of classes. A real problem with process-
other programs were designed to acquire free labor oriented essentials (evaluation measures based on
under the guise of an educational program. The new how things are accomplished) was justifying what was
field had a perplexing incongruence: Although the required: For example, are 50 books too many? Are
inhalation therapists dealt with some of the most 49 too few? Are they the right ones? In retrospect, these
critical medical situations, they often had the least processes clearly were not appropriate criteria for
formal education. judging the quality of the educational programs.
However, they did and still do have roles in terms of Inhalation Therapy (ARIT) took place in November
available resources. 1960, and 12 individuals successfully completed the
Beginning in 1980, the Joint Review Committee examinations. Because the ARIT did not complete
began to question the validity of the old process- incorporation until January 1961, the new therapists
oriented essentials and to plan for new product- did not officially receive their titles until the second
oriented essentials (evaluation measures based on examination, which took place in April 1961.
the quality of the product—in this case, program The first examination process consisted of two
graduates). The new essentials could also be described components, an objective written examination and an
as outcome-oriented essentials (measures of the oral examination. The successful completion of both
attainment of stated goals). A program would deter- exams was required to obtain the coveted credential of
mine its goals and then give evidence that it was American Registered Inhalation Therapist (ARIT), now
attaining them. Rather than allowing the essentials to called Registered Respiratory Therapist (RRT).
determine what was necessary, the programs would be The written examination tested basic knowledge in
justified based on how well they achieved their goals. areas such as gas laws, history, oxygen therapy theory,
Compared to process-oriented essentials, outcome- and infection control. The more controversial of the two
oriented essentials are clearly more in the mainstream test segments was the oral exam, which was divided
of modern programmatic evaluation and fairer to the into two tests. Usually, a physician in one room and a
programs. therapist team in another room administered the oral
However, the importance of passing Joint Review tests. In the physician’s room, the candidate was
accreditation would seem to be a powerful incentive questioned in areas concerning theoretical and profes-
for educators to be modest in setting their programs’ sional matters. In the therapist team’s room, the empha-
goals. Whether the new essentials will have a flattening sis was on practical equipment matters; the candidate
effect on innovation in respiratory therapy education is was asked to identify and troubleshoot equipment. The
yet to be determined. Nevertheless, the emergence of rationale for the orals was that, in the clinic, the
Web-based curricula, problem-based learning, and candidates were not going to face multiple-choice
online outreach programs are all reasons to be optimis- situations and given time to ponder their answers.
tic that creativity and innovation will remain strong Rather, they would be required to function under
attributes of respiratory care education programs. pressure and to make quick decisions. The orals there-
As of January 2011, there were 10 level-100 (entry- fore provided a means of simulating the conditions
level) programs and 362 level-200 advanced practice under which the therapists would actually practice.
(AS/AA, BS, or master’s) programs, for a total of 372
accredited RC/RT programs in the United States. Of Oral Exams. The oral examination system was at first
the advanced-level programs, 306 were at the associ- under the direction of Dr. Meyer Saklad, who worked
ates level, 53 were at the BS level, and 3 were at the to overcome the inevitable criticism of subjective
master’s degree level. Of the 10 100-entry level pro- examinations. After the death of Dr. Saklad, Dr. Robert
grams, 6 were stand-alone programs with no affiliation Lawrence became the director and continued in that
with an institution of higher learning (community or role until the orals were discontinued in 1978. Despite
4-year colleges or universities). By 2012, five of the six the tireless efforts of Drs. Lawrence and Saklad to make
stand-alones will have completed affiliation agree- the oral examinations fair, the system was inherently
ments with colleges or universities, and one has started flawed: The bar was not at the same level for all the
the process to voluntarily withdraw its CoARC accredi- candidates. Certain examiners were tough; others were
tation. The net effect of these moves is that all RC lax. Thus, becoming registered in the profession was a
programs will be capable of offering two years of CoA matter of the luck of the draw. Ironically, the last oral
RC education. examinations were given in November 1978 in Las
Vegas.12
The orals hold an interesting place in the hearts and
AMERICAN REGISTRY FOR INHALATION THERAPY minds of those who went through them. In a sense,
Concurrent with the development of AMA-approved they became a badge of honor for the therapists who
schools for inhalation therapy was the start-up of a shared the not-altogether-pleasant experience. Therapist
credentialing system to provide recognition for quali- gatherings were often and still are peppered with stories
fied inhalation therapists. The autumn 1959 AAIT of the orals, each more striking than the last.
Bulletin announced the development of a constitution
and bylaws for a nonprofit corporation that would be Clinical Simulation Exam. The orals were finally
created for registering individual practitioners.12 The replaced by a written clinical simulation, which
organizational meeting for the American Registry for resolved the inherent problem of unevenness in the
oral testing system. The shift away from oral examina- salary, the standard became entry level. Often, the two
tions enabled the Registry to review an essentially levels of qualifications became meaningless in the
unlimited number of candidates each year. In its clinics, and in times of cost containment clinical units
initiating trial in June 1979, the clinical examination began to find the lower-paid, entry-level practitioners
was given to 3176 candidates—over six times the preferable.
number of candidates who could be accommodated by
the orals.
THE 1970s: GROWTH AND UNREST
The AAIT entered the 1970s in a high-growth mode.
Certified Inhalation Therapy Membership grew from 5147 members in 1969 to
Technicians 7934 members in 1970. By 1975, the membership was
In the early to mid-1960s, registered inhalation thera- 23,448. As of 2009, membership exceeded 47,000.
pists were in short supply. The job market was in such a During this high-growth period, strains appeared
state of growth that therapists could move from position between the allied health practitioners and their
to position. They could pick the state, the city, and in physician supporters. As the field grew and the AAIT
many cases even the hospital they wanted. To fill the matured, the therapists’ views began to diverge from
need for trained personnel, in September 1968, the AAIT and in some areas conflict with those of many of the
announced the appointment of a committee for the supporting physicians, who had come to feel almost as
establishment of a second level in the field: certified if they owned the specialty.
inhalation therapy technician (CITT), now called These conflicts were unfortunate; physicians had
certified respiratory therapist (CRT). A pilot examination played and continue to play an important role in the
was provided for 99 candidates for the new certification development of the specialty. By the 1970s, the needs
at the annual meeting held in Kansas City in 1969.14 and views of the physician groups were not always
The recognition of certified inhalation therapy congruent with those of respiratory therapists in such
technicians (CITTs) was very successful in meeting the areas as licensure, accreditation, and federal policy. Yet,
clinical needs for more practitioners. These practitio- even in the turbulent 1970s, physician colleagues lent
ners graduated from programs that were about half the remarkable support in helping respiratory care escape
length of those for registered therapists. The CITTs, from some of the more stringent federal regulations
along with practitioners graduating from nontradi- directed toward hospital cost containment.
tional, entry-level (correspondence) programs, quickly In the mid-1970s the National Heart and Lung
filled the available positions. Institute (NHLI) and the American Thoracic Society
In 1974 the AART’s Technician Certification (ATS) cosponsored a conference on the scientific basis
Examination, and the ARIT’s Registry examination were for respiratory therapy.15 The meeting became known
placed under a single credentialing entity: the National as the Sugarloaf Conference, after its meeting place in
Board for Respiratory Therapy (NBRT), later renamed Philadelphia. Although the findings of the conference
the National Board for Respiratory Care (NBRC). took several years to be felt, they were to have a
A problem associated with the establishment of profound effect on the types of therapy provided. By
certified inhalation therapy technicians was how to the mid-1980s the IPPB devices, which had been a
differentiate technicians from registered inhalation standard for the profession, were generally replaced by
therapists in the clinics. One of the tasks accepted by volume-oriented postoperative devices.
the NBRC was to perform a national job analysis to
identify the specific job tasks that were expected of
the entry-level practitioners. The job analysis identi- THE 1980s: CHANGE IN MANY AREAS
fied two distinct levels of practice. Compared to Major advances in respiratory care in the 1980s were
entry-level (certified technicians) staff, advanced found in intensive care units, where the greater under-
practitioners (registered therapists) were expected to standing of cardiopulmonary pathophysiology was
handle a different set of tasks, to have a more matched by improved technologies for monitoring and
in-depth and diversified knowledge base, and to supporting the systems. The 1980s saw the pneumati-
operate at a higher level of complexity and with less cally controlled equipment evolve into microprocessor-
supervision. controlled ventilators, monitoring systems, and
Although it was easy to make such distinctions and diagnostic instruments such as blood gas analyzers.
even to write up a listing of job duties, the reality (See Chapters 16–19.)
remains that whoever is on duty at the time is expected To provide a comprehensive overview about a
to do everything. Small clinical units could not afford to dynamic aspect of pulmonary physiology, pulmonary
hire two sets of practitioners, and, given the difference in medicine, or clinical respiratory care, the AARC Program
TABLE 1-3 Donald F. Egan Scientific Lectures

1974 John F. Murray, MD: “Oxygen Transport: New Concepts, New Problems”
1975 Lynne Reid, MD: “New Perspectives in Pulmonary Hypertension”
1976 David Bates, MD: “Early Detection of Airway Obstruction”
1977 George Burton, MD: “How to Succeed in Respiratory Therapy by Really Trying”
1978 John Hedley-Whyte, MD: “Ventilatory Care”
1979 Albert Fishman, MD: “Changing Concepts of Pulmonary Edema and the Respiratory Distress Syndrome”
1980 Alan Pierce, MD: “Respiratory Therapy, State of the Art”
1981 John Severinghaus, MD: “Transcutaneous PO2 and PCO2 Monitoring”
1982 Reuben Cherniack, MD: “Pitfalls in Pulmonary Function Testing”
1983 Roger Bone, MD: “Adult Respiratory Distress Syndrome: Treatment in the Next Decade”
1984 Thomas Petty, MD: “Pulmonary Rehabilitation: Better Living with New Techniques”
1985 Irwin Ziment, MD: “Five Thousand Years of Attacking Asthma”
1986 Ronald Harrison, MD: “Ventilatory Support Techniques: A Resource for Discovery”
1987 David Dankzker, MD: “PEEP and Oxygen Consumption: Is O2 Delivery Really Our Goal?”
1988 John West, MD: “Severe Hypoxia: Lessons from High Altitude”
1989 Leonard Hudson, MD: “The Prediction and Prevention of ARDS”
1990 Mary Ellen Avery, MD: “Twenty-Five Years of Progress in Hyaline Membrane Disease”
1991 E. Regis McFadden Jr., MD: “Fatal Asthma”
1992 John Marini, MD: “Patient-Ventilatory Interaction: Rational Strategies for Acute Ventilatory Management”
1993 Lee Reichman, MD: “Tuberculosis: An Old Enemy Back”
1994 C. James Carrico, MD: “The Trauma Patient: Our Responsibilities in the ICU and in Society”
1995 Jerome Modell, MD: “What Have We Learned About Lung Injury from the Management of Near Drowning?”
1996 Luciano Gattinoni, MD: “How Does PEEP Work?”
1997 William Sibbaid, MD: “The Whys and Wherefores of Measuring Outcomes in Respiratory Critical Care”
1998 Gordon Bernard, MD: “ARDS: New Approaches to a Serious Respiratory Illness”
1999 Martin J. Tobin, MD: “Weaning from Mechanical Ventilation: What Have We Learned?”
2000 James K. Stoller, MD: “Are RTs Effective? Examining the Evidence”
2001 John E, Hefner, MD: “Chronic Obstructive Pulmonary Disease—On the Exponential Curve of Progress”
2002 John B. Downs, MD: “Controversial Aspects of Oxygen Therapy”
2003 Gordon D. Rubinfeld, MD: “MSc Translating Clinical Research into Clinical Practice”
2004 Arthur S. Slutsky, MD: “Ventilator Induced Injury: From Barotrauma to Biotrauma”
2005 Homer A. Boushey, MD: “Past and Future Therapies for Asthma”
2006 Bartolome Celli, MD: “COPD: From Unjustified Nihilism to Evidence Based Optimism”
2007 J. Randall Curtis, MD: “MPH Caring for Patients with Life-threatening Illness and for Their Families:
The Value of the Integrated Clinical Team”
2008 David J. Pierson, MD: “FAARC The Cardiopulmonary Physiology of Dinosaurs”
2009 Bruce Ruben, MD: “Air and Soul—The Science and Practice of Aerosol Therapy”
2010 Robert Kacmarek, PhD, RRT: “The Mechanical Ventilator—Past, Present and Future”
Committee established the Donald F. Egan Scientific therapy and one of its first major educators and authors.
Lectures in 1974. Each year, the lectureship is extended Table 1-3 provides a chronological listing of the lectures.
to a prominent investigator, clinician, or academician in A review of the subjects provides insight into the
the arena of interest. The lectureship honors Dr. Donald developing growth and maturity of the scientific and
F. Egan, an early champion and supporter of respiratory clinical interests of the profession.
Effects of Governmental collapse under the weight of rises in costs. Early

attempts at cost containment (actually wage and price
Programs controls) in the 1970s had proved disruptive and
Important engines for growth of the new allied health ineffective. In 1983, the government adopted a
field were the federal programs authorized in the prospective payment system (PPS), which was to
mid-1960s to increase citizen access to health care. Two have a dramatic impact on the respiratory therapy.
such programs were Medicare and Medicaid, autho- The basis of the Medicare prospective payment
rized in 1965 under the Social Security Administration system is the diagnosis-related group (DRG). For a
(SSA) of the U.S. Department of Health Education and given diagnosis, each institution is paid a set amount
Welfare (HEW). Medicare provides assistance to pay rather than the actual amount spent on the patient.
for health services for people 65 and older and for This system allowed rates of payment to be determined
persons who have been receiving Social Security in advance for a medical diagnosis. Because payments
disability benefits for 2 years. Medicaid authorizes for an illness were predetermined and fixed, regardless
federal matching funds to assist the states in providing of the amount of care or services actually rendered,
health care for certain income groups at or near the health care facilities had a powerful incentive to
federal poverty line.16 contain costs and to curb the amount of therapy
In 1977 both programs were administered by the provided. The most common forms of cost contain-
new Health Care Finance Administration (HCFA) of the ment were reduced services, decreased staff, and
U.S. Department of Health and Human Services. In shortened lengths of patient stay. In effect, the patients
1980 HEW was split into two agencies, the Department were being sent home “quicker and sicker.” Because the
of Education and the Department of Health and prospective payment system was initially focused on
Human Services (HHS), the latter of which became hospital costs, it caused a shift of services from the
HCFA’s new supervising agency. By 2001 HCFA was hospital to the physician’s office, to external clinics,
renamed the Center for Medicare & Medicaid Services. and to homes. This shift established a need for greater
The name change recognized the mandates to oversee respiratory therapist activity in the homecare market
not only Medicare and Medicaid but also the State and an increased scope of practice (the functions
Children’s Health Insurance Program, as well as the performed).
Health Insurance Portability and Accountability Act Thus, cost containment hinged on three major
(HIPAA) Standards and the quality standards for issues: patient acuity (how sick the patient’s were),
long-term care facilities (nursing homes) and clinical length of stay (how long the patients remained in the
laboratories. (For details of Medicare and Medicaid hospital), and manpower costs (wages and benefits
payments for individuals 65 and older, see Chapter 35.) costs for health care workers).
In their original formulation, both Medicaid and
Medicare were strictly fee-for-service systems. Hospi-
tals and physicians were reimbursed for whatever they CHANGING ACUITY LEVELS
spent on qualified patients. In that health care is one of The general acuity level in the hospital increased as
the few areas in which the sellers, not the consumers, patients who were not critically ill were moved from
make the buying decisions, health care providers had the hospital to other service venues. Patients who
an immense incentive to provide more and more required less technical, less complicated care were
services. This is not to say that physicians and hospitals considered to be at the subacute care level (see
exploited the new programs. However, the physicians’ Chapter 34). The heightened acuity level in the
and hospitals’ desire to provide services coincided hospital shifted the emphasis of respiratory care
closely with the consumer’s desire that all that could be services from the general patient floor to the intensive
done would be done. The result was an explosion in care units and to diagnostic areas, such as cardiology
health care costs. Specialty areas such as respiratory and pulmonary function.
care became highly profitable revenue centers for The patients being released from the hospital
hospitals, and services expanded well beyond any earlier than in the past needed to be serviced in other
justifiable need. venues, such as the home. As one of the major effects
of governmental attempts at cost containment, sub-
acute care (see Chapter 35) quickly became a specialty
COST CONTAINMENT area for respiratory therapists. As of 1997, it was
In the early 1980s, the federal government again projected that 30,000 to 50,000 practitioners were
significantly changed how it provided health care providing respiratory care in practice sites outside the
services to the poor and elderly. As fee-for-service hospital.17 Although this is a reasonable shift in
programs, Medicaid and Medicare were about to respiratory care priorities, to be fully successful,
respiratory care practitioners needed more complete can hold down health care costs in the long run
governmental recognition of the value of their services. without disrupting the quality of the services pro-
Over the past three decades, several bills have been vided. The issue is that, for many practitioners,
introduced in Congress that addresses the issues of managed care seems to place others between them
recognition and reimbursement for RTs who practice and the patients they serve. These others make the
outside of hospitals in skilled nursing facilities (SNFs), decisions about the type, length, and conditions of
in home care, and in subacute, intermediate, and acute the care to be provided. At least some of the medical
long-term care facilities. None of these bills has decision making seems to have been taken out of
successfully passed through the Congressional process, hands of the physician and given over to the clerks
but support appears to be gathering in both the House and accountants in the government and insurance
and the Senate. As a result of the 2008–2009 world- companies.
wide financial crisis it appeared that the then-current
initiative would be likely also to fail unless a compel-
ling case can be made for significant increases in the CRISIS IN CARE
quality of care and cost reductions associated with that The crisis in U.S. health care will not go away soon. At
care and RT reimbursement. In 2010 Congress passed a the beginning of the twenty-first century, the costs of
bill that provided RT reimbursement for BS-educated health care are too high and rising. Ways must be
RRTs. Although the bill passed and was enacted, the found to maintain quality, increase access, and control
rule-writing process by the administrative bodies is costs. Whether these changes occur as a result of
still ongoing. government intervention or market forces is an issue
that must be addressed.
The crisis will make for difficult times for respira-
The 1990s: A Maturing tory care providers, as well as for most health care
Profession practitioners and certainly for patients. Despite the
current practice dilemma, the respiratory care practi-
Cost control continues to be a major factor in how,
tioner must remain committed to providing the best of
when, and where respiratory care practitioners provide
care, in a system that is trying simultaneously to
services. The advent of managed care and case manage-
maintain provider and receiver choice and to contain
ment has greatly affected all facets of health care.
cost. The crisis is exacerbated by the fact that higher
Managed care is a system in which preventive services
survival rates and an aging population have resulted
and volume purchasing are emphasized in hopes of
from improved (and more expensive) technologies
providing quality care at lower costs. In the search for
and from heightened knowledge and understanding
less costly ways to provide care, however, both access to
of the disease process and treatment. At the same time,
care and the quality of it can suffer at times.
health manpower (the workforce) and monetary
resources have not kept pace with such improvements
MANAGED CARE in care.
The look of the future system is unclear, but its
Since the late 1990s, health care reform efforts have
requirements are not: It must contain costs without the
taken the form of managed care systems, which
loss of quality of care.
attempt to bring free-market restraint to spiraling
health care costs. Essentially, managed care is an
umbrella concept for plans that coordinate health Respiratory Care in the
care through primary care (generalist) physicians.
Managed care systems use a variety of approaches to Twenty-First Century
alter the practice behaviors of physicians and other Respiratory care enters the twenty-first century with
health care providers. The use of case managers to heightened professional maturity. Changes in the title
coordinate care, financial incentives to conserve of entry-level practitioners (individuals who complete
resources, and health care protocols to guide the the entry-level examination) reflect these changes.
delivery of care all seek to lower the expenditure of Certified Inhalation Therapist became Certified Inhala-
funds. Case managers review health care records and tion Therapy Technician (CITT) and then Certified
may deny payment for what they deem to be unneces- Respiratory Therapy Technician (CRTT). In recognition
sary services, and they seemingly ration certain of the increases in responsibility over the decades, the
services provided within the plan. National Board for Respiratory Care (NBRC) has
As a result, managed care activities have, in fact, recommended and approved that the name of the
lowered the rising costs of health care in the United credential be changed again to Certified Respiratory
States. However, it is unclear whether market forces Therapist (CRT). All respiratory care personnel are now
expected to have the knowledge and skills to perform a LICENSURE

common set of job duties, regardless of education level The mid-1980s to the late 1990s saw a surge of legisla-
or whether they are referred to as technicians or tive activity, with more than 40 states gaining licensure
therapists.18 for the practice of respiratory care. These licensure acts
The 2004 figures from the NBRC indicated that varied significantly in many ways, but they did not
172,113 professionals had received their CRT credentials restrict the growth of the profession or the scope of its
and that 88,384 had also qualified for the RRT creden- practice. While protecting the scope of respiratory care
tial since the inception of the credentialing process. practice, these laws allowed other health care profes-
AARC data for 2004 indicated a membership of sionals, with appropriate training, to perform some of
36,995, and 2005 reports indicate 47,000 plus mem- the duties of the licensed respiratory therapist. As
bers. The AARC’s 2010 membership report showed leaders in the field of respiratory care become more
51,343 as of December 2010. CoARC reported program adept at drafting, amending, and enforcing legislation,
enrollment of 6231 for the 2004 academic year with the strength of the profession should continue to grow.
3994 graduates in that year and an attrition rate of As of 2009, 48 states, Puerto Rico, and the District
35.9% and a 5-year attrition rate of 33–36%.19 of Columbia have established licensure or an other
form of legal credentialing. All of those jurisdictions
utilize the NBRC CRT (entry-level) examination as their
EDUCATION licensure requirement. Only Alaska and Hawaii have
To accommodate the need for a more broadly based not passed a legal credentialing act at the time of this
practitioner, the AARC and Joint Review Committee writing; although Hawaii has introduced legislation to
for Respiratory Therapy Education (JRCRTE) agreed do so.
to establish a new accrediting agency for respiratory
care educational programs, the Committee on SCOPE OF PRACTICE
Accreditation of Respiratory Care Programs
In 1991, the leadership of the profession undertook the
(CoARC). CoARC has proposed a new set of standards
task of providing a vision of the roles and responsibili-
for the education of practitioners, which requires a
ties of the practitioner in the twenty-first century. The
minimum of an associate’s degree in respiratory care
resultant document was titled “Respiratory Care
for entry-level practice.20
Practitioner 2001.”24 In addition to listing the clinical
Also, a movement in RT education circles is afoot
duties, required characteristics, attributes, nonclinical
to promote an increased education level to bachelor’s
duties, and practice settings (Table 1-4), the group
degree programs, and some programs are studying and
addressed the issues of medical direction and whether
implementing graduate degree (master’s) programs for
the future practitioner was to be a specialist or a
RTs. In a 2009 report, The Commission on Accredita-
generalist. Respiratory care scope of practice has been
tion of Allied Health Education Programs (CAAHEP)
legitimized through the licensure laws of most of the
lists 355 respiratory therapy education programs in the
states and other political bodies in the United States.
50 states.21 According to the AARC’s Coalition Bacca-
Each of these states or territories (plus Washington
laureate and Graduate Respiratory Therapy Education
D.C.) has included a scope of practice statement in its
(CoBgRTE), as of 2009, 54 of these were colleges and
legislation or regulation, making it a legal or regulatory
universities offering respiratory therapy programs
mandate. All of these bodies recognize and mandate
awarding baccalaureates (51) or master’s degrees (3)
that the NBRC Certified Respiratory Therapist creden-
with a major or concentration in respiratory therapy
tial is the minimum level of credentialing required to
(care). One of the master’s-level programs is an entry-
practice in their jurisdictions. None of these entities
level program requiring a previous bachelor’s degree
has enacted a restricted scope of practice, thereby
for admission.22
allowing the growth of the profession’s skills and
Additionally, on the education front, in 2004 the
practice. By the third quarter of 2010, the NBRC issued
AARC Board of Directors approved a document titled
11,677 new credentials and administered 29,119
“Standards for International Respiratory Care Educa-
examinations in seven areas:
tion,” which was developed in conjunction and
cooperation with the International Council for Respira- • CRT
tory Care (ICRC). This 21-page document sets forth • RRT Written
standards and evaluation criteria for three levels of • RRT, Clinical Simulations,
AARC recognition for educational programs based on • Pulmonary Function Technician (CPFT)
the quality and duration of the programs. This action • Pulmonary Function Technologist (RPFT)
recognizes the increasingly global interest in formal RT • Neonatal Pediatric Specialist (NPS)
education.23 • Sleep Disorders Specialist (SDS)
18
TABLE 1-4 Respiratory care practitioner 2001
Clinical Duties Characteristics Attributes Nonclinical Duties Care Settings

Be involved in direct patient care. Be a product of a multilevel Possess an ability to Participate in discharge Possess an ability to
educational system, with practice in all care settings. planning. render care across
Furnish monitoring for cardiopul-
entry level residing at the the entire health care
monary and other systems utilizing Have stamina, both physical Teach at both primary and
associate’s degree level and delivery spectrum,
sophisticated, high-tech devices. and mental. secondary levels within
advanced at the baccalaure- from critical care
the context of health care
Be positioned on the health care ate degree level. Possess a holistic caregiver’s on one extreme to
delivery.
delivery team in such a way as to perception. self-care in the home
Possess training and educa-
have the responsibility for refining Be responsible for on the other and all
tion in the following areas: Be compassionate.
broad or general physicians’ preventive medicine and points in between,
orders within the parameters of Critical thinking skills Have an ability to move wellness interventions. such as transitional
predesigned protocols. back and forth from high care settings, skilled
Liberal arts Expand involvement within
tech to high touch. nursing facilities, and
Administer medications via aero- the infrastructure of the
Basic sciences all outpatient venues.
sol, parenteral, IV, and IM routes Be an innovator and a health care delivery system.
of delivery. Communication skills creator.
Possess a leadership role in
Educate other caregivers, patients, Affective skills Be efficient and effective. allied health so as to bring
and family caregivers on methods (dependability) about change in health care
Be able to respond to
of self-administration and other Computer science change as well as to be a practices and health care
related subjects such as wellness change agent. policy.
and equipment maintenance. Have awareness of one’s
environment and an ability Possess skills as a Expand role in each organi-
Assess patients and their progress to be flexible and adaptable. negotiator. zation’s quality improvement
as it relates to the overall care process and data collection
plan. Possess human relations Act as a mentor. in order to improve resource
skills in order to work as accounting and document
Render clinical interventions Remain professionally
part of a team. efficiency and effectiveness.
over and above the traditional dynamic as manifested by
scope of practice, including Be a licensed professional. a commitment to being a Expand managerial skill
clinical interventions that rely lifelong student. base.
on a qualified patient evaluator, Be compensated com- Enlarge role in research.
competence with high-tech mensurate with skill level,
equipment, and interventions, responsibility, and authority. Possess an in-depth
both therapeutic and diagnostic, familiarity with other
Refuse to be a captive of allied health procedures and
that could readily be mastered
paradigms and be willing to interventions.
by qualified respiratory care
create new ones as needed.
practitioners.
Possess an awareness of
Perform invasive diagnostic and
cultural sensitivity and
monitoring procedures.
diversity.
From American Association for Respiratory Care. Proceedings of a National Consensus Conference on Respiratory Care Education. Dallas, Tx: American Association for Respiratory Care; 1992.
The NBRC has issued over 350,000 professional • The American College of Chest Physicians
credentials to more than 209,000 individuals since its (ACCP) has opened its active and associate
beginning in 1960. membership rolls to respiratory therapists.
Additionally, several respiratory therapists have
been elected as fellows of the college (FCCP).
SPECIALTY PRACTICE AND CREDENTIALS
This election represents recognition as an
One conclusion of the group was that the historically exemplary clinician, teacher, and/or researcher in
solid bond between respiratory care and its physician the area of chest medicine.
supporters has been an integral component of the • As of 2007, the Society of Critical Care Medicine
profession’s past successes and is the framework in (SCCM) has welcomed 172 RTs into membership
which the scope of practice should expand. Further- and inducted 21 RTs into its fellowship program
more, the group agreed that the field needs both (FCCM). With more than 14,000 member, SCCM
generalists and specialists. Generalists are felt to be is an international, multidisciplinary, multi-pro-
necessary as the specialty continues to move into fessional organization dedicated to the advance-
alternative practice settings. ment of critical care through excellence in patient
The development and implementation in 2002 of care, education, research, and advocacy. This
the Asthma Educator Certification (AE-C) course, organization includes physicians, nurses, RTs,
jointly sponsored with AARC, has opened another path pharmacists, physician’s assistants, architects, and
for professional growth and recognition. Successful veterinarians as well as research scientists. RTs
completion of the 12.5-hour course and its final exam have served at the highest levels of this organiza-
results in certification as a Certified Asthma Educator tion and as chairs of major committees.
(AE-C). • The 50,000 plus members in the AARC represent
Clearly, respiratory care practitioners will need to about 30% of the RT population. The National
increase their level of educational requirements to Board for Respiratory Care (NBRC) is the
practice effectively as members of multidisciplinary credentialing body for respiratory care profes-
teams and to assume the expanded roles demanded by sionals. The NBRC offers credentialing exams for
current health care practice. If the graduate is to be able the entry-level Certified Respiratory Therapist
to survive and to work collaboratively on the health (CRT) and advanced practice Registered Respira-
care team, curricula will need to focus on multiskilling tory Therapist (RRT) level. Additional credentials
and on a systems approach to the organization and include the Neonatal-Pediatric Specialist (NPS).
delivery of health care. Critical thinking, problem NBRC has issued over 180,000 credentials to
solving, oral and written communication skills, and more than 198,000 individuals and currently
skills in interpersonal relations and information tests nearly 18,000 candidates every year. In
technology will all be needed by the respiratory care 2009, a new Sleep Disorders Specialty (SDS)
practitioner of the twenty-first century. RTs can no exam was developed and released. In the last
longer afford to be the practitioners who work with the several years, preliminary planning and data
most critical patients while having the least formal gathering were done to examine the feasibility
education. of developing a similar credentialing exam in
Critical Respiratory Care, which will be given
Professional Recognition for the first time in mid-2012.
• Rapid Response Team (RRT) (also known as
Over the last decade, recognition by peers, colleagues,
Medical Emergency Teams [METs]) and Critical
and the government has done much to elevate the
Care Outreach Teams (CCOT) were developed to
professional status of respiratory care as a true profes-
“. . . . rapidly identify and manage seriously ill
sion. Consider the following examples:
patients at risk of cardiopulmonary arrest and
• In 1998, the AARC established a professional other high risk conditions.”25 The adoption of the
recognition program. The purpose is to recog- Rapid Response Team (RRT) concept in the United
nize RTs who have distinguished themselves in States in mid-2000 opened new doors for respira-
the professional practice of respiratory therapy. tory therapists. First developed in the 1990s in
From 1998 to 2006, 178 individuals have been Australia and the United Kingdom, the systems
inducted as fellows of the AARC (FAARC). These have reported success in reducing deaths, ICU
individuals are RTs, physicians, clinicians, stays, overall hospital stays, and all of the costs
educators, medical directors, and researchers associated with prolonged hospital and ICU stays.
from the United States and several other Their success made it easy for many U.S. hospitals
countries. to implement the system, even though debate is
ongoing as to whether the RRT system has all the Uniformed Branch of the U.S. government.
benefits that its supporters claim. The majority of Officers in the USPHS are also awarded reserve
papers and news articles published on the subject commissions in the United States Navy. To be
include the respiratory therapist as a member of granted commissioned status, therapists must be
this three- or four-person team. Their inclusion in Registered Respiratory Therapists and hold a BS
the system is recognition of RTs’ specialized degree or higher, among other qualifications.28
assessment skills and ability to rapidly apply
appropriate emergency interventions and stabiliza-
tion techniques and technology for fragile Summary
patients. RTs as a profession have thus enjoyed
Respiratory care practice is an emerging profession, but
excellent publicity and public exposure as valued
its roots extend back thousands of years to the works of
and vital members of the health care team.
Hippocrates, Aristotle, and Galen. Not until the 1600s
• The Joint Commission (formerly the Joint
did the role of oxygen begin to be understood. William
Commission on Health Care Organizations
Harvey demonstrated blood circulation. Robert Boyle
[JCAHO], the body that inspects and accredits
elucidated the volume and pressure relationships of
hospitals, long-term care facilities, and home
gases. Joseph Priestley experimentally produced
care organizations) has appointed six RTs to
oxygen. In the 1700s, Antoine Lavoisier gave oxygen its
serve on their Professional Technical Advisory
name and correctly described the basic physiology of
Committees (PTACs). These therapists serve on
respiration. Thomas Beddoes established the Pneu-
the home care, laboratory services, and the
matic Institute of Bristol, England, and was the first to
ambulatory care PTACs. The PTAC’s function is
use oxygen therapeutically. Growth of the field of
to advise, propose, and consult with the rule-
respiratory care burgeoned in the twentieth cen-
making bodies in the Joint Commission. Several
tury with rapid advancements in science and technol-
other RTs serve the Joint Commission as site
ogy, many of which resulted from research in World
visitors and inspectors for The Joint Commission
Wars I and II.
accreditation process.
Over the years, the role of persons who delivered
• In response to natural disasters, the federal
oxygen therapy changed from mere equipment techni-
government has enlisted the assistance of RTs to
cians (oxygen orderlies) to fully accredited allied health
provide short-term respiratory care procedures as
care providers. A national professional organization
part of the Emergency Mass Critical Care (EMCC)
developed a set of standards for requirements, educa-
initiative during the disaster period. A supple-
tion, and scope of practice.
ment to Chest details this program.26 Respiratory
Implementation of evidence-based practices and
Therapists act as part of a DMAT (Disaster
the refinement of protocol-based care methods will,
Medical Action Team). DMAT is defined as:
without a doubt, continue to expand the scope of
a group of professional and para-profes- practice. They will lead to the advancement of the
sional medical personnel (supported by a respiratory care practitioner’s ability to provide timely
cadre of logistical and administrative staff) and efficacious patient care with reduced morbidity
designed to provide medical care during a and mortality. They will also enhance the potential for
disaster or other event. NDMS recruits developing effective multidisciplinary care teams.
personnel for specific vacancies, plans for Future health care reform in the United States will
training opportunities, and coordinates the pose many challenges to the field of respiratory care as
deployment of the team. To supplement the the government attempts to contain rising prices while
standard DMATs, there are highly specialized preserving and increasing access for citizens. The
DMATs that deal with specific medical leadership of the specialty will need to be especially
conditions such as crushing injuries, burn, nimble in negotiating each of the legislative changes
and mental health emergencies.27 that affect practice sites.
The federal officials responsible for this
project specifically requested RTs as DMAT
members.
Study Questions
• A long-awaited change in federal policy has SHORT ANSWER
resulted in the approval to award officer status in 1. Of the three individuals associated with the
the U.S. Public Health Service (USPHS). The discovery of oxygen (Priestley, Scheele, and
USPHS is a part of the U.S. Department of Lavoisier), to whom would you give the credit for
Health and Human Services and is the 5th the discovery of oxygen? Explain your answer.
2. Briefly state the purpose and effect of the Sugarloaf 6. Which of the following pre–twentieth century
Conference. developments in science was the most important
3. What are some reasons for the close relationship for the modern allied health profession of
between physician groups and respiratory care respiratory care?
specialists? a. the development of the germ theory of
disease
4. It has been said that the lessons of war speed the
b. the study of cardiopulmonary anatomy by
development of medicine. Why is that?
Vesalius
c. the development of the dephlogistication
MULTIPLE-CHOICE QUESTIONS theory of respiration
d. the discovery and publication of the
1. Which of the following is true? gas laws
a. Much of the success of respiratory care is due to
7. The first organized clinical use of oxygen as a
its close relationship with physician supporters.
therapeutic gas was carried out by
b. Respiratory care ranks on par with nursing in
a. Thomas Beddoes.
terms of professional status.
b. Joseph Priestley.
c. The length of education or training is not an
c. Robert Boyle.
issue in obtaining professional status.
d. Galen.
d. Respiratory care can trace its roots to the
mid-1960s. 8. Which of the following is the correct chronological
sequence of the establishment of the listed
2. Which of the following entities deals with
agencies?
professional credentialing?
a. AARC, CoARC, NBRT
a. American Association for Respiratory Care (AARC)
b. JRCRTE, NBRT, AARC
b. Committee on Accreditation of Respiratory
c. AARC, CoARC, JRCRTE
Care (COARC)
d. AARC, NBRT, CoARC
c. State Boards of Healing Arts Regulation
(SBHAR) 9. Which of the following would appear to produce a
d. National Board for Respiratory Care (NBRC) cost-effective care model?
I. Evidence-based practice
3. Which are the major challenges that face the
II. Integrated care teams
profession in the twenty-first century?
III. Respiratory protocols
I. Determining the appropriate level of education
IV. Function-based care
II. Gaining government recognition
a. I, II, IV
III. Gaining recognition as an independent primary
b. II and IV only
care provider
c. I, II, III
IV. Determining the need for two levels of practi-
d. All of them
tioner professional credentialing
V. Delineating a standard scope of practice
a. I, II, III only CRITICAL-THINKING QUESTIONS
b. I, III, IV only
c. I, II, IV, V 1. How has respiratory care addressed the
d. All of the above extended education requirement for professional
status?
4. State licensure laws for the practice of respiratory care:
a. are unified, with the same requirements and 2. Only about 30% of respiratory therapists
scope of practice. belong to a professional organization. What
b. are in effect in all U.S. states and territories. can be done to increase the number of active
c. generally restrict areas of practice and skills. members?
d. allow nonrespiratory therapists to practice 3. How can the profession gain the level of
some respiratory therapist tasks. governmental recognition needed to ensure
5. From an organizational perspective, respiratory its place in the new collaborative health care
care had its beginnings team?
a. in New York City in 1930. 4. What is the value of aligning the profession with
b. in Chicago in 1947. other groups such as the Society for Critical Care
c. in San Francisco in 1963. Medicine and the American College of Chest
d. in Washington, D.C., in 1999 Physicians?
References 20. COARC lives! . . . accreditation for respiratory

care . . . questions about respiratory care program
1. Byrne P. Analysis and Science in Aristotle. New York: accreditation. AARC-Times. February 22, 1998;22–25.
State University of New York Press; 1917. 21. Respiratory therapy programs search. Commission
2. Brock A. Greek Medicine, Being Extracts Illustrative of on the Accreditation of Allied Health Education
Medical Writing from Hippocrates to Galen. New Programs (CAÁHEP). http://www.caahep.org.
York: Library of Greek Thought; 1976. 22. Barnes T, Beachy W, Black C. 2008 Roster: Respira-
3. Zhou C, Han Y. The Illustrated Yellow Emperor’s tory therapy programs awarding a baccalaureate or
Canon of Medicine. Beijing, PRC: Dolphin Books; masters degree. American Association for Respira-
1995. tory Care. 2009. www.aarc.org/education/
4. Bowman I. Historical Vignettes Brochure for John P. accredited_programs/bsrt_msrt_roster.pdf
McGovern Hall of Medical History. Galveston, TX: 23. Recognition guidelines for quality international
University of Texas; 1986. respiratory care education. International Education
5. Burton G, Gee G, Hodgkin J. Respiratory Care. Phila- Recognition System. http://www.aarc.org/iers/6/
delphia: JB Lippincott; 1977. index.cfm.
6. Hillar M. The Case of Michael Servetus. Lewiston, 24. American Association for Respiratory Care. Proceed-
NY: E. Mellen; 1997. ings of a National Consensus Conference on Respiratory
7. Yount L. William Harvey. Discoverer of How Blood Care Education. Dallas TX: American Association for
Circulates. Berkley Heights, NJ: Enslow Publishers; Respiratory Care; 1992.
1994. 25. King E, Horvath R, Shulkin DJ. Rapid response
8. Kaplan B. “Divulging of Useful Truths in Physick”: The teams: a bridge over troubled waters. White paper.
Medical Agenda of Robert Boyle. Baltimore, MD: Irving, TX: Voluntary Hospitals of America; 2007.
Johns Hopkins University Press; 1930. https://www.vha.com/Solutions/ClinicalImprovement/
9. Priestley J. As quoted in Levine, Edwin, eds., Pages/RapidResponseTeams.aspx
Effective Inhalation Therapy. Chicago: National 26. Definitive care for the critically ill during a disaster:
Cylinder Gas; 1953. from a task force for Mass Critical Care Summit
10. Eubanks D, Bone R. Comprehensive Respiratory Care. Meeting, January 26–27, 2007 Chest. Supp.
St. Louis: Mosby; 1990. May 2008;133,5:66.
11. Porter R. Doctor of Society; Thomas Beddoes and the 27. Public Health Emergency. http://www.hhs.gov/
Sick Trade in Late Enlightenment England. Atlanta: aspr/opeo/ndms/teams/dmat.html.
Rodopi Publishers; 1992. 28. Questions and answers regarding PHS service for
12. Personal communication CoARC and Paul RTs. http://www.aarc.org/headlines/07/11/phs/
Mathews, January 2011. siegal.cfm
13. Motley H, et al. Observations on the use of positive
pressure. J Avia Med. 1947;18:417.
14. Smith G. Evolution of a Profession. Lenexa, KA: Suggested Readings
Applied Measurement Professionals; 1989. Annas G, et al. The Rights of Doctors, Nurses and Allied
15. Conference on the scientific basis of respiratory Health Professionals. Cambridge, MA: Ballinger; 1981.
therapy: final report, summaries and recommenda- Eicher J. State overview. Pew Commission releases new
tions. Am Rev of Respir Dis. 1985;110:4–15. report on professional regulation. AARC Times.
16. Edge R, Krieger J. Legal and Ethical Perspectives in December 1998:22:12–13.
Health Care. Clifton Park, NY: Delmar Cengage Final draft report of the Advisory Panel for Allied
Learning; 1998. Health to the Pew Health Professions Commission.
17. Dunne PJ. Respiratory care for the homebound J Allied Health. 1992;21:1–74.
patient. Respir Care. 1997;42:133–140. Healthy America: Practitioners for 2005, an Agenda for
18. Ross B. NBRC approves new entry level credential Action for U.S. Health Professional Schools. San
designation. NBRC Bulletin. June 5, 1998. Francisco: Pew Health Prof Commission; 1991.
19. Mathews PJ, Drumheller L, Carlow JJ. Respiratory Van-Scoder LI, Johnson JC, Nyhuis AW. Frequency with
care manpower issues in Interface of Public Policy which staff respiratory therapists perform selected
and Critical Care Medicine; Model and Workforce. entry-level tasks. Respir Care Educ Annu. 2000;
Critical Care Medicine. Supp. March 2006;34,3: 9:3–17.
S32–S45.
CHAPTER 2
Legal, Professional, and Ethical Practice

Raymond S. Edge
OBJECTIVES
• Define the principle of stare decisis and state the benefits derived from it.
• List the major elements found in a practice act.
• Define the legal term tort and list the elements of a tort.
• Differentiate between libel and slander.
• Differentiate between intentional torts and negligent torts.
• Differentiate between morals and ethics.
• Identify the basic principles involved in health care ethics.
• List the legal requirements for breaking patient confidentiality.
• List the legal requirements found in HIPAA as it relates to patient access to medical records.
• Explain how the principle of informed consent is derived from the principles of autonomy and veracity.
• Differentiate among compensatory, procedural, and distributive justice.
• Differentiate between duty, consequence, divine command, and virtue as bases of ethical reasoning and list
the major criticisms of each.
• Solve an ethical dilemma using the following decision-making formats: utilitarianism, Kantian, virtue, and
divine command.
CHAPTER OUTLINE
Defining a Profession The Civil Lawsuit
Professional Obligations Initiating the Suit
Legal Aspects of Respiratory Care Practice Discovery
The Foundations of U.S. Law The Trial Process
Common Law The Appeal
Statutory Law Arbitration
Administrative Law
Private Law
(continues)
23
(continued)
The Duty of Ethical Practice Basic Decision-Making Models

Basic Principles of Health Care Ethics Consequence-Oriented Theories
Respect for Persons Duty-Oriented Theories
Beneficence Virtue Ethics
Nonmaleficence Divine Command Theory
Justice The Decision-Making Process
Role Duty Some Practical Advice
KEY TERMS
administrative law false imprisonment normative elements
assault felony plaintiff
autonomy harm principle practice acts
battery Health Insurance Portability private law
beneficence and Accountability Act respondeat superior
case law (HIPAA) role duty
common law informed consent slander
confidentiality interrogatory stare decisis
constitutional law invasion of privacy statutory law
defamation justice summary judgment
defendant liability tort
discovery libel utilitarianism
divine command ethics misdemeanor veracity
divine command theory morals virtue ethics
double effect negligence
ethics nonmaleficence
T
exts such as The Foundations of Respiratory Defining a Profession
Care are designed to assist individuals in
the process of enculturation into the One of the definitional elements of all professions is
profession. The practice of respiratory care that they are self-regulating. Professions provide
goes beyond the study of applied sciences, essential guidance for their members in regard to a set of norms
therapeutics, and technical competence. Important of behavior that go beyond technical or clinical
normative elements of professional conduct are expertise and are part of the ideology of the group. An
found in rules of professional etiquette, legal important element of professional self-regulation is the
requirements, and ethical codes. Members of the creation of a professional code of ethics and profes-
respiratory care profession are expected to accept a sional conduct. Figure 2-1 provides the current AARC
shared set of ideals, values, and standards of behav- Statement of Ethics and Professional Conduct. These
ior and practice. This chapter is intended to assist the normative prescriptions are intended to reflect and
practitioner in: promote the values and aspirations of the group.
Rules of professional etiquette are generally based
• Understanding the legal and ethical environ- on traditions of good practice and good manners. Rules
ments of health care. of professional etiquette are standards of behavior that
• Making appropriate legal and ethical choices in are socially approved but not generally ethically or
practice.
CHAPTER 2 ■ Legal, Professional, and Ethical Practice 25
AARC Statement of Ethics and Professional Conduct

In the conduct of professional activities the Respiratory Therapist shall be bound by the following ethical and
professional principles. Respiratory Therapists shall:
• Demonstrate behavior that reflects integrity, supports objectivity, and fosters trust in the profession and its
professionals. Actively maintain and continually improve their professional competence and represent it accurately
• Perform only those procedures or functions in which they are individually competent and which are within their
scope of accepted and responsible practice
• Respect and protect the legal and personal rights of patients they treat, including the right to privacy, informed
consent and refusal of treatment
• Divulge no protected information regarding any patient or family unless disclosure is required for responsible
performance of duty, or required by law
• Provide care without discrimination on any basis, with respect for the rights and dignity of all individuals
• Promote disease prevention and wellness
• Refuse to participate in illegal or unethical acts
• Refuse to conceal, and will report, the illegal, unethical, fraudulent, or incompetent acts of others
• Follow sound scientific procedures and ethical principles in research
• Comply with state or federal laws which govern and relate to their practice
• Avoid any form of conduct that is fraudulent or creates a conflict of interest, and shall follow the principles of
ethical business behavior
• Promote health care delivery through improvement of the access, efficacy, and cost of patient care
• Encourage and promote appropriate stewardship of resources.
Effective 12/94
Revised 12/07
FIGURE 2-1 American Association for Respiratory Care Statement of Ethics and Professional Conduct.
Courtesy of American Association for Respiratory Care, Irving Texas
morally significant. These rules help the specialty Legal requirements can be considered to be the mini-
maintain order and civility and create an environment mal standard of expected behavior. To ensure that
that promotes professional conduct and practice. They practitioners abide by this lowest standard of behavior,
often involve matters such as respect for persons, such many professional codes of ethics contain rules that
as the need to avoid talking ill about other members of require the practitioner to stay within the law in their
the health care team. Most often the new practitioner is professional conduct. The following statement from
mentored into an understanding of the etiquette the AARC Statement of Ethics and Professional Con-
requirements of the health care environment. These duct speaks to the need for practitioners to be law
rules of social behavior are often not formally written abiding in their practice. According to the AARC
and, when broken, do not generally evoke the same statement a practitioner shall:
level of negative response to infractions as do legal or
Refuse to participate in illegal or unethical acts,
ethical lapses. However, a practitioner who continues
and shall refuse to conceal illegal, unethical or
to break the rules of professional etiquette can face seri-
incompetent acts of others.
ous consequences, not the least of which is that one is
considered boorish by ones colleagues and, when Ethical standards and legal requirements are
possible, avoided. usually closely related, with our ethical obligations
Legal requirements are the formal body of rules or typically exceeding our legal duties. If a situation occurs
principles enacted and backed by the power of the where a practitioner believes a legal requirement is
state. Therapists can think of legal requirements as unjust or unethical, there is an obligation to work
being a set of principles and rules that command us or within the system to change the law or remove oneself
restrain us from doing or not doing certain things. from the process.
Like rules of professional etiquette, the rules of TABLE 2-1 Common legal and ethical issues
ethics are also designed to promote order and civility.
However, professional ethics generally doesn’t deal Common Legal Issues Common Ethical Issues
with something considered to be bad manners; profes- Falsification of Indiscriminate and
sional ethics deals with the rights and welfare of credentials unnecessary use of
another person. As a result, the sanctions for ethical resources
failure are more severe than for matters of etiquette. It False or incomplete Failure to protect patient
should be noted that a single act could have conse- patient records confidentiality
quences that involve an individual’s ethical, legal, and Performing duties Failure to report incom-
etiquette standing in the profession. beyond scope of petent, unethical, or
Appropriate ethical, legal, and etiquette behaviors practice illegal activities of
are necessary components of practice for every health colleagues
care provider. In their daily activities, respiratory
Performing nonpre- Failure to provide equal
therapists (RTs) serve clients and patients whose
scribed services care to all
condition has placed them in a position of high need
and vulnerability. As a result of their trust, RTs have Practicing under the Issues involving patient
available a great deal of personal and confidential influence of alcohol, advocacy (e.g., inade-
information. They are entrusted with expensive instru- drugs, or narcotics quate staffing for patient
ments, have access to controlled substances, and safety)
perform duties that are essential to patients’ health and Conflicts of interest Use of inappropriate
well-being. Their patients and clients come to them for research procedures
their clinical skills and for their commitment to Failing to practice at an Issues involving the dying
professional standards. It is a special relationship appropriate standard patient (e.g., DNR orders,
where all patients or clients have the right to expect advanced directives,
compassionate and competent care of the highest organ donations)
quality, indeed the very best RTs have to offer.
Our decisions involving professional etiquette,
ethical conduct, and legal matters have real conse-
quences for our patients, ourselves, our profession, and of agreement among the health care team. In the areas
the community at large. of professionalism, legal practice, and ethical conduct
there is often less consensus, often no clear right answer,
and yet, wrong decisions can be devastating to the
Professional Obligations patients, the reputation of the profession, and personal
To enter into the practice of respiratory care is to enter careers. Although the professional, legal, and ethical
into a social agreement not only with the patients arena in which respiratory therapists (RTs) practice
being served but also with the greater community at abounds with problems that have no clear right answer,
large and with all other health care providers. This there are clearly wrong decisions that must never be
social agreement will require a high level of personal made. Table 2-1 lists common legal and ethical issues
commitment to excellence of practice, continuing that often confront the respiratory therapist.
education and lifelong learning, and the acceptance of To avoid the legal and ethical pitfalls of profes-
a set of appropriate moral, legal, and social behaviors. sional life, one must have some understanding of the
Often the answers to the important questions that basics of law and ethical conduct as they relate to our
face respiratory care practitioners are the product of practice. For most of us, information regarding how to
evaluating, understanding, and utilizing scientific avoid legal, ethical, and professional pitfalls will be at
information. Most practitioners see their clinical least as important as having liability (malpractice)
competence as the measure of their professional insurance.
competence. It is these clinical competency skills that The ability to reason to a right ethical or legal
are judged in the teaching laboratories and clinical decision is a real strength for a practitioner. As health
portions of our educational programs. Although care professionals, RTs are responsible to their col-
respiratory care education programs make reference to leagues for appropriate professional conduct and
ethical, professional, and legal behaviors as being etiquette and for the maintenance of lawful and ethical
important to practice, unless a student strays far from standards. Table 2-2 compares the sanctions imposed
the path, grades are primarily given on the basis of for inappropriate legal, ethical, and professional
perceived clinical knowledge and skills quickness. Yet, behavior. As can be seen, the adoption of illegal,
when they enter practice, the clinical questions are often unethical, or unprofessional behavior is no small
the easy area, the area in which there is the highest level matter and can end a career.
TABLE 2-2 Comparison of sanctions for The U.S. system of law was generally derived from
illegal, unethical, and unprofessional that of Great Britain. Common elements of law that
have come to us from the English system are the
behavior concept of trial by jury, the use of grand juries, the
Area Judgment Sanctions appellate review of lower court decisions, and a
professional judiciary.
Legal Legal or Loss of professional
The basic sources of modern law are common law,
illegal reputation, loss of
which emanates from judicial decisions; statutory law,
professional affiliations,
which arises from legislative bodies; and administrative
punishments determined
law, which flows from the rules, regulations, and
under law
decisions of administrative agencies.
Ethics Right or Loss of professional
wrong reputation, loss of
professional affiliations,
COMMON LAW
personal remorse
Common law, as distinguished from law created by
Professional Proper or Professional
the enactment of legislatures, derives its authority
etiquette improper condemnation
solely from usages and customs. The source of com-
mon law is primarily case law (law resulting from
judicial interpretation of statutes). The set of common
principles entailed in common law has evolved from
Legal Aspects of Respiratory the practices of the past and continues to evolve and
expand from judicial decisions that arise from court
Care Practice cases. These decisions are often based on long-term
This chapter’s discussion of the legal aspects of the custom or are guided by ethical principles such as
profession is not an attempt to provide all the neces- fairness. One example of how the law changes over
sary information that the respiratory therapist may time can be seen in modern cases involving victims’
need to know. It is certainly not intended to provide rights and restitution, in which fines collected are paid
legal advice. Many activities of practice require legal to the victim rather than retained by a government
knowledge, and it is hoped that the basic knowledge agency, as they once were.
provided here will help the practitioner avoid perform- Common law represents the gradual accumulation
ing illegal acts. of decisions. Cases arise out of disputes between
Perhaps the most fundamental principle of law is a individuals and, in adjudicating these cases, the judge
concern for justice and fairness. An important second- examines earlier cases involving similar problems and
ary principle is plasticity and change. Although the law circumstances to discover general principles that can
appears to be a complete and solid structure from the be applied to the case at hand. This process has given
outside, it is a shifting process that reacts to its environ- rise to the principle of stare decisis, which translated
ment. The third principle is that acts are judged on the means “let the decision stand.” The use of the prin-
universal standard of the reasonable person. What ciple stare decisis has provided the system with needed
would a similarly trained, reasonable, and prudent stability and yet has allowed for the creation of
person have done in the particular situation? The new principles as new or changing patterns of facts
doctrine of personal responsibility is fundamental to have emerged. In addition to classification by source,
the rule of law. Every practitioner is liable for his or her the law has been classified as being either public
own actions. or private.
The Foundations of U.S. Law STATUTORY LAW

Under our federal constitution and the various state
We can think of laws as a set of principles and pro- constitutions, legislative bodies are given the power to
cesses by which people in a society seek to settle enact laws to govern the people. The U.S. Constitution
disputes and problems without resorting to force or is the supreme law of the land.
violence. In some sense, law can be considered the
minimum standard of expected performance by • Constitutional law deals with the organization,
individuals in a society. Laws can be thought of as granted powers, and framework of government
general rules of conduct whose compliance is enforced and sets limits on what the federal and state
by government-imposed penalties. governments may do.
• Statutory law consists of the rules and regula- correction. Examples of common misdemeanors
tions (statutes) set down in printed form by a are the theft of small amounts of money,
legislative branch of the government. Congress disorderly conduct, and breaking into an
establishes federal statutes, whereas state statutes automobile.
are established by the various state legislatures. • A felony is the far more serious breach of law
Examples of statutory law at the federal level and is punishable by death or imprisonment in
include the creation of such agencies as the a state or federal penitentiary.
Centers for Disease Control and Prevention, the
Legislatures enact laws that determine whether an act is
Social Security Administration, and the National
a crime and whether it will be considered a felony or a
Institutes of Health. Examples of important state
misdemeanor. Examples of felonies are fraud and
statutes that affect the provision of health care
forgery. Some activities, such as murder, rape, sodomy,
include health providers practice acts, Good
larceny, manslaughter, burglary, robbery, and arson
Samaritan laws, and child abuse laws.
have been determined by common law to be felonies.
Sometimes practitioners engage in illegal activities
Practice Acts. Respiratory care practice acts are
that have criminal penalties, such as falsifying their
examples of statutory law that seek to regulate the
application when applying for a state license to practice
practice of respiratory care. Practice acts will vary in
or placing false information on the medical record. All
emphasis, but the majority will address the following
practitioners have a legal and ethical obligation to
elements:
protect themselves and others in the professions. The
• Scope of professional practice general thrust of public law, in all of its forms, is to
• Exemptions assist the society in attaining its public goals.
• Grounds for administrative action
• Creation of an examination board and processes
ADMINISTRATIVE LAW
• Penalties for unauthorized practice
Administrative law is the body of rules and regula-
A board or council usually is designated to tions promulgated by administrative agencies of the
administer and enforce the statute that created the federal government and state governments. Medicare,
practice act.1 Medicaid, and OSHA, for example, are created by
statutory law, but their rules and regulations are
Criminal Law. Criminal law is an important aspect of examples of administrative law. Violation of a regula-
statutory law. It defines and prohibits conduct deemed tion generally carries with it the imposition of a
injurious to public order and safety and provides for penalty in the form of restricting or restraining the
punishment of persons found to have engaged in professional’s right to practice. As an example, a clinic
criminal practices. In general this includes the defini- that fails to comply with Medicare or Medicaid regula-
tion of specific offenses and general principles of tions may lose the right to claim compensation from
liability (a responsibility or an obligation). these programs for services provided. A more relevant
Crimes are divided by their seriousness and level of example for RTs is the failure of the therapist to earn
punishment. the minimum number of required continuing educa-
• A misdemeanor is a crime punishable by less tion units (CEUs) over the licensing period. This lapse
than a year’s incarceration in jail or house of breaks the RT-administrated regulations and may result
in suspension or revocation of the individual’s license
and perhaps right to work as an RT.
Spotlight
On
PRIVATE LAW
Licensure Private law, or civil law, deals with definition, regula-
As of January 2011 49 states have adopted tion, and enforcement of rights in cases between citizen
licensure or other legal requirements for the and citizen or between citizens and organizations. Two
practice of respiratory therapy in their jurisdic- basic types of private law are torts and contract law.
tions. Only Alaska has not passed a law regulat-
ing respiratory therapy practice. In addition to Torts. A tort is a legally defined wrong committed
the 49 states, the District of Columbia and the upon a person or property independent of contract that
U.S. territory of Puerto Rico have established renders the individual who commits it liable for
regulations governing these practices. damages in a civil action. Torts are the violation of
some private duty by which damages accrue to the
defective medical products. Tort law is often used by

CASE STUDY 2-1 the courts to influence the behavior of companies and
to encourage them to behave responsibly. As an
An intensive care nurse who was planning to example, if a medical product harms an individual and
move to North Carolina had a stroke and died the customer sues the manufacturer, the company is
before she could make all the arrangements. likely to provide additional instructions and warning
A respiratory therapist who had worked with the labels on the products in the future. Common forms of
nurse discovered the paperwork that she had intentional torts that have implications for respiratory
planned to send to the North Carolina Board of therapists are:
Nursing. In that the paperwork was complete, the • Assault and battery.
therapist forwarded the materials to North • Defamation of character.
Carolina, resigned from the respiratory therapist • False imprisonment.
position, and moved, assuming the name and • Invasion of privacy.
credentials of the nurse.
Unfortunately the preparation of a nurse is Common Forms of Intentional Torts Assault and
very different from that of a respiratory therapist, battery are tantamount to tort action, giving rise to
and the therapist soon had numerous incidents civil liability, but they also may be considered, under
of incompetence on her records in North Caro- certain circumstances, criminal activity. Assault is
lina. These records eventually aroused suspicion defined as the unjustifiable attempt to touch another
that this person was not what she said she was. person or threat to inflict injury on another, coupled
Her supervisor called the hospital from which the with an apparent present ability to inflict such injury.
new “registered nurse” had come. During the Battery is the intentional touching of another person
conversation, the supervisor discovered that the without that person’s consent. Harmful or offensive
nurse in question had recently died. touching or contact by another person is the essence
Questions of battery. It would be a rare instance in which the
respiratory therapist was involved in an assault; battery
1. Who bears responsibility for the risks to is a more common offense. Any unnecessary mishandl-
patients due to the respiratory therapist ing of the patient during a treatment may amount
being employed as a nurse? to a battery.
2. What actions should be taken by the state Defamation is an injury to a person’s reputation
board of respiratory care? or character caused by false statements made by
3. What message does this case send to another to a third party. Defamation includes both
employers? libel and slander. Libel involves false or malicious
writing that is intended to defame or dishonor
another. The libel must be published in such a way
that someone else other than the one defamed will
individual and for which the courts will provide a observe it. Along with written statements, libel can
remedy in the form of an action for damage. The legal also be presented in signs, cartoons, photographs,
wrong committed upon the person may be a direct e-mails, and so on. Slander is the spoken form of
invasion of some legal right of the individual, the defamation. It is defined as false oral statements that
infraction of some public duty by which special injure the character or reputation of another and
damages accrue to the individual, or the violation of that are made in the presence of a third person.
some private obligation by which the damages accrue Defamatory statements communicated only to the
to the individual. injured party and to no one else, while potentially
Every tort action has three basic elements: hurtful, are not grounds for action. As practitioners,
therapists must always be especially cautious
• A legal duty owing from defendant to plaintiff
about comments made about other members of
• A breach of that duty
the health care team, as hasty, and inappropriate
• Damages that are a proximate result of the
actions or comments may subject us to a defamation
breach of duty
action.
Torts are usually classified into three broad catego- Normally for a case of slander or libel to be
ries: intentional torts, negligent torts, and torts in actionable, injury must result. However, there are four
which the liability is assessed irrespective of fault (strict classes of exceptions in which the courts have held
liability), such as claims against the manufacturers of that no proof of actual injury is required to recover
damages:2 When statements fall in these categories, the unwarranted and brought mental suffering, shame, or
law presumes that damages will result and they need humiliation, then there would be grounds for action
not be proven: on invasion of privacy. Tort actions involving invasion
of privacy issues generally involve one or more of four
• Accusing someone of a serious crime.
classes:3
• Using words that tend to injure another in his or
her trade, business, or profession. • Misappropriation usually deals with the unpermit-
• Imputing unchastity to a woman. ted use of an individual’s name or likeness for
• Accusing the plaintiff of having a loathsome another’s benefit or advantage.
disease. • Intrusion usually involves encroachment upon
Truth and privilege are the two main defenses another’s solitude or seclusion: for example,
against a charge of defamation of character. When invasion of an individual’s home, persistent
someone is charged with defamation, after making unwanted telephone calls, or eavesdropping.
statements that harmed another’s reputation, that • Public disclosure of private facts of an objection-
person cannot be held for slander if indeed the state- able nature may give rise to legal action even if
ments can be proved to be true. The defense of privi- the information is essentially true.
lege is used in cases in which the statements, which • Presenting someone in a false light to the public
ordinarily may be considered defamatory, are made in usually involves the publication of information
circumstances under which the individual is charged that misleads the public. An example might be
with a higher duty. For example, practitioners may be an article about Medicare fraud that includes a
required under law to report certain health problems or respiratory care team who were not involved in
a state may have provided immunity for persons the case.3
involved in peer-review processes. In general, respiratory therapists have the right to
False imprisonment, the unlawful restriction of make fundamental choices involving their families,
another’s freedom of movement, is a tort. Actual ourselves, and our relationships with others. These
physical force is not necessary to prove this claim. A activities should under most circumstances be free
reasonable fear that force, which may be applied by from the scrutiny of others, so long as our assertion
words, threats, or gestures, will be used to detain a of these rights is consistent with law or public policy.
person is often sufficient. The health care provider who RTs have the right to maintain their private lives and
forces a patient to remain until a bill is paid or forms to restrict the collection, processing, use, and dis-
are signed may be liable under the tort of false impris- semination of data about their personal attributes
onment. Certain state statutes have allowed the deten- and activities. The law provides legal redress against
tion of mental patients who were considered a danger those who would infringe upon our legitimate
to themselves, to property, or to others and of persons privacy from motives of malice, greed, curiosity,
with a contagious disease. The mentally ill or conta- or gain.
gious may be restrained only to the degree necessary to
protect themselves from harm or to prevent them from Negligent Torts The salient difference between
harming others (minimum necessary restraint). In intentional torts and negligence is the element of
these cases it is wise for the practitioner to document intent, which is present in intentional torts and
clearly and carefully the reasons for the detention, the absent in negligence. A second important difference
harm that would arise from the patient’s leaving, and is that intentional torts involve a willful act that
the patient’s insistence on leaving. violates another’s interest, whereas in negligence,
The right to be left alone, free from unwarranted the problem is likely to be an omission of an act that
publicity, is considered an important freedom in is deemed reasonable. The most common forms of
American society and has found its way into both state negligence are:
and federal statutes. The phrase right to privacy is a
generic concept encompassing a variety of rights • Malpractice. Carelessness or failure to act with
thought to be necessary for an ordered democracy. The due care on the part of a professional.
standard to determine whether an invasion of privacy • Malfeasance. Execution of an unlawful or
has taken place is that of a “person of ordinary sensi- improper act.
bilities.” If such a hypothetical individual would • Misfeasance. Improper performance of an act that
find that the appropriation or exploitation of one’s leads to injury.
personality, the publicizing of one’s private affairs, or • Nonfeasance. Failure to perform an act, when
wrongful intrusion into one’s private activities was there is a duty to act.
• Criminal negligence. Reckless disregard for the almost no training to complex tasks requiring years of
safety of another. education and intensive internships. Physicians,
therapists, nurses, and aides are all held to the level of
Sustaining a claim of negligence requires the
practice that meets the prevailing standards for their
following forms of evidence, often called the four Ds of
group. For example, respiratory therapists are not held
a negligence claim:
responsible for the level of care expected of the physi-
• Duty. A provider-patient relationship must be cian. They are, however, held responsible for the level
established. A duty to care must exist. of knowledge, skill, and care ordinarily possessed and
• Dereliction of duty. There must have been a exercised by other respiratory therapists. In the case of
breach of duty; that is, the provider failed to act State University of New York v. Young,5 the therapist was
as an ordinarily competent provider would have suspended for using the same syringe for drawing
acted in a similar situation. blood from a series of critically ill patients even after
• Direct cause. The breach of duty must have been having been warned that the practice fell below the
the direct (proximate) cause of the injury, standard of care.
damage, or loss. Often in cases of negligence more than one person
• Damages. An injury or loss must actually have may be involved in causing a patient’s total injury. Under
taken place. the doctrine of joint liability, several individuals may be
held responsible for contributing to the injury. In these
Respondeat Superior Respiratory care is a specialty that cases the plaintiff may recover damages from one or all.
in its development has had a close and positive associa-
tion with physicians, especially those involved in Contracts. A contract comes into being when one
anesthesiology and pulmonary medicine. Practice by party makes an offer that is accepted by another party
respiratory therapists has traditionally been under the and consideration passes between them. In a contrac-
authority of the local state medical practice act of the tual arrangement, each party gives or does something
physician. The movement toward state licensure for the for what is exchanged; the thing given or action
profession has somewhat changed the relationship and performed is known as consideration. Most often in
shifted the responsibility more toward the respiratory
care practitioner.
In the early years of the profession, many respira- CASE STUDY 2-2
tory care practitioners felt that there was no need to
seek licensure for the profession, given that they
A therapist in a hospital was called upon to set
worked under the license of the physician. In that the
up a ventilator for a nonbreathing patient. The
therapist performed only those duties prescribed by the
therapist managed to hook the patient to the
physician it was felt that the physician was the one who
ventilator without an expiratory valve in place.
had the legal liability under a doctrine known as
The alarm began to sound with each attempted
respondeat superior, which means “let the master
cycle, and the therapist began to troubleshoot
answer.” The original intent of the doctrine, under
the device without taking the patient off the
English common law, was to make the Landed Lords of
ventilator. After 7 minutes of troubleshooting, the
the land liable for the acts of their servants. The
therapist figured the problem out. However, the
doctrine has evolved to include liability assessment
patient, who had been apneic for the 7 minutes,
against employers for negligent acts committed by
had suffered irreversible brain damage. The
employees, if the negligent conduct occurred in the
patient’s family claimed that the injury was due
course and scope of their employment duties. Liability
to the therapist’s negligence.
is often assessed against hospitals and physicians for
the negligent actions of allied health personnel on the Questions
basis of the fact that the employer placed these indi-
1. How does this case satisfy the four elements
viduals in a position and gave them the apparent
of a negligence claim?
authority to act on their behalf.4
Although respondeat superior allows for the assess- 2. What would an ordinarily competent provider
ment of vicarious (indirect) liability to be assessed have done?
against those with whom RTs have a master-servant 3. Under the doctrine of respondeat superior,
relationship, it in no way exempts respiratory therapists can the hospital be held responsible for the
from responsibility for their personal acts. Health care therapist’s actions? Explain your answer.
is practiced on many levels, from simple tasks requiring
medical practice, the consideration is the fee for service. on the defendant to give notification that a suit has
Contracts are relationships of mutual consent; the been initiated against him or her. There generally is a
party who makes the offer and the one who accepts it statutorily required period in which the complaint
must be saying and thinking the same thing. must be answered. In that the answer to the complaint
In a breach of contract, there is a failure, without will become part of the court’s record and the defen-
legal excuse, to perform any promise that constitutes dant will be held for anything stated therein, it is
the whole or part of the contract. The formal contract is important that the therapist gain the assistance of an
established when both parties have promised to be attorney before answering the complaint. The defen-
bound in the agreement. Thus, when one party offers dant, in the response to the complaint, will admit,
to do something in exchange for the other party’s deny, or plead ignorance to each allegation in the
agreement to do something, the contract is formed by complaint. This is a period in which there is often
the acceptance of the offer. anger and fear on the part of the defendant, but it is
Contractual duty can occur as the result of signing also important to understand that being “served with
formal documents, or it can arise out of implication. For process” is just a notice of a lawsuit and nothing more.
example, if a patient shows up at the blood gas labora- Once the answer to the complaint has been filed,
tory and is met by the receiving therapist, fills out the the defendant may file a motion to dismiss or motion
paperwork, and allows the therapist to palpate the vessel, for summary judgment, also known as a demurrer. A
it can be inferred that the patient is willing to allow the summary judgment is one made by a judge without
blood to be taken and also to pay for the services.6 there being a trial. The motion for summary judgment
may be directed at all or part of the claim. In that a
summary judgment is asking the judge to make a
The Civil Lawsuit ruling on a dispute of law, it is important that there be
When a claim goes to court, the first stage is complaint agreement between the parties as to the facts in the
and answer. The individual who begins the lawsuit or case. If there is a dispute in regard to facts, then a
action, claiming damage or harm, is the plaintiff; motion for summary judgment will not stand. The
the party against whom the suit is brought is the defendant may also bring a motion to dismiss based
defendant. It is hoped that the respiratory therapist on the belief that the plaintiff has not established a
would never be involved in a lawsuit, but it is useful to prima facie case in the complaint or that the complaint
explore the process by which a case proceeds through does not state a remedy for which the law provides.
the legal system. Either the motion for summary judgment or the
motion to dismiss can be brought any time before the
INITIATING THE SUIT trial begins.
It is the duty of the plaintiff to establish the elements
of a case, consistent with case law or statute. To initiate
the legal process, the plaintiff files a complaint with the DISCOVERY
court that addresses the elements of the prima facie The discovery period is usually the longest part of a suit
case and the number of offenses (counts) the plaintiff and is the stage at which most lawsuits end because
alleges the defendant is guilty of violating. (Prima facie often information is discovered that is detrimental to
means legally sufficient to establish a case.) The com- one party. Once the defendant has been notified of the
mon elements of a complaint are: complaint, and certain statutory procedures have been
complied with by both parties (e.g., scheduling confer-
• A short statement laying out the grounds on
ences to determine deadlines for discovery and trial),
which the court’s jurisdiction depends. In
the process of discovery can be begun by either party.
essence, the plaintiff tells the court why he or she
Discovery is basically the fact-finding phase,
thinks it has the authority to rule on the suit.
during which each party has the opportunity to
• A statement of the claims that call for relief for
discover the strength of the other party’s case. Informa-
the plaintiff. In this part of the filing, the plain-
tion that is normally private may be brought to light
tiff states how he or she was wronged.
(e.g., patient records, departmental records, and
• A demand for judgment for a relief to which the
personal histories). Because discovery is the only
plaintiff feels entitled. Here the plaintiff states
opportunity that both sides have to discover informa-
what he or she wants done to resolve the wrong.
tion that will help their case, great latitude is given to
In federal courts, this filing is called the complaint; both parties in their discovery efforts.
in most state courts it is called a petition. The major elements in discovery usually involve
A copy of the complaint, along with a summons, is interrogatories, document requests, and depositions.
served on the defendant. The complaint must be served Each of these elements should be posted and answered
court) have a jury. Once the jury has been impaneled,

Best Practice the trial begins with the attorneys’ opening statements,
with the plaintiff’s attorney leading. The opening
In the Event of a Suit … statements outline the facts that the attorneys hope to
establish in the trial process. The plaintiff has the
During dispositions and court testimony, do not
burden of proving the case to the jury. The defendant
answer:
does not have a burden of proof, has to prove nothing,
• Questions you do not understand. and could, technically, remain silent. After each side
• Compound questions. has presented its case and cross-examined the wit-
• Questions with double negatives in them. nesses, each is allowed time for a closing argument.
After the closing argument, the judge instructs the jury
For each of these, ask the lawyer to simplify
of any applicable law and any presumptions the jury
and restate the question.
should consider in their deliberations. Then the jury is
Do not answer questions that were not asked.
dismissed to deliberate. The trial usually ends with the
Answer only the question that was asked; do not
verdict.
expand on the answer. If the question can be
answered with yes or no, answer with a yes or no.
As soon as the RT receives notice that a suit THE APPEAL
is being contemplated, he or she should get an
The losing party may appeal a trial court decision to a
attorney. It can get complicated very quickly.
higher court in that particular jurisdiction, but only a
The therapist will need a lawyer. The hospital’s
final judgment may be appealed. The higher court will
lawyer’s primary job is to protect the hospital, not
accept appellate arguments from both parties, but an
the RT.
appellate court will not entertain any new issues. Essen-
Professional liability (malpractice) insurance
tially, an appellate court is a trier of law, reviewing the
is not only a good idea, but it is a necessary
processes of the lower court and the applicable deci-
action. RTs are more likely to be included in legal
sion of law rendered by the lower court.
action now that licensure is the common practice
nationally, and they are becoming more visible to
the public. ARBITRATION
A recently applied process for settling legal disputes is
the process of arbitration. In arbitration, the parties to
with the assistance of an attorney in that they will the potential suit meet with a mutually agreed-upon
become a permanent part of the court record. third party, the arbitrator. The arbitrator listens to
Depositions are the most common and effective statements, reads documents, reviews evidence pre-
methods of discovery because they provide an opportu- sented by each party, and proposes a compromise
nity for each side to question witnesses and parties to a settlement. It is felt that the arbitrator, as an unbiased
suit in order to elicit information about the case. In the party, can substitute for judge and jury. Arbitration can
deposition, the witness testifies under oath before a be either binding or nonbinding. With binding arbitra-
reporter, who transcribes the testimony. In that the tion the arbitrator’s findings are final and not appeal-
deposition can be used to impeach later testimony able. Nonbinding arbitration leaves the door open for
given in the trial, it is important that witnesses answer appeals and refusal to comply with the arbitrator’s
the questions exactly as if they were testifying in court. findings.
An interrogatory is a series of questions sent by Because arbitration generally is less time consum-
one side to the other. Document requests are just ing and less expensive than suit and trial proceedings,
that—requests for documents. Document requests are it is more appealing to both the legal system and the
often important in health cases because they provide parties in dispute. This process will likely be used more
access to medical records. The resulting information often as both civil and criminal courts become more
may provide overwhelming evidence for the plaintiff or crowded.
may show that the plaintiff cannot establish the
elements of a case. After discovery, either the case is
dropped or the parties proceed to trial or arbitration. The Duty of Ethical Practice
Moral and ethical decisions can be seen as a less
THE TRIAL PROCESS prescriptive standard of conduct than just obeying the
A case may be tried before a judge only or before a law. It is perhaps important in the beginning of this
judge and jury; most trials (except in small-claims section to distinguish between morals and ethics.
According to the ethicist Joseph Fletcher, “Morals are and torture would not necessarily be wrong. Fortu-
what people believe to be right and good. . . . Ethics is nately for the rest of us, this is not a position that most
the critical reflection about morality and the rational in society feel comfortable adopting.
analysis of it.”7 Van Rensselaer Potter, who is credited Slightly less troubling but far more common are
with coining the term bioethics, explained that this new those who ground their personal philosophy solely in a
discipline had as its focus the traditional task of hedonistic worldview. In this worldview, the guideposts
medical ethics, that of aiding the individual practitio- for decision making are personal desire and aversion,
ner in making value-laden decisions and living by and nothing can be right or wrong apart from them.
them.8 Ethics, then, is nothing more than a generic This attitude of total self-absorption is somewhat
term for the study of how people make judgments with captured in the bumper sticker slogan, “He who dies
regard to right and wrong. Ethics provides us with the with the most toys wins” Or “Its all about me.” Gross
framework to examine the moral life and the moral personal self-absorption provides an inadequate
practice of health care professions. framework for ethical decision making in health care.
Human babies are not born with a set of pre- In the provision of health care, RTs are often called on
scribed value rules or moral standards as to what they to make decisions in accordance with our better selves;
should do in any given situation. They draw from their an attitude of “anything goes” is unacceptable.
cultural environment a set of beliefs, attitudes, feelings, As health care providers, when RTs involve them-
and opinions that we develop into a rather consistent selves in unethical practices, they not only harm their
worldview, and it is with this that they judge the world patients, careers, and personal reputations, but also, by
around them—good, bad, right, wrong, positive, association, they harm all their fellow practitioners.
negative. Although each of us—in accordance with our Insofar as unethical practice lowers the general esteem
varying beliefs, experiences, and upbringing—has a in which health care providers are held, it harms the
unique overall view of the world, most people in a community at large. One analogy that is often used to
society hold similar sets of values and moral beliefs. describe the provision of health care is the community
These reflections from our worldview are all part of the commons. In earlier times, often, each small town had
individual’s personal values; they are reflections of the a common shared field in which to keep the animals.
individual’s moral life. This community commons was the shared responsibil-
The capacity to become ethical beings and to ity of all the townspeople. In this sense the health care
conform to some universal principles of cooperation environment where we practice is the shared responsi-
and altruism seems as old as the human species itself. bility of all practitioners, and each of us has an obliga-
One of the earliest anthropological findings of Nean- tion for its maintenance and upkeep. It is unthinkable
derthal remains was of an individual about 50 years of and unwise to believe that maintenance of the health
age. The skeletal remains showed that the individual care commons is the responsibility of some other
suffered from several debilitating conditions including group, such as a state legislature or physicians. Provid-
arthritis and could not have survived in the rough-and- ing ethical care, refining the quality of our practice, and
tumble environment of his time without the care and providing community service are not the obligations of
support of his group. Neanderthals may not have had a few; they are the obligations of all. It is a privilege to
the words to express such concepts as love, individual be a health care provider; it is a duty to conduct
respect, and altruism, but they certainly shared the ourselves in practice in such a manner that we can
behaviors by which people would describe such values. come again, and when we finally leave, to leave the
The philosopher Friedrich Nietzsche (1844–1900) commons healthy so that others can replace us in the
was correct in his assessment that humans are valuing labor. Nothing damages the community commons of
animals. However, in regard to our values, humans are health care as badly as does unethical practice.
not programmed, as are the beasts of the field, to a
proscribed set of correct actions but are condemned to
lives of freedom and choice. There are a few people in Basic Principles of
any society who use this freedom of choice to subscribe
to a philosophy of moral nihilism. Adherents to this Health Care Ethics
philosophical position believe that there are no moral Health care in the United States is aggressively patient
truths, no moral laws, no moral facts, no moral centered but has ancient roots. Two models of health
knowledge, and no moral responsibilities. In this sense care from the ancient Greeks that have significance for
nothing can truly be right or wrong in a moral sense. our times are the cults of Aesculapius and Hygieia. The
For the moral nihilist, morality, like religion, is a mere cult of Hygieia was developed on a broad public health
illusion. If one followed this philosophical position to and social model of prevention. The origin of the term
its conclusions, heinous acts such as child abuse, rape, hygiene means “good for health,” and the cult of
I swear by Apollo, the Physician, by Asclepius, by Hygieia, Panacea, and the gods and goddesses, making them
my witnesses, that I will fulfill according to my ability and judgment this oath and covenant.
To hold him who has taught me this art as equal to my parents and to live my life in partnership with him, and if
he is in need of money to give him a share of mine, and to regard his offspring as equal to my brothers in male lineage
and to teach them this art—if they desire to learn it—without fee and covenant; to give a share of precepts and oral
instructions all the learning to my sons and to the sons of him who has instructed me and to pupils who have signed
the covenant and have taken an oath according to the medical law, but to no one else.
• I will apply dietetic measures for the benefit of the sick according to my ability and judgment; I will keep them from
harm and injustice.
• I will neither give a deadly drug to anybody if asked for it, nor will I make a suggestion to this effect. Similarly I will
not give to a woman an abortive remedy. In purity and holiness I will guard my life and my art.
• I will not use the knife, not even on sufferers from stone, but will withdraw in favor of such men as are engaged in
this work.
• Whatever houses I may visit, I will come for the benefit of the sick, remaining free of all intentional injustices, of all
mischief and in particular of sexual relations with both male and female persons, be they free or slaves.
• What I may see or hear in the course of the treatment or even outside of the treatment in regard to the life of men,
which on no account one must noise abroad, I will keep to myself holding such things shameful to be spoken about.
• If I fulfill this oath and do not violate it, may it be granted to me to enjoy life and art, being honored with fame
among all men for all time to come; if I transgress it and swear falsely, may the opposite of all this be my lot.
FIGURE 2-2 The Hippocratic Oath.
Hygieia was directed toward the prevention of disease developed to assist health care providers in determin-
rather than therapy. In this sense it was more closely ing right from wrong in value decisions are respect for
related to the traditional practices of Chinese medicine persons, beneficence, nonmaleficence, justice, and role
than those of the West, although the modern HMO duty. Refer to Figure 2-1 for the AARC Statement of
system was originally based on a supposition that Ethics and Professional Conduct.
preventive care (preventing injury and illness) was less
costly and more effective than curing illness and the
effects of injury. RESPECT FOR PERSONS
The cult of Aesculapius (introduced in Rome from
The principles that speak to the patient-centeredness of
Greece 293 BCE) was strictly a patient–health care
our ethical practices are gathered under the general
practitioner affair aimed at getting the particular
principle of respect for persons. These include patient
individual patient physically well. In this light, health
confidentiality, veracity, and personal autonomy.
care would be patient centered and the practitioner
would not mix social, political, or economic consider-
Confidentiality. Confidentiality (the keeping private
ations with the care of the patients. It is clear that the
of information) is a principle that is perhaps the easiest
current health care model in the United States is more
to understand and the hardest to honor given the
based on the traditions of Aesculapius than on those of
problems associated with modern health care. Any
Hygieia, although our public health and wellness
breach of confidentiality, in essence an invasion of
efforts are more in keeping with the latter. The Hippo-
privacy, can create a wide gulf of distrust between a
cratic Oath (Figure 2-2) provides an early Aesculapian
patient and a respiratory therapist. Using knowledge of
model for professional ethics.
a patient’s condition as grist for the cafeteria gossip
A professional system of ethics, such as that found
mill is an inexcusable abuse of patient trust. Yet it is
in respiratory care practice and health-related law, can
important to understand that society has determined
be considered applied ethics. It is designed to promote
that there are conditions under which confidentiality
ethical and legal practice in the profession and to
must be breached for the public good. The following
promote the major purposes of the specialty. In health
are some situations in which there is a legal require-
care, the major good or purpose is usually expressed as
ment to break confidentiality:
the pursuit of good health, with the prevention of
death and the alleviation of suffering as secondary • Child abuse
goals. The basic operative principles that have been • Elder abuse
• Communicable disease • Request an accounting of all disclosures of their

• Births and deaths health information
• Wounds made with knives and guns
All health care providers have a duty to provide
• Criminal acts (e.g., attempted suicide, rape, drug
security for both paper and electronic transmission of
abuse)
individual health information: to become knowledge-
• Communicable disease in newborns (e.g.,
able in regard to the requirements of HIPAA, to
diarrhea and staphylococcal infections)
understand and comply with the institutions, policies
Beyond legal requirements that overcome our duty in regard to the complaint process, and to assist in
to provide confidentiality, there are situations in which investigations. Failure to comply with HIPAA regula-
confidentiality is overridden by more compelling tions is not only a breach of ethical conduct but also
obligations. The personal protective privilege of allows for both civil, monetary, and criminal penalties.
confidentiality is limited by the harm principle. This
principle requires that health care providers report Veracity. Although we are taught that honesty is the
information that is necessary to protect others who are best policy, the principle of veracity (truth telling), as
vulnerable to grave health and safety risks. As an an absolute, is difficult to fulfill. Yet veracity is an
example, if the practitioner knew that someone was important principle in health care provision because
HIV-positive, and that the patient was unwilling to telling lies cuts at the very heart of the patient-provider
inform his sexual partners while still determined to relationship. If the patient lies to the therapist, then the
continue sexual relations, there would be a duty to therapist has difficulty figuring out what is best for the
inform the vulnerable individuals. It would be unlikely patient. If the therapist lies to the patient, then the
that the respiratory therapist would have the direct patient, not having appropriate information, will have
obligation to tell the partners of their danger, but a hard time making appropriate decisions. Although it
someone in the health care system would have that is conceivable that lying to the patient may become
duty. The breaching of the obligation to maintain necessary to avoid some greater harm, it cannot be
confidentiality is recognized and is stated in certain entered into lightly because it interferes directly with
specialty codes of ethics, such as the 1992 Principles of the patient’s autonomy. Tolerance for lying damages
Medical Ethics of the American Medical Association health care delivery. Patients believe lies only because
statement: “A physician may not reveal the confidences truthfulness is the anticipated standard from health
entrusted to him in the course of medical attendance . . . , care providers. If patients begin to expect deceit an
unless he is required to do so by the law or unless it essential element of good health care delivery will have
becomes necessary in order to protect the welfare of the been lost.
individual or of the community.”9
With health care information being available to Autonomy. Patient autonomy is perhaps the most
great numbers of individuals throughout the hospitals important element under the respect for a person’s
via computer screens, confidentiality is very difficult to principle. The word autonomy comes from the Greek
maintain. Because of the difficulty to maintain confi- autos (“self”) and nomos (“governance”). In health care,
dentiality in modern health care, confidentiality has autonomy has come to mean a form of personal
been called the decrepit concept. On the other hand, liberty, where the patient is free to choose and imple-
perhaps confidentiality has become more important as ment his or her own decisions, free from deceit,
a personal duty of providers, requiring an extra effort, coercion, duress, or constraint. Informed consent
precisely because it has become so much more difficult (a patient’s authorization of medical intervention) flows
to maintain. Recognizing the growing problem in directly from the principles of autonomy and veracity;
1996, Congress enacted the Health Insurance patients can exercise self-determination in decision
Portability and Accountability Act (HIPAA) making only after they have appropriate information.
designed to encourage the use of electronic transmis- The common elements of informed consent are:
sion of health information (to assist in cost contain-
• Disclosure. The nature of the condition, the
ment) and provide new safeguards to protect the
various options, associated material risks, the
security and confidentiality of the information.10 Under
professional’s recommendation, and the nature
HIPAA, individuals have a right to:
of consent as an act of authorization.
• Request restrictions as to what information can • Understanding. Most states require that the
be given out and to whom physician provide information at the level that
• Receive notice of the health provider’s privacy a hypothetical reasonable person could
practices understand.
• Access to see, and get copies of their records and • Voluntariness. No effort toward coercion, manip-
request amendments ulation, or constraint is allowed. The patient
must be in a position to make an authentic harm, those involving nonmaleficence are stated in
autonomous decision. passive terms, as a duty to refrain from inflicting harm.
• Competence. Decisions in regard to competence Although it would seem only common sense that the
usually take into account experience, maturity, therapist would not inflict harm on patients, when
responsibility, and independence of judgment. stopping to consider how often in the use of modern
• Consent. An autonomous, authentic authoriza- technology there are serious side effects, at times doing
tion of medical intervention. some degree of harm seems inevitable. As an example,
morphine used as an analgesic will often suppress
Legal exceptions to the rule of informed consent
respiration.
have been allowed under considerations of therapeutic
Some scholars have advocated the principle of
privilege, especially in cases of emergency, of incompe-
double effect when the practitioner is faced with an
tence, of waiver, and in which there is implied consent.
ambiguous situation in which there are multiple effects
One ethically problematic use of therapeutic privilege
to an action. The following guiding elements are used
is in cases in which benevolent deception is used. In
in determining if an action is ethical when there are
such a case, the practitioner intentionally withholds
unintended but foreseeable negative side effects:
information because of his or her “sound medical
judgment” that to divulge the information would • The course chosen must be good or at least
harm the depressed or unstable patient. Benevolent morally neutral.
deception is a form of paternalism; the attitude that • The good must not follow as a consequence of
something is done for the patient’s own good. the secondary harmful effects.
Informed consent binds the physician to an adequate • The harm must never be intended but merely
disclosure and explanation of the treatment and its tolerated as causally connected with the good
various alternatives and consequences. It is the duty of intended.
the physician to obtain informed consent; other health • The good must outweigh the harm.
professionals may assist in the process, but it is the
To examine the complexity and limitations of the
doctor who must fully explain the procedures and
principle of double effect, consider the case of con-
treatment options.
joined twins. If the twins are not separated, both will
Emphasis on patient autonomy over practitioner
die. If they are separated, one will die because she does
paternalism is a relatively new, but expanding, phe-
not have lungs or adequate circulation and is depen-
nomenon in health care. The evolving body of infor-
dent upon the other. Can the one twin be ethically
mation regarding this subject has been away from
sacrificed to save the other? Must both die? The guiding
practitioner paternalism and toward patient autonomy.
elements of the principle of double effect would seem
As stated in the AMA’s 1992 Fundamental Elements of
to suggest that the surgery to separate the twins could
the Patient-Physician Relationship, the “patient has the
not be ethically justified because the perceived good
right to make decisions regarding the health care that is
(the life of one) would be the direct result of the death
recommended by his or her physician. Accordingly,
of the other. A court might allow the separation of the
patients may accept or refuse any recommended
twins, but it would not be able to do so on the basis of
treament.”11
the principle of double effect.
There is no clear consensus as to the value of the
BENEFICENCE principle of double effect. Many scholars feel that if a
The common English usage of the term beneficence side effect is foreseen, then it has become part of the
suggests mercy and charity. In health care usage the intended effects. Although there are arguments against
term is more in keeping with the Hippocratic Oath the double effect principle, it still provides a manner in
statement that the practitioner will “apply measures for which to examine these difficult decisions.
the benefit of the sick.” The obligation to benefit the
sick imposes upon the practitioner a duty to promote
JUSTICE
the health and welfare of the patient above other
considerations. Patients’ assumption that their provid- As are many of the basic principles of health care
ers are struggling incessantly on their behalf is of great ethics, the principle of justice is seemingly very simple
importance to their morale, especially those who are in the abstract and complex in application. Justice is
summoning all their energies to fight illness. the principle that deals with issues of fairness, just
deserts, and entitlements. In a just society, what is due
the individual?
NONMALEFICENCE Procedural justice, often known as due process,
Whereas statements involving beneficence are usually is the category of justice used in cases in which there
stated in active terms, as actions to prevent or remove is a dispute between individuals. For instance, if a
practitioner is accused of falsifying a patient record, represents a violation of patient trust, exploitation of
what due processes need be in place to ensure that the vulnerability and use of undue influence.12 In Heineche v.
practitioner is treated fairly, or justly? Department of Commerce,13 a male nurse lost his license
Distributive justice answers the question of how for having had a consensual sexual relationship with a
resources are to be distributed. Some common formu- patient, even though he had already resigned from the
las for distributive justice are: hospital where he had met her and she was no longer
a patient.
• To each an equal share.
• To each according to need.
• To each according to merit. Basic Decision-Making Models
• To each according to contribution. Our societal morals and legal rights develop from our
• To each according to effort. general worldviews. Ask almost anyone on the street to
• To each according to social worth. name some positive values, and the list would most
Which of the categories is best suited to distribute likely contain the following:
health care fairly? Is there justice in having the rich • Honesty
receive better care than the poor? Is there justice in • Love
having children receive less of the health care dollar • Lawfulness
than the elderly? • Equality
Another category of justice is compensatory justice, • Justice
in which individuals seek compensation for a wrong • Charity
that has been done. This has become a major issue as • Benevolence
the courts have struggled to provide justice to those
who have claimed harm from breast implants, asbes- Although few humans manage in their lives to
tos, and tobacco. If one considers the costs associated uphold all of these values all of the time, we generally
with lung cancer, chronic obstructive lung disease, and agree on them or at least agree that some things are
other problems directly related to cigarette smoking, right and some things are wrong. A morally neutral
how much money would be required to adequately society could not keep social order and would prob-
compensate the individuals or the society? Does the ably never progress.
warning label on the package overcome the claims, and We can gain an understanding of how value
therefore no compensatory justice is due? decisions are made by examining how we talk about
any controversial issue. Consider the following justifi-
cations of conflicting positions regarding abortion:
ROLE DUTY
1. I have a right to my body, I can make whatever
A role duty is a duty that exists owing to a person’s job
choice I want.
or position. In many cases, role duties are delineated in
2. Life is sacred; the Bible tells us that abortion is
the scope of practice section of the state legislation that
wrong.
governs respiratory care practice in the state. The nature
3. Abortion trivializes life. You start with the pre-
and traditions of the specialty are what define the role.
borns, and then it will be the elderly and helpless.
As an example, the respiratory therapist and the
4. People are breeding like rabbits; abortions are
physician are often both at the scene when patients are
environmentally necessary to stabilize world
acutely ill or have died. Yet, by tradition and duty, it is
population.
the physician’s role to explain to the patient’s family
5. Abortion is acceptable only in the case of rape or
the level of acuity of the patient. It is ethically and
incest; no baby should be born to someone who
legally important that specialists practice faithfully in
did not ask for it or want it.
the constraints of our role. There is no excuse for
6. Abortion is acceptable only to protect the health
respiratory therapists to overreach their scope of
of the mother or if the baby would be grossly
practice. When they do, the patients are poorly served
defective.
and the whole profession is brought into a poor light.
7. I don’t want this baby because it interferes with
Often, failures in the observance of role duty, such
my life plans.
as sexual improprieties with patients, will have not
8. A fetus is a human, and humans have the right to
only professional sanctions but also legal ramifications.
life, liberty, and the pursuit of happiness.
A significant number of health professionals have
been involved in litigated cases. Therapists who find Examination of these arguments shows that most
themselves sexually attracted to their patients must of them are based on the effects or consequences of the
seek personal help for themselves and must refer the actions (teleological, or consequence-oriented, argu-
involved patients to other therapists. Sexual misconduct ments). The others are based on an appeal to some rule
or principle (deontological, or duty-oriented, argu- making using utilitarian reasoning. Perhaps the greatest
ments). Statements 3, 4, 5, 6, and 7 are not appeals to difficulty to problem solving using act utilitarianism is
principles or rules but rather are justified on the basis that the individual must somehow predict and calcu-
of consequences, of what will happen if the decision to late all the various levels of pleasure gained and pain
allow abortion is made. These arguments are generally avoided for each potential action.
designed to increase general happiness and avoid pain. On its surface, utilitarianism appears to be a rather
Statement 1 appeals to the principle of the right of any hedonistic method of decision making as it might lead
individual to personal autonomy in making decisions to the majority group’s deriving pleasure from the pain
regarding her body. Statement 2 makes an appeal to of a minority and justifying the decision on the basis of
the religious principle of the sanctity of life, and the utility of the most good for the most people. To
statement 8 appeals to the principle of human rights. overcome these problems, most modern formulations
of consequence-oriented reasoning have inserted the
principle of “equal consideration of interest,” which
CONSEQUENCE-ORIENTED THEORIES
holds that each individual must be considered equally
The term teleological comes from the Greek word telos, in the process. The basic formulation for act utilitarian-
which means “end.” Teleological (consequence-oriented) ism then can be captured in the principle that one
theory then is the study of how things end, a study of should act in such a way as to produce the greatest
outcomes. Consequence-oriented theories judge the balance of happiness over unhappiness, everyone
rightness or wrongness of a decision by the outcomes or considered. Another interesting problem with utilitari-
predicted outcomes. Individuals following a consequence- anism is that if all one considered in the decision was
oriented theory would decide that the right decision was maximizing happiness and avoiding unhappiness, then
one that maximized some good. The right thing to do, it would be possible to consider that a happy, satisfied
then, is that which brings about the best outcome. pig might be on a higher moral plane than a dissatis-
The most common form of consequence-oriented fied Socrates. In order to overcome this criticism that
reasoning is utilitarianism, which is a philosophical utilitarianism was a “pig philosophy,” Mill defined
position first described by Jeremy Bentham (1748–1832) happiness as a set of higher moral pleasures such as
and John Stuart Mill (1806–1873). To the utilitarian intellectual, aesthetic, and social enjoyments rather
the good resides in the promotion of happiness or the than just sensual pleasure.14
greatest net increase in pleasure over pain. Rule utilitarianism overcomes some of the difficul-
The purest form of utilitarian reasoning is act ties of act utilitarianism in that it does not require the
utilitarianism, where the decision is made by listing all exact quantification of all the pleasure gained and pain
the potential alternatives for action and then weighing avoided with each option before making a decision.
each in regard to the amount of pleasure or utility it Rule utilitarianism is a theory that allows for rules to
provides and then selecting the choice that maximizes be prejudged using a measurement of utility. Utility
the pleasure. Figure 2-3 provides a format for decision would require that the rule would bring about positive
results when generalized to a larger context. As an
1. Describe the example, let us consider the rule regarding the freedom
problem of speech. No one thinks that free speech brings about
happiness and avoids pain in all cases, but, in general,
free speech has a high utility in that under most
2. List possible circumstances a rule that allowed free speech would
solutions bring about positive results.
Consequence-oriented reasoning is often very
persuasive in that it seems to support our modern
3. Determine
skepticism regarding absolute truths and rules and
the utility of speaks to our better selves in regard to tolerating the
each solution values and cultures of others. Although consequence
orientation appears persuasive, it is not altogether free
from problems in its usage. Several problems associ-
4. Choose the
ated with utilitarian reasoning are:
solution with • The calculation of all possible consequences of
the highest
utility
our actions, or worse, our inactions, appears
impossible.
• The theory does not give enough respect to
FIGURE 2-3 A flowchart for making consequence-oriented
persons. Under the theory, the ends justify the
decisions.
CASE STUDY 2-3 Describe problem
A certified therapist wished to pass himself off as

a registered therapist in order to move up in the List solutions
department. After considering falsifying his docu-
ments for a period of time, he decided not to
because he feared sanctions and the loss of his Compare solutions
position. with principles
Questions
1. On the basis of consequence-oriented One compliant Several compliant Conflicting
solution solutions principles
reasoning, is this therapist any different from
another therapist who never considered
fraud? Why? Correct Select among Rank
2. On the basis of virtue-oriented reasoning, are answer choices principles
they different? Why?
3. On the basis of duty-oriented reasoning, are Select from
they different? Why? solutions to the
highest-ranked
principle
means so it may be moral to use a person as a FIGURE 2-4 A flowchart for making duty-oriented decisions.
means to our ends.
• Using the theory it could be justifiable to
consequences of actions but rather from pure reason.
interfere with the personal liberty of others
He held that as rational beings we could derive prin-
especially to prevent them from harmful acts to
ciples that are universal. These universal truths would be
themselves. If smoking is bad, for the good of all
true for all people, for all situations, and for all times. An
legislators could ban it. Such a paternalistic view
action could be known to be true when it conformed to
could justify unacceptable governmental inter-
one of these universal principles, which he called
vention into the lives of individuals.
categorical imperatives. By “categorical” he meant that
• Utilitarianism is not sensitive to the agent
the rule did not permit exception, and by “imperative”
relativity of duty. As an example, we generally
he meant that it was a command derived from a prin-
believe that parents have special duties to their
ciple. These rules have three major components:
children and that physicians have special duties
toward their patients and that these special • Universal application
duties should prevent them from purposefully • Unconditionality
harming them. One could imagine a scenario in • Demanding an action
which harming patients and abusing children
Perhaps the most important of these categorical
would have a high utility.
imperatives relevant to health care ethics is that “one
must always treat others as ends in themselves and not as
DUTY-ORIENTED THEORIES means only.” According to Kant all people have an
absolute value, based on their ability to make rational
Deontological (duty-oriented) ethicists feel that the
choices. He felt that individual dignity was derived
basic rightness or wrongness of an act does not depend
from our capacity to reason and that it was violated
upon consequences or results but rather is part of its
when a person was treated as a means (a thing) and
intrinsic nature. Figure 2-4 provides a format for
not as a person.15 Kantian ethics has many detractors.
decision making using a duty-oriented system. In this
Several criticisms of Kantian reasoning are:
light, an act itself would be either right or wrong; it
could not be both. This particular worldview is codified • The exceptionless character of the philosophy is
in several major ethical systems and by many religions. too rigid for real life.
Perhaps the foremost formulation of duty-oriented • The disregard of consequences can lead to
reasoning is Kantian ethics, based on the work of disastrous results.
Immanuel Kant (1724–1804). Kant held that morality • The fact that people feel pain and pleasure is
is derived not from human nature or from the central to morality and the human experience. It
is unlikely that morality flows from pure reason The question then is how to gain the level of
alone. character at which one would, without analysis, make a
• It is possible to be in a situation in which two virtuous decision. The answer according to Aristotle is
duties conflict, yet are both equally supported by practice. Virtue is not the natural state of humans but is
an imperative. rather gained by the habit of doing virtuous acts.
Goodness of character is brought about by the practice
Duty-oriented theorists obviously wish to promote
of such virtues as courage, honesty, and justice. One
a good result; however, they believe that merely
becomes just and temperate by doing just and temper-
serving the good is not an adequate foundation for
ate things until justice and temperance become part of
ethics. For these theorists, the right action is one based
one’s natural character. In this sense Shakespeare’s
on a correct principle regardless of results. As an
Hamlet was correct: “If one would have virtue, one
example, if we choose a principle such as the sanctity
must first assume it.”
of life, then murder is wrong, and its wrongness
Every profession has its set of ideal practices or
cannot be modified by the situation leading to the
virtues of practice. This set of virtues is gained from the
action. Duty-oriented theorists argue among them-
practices of the past, especially from specialists who
selves as to how the principles are derived. Some claim
have expanded the profession. For nursing it would be
they are based on reason; others, on natural law,
individuals such as Florence Nightingale and Clara
intuition, social contract, or religious dictate. The
Barton; for respiratory care, it would be individuals
individual who believes that murder is wrong in all
such as Jimmy Young, Wilma Bright, and James
cases and the priest who maintains the confidentiality
Whitacre, who had distinguished careers and who
of the confessional even in cases of unreported
helped establish the foundations of the profession and
criminal activity are both following a duty-oriented
virtuous practices associated with what the good
form of reasoning.
respiratory therapist does in a value-laden situation.
With virtue ethics, if current respiratory therapists
found themselves in situations in which they needed to
VIRTUE ETHICS
make a value-laden professional decision, they would
It is clear that neither consequence nor duty ethics has not need to find a duty-oriented principle to apply or
produced a system that has been able to overcome its attempt to perform the mathematical calculations of all
major criticisms. Since the 1970s, several theorists have the potential pleasures gained and pains avoided.
begun to explore ethics not as a set of rules to guide Rather, the process would require that the practitioner
actions but rather as an attribute of character.16 rely on the traditions of earlier good practitioners to
In consequence-oriented reasoning the focus is on guide the decision. In some sense, it is asking oneself,
reasoning to an appropriate action rather than on the “What would a good respiratory therapist do in this
intent of the agent. In virtue ethics the focus is not on situation?” Figure 2-5 provides a decision-making
the action but rather upon the moral agent. The Greek format for virtue ethics.
philosopher Aristotle posed the problem in his A major problem with using virtue ethics in
Nicomachean Ethics when he avoided both duty- and making value-laden decisions in respiratory care
consequence-oriented reasoning and focused instead practice is that the field is changing so rapidly. Many of
on the intent and the heart of the moral agent. “We the issues surrounding managed care, organ donations,
may go so far as to state that the man who does not and genetic technologies are new to the health care
enjoy performing noble actions is not a good man scene and therefore there is no precedence of good
at all. Nobody would call a man just who does not
enjoy acting justly, nor generous who does not enjoy
generous action, and so on.” In this light it is not the Describe problem
weak person who is tempted and finally makes the
right choice who is to be admired but rather the
person who by virtue of his character is not tempted List solutions
in the first place.
Virtue-based decisions are motivated by what the
actor believes to be good and true. Duty- or role-based
Compare solutions
ethical decisions are motivated by stated or implied with traditions
rationales that say, “In my role as a [whatever specialty].
I have a duty to do____.” For example, “In my role as a
respiratory therapist, I have a duty to make vigorous Choose solution
attempts to treat all patients with equal care regardless
of my personal feelings for or about them.” FIGURE 2-5 A flowchart for making virtue-oriented decisions.
practice that can be brought forward. It is quite pos-

sible that responsible good practice under managed Describe problem
care is significantly different than in previous times.
Some major criticisms of virtue ethics are:
List solutions of
• Virtue ethics does not in general provide specific initial credibility
directions in regard to decision making.
• In that virtue ethics is based on traditional Compare solutions
practice, it does not respond quickly to new to divine commands
situations.
• A traditional emphasis makes morality depend FIGURE 2-6 Divine command decision flowchart.
on past experience rather than on reason. This
environment provides little respect for creative An important variant to divine command theory is
solutions or personal autonomy. the teachings of nondivine beings that are considered
• Practitioners often find themselves attempting to exemplary. Nondivine, but morally exemplary beings
address more than one set of idealized traditions, such as Siddhartha Gautama (Buddha) have also
which may come into conflict (e.g., the need to provided adherents with formal sets of rules that guide
be a team player versus the need to be a whistle- conduct. Rules such as The Noble Eight Fold Path, as
blower, as in a case of negligent care by a found in Buddhism, function with the same logic as
colleague). the divine command theory, with the important
difference being that their origin is the teaching of a
Even with the problems associated with virtue ethics
nondivine being.
decision making there is something persuasive about the
For followers of rules set forth by a divinity, or
process. Examination of how we make decisions as
exemplary but not divine individual, the logic of
practitioners shows how we often find ourselves follow-
Divine Command theory works the same. Both groups
ing the dictates of an idealized role. What would a good
follow rules that provide moral injunctions that
respiratory therapist do in this situation?
believers are to obey upon pain of divine retribution in
To understand the difference between virtue ethics
cases such as Judeo-Christian rules, or failure to achieve
and consequence oriented theories, consider that focus-
Nirvana for followers of Buddhism. Figure 2-6 provides
ing on consequences only would create the decision
a flowchart for making decisions using divine com-
that a therapist who contemplates fraud, but did not
mand theory. Divine command theory is similar to
carry it out, is no different from one who never consid-
most deontological theories with the exception that
ers it. Virtue-oriented reasoning would hold that
the answer is gained not from an appeal to reason but
because their intents, or hearts, were different the two
rather to revelation. Like theories such as Kantian
therapists were different.
Ethics, divine command rules generally have three
major components.
DIVINE COMMAND THEORY
• Universal application
An additional theory for ethical decision making, and
• Unconditionality
one often used in ethical discourse, is divine command
• Demanding of an action
theory. The idea is relatively simple and straight
forward. Divine command theorists hold that a divine There is no question that followers of divine
being has given a finite set of rules that adherents can command theory, whether derived from Judeo-
use to resolve most, if not all, moral dilemmas. One of Christian, Islamic, Buddhist, Hindu or other religious
the great examples of a divine command is the Ten frameworks, often find in their traditions a meaningful
Commandments, which are held to be moral impera- system for decision making. However, as health care
tives by followers of Judeo-Christian faiths. The Ten providers, we find ourselves in an increasingly complex
Commandments prohibit stealing, murder, adultery, world of believers and nonbelievers, in a world where
and so on, which also find condemnation in most of new questions, seemingly unimaginable by earlier
the world’s cultures. In that a set of finite rules are by generations, arise. It is difficult to see how ancient texts
their very nature finite and limited, adherents attempt can provide answers with a high degree of certainty
to extend them to find solutions to problems that seem involving questions such as cloning, or acceptable
related but are not directly covered, or covered only by limits to posthumanism, or whether a child should be
implication. Hence, some extend the prohibition conceived using frozen sperm taken from a deceased
against murder to include issues such as abortion, stem spouse. These new questions associated with the
cell research, physician assisted suicide, and euthanasia. continued development of science and technology
Obviously, many others believe that the basic rules threaten to stretch any absolutist theory such as divine
cannot be extended in this matter. command, to its very limit. Yet as seen in Figure 2-7,
Text not available due to copyright restrictions

when one examines the decisions by a variety of

religions with regard to organ donation, it is clear CASE STUDY 2-4
that divine command reasoning can be very
adaptive. Recently there has been a spate of cases where
As with the other systems of ethical decision health care providers have refused to provide
making, the divine command ethics format has not services based on their religious beliefs:
satisfied all scholars and critics. Some major criticisms
of divine command ethics are: • Does a pharmacist have a duty to provide
“day-after pills”?
• Divine command theories assume a belief in • Does a Catholic hospital have a duty to
either divine or exemplary individuals. To the permit obstetricians to perform steriliza-
extent that these beliefs can be questioned, so tions immediately after giving birth? Would
can the theory. the answer be different if they accepted
• Divine command theories generally have a “no any federal money?
exception” clause, either explicit or implicit. This • Can a physician be sued for violating state
is a problem for individuals living in morally anti discrimination laws due to his refusal
complicated times. to artificially inseminate a patient involved
• It is difficult to imagine that any set of religious in a lesbian relationship?
traditions could cover all possible cases of moral • Can health care providers be required
decision. This leads either to a fundamentalism, to remove hydration and nutrition from
in which one states that the extension of the patients for whom these seemingly
basic rules to other cases is unproblematic, ordinary and standard procedures have
or to differences in interpretation, and therefore been deemed “extraordinary care”?
differences in people’s decisions regarding these • If no other physician is available, can a
issues. physician refuse to participate in a request
• Divine command theory has been questioned for physician-assisted suicide where state
by what is known as the Euthyphro Problem, law permits the practice?
taken from the Platonic dialogue from which
it originated. The problem resides in how the Questions
divine or exemplary being came to the original In order to answer the preceding questions, the
decision for the rule. Did the divine or two freedoms at stake must be examined. For the
exemplary being decide arbitrarily that the patient, the case will most often be presented in
rule was correct, or is the divine or exemplary terms of personal autonomy, or relief of suffering.
being basing the decision on some justifying For the health care provider the issue will be a
reason beyond “I told you so.” If it is just right to act in accordance with his or her con-
“I told you so,” then it is difficult to imagine science. Can a just society force people to violate
why we should obey a rule so arbitrarily their personal consciences?
chosen. If it is based on some other underlying 1. Think of how you might answer these ques-
justifying reason, then perhaps we could tions, using whatever ethical decision-
refer directly to the justifying reason without making format you choose. Then consider
reference to the deity. In either case, one them using divine command.
could question assenting to divine
command rules. 2. How would you handle a work situation
where you were asked to perform a service
Regardless of the criticisms, divine command that went against your personal conscience?
theory seems to be very useful for personal decision
making and perhaps is an enhancement to the
process of ethical reasoning. Given that the answers
provided are from divine or exemplary sources, they
are also very effective in reaching agreement among they have revealed truth, often find it difficult to
the community of believers. The real problems arise explore options from other sources. Another unfortu-
when one is reasoning toward an answer with a nate side effect of divine command theory is that the
follower of a different belief system. If, after a person true believer often sees his or her answer as not only
consults his or her particular belief system and an being correct, but also good, which leaves the non-
answer is gained, how does the person explore or believer holding a position that is not only incorrect
value other options? Individuals, who perceive that but perhaps bad.
The Decision-Making Process 5. Make the decision and act on it. In that these are
decisions regarding values with which others may
Whatever ethical framework chosen, whether duty, con- disagree, prepare a defense for the decision
sequence, divine command, or virtue, the respiratory should it be questioned.
therapist will find he or she will need to proceed 6. Assess and evaluate the results.
through certain steps as decisions are made. There are
several problem-solving formulas from which to choose;
however, most will include the following six steps:
1. Identify the characteristics of the problem. Describe
Some Practical Advice
the problem, identify the principles involved. Ethical, legal, and professional practice is something
Who are the concerned parties? Who is charged that is gained by serious reflection, constant vigilance,
with making the decision? continued study, and honest self-evaluation. It is an
2. Gather the facts of the case. What is fact? What is area of practice that calls upon the practitioner to be a
opinion? What are the legal ramifications? Has critical thinker and a systematic decision maker. Here is
the issue been decided by the courts before? What some practical advice on issues that have both legal
documentation exists that outlines the problem? and ethical implications.
3. Examine and list the options of initial credibility. One
• Practice in your comfortable scope of
of the real problems with decision making in the
practice. Seek consultation when you have
area of values is a rush to judgment. The more
questions.
options considered, the more likely the respira-
• Provide care in accordance with good medical
tory therapist is to find one to support and
practice and national standards.
defend.
• Maintain accurate and complete records. Verify
4. Weigh and evaluate the potential options. What will
all telephone medical orders.
happen to the individuals involved, given each
• Maintain the confidentiality and privacy of
option? Has everyone been considered equally?
patients.
What basic principles were favored? Were any
• Do not disparage the professional skills of
sacrificed? What basic system is being used to
colleagues. When the practice of another
make the decision—duty, consequence, divine
warrants criticism, use appropriate reporting
command, or virtue?
mechanisms.
• Investigate all patient complaints thoroughly
CASE STUDY 2-5 and promptly. Allow the patient to fully explain
the nature of his or her concerns.
• Remain current in your practice. Continue
Dr. S. is a very senior surgeon at a hospital. It is
professional growth and development through
common talk around the hospital that Dr. S.’s
continuing education and association with your
patients have a higher level of hospital-borne
professional organization.
infection after surgery than do other doctors’
patients. In this case, the patient is a 38-year-
old female who has undergone a full mastectomy
for breast cancer. During postoperative care, you Summary
have found her to be very quiet, seemingly
depressed, and not talkative with you or the Respiratory care is a clinical practice and for the most
family members who come to visit. She seems to part our careers are involved with technical and
be in some pain during the treatments and has a scientific issues. However, in order to truly be successful
low-grade fever. After a treatment, she asks you, in practice, RTs must ensure that our performance is
“Is Dr. S. a good surgeon?” not only technically correct but also legally, ethically,
and professionally correct. As health care providers,
Questions RTs draw from a vast well of trust that has been formed
1. What are some answers you could give? by the past practices of the specialists who have come
before us. The patient’s trust—that the provider is
2. What principles are involved?
working single-mindedly on his or her behalf, that
3. Which of the ethical systems will you use— there are no conflicts of interest, that no secrets are
consequence, duty, or virtue? being hidden, and that the provider’s behavior is both
4. Which answer will you give? ethical and legal—is an important part of the therapeu-
tic relationship.
The provision of ethical and legal practice is not 2. A respiratory therapist who refuses to accept a
negotiable; it cannot be set aside because of sched- gratuity is attending to which of the following
ules or personal preference or in an effort to be more basic principles?
efficient or productive. Performing ethically and a. autonomy
legally is not just a nice way to practice; it is the only b. justice
way to practice. In some sense, ethical, lawful behav- c. beneficence
ior lies at the very heart of what is meant by being d. nonmaleficence
professional. 3. When the large tobacco companies are forced to
pay the health costs for smokers, the ethical
principle being applied is:
Study Questions a. compensatory justice.
b. nonmaleficence.
REVIEW QUESTIONS c. retributive justice.
1. List three major criticisms to the use of utilitarian- d. beneficence.
ism in making ethical decisions. 4. Informed consent flows mainly from the basic
2. List four legal requirements for breaking patient ethical principle of:
confidentiality. a. autonomy.
b. beneficence.
3. List three forms of intentional torts that a respira-
c. justice.
tory therapist might be involved with.
d. role duty.
4. List three major criticisms to the use of Kantian
5. In its best sense, paternalism is a contest between
ethics in making ethical decisions.
which of the following principles?
5. List and define the basic principles of a. autonomy and beneficence
healthcare ethics. b. justice and role duty
6. List three major criticisms to the use of the c. veracity and nonmaleficence
divine command theory in making ethical d. role duty and autonomy
decisions. 6. Which of the following ethical decision-making
7. Define the basic function of normative ele- formats is focused on the moral agent rather than
ments (as found in our rules of professional on the decision?
etiquette, legal requirements, and ethical a. utilitarianism
codes) as they relate to the practice of b. duty-oriented theories
respiratory care. c. virtue ethics
8. What were the two general goals of the 1966 d. divine command theories
HIPAA legislation? 7. The criticism that it is exceptionless is most
9. Take the common ethical dilemma faced by all meaningful in which ethical decision-making
practitioners (Should I take a gratuity from a format?
patient?) and using the flowcharts for decision a. Kantian ethics
making provided in the chapter work out the b. utilitarianism
solution using utilitarian, Kantian, virtue ethics, c. virtue ethics
and divine command reasoning. d. situation ethics
8. Which form of law would not include a state’s
respiratory care scope of practice?
MULTIPLE-CHOICE QUESTIONS a. constitutional law
1. According to the philosopher Joseph Fletcher, b. statutory law
“[M]orals are what people believe to be right c. administrative law
and good,” whereas ethics is concerned with: d. common law
a. critical reflection and rationales for judging 9. The highest form of public law in the United States is:
value problems. a. administrative law.
b. legal policies and procedures. b. criminal law.
c. professional issues only. c. constitutional law.
d. both legal and moral issues. d. legislative law.
10. The legal principle stare decisis means: 17. Which of the following statements reflects a virtue
a. “Let the buyer beware.” ethics format?
b. “Let the master answer.” a. If it is good for me, I should do it regardless of
c. “The thing speaks for itself.” what others think.
d. “Let the decision stand.” b. Only actions that are desired by a consensus of
11. You are trying to give a patient a treatment, the group are good.
and he tells you to leave him alone. Because c. The outcome will be good if the agent making
the doctor has ordered the treatment, you the choice is good.
push the patient’s hands away and apply the d. Situations change what is good or bad: What I
mask. What tort might you just have am allowed to do today I might not be allowed
committed? to do tomorrow.
a. assault 18. In which of the following situations could you
b. battery legally break patient confidentiality?
c. defamation of character a. A child is brought into your ER with many
d. false imprisonment bruises, both old and new.
12. Morals pertain to: b. A father wants the results of his 18-year-old
a. beliefs about right and wrong. daughter’s pregnancy test.
b. legal policies and procedures. c. A researcher wants the names, ages, and
c. professional issues only. diagnoses for a sequential group of patients
d. legal and value issues. visiting your clinic.
d. The police request the medical records of a
13. Which of the following is not among the basic
suspected hit-and-run driver.
principles involved in health care ethics as
applied to respiratory care? 19. Which is an intentional tort?
a. nonmaleficence a. An automobile accident is caused by an oil spill
b. autonomy during a violent thunderstorm.
c. polymorphism b. A neighbor’s tree has fallen across your drive-
d. beneficence way, preventing you from attending a World
Series baseball game.
14. In which of the following cases is one likely to
c. In order to save money, your car dealer
receive compensatory justice?
substitutes used tires for new ones on the
a. a criminal case regarding bank robbery
car you just bought. The tires fail, causing
b. a suit for slander
damage to your car.
c. a case involving traffic tickets
d. Because of mail delays, you miss your invitation
d. an administrative hearing regarding application
to a free cruise. Now your vacation will be at
of rules
the local mall.
15. An indication that informed consent is derived
20. All of the following are major elements found in a
from the principle of autonomy is:
practice act except for:
a. the patient’s right to refuse.
a. setting of reimbursement rates.
b. the patient’s being asked to sign the
b. description of scope of practice .
forms.
c. reasons for administrative action.
c. the presence of witnesses.
d. exemptions from the act.
d. the institutional representative’s power to
make agreements. 21. Which is a benefit derived from the principle of
stare decisis?
16. In order to differentiate between duty, conse-
a. Provides the system with stability and
quence, divine command, and virtue as forms of
allows for the creation of new
ethical reasoning, one must:
principles.
a. look at the outcomes of the situation.
b. Does not require judicial input or
b. project the distribution of costs among those
action.
affected by the action.
c. No one is found to be at fault.
c. determine the philosophical grounding of the
d. Only a six-person jury is required.
decision maker.
d. determine the legality of an action.
22. Which of the following is a tort? of your personal responsibility in the matter?
a. I contract with another health professional to Explain your answer.
share an office; she never pays her share of 5. Examine the following moral dilemma using a
the rent. duty, a consequence, divine command, and then
b. While caring for a ventilator case, I fail to drain virtue ethics format: Joe is a therapist on the
the ventilator tubing and the patient aspirates evening shift. In a bit of horseplay with his col-
and dies. league, Jim, he pushes a standby ventilator over and
c. Owing to a programming fault, the record breaks the device. He quickly changes the device
function of the IV controller reads high under and tags the broken device for repair. Joe asks Jim
certain conditions. No patients have been to keep the cause of the broken device confidential
harmed because the company warned all because he does not want to get into trouble. In the
customers. morning the supervisor notices the broken device
d. John goes to a bookie each week and bets $200. and asks Joe what happened. Joe says that he does
After 2 years he finds that Joe, the bookie, was not know, and then the supervisor turns to Jim and
cheating him. asks the same question. What should Jim say?
23. If I speak falsely and badly about you to others, 6. In what ways do HMO and managed care systems
which of the following statements is true? follow the precepts of the Hygieian system of the
a. I have both libeled and slandered you. ancient Greeks? In what ways do they differ from
b. I have defamed and libeled you. the Hygieian system?
c. I have not libeled, slandered, or defamed you.
7. How might telling a small child that an injection
d. I have defamed and slandered you.
“won’t hurt” affect the child’s future interactions
24. Divine command theory seems to be least like which with health care providers? What approach to this
of the following ethical decision-making systems. situation should be taken?
a. Kantian ethics
8. Generally for every set of rights there is a concur-
b. utilitarian ethics
rent set of obligations. Review the patient’s rights
c. virtue ethics
to their health care information as outlined in the
d. deontological ethics
HIPAA regulations, and create a set of practitioner
25. HIPAA requirements enhance and provide duties obligations that support those rights.
in regard to which of the basic principles of
9. Compare and Contrast the early Hippocratic
health care ethics?
Code with that of the AARC statement of ethics
a. veracity
and professional conduct as found in the chapter.
b. justice
c. confidentiality 10. Review the AARC statement on ethics and profes-
d. autonomy sional conduct. List those that you think promote a
more Hygieian form of health care provision.
CRITICAL-THINKING QUESTIONS
1. When you are moving between two beds you
References
knock a carafe of water onto a patient. The patient 1. Roach W, Chernoff S, Eslley C. Medical Records and
is wet but otherwise unhurt. Have you created the the Law. New York: Aspen Publications; 2006.
situation of an actionable tort? Defend your answer. 2. Pozgar G. Legal Aspects of Health Care Administration.
New York: Aspen Publications; 2006.
2. You wait in an empty parking lot for a therapist
3. Edge R, Krieger J. Legal and Ethical Perspectives in
who is giving you trouble to get off shift. As he
Health Care. Clifton Park, NY: Delmar Cengage
approaches his car, you walk over to him and tell
Learning; 1998.
him off; you call him a “backbiting ###” who
4. Smith G. Respiratory Care. Lenexa, KA: Applied
gossips about the patients and other staff mem-
Measurement Professionals; 1989.
bers. Have you committed either libel or slander?
5. State University of New York v Young, 170 AD2d 510.
Defend your answer.
6. Flight M. Law, Liability, and Ethics for the Medical
3. An FBI agent comes into the clinic, shows his Office Professional. 4th ed. Clifton Park, NY: Delmar
credentials, and demands that he be allowed to Cengage Learning; 2004.
make copies of a patient’s records. The practitioner 7. Fletcher J. The Ethics of Genetic Control. Garden City,
should ___________. NY: Anchor Books; 1988.
4. You are a student in a clinic and make a grave error. 8. Potter VR. Bioethics: Bridge to the Future. Englewood
To what extent does respondeat superior relieve you Cliffs, NJ: Prentice Hall; 1973.
9. Council on Ethical and Judicial Affairs. Code of 17. Bolton DL and Mock K, (eds). An Organ Donation
Medical Ethics, Current Opinions. Chicago: American Guide for Faith Leaders and Health Care Professionals.
Medical Association; 1992. Theological Perspective on Organ and Tissue Donation.
10. U.S. Department of Health and Human Services. 2007;114–151. UNOS: Richmond Virginia.
Fact Sheet: Protecting the Privacy of Patient’s Health
Information, May 9, 2001.
11. Council on Ethical and Judicial Affairs. American Suggested Readings
Medical Association. AARC Position Statement: Respiratory Care Education.
12. American Dental Association. Licensing boards AARC Position Statement: Requirements for the
confront sexual misconduct. Am. Dent. Assoc. Provision of Respiratory Care.
2004;135,9:1326–1329. AARC Position Statement: Scope of Practice.
13. Heineche v Department of Commerce, 810 P2d 459 AARC Position Statement: Role of the Respiratory
(Utah App 1991). Therapist in the Hospital and Alternate Sites.
14. Pojman L. Ethics: Discovering Right and Wrong. Carroll C. Legal Issues and Ethical Dilemmas in Respira-
Belmont, CA: Thompson, Wadsworth Publishing tory Care. Philadelphia: F.A. Davis; 1996.
Co; 2004. Edge, R, Groves, R. Ethics of Health Care: A Guide for
15. Johnson O, Reath A. Ethics. Philadelphia: Harcourt Practitioners. Clifton Park, NY: Delmar Cengage
Brace College Publishers; 2006. Learning; 2006.
16. Edge R, Groves R. The Ethics of Health Care. Clifton Pozgar, George. Legal and Ethical Issues for Health
Park, NY: Delmar Cengage Learning; 2006. Professionals. Boston: Jones & Bartlett Publishers; 2005.
SECTION II
The Applied Sciences

CHAPTER 3
Applied Physics
Paul J. Mathews
OBJECTIVES
• Understand each of the physical laws presented in this chapter and relate its application in the practice of
respiratory care.
• Perform simple physics calculations.
• Provide the correct formula for each of the gas laws.
• Calculate solutions to gas law problems.
• Define each physical law discussed in the chapter, and give its correct mathematical formula.
• Perform conversions from one measurement system to another.
• Convert data from ordinary numbers into scientific notation or vice versa.
• Apply physical laws to clinical situations using clinical case study data.
CHAPTER OUTLINE
Scientific Discovery and Belief Liquids
Measurements and Nomenclature Vapors
The International System of Units Gases
SI Prefixes, Dimensional Analysis, and Changes of State
Scientific Notation Mass, Weight, and Density
Mathematical Operations Mass
Order of Operations Weight
Mathematical Coupling Density
Heisenberg’s Uncertainty Principle Basic Electrical Theory
Occam’s Razor Electricity
Physics Circuits
Mechanics Ohm’s Law
States of Matter Capacitance
Solids Frequency
Plasma
(continues)
53
54 SECTION II ■ The Applied Sciences
(continued)
Light Waves Gay-Lussac’s Law

Fluid Physics The Combined Gas Law
Viscosity Dalton’s Law
Pressure Gradient Henry’s Law
Driving Pressure Avogadro’s Law
Types of Flow Graham’s Law
Bernoulli’s Principle Surface Tension
The Coanda Effect Laplace’s Law
Gas Laws Thermodynamics
Boyle’s Law Conservation of Matter and Energy
Charles’s Law Heat and Other Forms of Energy
KEY TERMS
acceleration fluid physics principle
Boyle’s law fractional concentration quantity equations
Charles’s law Gay-Lussac’s law Reynolds number
Dalton’s law Hooke’s law scientific notation
derived units inverse square law specific gravity (SG)
dimensional analysis law sublimation
dimensionless number mass effect Système International d’Unités
distending pressure mathematical coupling (SI system)
equal reactions MKSD theory
exponent physics triple point
flow Poiseuille’s law vector
T
his chapter introduces the physical laws, physiological balance. A thorough understanding of
principles, and theories especially pertinent these basic sciences is necessary for an understanding
to the scientific foundations of respiratory of the practice of respiratory care.
care, pulmonary anatomy and physiology, Distinctions among the basic sciences have
and pulmonary pathology. Physics is the science of become, and will continue to be, blurred in modern
how and why energy and matter interact to produce scientific society. The overlaps between biology and
what we see and experience in our universe. The chemistry (biochemistry), physics and chemistry
preceding words are chosen very carefully because (physical chemistry), and physics and biology (bio-
modern physics suggests the possibilities of other physics) have become more pronounced as our knowl-
universes in which physics may not work quite the edge of the structure and function of the body systems
same way as we think it does here. This chapter has improved. Regardless of the complexity and diverse
explores the physical principles governing the condi- interactions among the sciences, however, having a
tion of the patient and affecting the equipment and strong grasp of the elemental truths of the basic
procedures used in respiratory care, as well as the sciences is still a necessity.
relevant general mathematical concepts, measurement
systems, and analysis methods.
The art and science inherent in the practice of
respiratory care are based on the principles of physics, Scientific Discovery and Belief
chemistry, and mathematics. These principles act There is a general hierarchy of thinking in any science,
within the human body and within the equipment and and physics is no exception. The highest order of
techniques we use to maintain or alter the body’s thought is the scientific law, which, in science, is a
CHAPTER 3 ■ Applied Physics 55
statement that describes a scientific truth—something TABLE 3-1 SI base units

that has never been disproven either in the past or at
the current state of knowledge. This definition should Base Quantity Name Symbol*
not be taken to mean that the description will never be Length Meter m
disproven but only that the possible proof has not Mass Kilogram kg
been yet discovered. Theories are statements that are Time Second s
believed to be true but that are still being tested or are
Electrical current Ampere A
doubted in some scientific circles. Principles are
statements of perceived truths about defined situations. Thermodynamic temperature Kelvin K
An example is the Munroe-Kellie principle (or hypoth- Amount of substance Mole mol
esis, or sometimes doctrine), which states that, in a Luminous intensity Candela cd
confined or closed space changes in the size or mass
of one component of the contents of the space will *Both the symbol and whether it is uppercase or lowercase are critical
when using the SI system. Failure to use the right symbol and case can
cause a reciprocal change in the sizes of the other lead to serious errors and misunderstandings.
contents. This principle is sometimes referred to as
the mass effect.
obtained by using the base units in specific formulas
Measurements and Nomenclature called quantity equations. Examples of these units
and formulas are shown in Table 3-2. A derived unit
The language of science and mathematics by necessity
consists of two or more base units or, more properly,
must be precise, understandable, and easily communi-
the interactions of the expressions of two or more of
cated across a broad spectrum of fields and in a
the base unit properties.
multitude of languages. The language of physics is
mathematics. For clarity and understanding, concepts
in physics must be expressed mathematically. To do SI PREFIXES, DIMENSIONAL ANALYSIS,
this in a comprehensive and coherent manner, we AND SCIENTIFIC NOTATION
speak a common mathematical language. Based on
Because the numbers and units can get very large or
mid-eighteenth-century work, the medical and scien-
very small, they can be difficult to refer to, use, and
tific community has accepted and adopted the Interna-
manipulate in their original state. Three systems have
tional System of Units.
been developed to make them easier to use and
comprehend: SI prefixes, dimensional analysis, and
THE INTERNATIONAL SYSTEM OF UNITS scientific notation.
To ensure that the mathematical expressions of physi-
SI Prefixes. Table 3-3 presents a series of prefixes that
cal and other scientific concepts are identical through-
modify the magnitude of the base or derived SI units.
out the scientific and medical communities, a unified
Units whose magnitudes (sizes) are larger than the
system of mathematical and measurement systems was
base are labeled with Greek prefixes; those whose sizes
introduced and accepted by the world’s scientific
are smaller than the base are labeled with Latin pre-
community (with some local exceptions). This system
fixes. These prefixes can be used with any of the SI base
is called the MKSD (meter, kilogram, second, degree)
units except the kilogram (mass), because that unit
system, or metric system. A more proper name is the
already has the descriptor kilo as part of its name and
Système International d’Unités (French for Interna-
symbol. For units of mass, we use the prefixes with the
tional System of Units). The abbreviation “SI” units is
symbol “g” for gram.
commonly used.
Units of Measure. All measurements should be

referred to in SI units. There are seven base units on Best Practice
which all other measures depend and from which all
other measures are derived (Table 3-1). The seven base
units are length, mass, time, electrical current, tempera- Role of Physics
ture (based on absolute zero), amount of a substance, Physical phenomena occur because of the
and luminous (light) intensity. These units are further interaction of the basic properties of matter and
defined in this chapter. energy. The business of physics is to express
those interactions in meaningful and understand-
Derived Units. In addition to the base SI units, other able terms.
units are called derived units. Derived SI units are
TABLE 3-2 Examples of derived SI units

Derived Quantity Name Symbol Formula
Area Square meter m2 m·m
Volume Cubic meter m3 m·m·m
Speed, velocity Meter per second m/s m/s
Acceleration Meter per second squared m/s2 m/(s·s)
Mass density Kilogram per cubic meter k/m3 k/(m·m·m)
Specific volume Cubic meter per kilogram m3/kg (m·m·m)/kg
Substance concentration Mole per cubic meter mol/m3 mol/(m·m·m)
Special Derived Units
Frequency hertz Hz s–1
Force newton N m·kg·s–2
Pressure, stress pascal Pa N/m2
Energy, work joule J n·m
Power watt W J/s
Quantity of electricity coulomb C s·A
Electrical potential volt V W/A
Electrical resistance ohm V/A
Celsius temperature degree Celsius °C K – 273.15
TABLE 3-3 SI prefixes In what unit of measurement will the outcome be?
To perform the dimensional analysis, use the following
Increasing Magnitude Decreasing Magnitude process:
Factor Name Symbol Factor Name Symbol Where kg kilogram, m meter and s second
109 giga G 10–9 nano n 1. Write down the formula or equation:
106 mega M 10–6 micro μ
9.765 kg 1.056 m
__________________
103 kilo k 10–3 milli m 5.0 s
102 hecto h 10–2 centi c
2. Cross out the numbers, retaining the units and
101 deka da 10–1 deci d mathematical symbols:
kg m
_______
s
Dimensional Analysis. Mathematics in and of itself 3. After determining the correct units for the
can be a source of anxiety for many people. Couple outcome, simply perform the mathematical
that feeling with the need for mathematical values to functions:
have defining labels, and the difficulty level seems to
rise rapidly. Because many of the physics and physi- 9.765 1.056 10.31184
ological formulas used in respiratory care contain 10.31184 2.0624
________
specific measured variables, labeling can be problem- 5.0
atic. This is where dimensional analysis (the
4. Merge the mathematical results and the unit
reduction of units of measure) comes into play to
results to complete the problem and the dimen-
minimize confusion and to provide a clue as to the
sional analysis:
outcome of the mathematical formulas. For instance,
consider the following hypothetical example of a 2.0624 kg/m/s
mathematical equation that involves various forms
When the values are divided, so are the labels:
of measured data:
for example, meters/second. When the values are
9.765 kg 1.056 m
__________________ multiplied, the labels are merged: for example,
5.0 s kilogram-meter.
This equation indicates that a force is capable of TABLE 3-4 Examples of scientific notation
moving a mass of 2.0624 kilograms 1 meter in 1 second,
but in some cases, dimensional analysis can result in the Scientific Notation
cancellation of all unit values. Number Root Exponent Notation
In some cases, dimensional analysis results in the 0.00987 9.87 10–3 9.87 10–3
cancellation of all unit values. These cases yield what
1.007 1.007 — 1.007*
are termed dimensionless numbers, or dimensionless
variables. An example is the Reynolds number, a 1,230,000 1.23 106 1.23 106
description of fluid flow characteristics, described later 0.01 1.00 10–2 1.00 10–2
in this chapter. 230 2.3 102 2.3 102
*Numbers such as this cannot be further reduced by scientific notation.
Scientific Notation. The third system designed to
make the SI system easier and more convenient to
use is scientific notation. This is a system of recording
The same procedure and rules can be applied in
numerical data in a shorthand format, similar to an
the second example involving a very small number:
abbreviation. The notation is based on two simple
0.00000000014686. Convert the number to a value
rules: first, only numbers from 1 to 10 are allowed;
between 1 and 10. To do that, move the decimal point
second, an exponent of 10 indicates the magnitude
to the right until only a single digit remains to the left
of a number. These exponents may be either positive or
of the decimal point: 1.4686. The original number had
negative depending on the size of the numerical data.
10 places after the decimal point.
This system allows scientists to express both very large
numbers (e.g., 1,984,000,000) and very small numbers 0.00000000014686
(e.g., 0.00000000014686) logically, efficiently, and
precisely. Scientific notation allows mathematical
operations involving large or small numbers or So the scientific notation is 1.4686 1010. In other
combinations of both to be performed simply and words, to get the original number back, move the
clearly. decimal 10 places to the right as indicated by the minus
Consider the preceding examples. The first is a very sign. Table 3-4 presents further examples.
long and large number: 1,984,000,000. The first step is
to reduce the number to a value between 1 and 10; so
the number becomes 1.984. Next, the magnitude, or Mathematical Operations
size, of the number is shown as an exponent of 10. In Most of the mathematics used in respiratory care
this case, the number is larger than 1. Therefore, to involves the four basic mathematical operations—
determine this exponent, count the number of places addition, subtraction, multiplication, and division—
before, or to the left of, the decimal point. (In the next and a few formulas that require the use of exponents
example [0.00000000014686], we move the decimal to (powers and roots). Fortunately, these operations are
the right until the number is between 1 and 9. Because the familiar ones, and we need only review a few simple
original number was less than 1; so the places after rules. Addition, subtraction, multiplication, and
the decimal point are counted.) division have four rules in common:
1,984,000,000 1. Use only like entities (e.g., meters plus meters,
not meters plus centimeters).
2. Reduce measurements to the lowest common
There are 10 places to the left of the decimal, but the denominator.
number must be from 1 to 9 because the exponent 3. After completing the operation, restate the answer
shows the number of places the decimal has to move in in the most reasonable form for the task at hand.
order to increase or decrease the written value to the 4. Line up decimals one over the other.
original number. In this case, the exponent is 9; the
Multiplication is essentially a shorthand form for
decimal has to move 9 places to the left.
addition, and it follows the same basic rules as addi-
A positive exponent means the decimal moves to the
tion. However, here are six helpful hints for multiplica-
right (increasing the value), and a negative exponent
tion problems:
means that the value of the number must decrease by
moving the decimal to the left. For 1,984,000,000, the 1. When positive values are multiplied by positive
scientific notation is 1.984 109. The multiplication sign values or negative values are multiplied by negative
indicates that we are multiplying the value (1.984) by the values, the results are always a positive number: for
exponent (power) of 10, or raising 10 to the ninth power. example, () () (), () () ().
• When subtracting numbers with exponents, find

Best Practice the value of each number; then subtract the
results: for example:
Use of Signs (32) (43) (9) (64) 55
By convention, positive signs () are not gener-
• When multiplying numbers with exponents,
ally used; only negative values are signed ().
multiply the numbers; then add the exponents:
for example:
(24) (52) (2 5)42 or (10)6
Best Practice
• When dividing numbers with exponents, divide
the numbers and subtract exponents: for example:
Leading Zero
Always write decimals with a leading zero (0.xxx). (63 22) (6 2)32 (31) 3
Use of the leading zero can prevent tragic drug
errors in the case of medication calculations. The ORDER OF OPERATIONS
leading zero is much more than a placeholder; it
The order of operations relates to the approach to
is a very important safety tool.
mathematical formulas. Complex formulas contain
numbers that must be added, subtracted, multiplied,
and divided in various sequences and combinations.
2. When negative values are multiplied by positive The general approach is to work from the inner ele-
values, the results are always a negative number: ments of the formulas to the outer elements. Parenthe-
for example, () () (). ses ( ), brackets [ ], and braces { } are used to separate
3. When numbers containing decimals are multi- portions of the formula and are used in that order from
plied, the results should have at least as many the inside out. For example, a formula with the num-
decimals as the original number with the most bers removed might look like this:
decimal points: for example, 2.4 3.34 8.016.
4. When whole numbers are multiplied, their { [ ( ) ] [( )] } ( )
absolute value (the plus and minus signs are
Let’s put some numbers in the formula and see how it
disregarded) are always equal to or larger than
works:
either of the numbers multiplied.
5. Multiplying decimal numbers always results in a {[4(3 2)] [2(5 1)]} (7 2)
number that is smaller than either of the original
numbers: for example, 0.4 0.3 0.12. First, solve, or clear, the ( ):
6. If a whole number and a decimal number are {[4(3 2)] [2(5 1)]} (7 2)
multiplied, the result is always a number smaller
than the whole number and larger than the Next, clear the [ ]:
decimal: for example, 14 0.5 7.0. {[4(5)] [2(4)]} 9
Division is essentially a sophisticated form of
Then clear the { }:
subtraction, so it follows the four basic rules. The hints
for multiplication also apply, with one additional hint: {20 8} 9
Answers in division have at least one more decimal Finally, solve the problem:
place than the longest number in the problem: for
example, 285.68 1334.379 0.214092. 28 9 Solve the problem.
Exponents, or powers, are shown as superscripts. 19 This is the answer.

The superscript represents the number of times that the
number (or base) is multiplied by itself (i.e., raised): for MATHEMATICAL COUPLING
example, 24 2 2 2 2 16. The rules that apply Mathematical coupling deals with errors and
to mathematical operations involving exponents are: their effect on subsequent measurements and
calculations. The effects of undetected errors or
• When adding numbers with exponents, find the
inappropriate rounding in calculations move down
value of each number; then add the results: for
the chain of subsequent calculations that use the
example:
result of the erroneous calculation. The effect of the
(32) (43) (3 3) (4 4 4) (9) (64) 73 error grows larger with each step in the flawed
sequence of calculations. For example, if an exponent get the arterial blood can alter the results of the test. In
of 3 (e.g., 53) is mistakenly used instead of 2 (52) early other words, the ABG values are not as they existed
in a series of calculations, all subsequent calculations before the arterial puncture, but rather they have been
will be based on the wrong number (125 instead of altered by the test. (Of course, there are remedies to
25). For instance, one of the National Aeronautics and offset this effect.)
Space Administration’s (NASA) Mars probes missed the
planet Mars! An early error in converting from miles to
kilometers caused a coupling effect that multiplied a OCCAM’S RAZOR
small error in angle of flight into a planet-missing Occam’s razor, so named because the Razor was held
error. to “cut the truth finely,” is another rule of science and
math. It was named after a late Middle Ages English
theologian, philosopher, and mathematician named
HEISENBERG’S UNCERTAINTY PRINCIPLE William of Ockham (an alternate spelling) (1285–
1349). The paraphrased rule states, “When given a
The work of Werner Heisenberg in atomic physics choice of solutions, select the obvious (or simplest)
during the closing years of World War II led to one.” In other words, do not complicate matters.
important understandings about energy, materials, Put another way, the simplest explanation or solution
and measurement. Heisenberg was a German- for a problem is often the best one. The Razor is
American physicist and a member of the World War II popularly called the KISS principle: Keep it simple,
Manhattan Project, which developed the first nuclear stupid.
weapon. In the process of studying radioactivity,
Heisenberg needed to determine and understand the
atomic structure and activity level of high-energy
radioactive substances. After many failed attempts Physics
to determine the speed of movement and the Physics is a scientific discipline that studies the
position of electrons in the substances being relationships between matter and energy. Classical
studied, Heisenberg made a very enlightened physics was devoted to describing how things work
observation that has had implications far beyond (descriptive physics) and to the interactions of matter
nuclear physics. and energy (theoretical physics). In fact, the ancient
The following is a paraphrase of what Heisen- Greek and Roman schools of philosophy devoted
berg said: “The mere act of observing something much time and effort to describing how the world
changes the nature of the thing observed.”1 Known functioned and how things interacted. This inquisitive
as Heisenberg’s Uncertainty Principle, the statement activity eventually resulted in the rise of all modern-day
means that a given instrument can tell you either the science.
speed or the position of an electron—but not both From a clinical standpoint, the application of
simultaneously. The Heisenberg principle has shown physical laws to diagnostic and therapeutic problems
that the observations themselves change the proper- has led to today’s highly sophisticated and functional
ties of matter; the measure becomes part of the biomedical technology. This technology is spread
measurement. In other words, the very act of intro- across the entire spectrum of medicine, affecting
ducing a measurement instrument into a system patients of all ages and with every injury or disease.
changes the system from what the scientist wishes to Without an in-depth understanding of technology and
measure. its effects on the patient, the care provided would be
The keys to the accuracy of measurement are ineffective and even dangerous. The interaction of
twofold. First, choose the instrument or method with physics and biology (both normal and abnormal) must
the least likelihood of altering the system to be mea- be understood and utilized correctly to provide the best
sured. Second, choose the method of data collection possible patient care.
that is capable of providing the data desired within an Examples of the presence of classical physics in
acceptable degree of accuracy. medicine and respiratory care are the gas laws and the
An example is the drawing of an arterial blood gas concepts governing flow through tubes (such as blood
(ABG). For this test, an artery has to be punctured with vessels and airways). Examples of clinical physics are
a needle to obtain a blood sample. Patients may tend blood pressure measuring devices, thermometers,
either to hold their breath or to breathe deeply and oxygen supply equipment, heart-lung machines, and
quickly in anticipation of or in response to pain or radiology equipment. Largely due to the understanding
anxiety. Any of these actions can affect the blood gases and utilization of physical concepts has progress in the
(see Chapters 4 and 16) by altering the carbon dioxide diagnosis and treatment of disease and injury been
levels in the arterial blood. So the instrument used to made possible.
TABLE 3-5 Equivalent pressures for one Power is the time or rate of doing work (W/s); that
standard atmosphere is, it expresses the amount of work done over a given
period of time. Power units include the watt (1 joule of
760 mm Hg: 1 standard atmosphere at 0°C work per second) and the horsepower (550 foot-pounds
29.92 inches of Hg of work per second).
10.332 meters of H2O Energy, another term used to represent power or
force, is the power that can be used to do work. Energy
406.78 inches of H2O
exists in one of two states: kinetic or potential. Potential
33.899 feet of fresh water, 33 feet of sea water energy is the energy that can be translated into work of
14.696 pounds per square inch (psi) or pounds per some type—moving an object, overcoming resistance,
square inch gauge (psig) or affecting a chemical or physical energy change—but
1.033 kilograms per square centimeter that is not doing so at present. An example of potential
101.325 kilopascal
energy is a 20-lb rock sitting at the edge of a 50-ft-high
cliff. Despite the conditions of mass (200 lb) and
distance (50 ft), there is no active energy until some
outward force makes the rock topple and fall the
MECHANICS 50 feet, turning the potential force into a kinetic force.
Kinetic energy is energy in motion—energy that is
Mechanics is the branch of physics that studies force
doing something (like the rock falling off the cliff).
and movement, that is, all the phenomena that can
Kinetic energy can assume several forms, such as electri-
influence, by retarding or augmenting, the application
cal, thermal (heat), mechanical, chemical, or radiant.
of force and the inception of motion. Mechanics
Energy used to do work can be defined in terms of
includes such diverse variables as the flow of fluids
many descriptive units. Derived from combinations of
through tubes, the resistance of the chest wall to
force units and distance units, some commonly used
movement, and the causes of injury in falls and
energy units are joules, ergs, and foot-pounds. Likewise,
automobile accidents.
combinations of power and time units are commonly
used to indicate work or work potential. Examples of
Force and Motion. Issues of pressure and flow are these units are horsepower-hours, watt-hours, and
determined by reference to force and motion equa-
kilowatt-hours.
tions, which are direct descendants of Sir Isaac New-
As energy changes form, some of it becomes “lost”
ton’s observations and the natural laws he developed
to the system and cannot be used again. The loss is
from them. Air (gas) pressure is measured in many
generally in the form of heat. Therefore, any calcula-
units, which are listed in Table 3-5.
tions of energy, work, or force equations in terms of
Force is defined as the energy that originates or
energy expenditure must account for heat loss or the
arrests motion or other activities. Force can further be
equations will not balance.
defined according to its type or source, such as electro-
motive force (EMF, the difference in electrical potential energy in energy out heat loss or
across an electrical circuit) and mechanical force. energy out energy in heat loss
Other types of force are more commonly referred to as
To demonstrate this concept, briskly rub one hand
energy. The equation for force (F) is mass (M) times
against the other. Work (the movement of the hands) is
acceleration (a):
produced, but also produced is a significant amount of
F Ma heat, which is absorbed by the skin. The heat represents
energy loss due to friction.
Acceleration is the change in velocity over time.
Velocity is defined as distance (d) per unit of time (t).
Force units, then, are M(d/t) for simple constant linear Newton’s Laws of Motion. Sir Isaac Newton (1642–
acceleration. Examples are units such as kilogram- 1727), an English scientist and mathematician, was a
meter per second (kg-m/s), gram-centimeter per prolific discoverer. Not only did he develop the field of
minute (g-cm/min). differential calculus, but he also was responsible for the
Work (W) is the amount of energy expended to discovery that white light is composed of many colors.
move a mass a given distance. It is the transfer of Newton also discovered the three laws of motion.1
energy that occurs when a force is exerted on a moving
body in the direction of the body’s movement. Classi- Newton’s First Law of Motion (Inertia) The law of inertia
cally, the unit used to describe work is the kilogram- or Newton’s first law of motion, states that “a body at
meter (kg-m). The kg-m describes the mass (kg) and rest tends to stay at rest and a body in uniform motion
the distance moved (m). tends to stay in motion unless acted upon by an
1 kg-m/sec
FIGURE 3-1 Newton’s first law of motion: A body in motion tends to stay in motion
unless it is acted upon by an outside force.
outside force.” The assumption is that an ideal state sured in units called Newtons, abbreviated N in the SI
exists when forces do not act on objects unless system. More commonly, force is expressed in terms of
imposed by the observer. Intuitively, the first statement the mass equivalent per unit of area affected, such as
in the law is easy to grasp. If an object is securely kilograms times meters per second squared (kg·m/s2) or
positioned in a certain place, it remains there unless grams times centimeters per second squared (g·cm/s2).
someone or something moves it.
The second statement in the law is not as intuitive 2
and, in fact, may be counterintuitive. Casual observers
of nature know that everything that moves eventually 1
comes to a stop. The reason, however, is that all
movement is affected by an outside retarding or
resistive force—friction. Friction is a type of resistance Mass
or counter movement force (Figure 3-1). (kg)
The next logical question is, “If there are forces that
slow and stop movement, do other forces promote or
increase movement?” Newton addressed that question
in his second law of motion.
Newton’s Second Law of Motion (Acceleration) The Acceleration

law of acceleration (Newton’s second law) states that (m/s2) 4 2
“if a net force acts upon an object that object will
accelerate.” If the sum of the pushing and the pulling
forces is other than zero, the object moves, and the

movement is in the same direction as that of the
greatest force (i.e., toward the lesser force). This quality
of direction is called a vector. These concepts are Force
4 4
(kg m/s2)
shown in Figure 3-2.
The formula for this law is F Ma, where F FIGURE 3-2 Newton’s second law of motion: The force acting
force, M mass, and a acceleration. Force is mea- on an object is equal to its mass times its acceleration.
force. Adding an engine and a propeller at the rear of

CASE STUDY 3-1 the blimp gives a propulsive force to push the craft
forward, through the atmosphere’s gases, thus causing
Think of a car parked on a hill. With the car in a resistance to the forward motion.
neutral and the brake off, a little shove starts it Here is a question for thought and discussion:
rolling down the hill. The tendency of the car is What would the effect be if the blimp was shaped not
to keep rolling downhill until it hits something or like a bullet but like a railroad boxcar?
has to go uphill and loses its forward momentum.
Momentum. Momentum relates the part of Newton’s
Questions first law that says that a body in uniform motion tends
1. Given no crashes, what happens if the next to stay in motion. Momentum is the object’s tendency to
hill is as high or higher than the hill the car continue to stay in motion in the same direction
started on? (vector) unless or until it is acted on by outside forces.
2. What happens after that? As Figure 3-4 illustrates, mass, vector (direction), and
energy (force) are not changed; only their distribution
3. What is the final outcome?
in the system is altered. Note the effect of the small
force on the mass accelerated by the large force in the
figure (we will talk about his further when we discuss
Newton’s Third Law of Motion (Equal Reactions) The conservation of matter and energy). Can you think of
law of equal reactions (Newton’s third law) states some common applications of this law?
that “for every action there is an equal and opposite
reaction.” If a weight is pushed with a given amount of Gravity. Gravitation relates to the forces of attraction
force, an equal and opposite force will resist that push. between objects. The theory of gravitation holds that
These forces are in the form of friction, resistance, and all objects are attracted to all other objects. The force
heat, among others. Figure 3-3 illustrates the principle. of attraction is a factor of the product of their masses
The helium in the blimp is less dense than air and (M1 M2) and the inverse of the square of the distance
causes the blimp to rise (lift) to the altitude where the between the objects (d2). The complete formula for
gas is at the same density as the surrounding atmo- the force (F) of gravitation (G) is:
sphere, the blimp is held at that altitude by the balance
of the downward force of gravity and the upward lift F G(M1 M2) d2
Gravity
Propulsion Resistance
Lift
FIGURE 3-3 Newton’s third law of motion: For every action, there is an equal and
opposite reaction.
Original vector penetrate the lung) and large enough to rain out in the
Final vector
lung before being exhaled.
0.5 kg
Point of Impact 1 kg Elasticity. Elasticity is an important topic. For example,
suppose a person takes in a big breath, holds it, and
then exhales. While breathing in and holding the
breath, the body was actively using its respiratory
1 kg
muscles. When air is exhaled, the body only has to stop
Original vector 1 kg using those muscles, and the muscles relax into a
resting state. That is the elastic recoil of the lungs and
chest in action. Exhalation is normally a passive,
non-energy-consuming function.
0.5 kg
Diseases that modify the tissues of the chest wall
0.5 kg and the lungs can adversely affect this elastic recoil
Final vector
mechanism. The effect can lead to inadequate
FIGURE 3-4 Newton’s law of conservation of momentum: emptying of the lungs, trapping of air in the lungs,
At the point of impact, the first object changes direction and increased energy use for breathing. This is
(vector), as does the second object, imparting its force referred to as an increased work of breathing (WOB).
acting on the first object. In the absence of friction or Exhalation may become an active rather than a
gravity, the sum of the forces remain unchanged, and the passive function. Loosely defined, elasticity
net deviation in the sum of the pre- and post-impact might be seen as a form of stored or potential
vectors are constant. energy.
Hooke’s law, named after Robert Hooke (1635–
1703), an English physicist, describes the effects of
elastance. It states that the stretching of a solid is propor-
The gravitational constant, G, can be safely ignored tional to the force exerted on it. Figure 3-5 shows that an
because it is constant within the environment. The elastic (distensible) structure stretches linearly with
equation thus takes the form: increasing force until, at its elastic limit (tensile limit),
F (M1 M2) d2 stretch is no longer possible, and the structure breaks. A
simple example is an elastic band that snaps when
This formula, sometimes referred to as the inverse stretched too far.
square law, tells us two things. Figure 3-6 depicts the linear relationship
• First, the force of attraction decreases inversely with between pressure change and volume change in a
the square of the distance between objects. If the lung model. This is termed elastance (P/V). Its
energy or force exerted by one object on another reciprocal, volume change per unit of pressure
has a value of, say, 10 units and the objects are change (V/P) is called compliance. At the limits of
moved twice as far apart, the force exerted elastance, the application of more pressure does not
decreases by a factor of 4 to 2.5 units. This fact result in increased volume change (stretch) but does
also applies to bacterial contamination, radia- risk rupture of the lung unit.
tion, and many other physical phenomena.
• Second, small objects are more strongly attracted
to large objects than large objects are to small
ones. This is why something that is dropped falls CASE STUDY 3-2
to the ground. The ground (the Earth) does not
rise to meet the dropped object. This second Ms. T. S., age 25, fell while attempting a Waldo
effect also explains why some aerosol particles on her inline skates. Among her considerable
remain suspended for long periods of time while injuries were a fractured right wrist, three
others rain out relatively quickly. This concept of fractured ribs, and four amputated artificial
fallout or sedimentation occurs in response to fingernails. Because of the fractured ribs, she is
gravitational attraction. having difficulty breathing.
The effects of gravity you are in play when the
Question
respiratory therapist chooses appropriate devices to
ensure that aerosols will not only be in the therapeutic Explain why fractured ribs (other than for reasons
size range but also control particle retention in the of pain) would interfere with breathing.
lung. The particle must be respirable (small enough to
Increasing Force Increasing Alveolar Pressure
5 cm 10 cm 15 cm 20 cm 25 cm 30 cm
Alveolar Volume
H2O H2O H2O H2O H2O H2O
Increasing
Volume
Level
Volume
Level Doubles
Rupture
Volume
Level Triples
Increasing
Volume Level
Distance
Increases Very Little

Volume Level Beyond
The Elastic Limit Of The Lung Unit
Increasing Volume
Increasing Pressure
FIGURE 3-6 Hooke’s law related to the elastic properties of

the lung: Note the linear relationship between pressure
change and volume change. Beyond the limits of stretch,
the system breaks down and ruptures.
Increasing
Distance
States of Matter
Matter exists in one of three states: solid, liquid, or gas.

Each state imparts specific characteristics to the mate-
rial. In addition to those three states, a transition state,
called plasma, exists between solids and liquids. Also,
Increasing Force
some people consider vapors to be a transition state
FIGURE 3-5 Hooke’s law: Within the elastic limits of an
between liquids and gases. Plasmas, liquids, vapors,
elastic structure, the amount of stretch produced is and gases can all be classified as fluids, and the laws of
directly and linearly proportional to the force exerted fluid physics (the physical properties of materials that
on the object. Beyond the elastic limits, stretch quickly flow) apply to these substances to a greater or lesser
declines until a breaking point (tensile limit) is reached. degree. These laws, however, do not apply to solids
under circumstances we are likely to encounter.
Respiratory caregivers are often concerned with
Age-Specific Competency the transition of matter from one state to another.
Figure 3-7 presents a conceptual view of the bond
strength of each of the three main types of matter.
Elasticity The therapeutic use of humidifiers, vaporizers, liquid
Elasticity of the chest wall varies considerably and gaseous oxygen, mists, and aerosols all demand
over the life span. The ribs of infants are mainly a sound grasp of the general attributes of matter in
cartilage. Those of older children and of adults each of its states, of the changes that occur when matter
to late middle age retain flexibility, but flexibility changes form, and of the factors that influence or cause
deceases with age, and the ribs become rigid changes of state.
and brittle. When evaluating chest wall injuries,
performing assessments, and initiating treatment
regimes, be mindful of the elastic properties of SOLIDS
the chest wall relative to the patient’s age. Solids are substances in which the molecules are very
close to one another. The forces that cause the molecules
Solid Liquid Gas

CASE STUDY 3-3
Ms. I. R. presents to the emergency room
complaining of shortness of breath, fever, and
headache. Tests indicate that her blood oxygen
level is down, as is her blood carbon dioxide
molecule moderate bond
level. (Chapters 14–19 provide more detailed
weak bond strong bond information on laboratory tests.) She needs
FIGURE 3-7 States of matter: States in which matter exist
oxygen delivered by as accurate a means as
are in large measure determined by the type and strength possible. This means her peak (maximum)
of the bonds between atoms of the components of the inspiratory flow rate (PIFR) must be determined.
substance and the strength of the intermolecular forces
of attraction. Questions
1. How will PIFR help the respiratory therapist
decide how to deliver oxygen to Ms. R.?
to become closely positioned are called van der Waals 2. What other information regarding Ms. R.
forces. Solids are not compressible; they retain their does the therapist need to solve this
shape and mass unless acted on by outside forces. problem?
Solids are thought to be the densest form of matter
(density is mass per unit volume, for example, grams
per liter or mg/cc). Examples of solids are rocks, blocks
Because gases are also fluid, we can refer to the
of wood, steel beams, and ice.
movement of gases in terms of flow also. For example,
in the calculation of respiratory flow, it is customary to
PLASMA differentiate between inspiratory (I) and expiratory (E)
flow. Calculating these variables requires determination
Plasma is a type of matter that can be said to be transi-
of the respiratory rate (RR), which is breaths per
tional; that is, it exists in a state between a solid and a
minute (bpm), and of the duration of the average
liquid. It has some of the properties of a solid and
breath in seconds. The duration of a breath is then
some of the properties of a liquid. In plasmas, the van
subdivided into inspiratory (I-time) and expiratory
der Waals forces of attraction are a bit less intense,
(E-time) components. Combined and expressed as a
allowing some adjustment of shape and position. The
ratio of total breath time, this information, when
density of a plasma is a little lower than that of a solid.
reduced to its lowest common denominator, provides
An example of a plasma is glass, which, over time,
us with the inspiratory-to-expiratory ratio, or the I/E
deforms and flows to its lowest point. Another example
ratio. The normal value is 1:2. Once the I/E ratio has
is an egg yolk, which deforms but does not flow unless
been determined, finding the inspiratory flow is a
broken.
simple matter.
LIQUIDS
VAPORS
Liquids are substances that have moderate molecular
Vapors are seen as either gases that act as liquid or as
forces of attraction and that can take the shape of a
liquids that act as gases. Water vapor is the most
container in which they are placed. They are denser
common vapor, but others exist. They may flow coher-
than gases but less dense than plasmas or solids.
ently or have high resistance to compression, or they
Examples of liquids are water, gasoline, and blood
may not mix freely with other fluids.
plasma.
Liquids are also known as fluids. When liquids are
given an opportunity to move from one place to GASES
another, the molecular attraction is great enough that
A gas has the lowest density and the lowest strength
they tend to move in mass quantities. This movement
of attraction of the three classical, or standard, states of
is called flow. Flow is defined as volume moved per
matter. Like liquids, gases can take the shape of a
time period: for example, gallons per minute, cubic
container into which they are placed, and they are
centimeters per second, or liters per minute: The
fluid. Examples of gases are helium (He), hydrogen
formula for calculating flow is:
(H), oxygen (O), nitrogen (N), and water vapor (H2O).
flow volume time Air is a mixture of gases (Table 3-6). Gas mixtures have
TABLE 3-6 Constituents of air at

standard temperature and pressure CASE STUDY 3-4
(to 0.00 decimals) in the lungs
On a hot, hot summer day, a tall, cold drink of
Vol% Pressure iced tea, with lots of ice in a sweaty glass, is very
Substance Symbol Composition (mm Hg) welcome. Thank the triple point of water for that
Nitrogen N2 78.084 556.74 pause that refreshes. Ice (solid water), tea
Oxygen O2 20.947 149.35 (mostly liquid water), and a sweaty glass (con-
densed gaseous water vapor) all existed at once.
Argon Ar 0.934 6.66
Carbon dioxide CO2 0.033 0.24 Questions
Subtotal of air 99.998 712.99 1. What is the value of knowing a substance’s
Water (vapor) H2O 47.00 759.99 critical temperature, critical pressure, and
triple point?
Trace gases ~0.002 760.00
2. Name three devices used in respiratory care
that take advantage of the transition points
certain characteristics that are discussed elsewhere in of materials.
this chapter.
CHANGES OF STATE industrial gas delivery systems. Both the large-capacity

Each material is capable of changing its state given an liquid systems used to supply oxygen to hospitals and
appropriate temperature (critical temperature) and an industry and the smaller nitrous oxide (NO2) cylinders
appropriate pressure (critical pressure). For each depend on using pressure and temperature changes to
substance, a phase diagram can be constructed to turn liquid oxygen and nitrous oxide into their gaseous
illustrate this capability (Figure 3-8). The phase diagram states.
is a graph that plots temperature versus pressure. It The transition points have special but familiar
shows the effects of changing pressures and tempera- names. The point of transition from solid to liquid is
ture on the state of matter in which a given material the melting point. The point at which a liquid turns into
can exist. At any given point where temperature and a solid is its freezing point. The point of transition from
pressure intersect, the material will be liquid, solid, or liquid to gas is called the vapor point, or point of
gaseous form or in a state of equilibrium between the vaporization, and the point of change from gas to
various states of matter. This fact comes into good use liquid is the dew point. Some materials skip the liquid
in the fractional distillation of air to create gaseous phase and go directly from solid to gas; this type of
oxygen (O2). The theory is also applied in medical and change is called sublimation. Dry ice is a good
example. Dry ice is solid carbon dioxide (CO2), which,
at normal room temperature and pressure, turns from
218 B
its solid (ice) state directly into gaseous CO2.
Another important point on the graph is the place
Pressure in atmospheres
C where all three curves come together, the so-called

triple point. The triple point is significant because at
Liquid that point a substance can exist in all three states of
ints
ts
matter simultaneously. Water is one of the few materi-

Melting poin
Freezing po
ts als that can do this within our preferred temperature

in
e
ur
1 po and pressure range.

ss
g
re
Solid ilin
p
Bo
por
Mass, Weight, and Density

Va
0.0063 ion Vapor

at
(4.8 mm. Hg) m A Mass, weight, and density are separate but interrelated
bli
Su concepts that, in some conditions, can be difficult to
D
distinguish.
0.01 100 374
t° C MASS
FIGURE 3-8 Example of a phase diagram. Point A is the Mass is a difficult concept to define. One definition
Triple Point of this substance. is that mass is the quality of matter that defines the
amount of matter in an object. If this definition is DENSITY

accurate, then mass is an expression of the number of Density is the expression of a substance’s weight per
molecules or atoms that make up an object or sub- unit of volume. To determine a substance’s density,
stance. Until relatively recently, mass and weight have weigh a given volume of the material. This is not
been treated and thought of as essentially identical difficult for liquids or gases because they adopt the
concepts. However, it is now known that mass is shape of the container they are in. For solids (and
independent of the location of the substance, whereas plasmas), getting a weight is a bit more complex; that
weight is dependent on the substance’s location. Mass is, it might be difficult to measure the volume of an
is said to be an invariant quantity; if we do not add or irregularly shaped solid or plasma. The problem was
remove a quantity of matter, mass remains constant. solved by a Greek philosopher named Archimedes
Mass is measured in units of kilograms. The force (c. 287–212 BCE), who discovered that, when a solid
needed to move one kilogram of matter 1 meter per body is immersed in water, it displaces an amount of
second per second is called a newton (N kg m/s2). water equal to the volume of the immersed solid. This
is called Archimedes’ principle. Determining the volume
WEIGHT of the displaced water, an easy determination to make,
Weight on the other hand is a variable quantity whose indicates the volume of the solid in question. Given
value is dependent on position or location. Weight (W) the volume and the weight of the substance, its density
is the quality of matter expressed by its mass (M) and can be calculated.
the force of gravity (G) acting on the mass: Specific gravity (SG) is a ratio of the density of
one substance to the density of a standard substance.
W MG For solids and liquids, the standard substance is water.
The relationship between mass and weight is illustrated For gases, the standard substance is air. For example,
in Figure 3-9. An object with a mass of 70 kg on the the specific gravity of oxygen can be calculated as
Earth will also have a weight 70 kg on the Earth. On
specific gravity of oxygen density of oxygen
the moon, however, although its mass remains 70 kg,
density of air
its weight is only 11.9 kg. The difference is due to the
1.429 g/L 1.293 g/L
effects of gravity. Thus mass is invariable, and weight is
1.105
location dependent, positional, and variable. In space,
the weight of an object is even lower, although the Note that the units canceled. Because the units are the
mass remains constant. According to inverse square same for both substances, they cancel out, and the
law, the farther two masses are from each other, the less values for specific gravity are dimensionless, that is,
the attraction (the effect of gravity) is of one mass for have no units.
the other. How much less depends on the distance
between them.
Basic Electrical Theory

Knowledge of electrical theory is important for
several reasons. First, many of the respiratory thera-
pist’s tools are powered by electricity. Second, the
theories and behaviors of electrical circuits and the
laws that govern those behaviors are in many cases
identical to the laws and application in fluid physics.
Several facts about electrical charges are important to
Earth Moon Space keep in mind:
Weight 70 kg 11.9 kg 0.09 kg • Like charges repel. Two positively charged
objects attempt to move away from each other.

Mass 70 kg 70 kg 70 kg
Conversely, unlike charges attract each other.
Gravity* 1.00 0.17 0.001 Thus, a positively charged object is attracted to a
negatively charged one, and vice versa.
*Relative to the earth. • Charge is conserved. In a closed system, the total
FIGURE 3-9 Mass versus weight: Weight is gravity amount of charge is stable and neutral. The
dependent, whereas mass is independent of gravity. number of positive charges equals the number of
As the force of gravity decreases, so does weight, but negative charges. Therefore, the system is both at
mass remains constant. equilibrium and electrically neutral.
ELECTRICITY illustrates a simple electrical circuit. The movement of

Electricity is the movement of electrons (negatively electricity depends on the power and resistance to flow
charged subatomic particles) from one portion of space in the circuit. Power in this sense refers to the differ-
to another. Electricity, like other forms of energy, exists ence between the electron concentration (charge) at the
in one of two states: active (kinetic) and resting source of power and the concentration at the receiver
(potential). Electricity changes from the passive to the (the light bulb in this case).
active state when two conditions are met:
1. There is an electrical potential, also known as a OHM’S LAW
charge difference. In this case, potential means that
The movement of electricity through the electrical
there is a difference between the number of
circuit is summarized by Ohm’s law, which states
electrons (negatively charged particles) at one
that current (I) is equal to power (E) divided by
part of a circuit and the number of electrons at
resistance (R):
another part. So, if one area (D) has 1000 elec-
trons and another area (H) has only 500 elec- IER
trons, there is a net electron difference between
Current (I) is the amount of electrical flow per
D and H of 500 electrons. Electricity always
unit of time passing a given point in the circuit. Flow
moves from areas of high electron concentration
is influenced by the difference in electrical charge
to areas of low concentration.
(pressure) at each end of the circuit. This charge
2. A conductor connects D and H. A conductor, or
difference is directly proportional to the resulting
medium, allows electrons to flow through it
flow (or current) and is inversely proportional to
without altering it. This flow of electrons occurs
the resistance of the circuit to the flow. The charge
with varying degrees of ease through different
difference is measured in volts (V). A volt is the
materials. Factors that impede the movement of
amount of charge differential needed to send
electrons are said to cause increased electrical
1 ampere (A) of current through a circuit having
resistance in that material. The opposite of a
1 ohm (Ω) of resistance.
conductor is an insulator, which is a substance
Power, or electromotive force (E), is the ability to do
through which electricity cannot easily flow.
work. It is usually rated in base units of watts (W) or
the more common kilowatts (kW).
CIRCUITS Resistance (R) is an expression of the forces that
impede or restrict current flow. It is measured in ohms
Electrical circuits are devices designed to carry an electrical
(Ω). Electrical circuits use the inherent resistance of
charge from one site to another. Circuits can be very
certain materials to electrical flow to perform desired
simple or exceedingly complex. A simple circuit might
tasks: for example, toasters, incandescent lights, space
consist of an electrical source, two lengths of insulated
heaters, and soldering guns. All these examples depend
copper wire, a switch, and a light bulb. Figure 3-10
on electrical resistance to produce heat—and, in the
case of light bulbs—light plus heat, in response to
current flow.
Wire
CAPACITANCE
- Capacitance is the ability of a device to store an electri-
cal charge for later use or to stabilize power in a circuit.
Battery
This term is also used to refer to the potential differ-
Light
power ence between the two sides of a circuit.
bulb
source
+ FREQUENCY
Frequency is another factor to be considered when
dealing with electricity or electrical devices. In circuits
like the simple one in Figure 3-10, frequency is not a
Switch problem because the battery power is consistent,
FIGURE 3-10 A simple electrical circuit consists of a power within reason. This type of current is called direct
source, a conductor, a device to use this power, and a current (DC). Direct current is mostly reserved for
switch to control the flow of electrons. low-power, low-duration needs such as flashlights,
Best Practice Light Waves

The respiratory therapist needs to be familiar also
AC Versus DC with light wave characteristics. Several monitoring
and analysis instruments depend on the ability
Equipment to be connected to AC or DC circuits to differentiate various types of light waves
must be rated—that is, approved—for use on (see Chapter 16).
these types of circuits. Devices designed for use Light waves range from ultraviolet to infrared. A
with AC circuits must be matched to the fre- particular light wave’s position in the light spectrum is
quency and power output of the circuit. Failure a result of its wavelength, its amplitude, its period, and
to match the type of equipment with the circuit its frequency.
can result in damage to both the circuit and the
device and, in some cases, in injury to patients • Wavelength (lambda, ) is the distance from the
or staff. peak of one wave to the peak of the next wave.
Wavelength is measured in nanometers (109).
• Amplitude (A), the displacement of the wave
particles, is the height of the wave from top to
bottom. It represents the strength, energy,
CD players, or car starters. However, the current we use intensity, or power of the wave.
to run our household appliances, medical devices, and • Period (T) is the time it takes a wave to travel a
electric lights is alternating current (AC), that is, power is given distance (i.e., the time between two peaks).
turned on and off many times a second. It is described Another more common term for this charac-
in terms of cycles per second, or hertz (Hz). Although teristic is “cycle.”
not important to our discussion, alternating current is • Frequency (Hz) is the number of waves that
used to reduce resistive forces and thus strain on the pass a given point per period of time or the
system. number of periods divided by the time period.
The concepts embodied in Ohm’s law are critical Frequency is generally expressed in terms of
both to electrical flow and to the movement of gases in hertz (Hz). One hertz equals 1 cycle per
respiratory care equipment and the lung. Additionally, second (cps).
Ohm’s law plays a large role in how blood circulates in Figure 3-11 illustrates these characteristics.
the body. Ohm’s law is another critical theory that the
RT must master.
600 nm
wavelength
CASE STUDY 3-5
Different areas of the world use different mix- one cycle
tures of power and frequency. At some power a b
levels, motors and electrical devices operate at
faster or slower rates than at others. Some
countries use higher-frequency power than is
Intensity
used in the United States.
Questions
1. What advice would you give your boss, who
wants to donate some old ventilators to a
medical mission in another country?
0 Time (s) 1
2. What would be the effect if a lower-power
level were applied to a heater that worked on Frequency cycles/s (10 cps)
a resistor system?
FIGURE 3-11 Characteristics of light waves: Intensity is
3. How might you check to see whether equip- essentially a power rating. Frequency is the number of
ment you wanted to donate would work cycles per time period, usually measured in seconds, and
where they would be sent? wavelength is the distance from one wave crest to the next.
From Mathews PJ. Co-oximetry. Respir Care Clin N Am. 1995;1:61
Fluid Physics Pressure Pressure Pressure Vector
Fluid physics is the study of why fluids (matter that

50 mm Hg 30 mm Hg 50 mm Hg
flows) act as they do and of the forces that prompt
those actions. Fluids include gases, liquids, and plas- 13 mm Hg 26 mm Hg 13 mm Hg
mas. The factors that influence or cause flow are varied
both in effect and in strength. 100 cm H2O 60 cm H2O 40 cm H2O
90 cm H2O 90 cm H2O 0 No flow

VISCOSITY
FIGURE 3-12 Driving pressure gradients and flow: Three of
Viscosity is a primary factor influencing the flow of
the pipes have different pressures on their ends, result-
fluids. Viscosity is often thought of as thickness (e.g., ing in a pressure gradient (P) and flow in one direction
ketchup is thicker—has a higher viscosity—than water). (vector). Note that equal pressures result in P 0 and
The formal definition in a sense reinforces this com- no flow.
monly held conception. Formally, viscosity is the
resistance that a gaseous or liquid system offers to
flow when subjected to a shear stress. (A shear stress is
what occurs when two or more parts of a system are DRIVING PRESSURE
moving at different speeds or in separate directions Driving pressure is another term used to refer to pressure
or both.) As a result, fluids become less viscid (thick) gradient. Figure 3-12 provides several examples of
as they are stretched and pulled. Once rendered pressure gradient, or driving pressure. The term
less viscid—having a lower viscosity—they flow “driving pressure” is used when the pressure provides
more easily. the force, or drive, to overcome all the resistive forces
Viscosity is measured in SI units called poises. that impede movement or, in the case of fluids, flow.
Simple gases have a low viscosity, ranging in the area Driving pressure is also a vector force, having both
of 100–200 micropoise at STP (standard temperature magnitude and direction.
and pressure). Simple liquids have viscosities two Hagen-Poiseuille’s law, better known as Poiseuille’s
orders of magnitude higher, in the centipoise range. law, describes in mathematical terms the factors that
influence the flow of fluids through tubes. It explains
PRESSURE GRADIENT the effects of tube geometry on resistance and flow in
tubes. The formula for this description is:
The pressure gradient in the fluid system is another
primary factor in flow dynamics. A pressure gradient is V
______
Pr 4
the difference in pressures from one area to another 8L
in the system. Pressure gradients are commonly
where V fluid flow rate (volume per unit of time).

thought of in terms of two areas of the respiratory
system: between the ends of a tube or between the P driving pressure
respiratory system and the external environment. r4 radius of the tube to the fourth power
The pressure gradient has both quantity and vector viscosity of the fluid
components; that is, pressure gradients are forces /8 mathematical constant ( 3.14)
applied in a direction. The formula for pressure L length of the tube
gradient (P) is This formula states that flow is directly propor-
P P1 P2 tional to the driving pressure and the radius of the
tube and inversely proportional to the length of the
where P1 is the higher pressure and P2 is the lower tube and the viscosity of the fluid. For clinical
pressure. For example, the pressure at end A of a tube purposes, the mathematical constant /8 and the
is greater than the pressure at end B. As an example, viscosity constant can be eliminated. The restated
calculate the pressure gradient if A equals 70 mm Hg formula is:
and B equals 42 mm Hg. Indicate the direction (vector)

Pr 4
of force. V _______
L
P P1 P2
The restated formula now relates flow (V) directly to

P 70 42 mm Hg
the pressure gradient and to the radial size of the tube
P 28 mm Hg (A to B)
and inversely to the tube’s length. The formula can be
Fluids therefore exhibit directionality (vectors)— further rearranged to find P:
movement—from high-pressure areas to low-pressure LV
P ___
areas. r4
One more step reveals an interesting conclusion. Move flow, it comes out of the hose in a smooth clear stream.
V
to the other side of the equation so that In fact, laminar flow is also called streamlined flow.
P __
___ L

r4 Turbulent Flow. Turbulent flow, on the other hand, is a
V
type of flow that swirls and eddies, causing increased
but resistance and requiring increased pressure gradients
P resistance (R)
___ to move the same amount of fluid as laminar flow

would. In Figure 3-13, turbulent flow is caused by
V
So resistance (R) is directly related to length of the sidewall obstruction and changes in both the velocity
tube (I) and inversely related to the fourth power of the and direction of flow caused by the obstructions.
tube’s radius (r 4). This conclusion suggests that short,
wide tubes have lower resistance to flow than do long, Transitional Flow. Tracheal-bronchial, or transitional,
narrow ones. flow has elements of both laminar and turbulent flow.
Figure 3-13 illustrates transitional flow in a branching
tube. The branch causes a slowing of flow and a change
TYPES OF FLOW of vectors in parts of the flow while other parts of the
Flow is dependent on the density and viscosity of the flow remain laminar. For example, if a finger is placed
fluid and on the pressure gradient in the system.2 The into the water stream about an inch from the hose
three most common types of flow are laminar, turbu- outlet, the stream splits in two. However, there is also
lent, and transitional or tracheal-bronchial (Figure 3-13). some spray to the top and bottom as the turbulence
from the finger takes effect. Another example is water
Laminar Flow. Laminar flow is flow that runs parallel to running over a smooth stretch of streambed and then
the walls of smooth tubes. It is a smooth, relatively coming upon a rocky bottom with a few obstructions
low-resistance flow. Laminar flow requires less force to leading to rapids. The flow of the smooth-running
move a given quantity of fluid through the tube than stream is laminar, the rocks on the bottom cause
do the other two types of flow. Laminar flow is transitional (tracheal-bronchial) flow, and the rapids
enhanced if low pressure gradients and low flow rates produce turbulent flow.
are used. Think of a garden hose with the spray attach- Type of flow is determined by the Reynolds
ment removed; when the water is turned on at a low number, a dimensionless factor determined math-
ematically and based on density, velocity, viscosity, and
the inertial force applied on the fluid. Flows with a
Reynolds number greater than 3000 are turbulent;
Laminar
those with a Reynolds number below 2000 are laminar.
Flows with a Reynolds number between 2000 and 3000
are transitional.
BERNOULLI’S PRINCIPLE
Turbulent Bernoulli’s principle is based on the law of continuity.
The law of continuity, in effect, says that the product of

flow (V) times the cross-sectional area (A) of a tube is

constant if the flow is constant. Therefore, at a given

flow rate (indicated by V, which means volume per

unit of time—the definition of flow), if the size of the
tube is increased, the velocity of the flow must decrease.
Transitional For the net product of flow times cross-sectional area to
remain unchanged, a change in cross-sectional area
somewhere along the tube requires a change in velocity
(distance in some direction in a period of time). This

principle is diagrammed in Figure 3-14. The Bernoulli
equation allows the approximation of the effect of
changing one or more of these factors.
V
A ⬇ V
A
1 1 2 2
FIGURE 3-13 Flow types: The three basic types of flow are
laminar (smooth), turbulent (rough), and transitional or where V
is velocity and A is the cross-sectional area of
tracheobronchial (a combination). the tube. The approximation symbol (⬇) is used to
P1 P3
P2
V1 v1 v2 v3 V3
2
Separation
1 3 bubble
FIGURE 3-14 Bernoulli’s principle: A system with constant

flow (V 1V 3) exerts a side (lateral) wall pressure (P1) and

has a velocity (v1) along segment 1. If the tube cross- FIGURE 3-16 The Coanda effect: Given a high enough flow
sectional area (segment 2) decreases, the pressure (P2) through a tube, the lateral wall pressure drop forms a
also decreases and the velocity (v2) increases. As the separation bubble, which permits the flow to attach to
cross-sectional area increases again (segment 3), the one wall of the tube. Unless acted on by another force,
pressure (P3) once more increases and the velocity (v3) the flow remains attached to that wall.
decreases. If the changes in cross-sectional areas are
equal, the implied relationship is that Pv k (k is
constant). high velocities through tubes, fluids attach to one of
the sidewalls due to the formation of a high-pressure
fluid separation bubble on one wall. The result is the
recognize that frictional and other resistance forces act formation of a low-pressure boundary layer with slower
to slow velocity and to remove energy from the system. flows at the walls and faster laminar flow in the center
Therefore, if the flow V
through the tube is constant, of the tube. See Figure 3-16. This attachment persists
then, when the cross-sectional area (A) decreases, the until another force acts on the flow.
velocity (v) must increase to allow the equation to Another effect of the Coanda or boundary layer
work. When applied to the Bernoulli equation (the phenomenon is that, in smooth tubes, the laminar
lateral pressure of flowing fluid or gas is inversely flow forms a ballistic or bulletlike profile, as shown in
proportional to the velocity), as the velocity increases Figure 3-17. Ballistic, or parabolic, flow patterns are
due to the decrease in cross-sectional area, the lateral known to reduce resistance to flow because of their
pressure also decreases. wedgelike shape, which can be thought of as opening a
An application of Bernoulli’s principle and its path in the opposing material.
effect is a device called a Venturi. The Venturi uses the
sidewall pressure drop to add a secondary entrained
gas to the system, as shown in Figure 3-15. Gas Laws
The area of physics that is perhaps of greatest concern
and interest to respiratory therapists is that of the gas
THE COANDA EFFECT
laws. The gas laws are a series of equations that explain,
Closely related to Bernoulli’s principle is the Coanda
(or sidewall attachment) effect. In the Coanda effect, at
A
P3
P1
P2
A2 C
A1 Angle of A3
2 divergence
1 B 3
B
FIGURE 3-15 A Venturi device: The Venturi device makes
air entrainment possible by the pressure drop in segment 2. FIGURE 3-17 Ballistic flow profile: The characteristic
Three factors are critical in the design. There must be a laminar flow forms a bulletlike, or ballistic, velocity
gradual tapering from segment 1 to segment 2; the angle profile. In this profile, A and B (called boundary layers),
of divergence from segment 2 to segment 3 must be less are slower-moving gas streams than those of section C
than 15°; and the cross-sectional area of segment 3 must (axial flows) because of the relatively higher resistance
be large enough to accommodate the increased volume of to flow on the wall surfaces compared with the center of
gas introduced from the entrainment port (B). the lumen.
TABLE 3-7 Gas law symbols and units BOYLE’S LAW

Name Symbol Unit Boyle’s law, developed by Robert Boyle in 1662, states
that if the temperature of a gas is constant in a sealed
Volume V mL
container, its pressure (P) varies inversely with its
Pressure P mm Hg volume (V). In other words, at any given temperature,
Temperature T degrees Absolute (°A) if a gas is pressurized, its volume will be reduced
or Kelvin (K)* proportionately to the pressure change; if we increase
Moles of gas the volume of a gas, its pressure will increase. Figure 3-19
illustrates this law. The formula representing for
Gas constant R J/°A Boyle’s law is:
Initial value (subscript) 1
Final value (subscript) 2 P1 V1 P2 V2
*K °C 273.15; no degree symbol is used with the unit K. Another way to express Boyle’s law is:
through the use of physics and mathematical formulas, PV k

the manner in which gases act under normal environ-
where k is a constant. Any increase in V must be offset
mental conditions. Gas physics forms the groundwork
by a reduction in P, and any reduction of V must be
and is the supporting structure of the art and science of
offset by an increase in P. For example, at a constant
modern respiratory care. Without a strong command of
temperature, and with three known values, we can
these principles, the respiratory therapist’s success in
solve for the unknown value:
the care and treatment of patients is severely limited.
In gas law problems, certain conventions, standard P1 25 mL
symbols for physical values, and specific units are used
(Table 3-7). These units and conventions are frequently V1 100 mm Hg
used in respiratory therapy and should become very V2 50 mm Hg
familiar to therapists before long. P2 ?
There are three major gas laws: Boyle’s law,
Charles’s law, and Gay-Lussac’s law. Memorize them Thus:
and the combined gas law, which is a modification of
the ideal gas law. The combined gas law allows the P1 V1 P2 V2
examination of all of the variations in the other three 25 100 50 V2
gas laws. These modifications take into account the fact
that we generally work and live in a relatively constant 25 100
V2 _________
physical environment. The major variables in the gas 50
laws are gas pressure, gas volume, and gas temperature 2500
V2 _____
(Figure 3-18). 50
V2 50 mL
Temperature
T1 T2
Gas volume Pressure

P1 P2
V1 V2
FIGURE 3-18 Elements of the gas laws: At physiological

conditions, all gas laws can be stated as equations involv- FIGURE 3-19 Boyle’s law: If the temperature is kept
ing pressure (the gauge), temperature (the thermometer), constant, the volume of a gas varies inversely with the
and volume (the box). pressure of the gas.
Best Practice T1 T
Temperature
All temperatures in gas law equations must be
stated in absolute (A) temperatures or kelvins (K).
P1 P2
V1 V2
CHARLES’S LAW
Charles’s law, developed in the 1760s by Jacques
Charles, is an extension of Boyle’s law. Charles FIGURE 3-21 Guy-Lussac’s law: Given a constant volume,
per formed a series of experiments designed to test pressure varies directly with temperature.
Boyle’s law and to determine the effect that tem-
perature changes have on gases. Charles found
that, if pressure (P) is held constant, volume (V) GAY-LUSSAC’S LAW
changes directly with temperature (T). Therefore, if
Gay-Lussac’s law states that, if the volume (V) of a gas
a volume of gas is heated while the same pressure
is kept steady, temperature (T) will change in the same
is maintained, the volume (V) of that gas will
direction as pressure (P). That is, the change in pressure
increase or expand (Figure 3-20). The relation ship
of a given volume of gas is directly related to the
between T and V is direct and equals a constant
change in temperature (Figure 3-21). This law can be
such that V/T ⫽ k. The formula representing
expressed symbolically as P ⫼ T ⫽ k. The equation
Charles’s law is:
illustrating Gay-Lussac’s law is:
V V
1
⫽ ____2
____ P P2
T1 T2 1
⫽ ____
____
T1 T2
For example, if P is constant, V1 ⫽ 1200 mL, T1 ⫽ 320°A, For example, letting P1 ⫽ 780 mm Hg; T1 ⫽ 310°A;
and T2 ⫽ 290°A, then we can solve for V2: T2 ⫽ 315°A; and V ⫽ a constant, solve for P2.
V V P P2
1
⫽ ____2
____ 1
⫽ ____
____
T1 T2 T1 T2
V1
1200 mL ⫽ _____ P2
780 ⫽ ______
______
________
320° 290° 310°A 315°A
1200 ⫻ 290 ⫽ _______

348000 ⫽ 1087.5 mL 780 ⫻ 315 ⫽ P
__________
V2 ⫽ ___________ 310 2
320 320
245700 ⫽ P
_______
310 2
T1 T2 P2 ⫽ 792.58 mm Hg
THE COMBINED GAS LAW

The combined gas law provides us with a method of
comparison and analysis of various gases at widely
P1 P2 varying times and conditions. Figure 3-22 depicts the

combined gas law, which involves two other laws: the
V1 V2 ideal gas law and the clinical gas law.
Ideal gases are a theoretical construct used to
analyze the mathematical relationships among the
FIGURE 3-20 Charles’s law: If the pressure is kept physical forces acting on gases. Ideal gases do not exist
constant, the temperature of a gas varies inversely with in nature. Nevertheless, they serve an important
the gas’s pressure. function because they allow us to imagine what would
is needed, although, if a factor is constant, we can

T1 T2
use it.
For practice with this concept, solve the following
problem for T2:
P1 770 mm Hg
V1 500 mL
P1 P2
T1 312°A
P2 750 mm Hg
V1 V2
V2 550 mL
P V P2 V2
_______
1 1
_______
T1 T2
P1V1 = P2V2
T1 T2 (750)(550)
(770)(500) ___________
__________
FIGURE 3-22 Combined gas law: The combined gas law 312 T2
illustrates the interrelationship among three variables. By
(750)(550)(312)
using the formula presented, we can solve any gas law T2 _______________
problem for which we know any five of six possible vari- (770)(500)
able values.
128700000
T2 ___________
385000
happen to a gas or a mixture of gases if we altered the T2 334.29
physical conditions acting on them.
The Ideal Gas Law. The ideal, or perfect, gas law states As shown, even complex problems with many
that the product of a gas’s pressure (P) and its volume (V) changing variables can be solved using the combined
is equal to the product of its temperature (T) and the gas law.
number of moles () of the gas times the universal gas
constant (R):
DALTON’S LAW
PV RT
Air is a mixture of several gases, each of which
The Clinical Gas Law. The molar concentration of imparts its own characteristics to the inhaled vol-
an ideal gas is constant (22.4 L; see the discussion of ume. Because respiratory therapists alter the mix-
Avogadro’s number later in the chapter). The energy ture’s composition for therapeutic reasons, it is
value of gases (universal gas constant, R) within important to know how the characteristics of the
physiological ranges is also constant (R 8.31 joules/ mixture are influenced by changes in composition
mole/°A). That is the number of energy units and by changing conditions. Dalton’s law describes
released or absorbed per mole per degree of tem- the effect of gas composition on the pressures that
perature change. Thus, molar concentration and the gas exerts on its surroundings.
energy value can be ignored. So, the combined gas Dalton’s law of partial pressures states that the
law is used. total pressure of a mixture of gases is equal to the
sum of the pressures exerted by the individual gases.
The Combined Gas Law. The combined gas law Each gas in the mixture exerts a pressure equal to the
combines the laws of Boyle, Charles, and Gay-Lussac fractional concentration of that gas. Fractional
with the definition of a mole in a single equation that concentration means the percentage of the total gas
describes the actions of gases when one or more of the volume made up of a given gas. In other words, if a
gas’s physical characteristics undergo change. gas mixture is made up of four gases (A, B, C, and
D), the pressure of the gas mixture (pT) equals the
P V P2 V2 total of all the gas pressures: Pressure A (pA)
_______
1 1
_______
pressure B (pB) pressure C (pC) pressure D (pD)
T1 T2
equals pT.
This formula can be solved for an unknown of any of However, the law is not quite that simple because
the incorporated factors. For this equation, no constant we have to account for the amount of each gas in the
mixture. This is easy if the proportion or percentage of TABLE 3-8 Partial pressure (in mm Hg)
each gas is known. For example: of gases in the air, alveoli, and arterial
blood at STP
pT 200 mm Hg
Alveolar Arterial Venous
Gas A is 30% of the mixture: 200 0.3 60 mm Hg
Gases Dry Air Gas Blood Blood
Gas B is 10% of the mixture: 200 0.1 20 mm Hg
PO2 159.0 100.00 95.0 40.0
Gas C is 40% of the mixture: 200 0.4 80 mm Hg
PCO2 0.2 40.0 40.0 46.0
Gas D is 20% of the mixture: 200 0.2 40 mm Hg
pH2O (vapor) 0.0 47.0 47.0 47.0
Total % 100% Total pressure (pT) 200 mm Hg
pN2 (and
trace gases) 600.8 573.0 573.0 573.0
The pressure exerted by each gas in the mixture is
Total 760.0 760.0 755.0 706.0
called its partial pressure (p or P). So gas A has a partial
pressure of 60 mm Hg, and gas C has a partial pressure
of 80 mm Hg. TABLE 3-9 Standard temperatures and
A refinement of this technique is to determine the partial pressures of oxygen at selected
composition of the mixture of gases and then multiply elevations
the total pressure by the percentage concentrations of
the individual gases to arrive at the fractional concen- U.S. Std. Atmosphere
Elevations Temp. (mm Hg, Oxygen
tration of the gas (F). In the example, gas B has a
fractional concentration of 10.0%, or more properly m Ft (°C) dry) (mm Hg)
FB 0.100, where F fractional concentration and –1000 –3280 70.7 854.08 179.36
B gas B. Likewise, gas D has an FD of 0.20, or a –500 –1640 64.9 806.00 169.89
concentration of 20.0%, and gas A has a concentration 0 0 59.0 759.99 160.00
of 30.0%, with an FA of 0.30. Note that the F values for
the gases are simply decimal equivalents of the percent- 250 820 56.1 737.24 154.82
age concentrations of each gas; that is, 15% equals 500 1640 53.2 715.53 150.26
0.15, 6% equals 0.06, and 99% equals 0.99. Of course, 750 2461 50.2 694.85 146.92
100% equals a fractional concentration of 1.00. 1000 3281 47.3 673.65 141.47
Knowing the fractional concentrations of the gases and
1500 4921 41.5 633.84 133.11
the total pressure of the mixture, we can determine the
partial pressure of each gas. 1750 5742 38.5 614.71 129.10
The composition of the Earth’s atmosphere is fairly 2000 6562 35.6 595.58 125.07
constant. The fractional concentrations of the gases 2500 8202 29.8 559.91 117.58
change little over the surface of the earth. What does
3000 9843 23.9 525.79 110.42
change is the total pressure of the atmosphere and
therefore the partial pressures of the gases making up 3500 11483 18.1 493.22 103.58
the atmosphere. Table 3-8 lists the partial pressures From Glover TJ. Pocket Ref. Littleton, Colo: Sequoia Publishing Inc; 1997
of the four gases that account for 99.9% of the total
volume of atmospheric gases. Table 3-9 lists the
changes in atmospheric pressure and oxygen pressure gases. This subtraction results in an adjusted partial
as elevation changes from 1000 m (3280 ft) below pressure (padj).
sea level to 3500 m (11,483 ft) above sea level. The pbar pH O padj
2
temperatures are the standard temperature of air at
760 mm Hg 47 mm Hg 713 mm Hg
these altitudes.
Note that water vapor pressure is not affected by So, assuming a gas mixture that is 20.93% O2, 78% N2,
its fractional concentration. Water vapor, within 0.3% CO2, and 0.1% trace gases, what are the fractional
physiological ranges, changes only in response to concentrations (FI) and partial pressures (PI) of this
temperature changes. Water vapor pressure at normal inspired gas mixture at body temperature and 100%
body temperature (98.6°F, 37°C) and sea-level atmo- body humidity? The fractional concentrations are:
spheric pressure (760 mm Hg) is 47 mm Hg. To FIO2 0.2093
account for the water vapor in the saturated gases
FIN2 0.78
in the respiratory system, we must subtract pH O
(47 mm Hg) from the total pressure (760 mm Hg)
2
FICO2 0.003
before calculating the partial pressure of the other FItrace 0.001
where FI is fraction of inspired. The partial pressures terms of the solubility coefficient of the gas, and the
are: solubility coefficient depends on the interaction of
three factors:
(713 0.2093) 149.2309 mm Hg PIO2
• The nature of the solvent (the median in which
(713 0.7800) 556.14 mm Hg PIN2 the gas dissolves)
(713 0.003) 2.139 mm Hg PICO2 • The temperature of the solvent (and to a very
(713 0.0001) 0.713 mm Hg PItrace small extent that of the gas)
• The pressure of the gas
As these atmospheric gases travel down to the The solubility coefficient, then, is the amount of
alveoli, they mix with a combination of end-expiratory gas that dissolves in 1 mL of a given solvent at standard
gases and deadspace gases, which modify the actual pressure (760 mm Hg) and a given temperature
alveolar gas concentrations and therefore the alveolar (37°C). As temperature increases, so does the solubility
partial pressures. The actual alveolar partial pressures coefficient; as temperature falls, so does the solubility
depend in part on the amount of ventilated but coefficient.
nonperfused alveoli (deadspace units) and on the
number of perfused but not ventilated alveoli (shunt
units). Also, the amount of carbon dioxide production AVOGADRO’S LAW
plays a role in the final alveolar and arterial partial Avogadro (1776–1856) formulated what became his
pressures of inhaled gases. famous law in 1811. Avogadro’s law states that equal
Dalton’s law has many applications and is one of volumes of gases contain equal numbers of molecules
the most important biophysical concepts to master in at the same temperatures and pressures regardless of
the study of pulmonary physiology, medical gas their masses. Further investigations of this statement
administration, ventilator care, arterial blood gas and proved it to be true. It was shown that, at STP, each
acid-base analysis and interpretation, and pulmonary gram molecular weight (gmw) of an ideal gas consists
pathophysiology. of a volume of 22.4 L and contains 6.02 1023
molecules (Avogadro’s number). Further, this was a
constant across all gases tested.
HENRY’S LAW
Henry’s law (of solubility) states that, given a con- GRAHAM’S LAW
stant temperature and a state of equilibrium between
Graham’s law of diffusion deals with the movement of
the gas pressures within and outside the liquid, the
gases from one part of a system to another. This process
amount of gas dissolved in a liquid is directly
is random; that is, where any given molecule will go is
proportional to the pressure of the gas on the surface
unpredictable. Because gas molecules move quickly
of the liquid. In other words, if the pressure of a
(over 1000 mph) and independently, there are many
gas A, which is in contact with a liquid surface, is
collisions, resulting in random vectors and accelera-
double, then the amount of the gas A dissolved in
tions. The tendency over time is for the gases to
the liquid increases. If the original value is halved,
become evenly distributed (homogeneous) throughout
the dissolved gas decreases proportionally.
the area.
Remember two things. First, dissolved gases are not
chemically bound to their carrier mediums.
General Movement of Gases. The general movement
Second, dissolved gases exert a partial pressure
of the gases is from areas of high concentration to areas
equal to their gaseous partial (fractional) concentra-
of low concentration. A moment’s reflection makes it
tion. This is the case with oxygen in the alveolus and in
clear that the areas of high concentration allow more
the blood plasma. (Although no direct contact takes
collisions and direction changes, thus spreading the gas
place across the alveolar-capillary membrane, the 2- or
molecules out. Graham’s law of diffusion, as it applies
3-cell separation has only a small and, in most cases,
to gas mixtures, says that the rate of diffusion (r) is
clinically insignificant effect.) As FIO2 changes, the
inversely proportional to the density of the gases.
dissolved oxygen in the plasma (PaO2) should undergo
Specifically, Graham determined that the rate was
changes that are proportional to and in the same
inversely related to the square root of the density.
direction as the change in FIO2.
Mathematically, this relationship is represented by the
Another way of stating this principle is as
equation:
follows: The amount of dissolved gas in a mixture
is proportional to the pressure of that gas on the 1
r ___
__
liquid surface. The proportionality is defined in √D
As you can see, each gas has its own value for r, LAPLACE’S LAW
called its diffusion coefficient. A comparison of these Pierre-Simon Laplace (1749–1827) found that the
coefficients indicates which gases diffuse most rapidly interrelationship of the surface tension forces and the
and by what amount. For example, assume that gas A forces acting to disrupt or break the liquid sphere
has a density of 1.5 g/L and that gas B’s density is varied inversely with the radius of the sphere. This
1.46 g/L. An equation (a proportionality) can then came to be known as Laplace’s law, which describes
be set up: surface tension in relation to liquid spherical bodies. In
____ other words, the smaller the sphere is, the higher the
√____
DA
rA _____
___
rB surface tension is and the smaller the sphere wants to
√ DB
_______ get. Laplace’s law says that the distending pressure
√________
1.5 g/L
rA _________
___ (P, the pressure required to expand volume by a given
rB √1.46 g/L amount) is directly related to the surface tension (ST)
and inversely related to the radius (r) of the sphere.
rA ______
___ 1.225
rB 1.208 Distending pressure is defined in units of dynes per
square centimeter, the surface tension in dynes/per
rA 1.014 centimeter, and the radius in centimeters. Stated as an
equation, the law reads:
This shows that gas A diffuses 1.014 times as fast as gas B.
2ST
P ____
Brownian Movement. The diffusion of gases in other r
fluids is erratic and seemingly random. This statement As an example, assume a liquid has a surface tension of
is especially true in the case of gas-to-gas diffusion 250 dynes/cm and a radius of 0.3 cm. What is the
systems, in which the molecules of the two gases distending pressure?
randomly strike each other and thus alter the other
molecules’ path or trajectory. This random motion is 2ST
P ____
called Brownian motion or Brownian movement. Because r
of the erratic and unpredictable movements of the 2(250 dynes/cm)
molecules of gas, this process is sometimes referred to ________________
0.3 cm
as the “drunkard’s walk.” 500 dynes/cm
_____________
0.3 cm
Diffusion through Liquids. For the diffusion of gases
through liquids, one must consider the solubility P 150 dynes/cm2
coefficient (Cs) of the gas. This requires only a simple
modification of the formula:
________ Thermodynamics
___ √DA(Cs )
rA _________
A
________ Thermodynamics is the study of the interrelationship
rB
√DB(Cs ) B
between matter and energy. Familiarity with basic
thermodynamic concepts aids in the understanding of
Simply solve the square root terms and multiply them
by the respective solubility coefficients and then solve
the proportionality as in the earlier problem.
Age-Specific Competency
Surface Tension Laplace’s Law
Surface tension is why bubbles form, why water collects Laplace’s law explains why newborns need
in droplets, and why rain is globular or shaped like higher ventilating pressures than adults do. Their
teardrops. The water or other fluid forms tight bonds alveoli are bubblelike and very small compared
between molecules where the gas and fluid meet. These with those of a child or an adult. Surfactant is a
bonds have the effect of a skin covering the liquid. The biochemical, surface-active compound that alters
tighter the bonds get, the stronger the skin is, and the the surface tension of the alveoli. The addition
harder it is to disrupt the bubble, or skin, effect. The of surfactant by direct instillation reduces the
cohesive forces of the liquid tend to want to shrink the collapsing forces, allowing better alveolar
size of the liquid. Surface tension is a strong cohesive expansion. Commonly used in neonatal patients,
force. Disruptive forces are forces that tend to expand surfactant may prove valuable in the treatment of
and eventually break the skin, allowing the liquid to adults with severe lung disease.
move in any direction.
metabolic processes, both normal and abnormal. In o

F
o
C K(A)
addition, concepts such as entropy relate to the degra-
dation of biological and electromechanical systems
Boiling point 212.0 100.0 373.16
over time. H2O
Body 98.6 37.0 310.16

CONSERVATION OF MATTER AND ENERGY temperature
According to Einstein’s famous equation E MC2, if
Melting point –32.0 0.0 273.15
the speed of light (C) is a constant, then the ratio of H2O
energy (E) to matter (M) must always remain constant
(C2 E/M). This statement suggests that, in any system
where C is constant, changes in the amount of energy 0.0
Absolute zero – 459.69 – 273.15
must be offset by proportional changes in matter.
Hence the conservation of matter and energy. The total
o o o o
amount of energy and matter in a system must remain F = 9/5 C + 32 C = 5/9 (F – 32) K = C + 273.15
constant, although their proportions may change. FIGURE 3-23 Comparison of temperature scales.
Law of Entropy. Entropy is a concept that at first

glance appears to be at odds with the law of conserva- Kelvin (K) scale. The United States and, to a lesser
tion of matter and energy. The law of entropy states that, degree, Great Britain commonly use a third system: the
in a closed system, everything moves toward a state of Fahrenheit system (°F). The presence of this third scale
equilibrium. In other words, the entropy (entropic causes confusion and error when people are trying to
condition) is such that everything (matter and energy) communicate effectively in scientific and medical
is equally distributed. On the largest possible scale, the communities. The respiratory therapist must become
implication is that, at some far future date, all of the familiar with and fluent in the Kelvin and Celsius
matter and energy in the universe will be evenly distrib- temperature scales.
uted. And if all things are evenly distributed, there will Figure 3-23 illustrates the three scales in reference
be no movement of either matter or energy. Carried to some important conditions. Note that the numbers
further, without any movement or potential for move- associated with these events vary widely depending on
ment, there is no energy. If there is no energy, there can the temperature system referenced. Points of special
be no matter—for energy is needed to hold matter interest are body temperature, the boiling point of
together. Therefore, at the moment of total entropy, the water, the freezing (or melting) point of water, and the
universe will cease to exist. point at which molecular activity ceases (absolute
zero). Table 3-10 shows the calculations used to convert
from one scale to another.
HEAT AND OTHER FORMS OF ENERGY
As seen earlier in this chapter, heat is a product of Radiation. Because radioactive substances are widely
molecular movement and a by-product of biochemical used in both therapeutic and diagnostic procedures, all
physiological processes. The process of measuring and health care workers should have at least a basic com-
recording temperature is not as simple as one would prehension of them. Radiation exists in two forms:
think. ionizing and nonionizing. Sunlight, heat, and radio
waves are forms of nonionizing radiation, and they are
Physiological Temperature. Human beings—and all generally no threat to humans. Ionizing radiation—
living things for that matter—live and survive in a very X-rays, radioactive isotopic implants, and certain
narrow temperature range. Slight variations of that radioactive markers (contrast media)—are helpful
range cause havoc not only with biological systems but in our practice of patient care. However, ionizing
also with social and economic systems. Just think of radiation can be hazardous if improperly used.
heat waves and blizzards to realize how poorly A radioactive material is a material that emits
equipped humans are at surviving outside their particulates of electromagnetic radiation as a conse-
comfort range. quence of nuclear decay. This decay results in the
release of high-energy electrons (beta particles),
Temperature Scales. Globally, the vast majority of electromagnetic energy (photons), or helium ions
nations, as well as the entire scientific and medical (alpha particles). The unit of measurement for radia-
community, have two common temperature reference tion is the curie (Ci), which equals 37 billion disinte-
systems: the Celsius scale (C) and the Absolute (°A) or grations per second. One-millionth of a curie is a
TABLE 3-10 Temperature scales and Summary

conversion formulas Physics, especially of fluids and gas, is among the most
Scale Description Formula useful studies a respiratory therapist can undertake. An
°F 1/180th of the °F 9/5 (°C + 32) in-depth understanding of the principles of physics
(Fahrenheit) difference between enables the respiratory therapist to understand the
the melting point of interactions among physics, physiology, and patho-
water and its boiling physiology. In addition to the gas laws, the laws
point at standard governing electricity, elasticity, force, and motion are all
pressure and relevant to respiratory care. The respiratory therapist
temperature. must be competent in the use of scientific notation, the
metric system, and dimensional analysis because the
°C 1/100th of the °C 5/9 (°F – 32)
solving of physiological equations plays a large part in
(Celsius) difference between
the science of respiratory care.
the melting and
As experts in the application of technology to the
boiling points of
seriously ill or recovering patient, respiratory specialists
water at standard
must understand how both patient and equipment work
pressure and
and interact if they are to be at the peak of their profes-
temperature.
sion. Having a grasp of physical principles and their
K Based on the average K °C + 273.15 application to both technology and humanity is a never
(Kelvin) kinetic energy per ending duty owed to patients. Many people understand
molecule of a physics and many understand patients, but relatively few
perfect gas. Zero on understand how to manage the interface where patient
this scale is the and technology meet. That is a respiratory therapist’s skill.
temperature at
which a perfect gas
loses all its energy. Study Questions
Sometimes called
REVIEW QUESTIONS
Absolute tempera-
ture. The degree 1. Name the traditional and transitional states of matter.
sign (°) is not used 2. Write the formula for the combined gas law and
in this scale. the ideal gas law. Why are they different?
3. Explain Dalton’s law.
4. Cite two uses for Boyle’s law.
microcurie, which is the unit used to calculate dosage 5. Convert 2 yd to meters and 3 lb to kilograms.
and exposures. 6. Change the following numbers into scientific
The emission of these radioactive particles notation: 195,000, 0.0085, 0.012.
diminishes over time. A critical piece of knowledge
7. Change the following scientific notations into
about a radioactive substance is its half-life: the
numbers: 1.45 103, 2.568 103, 7.16 105.
amount of time it takes for the substance’s radioactivity
to be halved.
MULTIPLE-CHOICE QUESTIONS
1. Which of the following formulas would you use to
determine volume changes at various pressures and
Best Practice temperatures?
a. Boyle’s law
Radiation b. Charles’s law
Persons who work in areas where the potential c. Hagen-Poiseuille’s law
for exposure to ionizing radiation sources is great d. the combined gas law
and prolonged should wear dosimeters, which 2. To determine the water vapor pressure of a gas
are devices that measure and record exposure mixture, what information do you need?
levels. Persons who work in intensive care units, a. identity of the gases in the mixture
emergency rooms, and radiology departments are b. pressure of the mixture of gases
among those who should have dosimeters. c. temperature of the mixture
d. volume of the mixture
3. Which of the following measures would lower 9. The triple point is defined as
resistance to flow in a linear tube such as an airway? a. the point at which the freezing, boiling, and
a. using a ballistic flow pattern vaporization temperatures of two substances
b. employing a square-wave flow pattern coincide.
c. Flow pattern is not a factor in resistance. b. the time when the values of temperature,
d. using a ramp-shaped flow pattern pressure, and volume are at equilibrium.
4. Why is the ideal gas law different from the clinical c. the point at which a substance can exist as
and combined gas laws? solid, liquid, and gas at the same time.
a. The combined gas law assumes that water vapor d. the partial pressure of a gas when the fractional
is inconsequential. concentration passes 100.
b. The clinical gas law assumes that the number of 10. Which is the correct and safest way to write the
molecules remains constant. number nine-tenths?
c. There is no difference between the two laws a. 0.9
other than their names. b. .9
d. The ideal gas law fails to account for temperature c. 009
changes over the narrow physiological range. d. 9.0
5. In a gas mixture with a pressure of 200 mm Hg at
37°C 100% saturated with water vapor, what is the
water vapor pressure?
a. 47 mm Hg 1. How does the science of physics specifically apply
b. 100 mm Hg to respiratory therapy?
c. 35 mm Hg 2. Look up the relationship between the terms
d. 760 mm Hg “physics” and “physician” and between “physics”
6. A gas mixture has a pressure of 300 mm Hg at and “physic.”
37°C 100% saturated. What is the pressure of gas A, 3. Why should a respiratory therapist have a solid
one of the gases in the mixture, if its fractional understanding of physical principles?
concentration is 30%?
4. What area of physics is most applicable to respira-
a. 90 mm Hg
tory care?
b. 100 mm Hg
c. 76 mm Hg
d. 47 mm Hg References
7. As the oxygen in a liquid O2 storage vessel evapo- 1. Macmillan Visual Desk Reference. New York:
rates and turns into a gas, heat is extracted from the Macmillan Publishing Co; 1993.
surrounding environment. What happens to the 2. Eckhardt B. A critical point for turbulence. Science.
pressure in the storage vessel during this process as July 8, 2011;333:165–167.
gas is formed?
a. Pressure is not affected.
b. Pressure decreases. Suggested Reading
c. Pressure fluctuates randomly. Branson RD, Hess DR, Chatburn RL. Respiratory Care
d. Pressure increases. Equipment. 2nd ed. Philadelphia: Lippincott,
8. If we consider roads as airways and cars as gas Williams & Wilkins; 1999.
molecules, which of the following is most likely to
represent a situation demonstrating transitional flow?
a. An interstate highway passing through sparsely
settled land
b. Entrance ramps and an adjacent interstate
highway at midday
c. Streets in New York City during rush hour
d. Traffic stalled by gridlock or an auto accident
CHAPTER 4
Applied Chemistry
Ingo S. Kampa
OBJECTIVES
• Understand the physiological applications of acids and buffers.
• Define physiological acids, bases, and buffers.
• Explain the regulation of pH (hydrogen ion concentrations) in various cellular and intracellular
compartments.
• Describe the functions of various physiological buffers.
• Calculate pH and use the Henderson–Hasselbalch equation.
• Outline the physiology of acid–base disturbances.
• Recognize and understand the causes of acidosis and alkalosis.
CHAPTER OUTLINE
Review of Atoms and Molecules How Acids, Bases, and Buffers Affect Respiration
Atoms Transport of Carbon Dioxide to the Alveoli
Atomic Bonds Processing of Noncarbonic Acids
Molecules Regulation of Alkali in the Body
Acids, Bases, and Buffers Disturbance of the Acid–Base Balance
Definitions of pH, Base, and Buffer Respiratory Acidosis
Concept of pH Respiratory Alkalosis
Concept of Acids and Their Physiological Metabolic Acidosis
Application Metabolic Alkalosis
Concept of Bases
Concept of Buffers
82
CHAPTER 4 ■ Applied Chemistry 83
KEY TERMS
bicarbonate buffer system pH respiratory acidosis
hemoglobin buffer system phosphate buffer system respiratory alkalosis
isohydric principle physiological acid strong acid
metabolic acidosis physiological base weak acid
metabolic alkalosis physiological buffer
nonvolatile acid protein buffer system
T
his chapter begins with a review of certain table is organized into groups that consist of represen-
aspects of atoms and molecules relevant to tative elements, transition elements, inner-transition
respiratory therapy. It also provides the basic elements, and noble gases. The information provided
concepts of chemistry that will help the for each element consists of the atomic number,
reader learn and integrate the information throughout symbol, name, and mass number.
the book. The respiratory therapist must have a basic
understanding of chemical structure, molecular
bonding, and the four major groups of biological ATOMS
compounds and their interaction in a physiological An atom consists of a nucleus and one or more
organism. electrons (Figure 4-2). The nucleus consists of two
All body fluids contain hydrogen ions (H+). To different kinds of particles, protons and neutrons.
sustain life, the hydrogen ion concentration (pH) in The major difference between these two particles
body fluids (which is a result of the acid–base balance) is that the proton has a positive electrical charge and
must be maintained within a relatively narrow range. the neutron has no electrical charge. Electrons are
Optimal metabolic function requires a pH in an even negatively charged particles located outside the
smaller range. nucleus. Protons and electrons carry opposite
When hydrogen ions accumulate or are signifi- charges; so a neutral atom has the same number of
cantly decreased, the functioning of a multitude of protons and electrons. The electrons move around
metabolic pathways deteriorates. Physiological the nucleus in specific volumes of space called
compensatory mechanisms are initiated to avert atomic orbitals, which have different shapes depend-
potentially disastrous consequences. Physicians, ing on the energy of the electrons they contain. The
assisted by respiratory therapists, laboratory scientists, lowest-energy orbital in any atom is spherical and is
and technicians, must assess the acid–base status and called a 1s orbital. Other spherical orbitals are also
take steps to correct any imbalance. This chapter called s but have higher energies and thus are
defines acids, bases, and buffers and discusses the designated as 2s, 3s, 4s, and so on. Orbitals with
concept of pH. It will also show how these concepts characteristics different from s orbitals are desig-
apply to respiration and discuss common acid–base nated as p, d, and f. The shapes of these are different
balance disturbances. from the shape of s orbitals. For example, p orbitals
have a dumbbell shape, and d orbitals look like
three-dimensional four-leaf clovers.
Review of Atoms and Molecules The number of electrons in a neutral atom deter-
In the nineteenth century, scientists looked for order in mines the chemical properties of an element. The
the chemical information gathered about elements. In atomic number is identical to the number of protons in
1869, two scientists, Dmitry Mendeleyev and Julius the nucleus of an element and to the number of
Lothar Meyer, independently produced a classification electrons outside the nucleus. For example, hydrogen
scheme for the elements. The scheme was based on the (H), which has the atomic number 1, has one proton
periodic law, which in its present form is an arrange- and one electron; sodium (Na) has the atomic number
ment of all the elements in order of increasing atomic 11 and contains 11 protons and 11 electrons. Protons
number. The result is that elements with similar and neutrons have approximately the same mass. The
properties occur at regular (periodic) intervals. A mass of electrons is negligible and does not add to the
convenient way to compactly represent such behavior total mass of an element. As a result, the total mass of
on the basis of the periodic law is in a table, which is an element is approximately the total mass of the
called the periodic table (Figure 4-1). The periodic protons and neutrons.
1 IUPAC 18
1 Periodic Table of the Elements 2
K or 1 H He
hydrogen 2 13 14 15 16 17 helium
1.007 94(7) Key: 4.002 602(2)
3 4 atomic number 5 6 7 8 9 10
L or 2 Li Be symbol B C N O F Ne
lithium beryllium name boron carbon nitrogen oxygen fluorine neon
6.941(2) 9.012 182(3) standard atomic weight 10.811(7) 12.0107(8) 14.0067(2) 15.9994(3) 18.998 4032(5) 20.1797(6)
11 12 13 14 15 16 17 18
M or 3 Na Mg Al Si P S Cl Ar
sodium magnesium 3 4 5 6 7 8 9 10 11 12 aluminium silicon phosphorus sulfur chlorine argon
22.989 770(2) 24.3050(6) 26.981 538(2) 28.0855(3) 30.973 761(2) 32.065(5) 35.453(2) 39.948(1)
19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36
N or 4
K Ca Sc Ti V Cr Mn Fe Co Ni Cu Zn Ga Ge As Se Br Kr
potassium calcium scandium titanium vanadium chromium manganese iron cobalt nickel copper zinc gallium germanium arsenic selenium bromine krypton
39.0983(1) 40.078(4) 44.955 910(8) 47.867(1) 50.9415(1) 51.9961(6) 54.938 049(9) 55.845(2) 58.933 200(9) 58.6934(2) 63.546(3) 65.409(4) 69.723(1) 72.64(1) 74.921 60(2) 78.96(3) 79.904(1) 83.798(2)
37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54
O or 5 Rb Sr Y Zr Nb Mo Tc Ru Rh Pd Ag Cd In Sn Sb Te I Xe
rubidium strontium yttrium zirconium niobium molybdenum technetium ruthenium rhodium palladium silver cadmium indium tin antimony tellurium iodine xenon
85.4678(3) 87.62(1) 88.905 85(2) 91.224(2) 92.906 38(2) 95.94(2) [97.9072] 101.07(2) 102.905 50(2) 106.42(1) 107.8682(2) 112.411(8) 114.818(3) 118.710(7) 121.760(1) 127.60(3) 126.904 47(3) 131.293(6)
55 56 57-71 72 73 74 75 76 77 78 79 80 81 82 83 84 85 86
P or 6 Cs Ba lanthanoids Hf Ta W Re Os Ir Pt Au Hg Tl Pb Bi Po At Rn
caesium barium hafnium tantalum tungsten rhenium osmium iridium platinum gold mercury thallium lead bismuth polonium astatine radon
132.905 45(2) 137.327(7) 178.49(2) 180.9479(1) 183.84(1) 186.207(1) 190.23(3) 192.217(3) 195.078(2) 196.966 55(2) 200.59(2) 204.3833(2) 207.2(1) 208.980 38(2) [208.9824] [209.9871] [222.0176]
87 88 89-103 104 105 106 107 108 109 110 111
Q or 7 Fr Ra actinoids
actinoi
tinoids Rf Db Sg Bh Hs Mt Ds Uuu
francium radium rutherfordium dubnium seaborgium bohrium hassium meitnerium darmstadtium unununium
[223.0197] [226.0254] [261.1088] [262.1141] [266.1219] [264.12] [277] [268,1366] [271] [272]
7
57 58 59 60 61 62 63 64 65 66 67 68 69 70 71
a
La Ce Pr Nd Pm Sm Eu Gd Tb Dy Ho Er Tm Yb Lu
lanthanum
lanthan
num cerium
m praseodymium neodymium
um promethium
um samarium
m euopium
um gadolinium
olinium terbium
erbium dysprosium holmium
ium erbium
bium thulium
hulium ytterbium
terbium lutetium
138.90555(2)
138.9055(2) 140.116(1)
(1) 140.907 65(2) 144.24(3)
3) 7)
(144.9127) 3)
150.36(3) 151.964(1)
4(1) 157.25(3)
7.25(3) 158.925
925 34(2) 162.500(1) 164.930
0 32(2) 167.259(3)
259(3) 168.934
934 21(2) 173.04(3)
73.04(3) 174.967(11)
174.967(1)
89
9 90 91 92 93 94 95 96 97 98 99 100 101 102 103
c
Ac Th Pa U Np Pu Am Cm Bk Cf Es Fm Md No Lr
actiniu
um
actinium m
thorium protactinium
um m
uranium neptunium
um plutonium
um americium curium berkelium
m m
californium m
einsteinium fermium
um evium
mendelevium nobelium
lium lawrencium
m
(227.0277)
(227.02277) 232.0381(1) 8(2) 238.028 91(3)
(1) 231.035 88(2) (237.0482)
482) (244.0642)
42) (243.0614) (247.0704)
4) (247.0703)
3) (251.0796)6) (252.0830)
0) (257.0951)
951) (258.0984)
984) (259.1010)
1010) (262.1097))
(262.1097
FIGURE 4-1 The Periodic Table of Elements

Copyright © 2003 IUPAC, the International Union of Pure and Applied Chemistry
number of neutrons). Atoms of the same element

with different mass numbers are called isotopes. For
ee–– ee–– example, carbon exists as three isotopes containing
six, seven, and eight neutrons. Because these isotopes
exist in various quantities, carbon has an average
ee–– mass number of 12.011.
ee––
+
+ +
ee–– +
+ ATOMIC BONDS
+ +
+ Substances consist of atoms that are held together by
ee–– bonds. The type of bond that holds atoms together
e–
determines in part the chemical property of a sub-
ee––
stance. A bond is an attractive force that exists between

two atoms. The two most common types of bonds are
ionic and covalent bonds.
The ionic bond is formed by the electrostatic
attraction between a positive and a negative ion. A
positive ion results from an element losing one or
FIGURE 4-2 A three-dimensional diagram of an atom of more electrons, giving it a positive charge. Such an ion
oxygen, which contains eight protons, eight neutrons is referred to as a cation. A negative ion results from an
located in the center nucleus, and eight electrons in the
element gaining an electron, giving it a negative charge.
orbital shells moving around the nucleus.
It is referred to as an anion. For example, sodium and
chloride exist in tissue fluids as ions (Nav+ and Cl−).
The number of neutrons in the nucleus of an When they are allowed to combine, however, they form
element may be different. Thus, the same element an ionic bond, and sodium chloride (NaCl), a salt, is
may have different mass numbers (i.e., different formed (Figure 4-3).
Na Cl NaCl
-
ee– -
ee–
- -
ee– - ee– - - - - - -
ee–
- ee– - - ee– ee– ee– ee– ee–
ee– -
ee– -
ee– - ee– ee–
ee– -
-
ee– ee– -
ee– - -
- ee– ee–
11 +
p+ ee– 17 +
p+ 11 +
p+ 17 p++
- 6p - 6p - 6p - 6p - -
ee– 12 no
-
ee– ee– 19 n o ee– 12 no
-
ee– ee– 19 o ee– ee–
- 6 n° - 6 n° 6 n° 6 nn°
ee– ee– - - - - -
ee– ee– - ee– ee– ee–
- -
ee– ee–
- ee– - -
ee– ee– ee–
- - - - -
-
ee–
-
ee– ee– ee– -
ee– ee– ee– ee–
- -
ee– ee– -
ee– -
ee–
1 Sodium atom 1 Chlorine atom

1e– in outer shell 7e– in outer shell Sodium Chloride (salt) NaCl molecule
valence of +1 valence of _1
FIGURE 4-3 An ionic bond is formed between sodium (Na) and chlorine (Cl) to form table salt, sodium
chloride (NaCl).
Covalent bonds are the result of sharing electrons MOLECULES

between atoms. There are two types of covalent bonds: Biological molecules are usually classified into four
nonpolar and polar. For example: groups: carbohydrates, lipids, proteins, and nucleic
• In hydrogen gas (H2), the two atoms share the acids. Many important biological molecules are very
electrons equally. The attraction between the two large and are called macromolecules.
atoms results in a molecule held together by a
nonpolar covalent bond. Carbohydrates. Carbohydrates are complex organic
• In a water molecule (H−O−H), the electrons compounds that can be further classified into mono-
between the hydrogen and the oxygen are shared saccharides, disaccharides, and polysaccharides.
unequally and are closer to the negatively • Monosaccharides are single polyhydroxy
charged oxygen atom (Figure 4-4). This arrange- aldehydes or ketones.
ment results in a net negative charge on the • Disaccharides are two monosaccharides linked
oxygen and a net positive charge on the two together.
hydrogens, resulting in a polar covalent bond. • Polysaccharides are long chains of monosaccharides.
The H2O molecule is a dipole.
1 p+
1 p+
e- e-
e- e-
e-
e-
e- e-
1 p+ 1 p+ 8 p+ e- 8 p+ e-
e-
8 no e- 8 no
e- e- e- e- e- e-
e- e-
2 Hydrogen atoms 1 Oxygen atom Water molecule (H2O)

1e– in outer shell 6e– in outer shell
valence of _1 valence of _2
FIGURE 4-4 A covalent bond is formed between two hydrogen atoms and one oxygen atom to form water (H2O).
The most important monosaccharides are glucose, Probably more than 200 peptides are essential for
fructose, and galactose, which are important energy the proper functioning of an animal or human body.
sources in living organisms. Disaccharides are hydro- Many of the important peptides are hormones—such as
lyzed to yield monosaccharides and are important insulin, prolactin, and glucagon—that regulate various
energy sources as well. Important disaccharides are metabolic processes essential for survival. Proteins or
sucrose, lactose, and maltose. [Hydrolysis occurs when polypeptides have many functions, including structural,
a compound is altered by the breakdown of a water storage, regulatory, transport, and movement functions.
molecule into H+ (hydrogen) and OH− (hydroxide The structural components in animals other than
ions).] Important polysaccharides are starch and inorganic substances (e.g., calcium in bones or iron in
glycogen. Both are polymers consisting entirely of hemoglobin) are proteins. Many essential stored sub-
glucose. Starch is the storage form of glucose in plants. stances, such as iron and hormones, are bound to
When animals digest starch, it is hydrolyzed to pro- proteins. Regulatory functions involve hormones (pro-
duce the monosaccharide glucose. Glycogen is the tein hormones such as growth hormone and thyrotro-
storage form of carbohydrates in animals, and it is pin) that regulate metabolic processes in the body. Many
abundant in liver and muscles. In humans, stored liver substances—such as ions, oxygen, and carbon dioxide—
glycogen maintains a normal blood glucose level for are transported while bound to proteins and are released
several hours after a meal. In a process known as from proteins at specific sites. Proteins also function in
gluconeogenesis, the liver produces glucose from catalysis (enzyme activities), protection (antibody
nonglucose substances and maintains long-term formation), and the transmission of nerve impulses.
normal blood glucose levels.
Nucleic Acids. Nucleic acids consist of two major
Lipids. Lipids can be simple or complex. Simple lipids classes: ribonucleic acid (RNA) and deoxyribonucleic
contain only two types of components. For example, acid (DNA). RNA is found in the cytoplasm of cells;
the simple lipid triglyceride consists of fatty acids and DNA is found in the nuclei. Nucleic acids are involved
an alcohol. Waxes are another group of simple lipids. in the transfer of genetic information from existing cells
Complex lipids contain more than two components. to new cells. Nucleic acids are composed of nucleotides.
Phospholipids and spingolipids are typical examples. Nucleotides consist of either a purine or a pyrimidine,
Under basic conditions, these compounds can be either ribose or 2-deoxyribose, and phosphate. There
saponified [i.e., hydrolyzed to an ester, a class of are three types of RNA: messenger RNA (m-RNA),
organic compounds that react with water to produce ribosomal RNA (r-RNA), and transfer RNA (t-RNA).
alcohols and organic or inorganic acids (see anion gap
• Messenger RNA transfers genetic material from
in Chapter 16)]. Typical classes of lipids that cannot be
the nucleus of a cell to the cytoplasm, where
saponified are steroids and prostaglandins.
protein synthesis occurs.
• In the cytoplasm, protein synthesis involves the
Proteins. Proteins are polymers consisting of amino
r-RNA.
acids. Amino acids are compounds consisting of an
• Specific t-RNA molecules bind with amino acids
amino group (NH3+), the carboxylate group (COO−),
and are transferred to the r-RNA site.
and a side chain (R group). These three groups are
attached to a carbon (the alpha carbon). The properties
of the amino acids depend on the nature of the Acids, Bases, and Buffers
R group. Twenty amino acids are found in naturally
Key to understanding many of the body’s metabolic
occurring proteins. The amino acids are bound to each
functions is knowledge of the role of acids, bases,
other by peptide bonds. The properties of the protein
and buffers.
depend on the number and kinds of amino acids
found in the protein as well as their sequence. The
resulting compounds can be classified as peptides, DEFINITIONS OF pH, BASE, AND BUFFER
polypeptides, and proteins.
Historically, acids and bases were first recognized
• Peptides are amino acid polymers of short-chain simply by taste: Acids were sour and bases were bitter.
length. Since the late nineteenth century, acids and bases have
• Polypeptides are polymers of intermediate lengths been defined according to their molecular characteris-
of up to 50 amino acids. tics. Organic chemists have embraced the definitions
• Proteins are very large polymers of amino acids offered by American chemist Gilbert Lewis because
consisting of more than 50 amino acids, with they are the most useful in organic chemistry. Accord-
molecular weights up to several millions. ing to Lewis, an acid is an electron pair acceptor,
whereas a base is an electron pair donor. This concept (where some protons are not present and the weak acid
is useful to the organic chemist because it adequately is transformed into a base), known as a conjugate base
describes sharing electrons in an acid–base reaction (A−). Buffer actions can best be explained using the
in nonaqueous solvents.1 Very simply, acids can be Henderson–Hasselbalch equation (Chapter 16) and
defined as a substance that gives off hydrogen ions, and the isohydric principle (discussed in the section
bases are substances that absorb or neutralize hydrogen “Concept of Buffers”). The important physiological
ions. An increase in hydrogen ions results in changes in buffers are the bicarbonate and phosphate buffers,
the pH. Buffers are substances that resist changes in pH hemoglobin, and plasma proteins.
whenever hydrogen ion concentrations change.
Another definition is the Bronsted–Lowry concept,
which defines acids as proton (H+) donors and bases as CONCEPT OF pH
proton acceptors.2 In this context, a proton is a hydro- The pH is the measure of the acidity or alkalinity (base-
gen atom without orbital electrons. According to this ness) of a solution. More technically, it is the negative
definition, a variety of compounds, including glucose, log of the hydrogen ion concentration, ranging from
ethyl alcohol, and triglycerides, are classified as acids 0–10−14 M, and it is commonly expressed as a range
because of their potential to donate protons. In physi- from 0 to 14.3 Neutral solutions have a pH of around 7.
ological systems, however, for a substance to be consid- Lower numbers indicate increasing acidity, and higher
ered an acid or a base, it must donate or accept protons numbers indicate increasing alkalinity (Figure 4-5).
in an aqueous system. These conditions exclude Mathematically, pH is calculated as pH = −log [H+]
glucose, ethyl alcohol, triglycerides, and many other where [ ] indicates concentration.
compounds. Thus, the Bronsted–Lowry concept of acids Because pH is an approximation, not an absolute
and bases is restricted to compounds that can donate or measure, of hydrogen ion concentrations in physiologi-
accept electrons in an aqueous body and buffer system. cal fluids, it has been suggested that the hydrogen ion
Therefore: concentration of blood be expressed in terms of
millimoles per liter (mmol/L). The pH concept,
• A physiological acid is a substance that can
however, is widely used in physiology and medicine.
donate electrons in a living physiological system.
• A physiological base is a substance that can
accept electrons in a living physiological system. CONCEPT OF ACIDS AND THEIR
In simple terms, physiological buffers are sub- PHYSIOLOGICAL APPLICATION
stances that resist changes in the hydrogen ion concen- Body fluids are contained in two main fluid compart-
tration when an acid or a base is added. Most buffers ments: the intracellular and the extracellular com-
consist of a weak acid (HA) and its unprotonated form partments.4 The extracellular compartment can be
Acidic Alkaline
Hydrogen ion (H+)

concentration 0.000001 0.0000001 0.00000001
(moles/liter)
pH 6 7 8
FIGURE 4-5 Schematic illustration of the relationship between hydrogen ion concentration,
pH, and acidity and alkalinity. Dots represent hydrogen ions.
subdivided into plasma and interstitial fluid. The Since more H2O is present, as compared with H+,
concentrations of electrolytes, acids, buffers, and A−, and HA, its concentration remains constant,
water differ significantly in each of these compart- resulting in
ments. For example, plasma and interstitial fluid
have high concentrations of Na+ and bicarbonate [H⫹] [A⫺]
k´ = _________
(HCO3−) ions, whereas intracellular fluids have high [HA]
concentrations of potassium (K+) and phosphate
(PO4−) ions. Plasma, approximately 1300–1800 mL/m2, Acids of Physiological Importance. Physiologically
represents about 15% of the total fluid volume. important acids fall into two categories: bicarbonic
Acids are classified as strong or weak depending on acids and noncarbonic acids. The first group consists
their degrees of ionization. Strong acids are repre- only of carbonic acids, which can readily permeate cell
sented by the following equations: membranes, thus affecting hydrogen ion concentra-
HA + H2O → H3O+ + A− tions and cellular pH.
The noncarbonic group consists of a variety of
H3O+ → H+ + H2O
acids, including sulfuric, lactic, and acetoacetic acids.
The hydronium ion (H3O+) results from the Noncarbonic acids are often referred to as fixed acids.
reaction of a hydrogen ion (H+) with water in an Nonvolatile acids (fixed acids), or nonvolatile acids,
aqueous solution. Thus a strong acid such as HCl such as sulfuric and phosphoric acids, which are
ionizes completely as follows: produced at a rate of 70–100 mmol daily and are
eliminated through the kidneys.
HCl + H2O → H3O+ + Cl−
Hydrogen ions are continuously produced in a
H3O+ → H+ + H2O living organism from the formation of carbon
A weak acid is only slightly ionized in an aqueous dioxide (CO2) and must be eliminated in a manner
solution. Weak acids are represented by the following that leaves the living organism unharmed. An
equation: individual weighing 70 kg produces approximately
15–20 moles (weight in grams/molecular weight) of
HA + H2O ↔ H3O+ + A− carbon dioxide daily that need to be eliminated
H3O+ → H+ + H2O through the lungs. When elimination is not accom-
plished, the physiological acid–base balance is
All gradations can be found between a strong and
disturbed.
a weak acid. The tendency of acids to dissociate or
The main hydrogen ion production results from
ionize into H3O+ is expressed as the dissociation
the metabolism of carbohydrates, fats, and proteins,
constant (k). At equilibrium, when the hydrogen ion
forming large quantities of CO2: for example, when
and conjugated base pair are present in equal concen-
glucose is converted to CO2. The resulting CO2
trations, the hydrogen ion concentration is equal to
transfuses across cellular membranes into interstitial
the dissociation constant. Thus, the dissociation
fluid to blood plasma and red blood cells and is
constant is related to the hydronium ion concentra-
finally eliminated in alveolar air. The reaction of CO2
tion (H3O+). In the remainder of this chapter, the
with H2O in these compartments results in hydrogen
term “hydrogen ion” and the symbol H+ will be used
ion production.
for the hydronium ion (H3O+) since H+ is more
commonly used. Remember, however, that hydrogen CO2 + H2 ↔ H2CO3 ↔ H+ + HCO3−
ions in aqueous solutions react with water to form the
Hydrogen ions produced in the various tissues must
hydrated hydronium ion.
be buffered in a physiological organism. The overall
At equilibrium, the constant k1 [HA] [H2O] =
process of these reactions is illustrated in Figure 4-6.
k2 [H+] [A−]. The numerical value of k is defined for a
Noncarbonic acids, such as lactic acid, beta-
specific temperature and changes if the reaction occurs
hydroxybutyric acid, and acetoacetic acid are interme-
at a different temperature. The dissociation constant of
diate products of carbohydrate metabolism. These
an acid can then be expressed as
hydrogen ions are normally converted to carbon
k dioxide and water before excretion.
K = __1
k2
or CONCEPT OF BASES
[H+] [A−] Bases are substances that accept electrons under
= ___________
[HA] [H2O] physiological conditions. A base can also inactivate
The mathematical relationship between pH and

CELLS PLASMA ERYTHROCYTE hydrogen ion concentration can be expressed by the
H
equation
H
CO2 CO2 CO2 + HbNH HbNCOO-
pH = −log[H+]
+ H2O The log[H+] in the equation can be converted to
−log[H+] by multiplying each term by −1. Substituting
H+ H2CO3 H2CO3 H+ pH for −log[H+] and pka for −log ka results in the
HHb
+ Pr - Hb- following equation:
HPr Na+ HCO3- HCO3- [A−]
pH = pka + log _____
CI- CI- [HA]
O2 O2 O2 HbO2- (The pka is a physiologic constant for each species
hemoglobin; for humans, pka = 6.3. It is essentially
FIGURE 4-6 Transport of carbon dioxide. the dissociation constant for the physiologic acid/
base pairs.) The Henderson–Hasselbalch equation is
extremely useful for calculating the pH of a buffer
system. Since [HA] represents undissociated acid and
an acid. In nonphysiological conditions, substances [A−] represents the completely dissociated salt (for
like the dihydrogen phosphate (H2PO4−) ion theo- example, A−), the equation can be rewritten as
retically can act as acids or bases; that is, they are able
to donate or accept electrons. Under physiological [salt]
conditions, however, body fluids such as blood pH = pka + log __________________
[undissociated acid]
would have to have a pH of 4 or less to act as a base.
Clearly, H2PO4− cannot act as a base in blood. Two
key physiological bases are bicarbonate and hemo- Buffers of Physiological Importance. Buffers in a
globin, which are discussed here as they function in physiological system can be divided into two broad
buffer systems. categories: bicarbonate and nonbicarbonate. A series
of buffer “events” is often referred to as a buffering,
or buffers, system. The bicarbonate system consists of
CONCEPT OF BUFFERS a single member, the bicarbonate–carbonic acid pair.
A buffer is any substance that resists change in pH5 and This is the most important buffer of plasma. The
usually consists of a weak acid and its conjugate base. nonbicarbonate buffer systems consist of the phos-
In a physiological system, a number of buffers in the phate buffer system (HPO42−−H2PO4−), the plasma
plasma compartment, body fluids, and red blood cells protein buffer system (Pr−−HPr), and the
maintain and regulate the pH. hemoglobin (Hb−−HHb and HbO2−−HHbO2)
buffer system.
Calculating the pH of a Buffer. The Henderson–
Hasselbalch equation can best calculate the pH of Bicarbonate Buffer System. The bicarbonate
buffers. Beginning with the equation buffer system is unique in a variety of ways. Con-
tinuously being formed, HCO3 thus exists in high
[HA] → [H+] + [A−]
concentrations and can readily be controlled by the
the dissociation factor for a weak acid can be calculated: lungs by either eliminating or retaining carbon
dioxide. In addition, concentrations are regulated in
[+H] [A−]
ka = _________ the kidney by increasing or decreasing reclamation
[HA] of bicarbonate ions from the glomerular filtrate.
Solving for [H+] results in Carbon dioxide is continuously formed in the cells
as a result of carbohydrate, fat, and protein metabo-
[HA]
[H+] = ka × _____ lism. As it passes through different cell membranes,
[A⫺] it reacts with water to form H+ and HCO3⫺. This
Converting the equation into a log form yields process is summarized in the following equation:
[HA] ↔ CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3−
log[H+] = log ka + log _____ CO2
[A−] (gas) (aqueous)
Since this reaction is bidirectional, CO2 is released The following equation shows how buffers resist a
in the lungs and expelled, thus eliminating the con- change in pH when acid is added. If 2 mmol/L of H+ is
tinuously produced CO2. If more hydrogen is retained, added, the following change of pH occurs:
then the substance becomes more acidic.
22
7.36 = 6.1 + log _________
The carbonic acid (H2CO3) exists only in trace 0.03 × 40
quantities because it readily dissociates into the
dissolved CO2 and HCO3−, which are in equilibrium Since the PCO2 is kept at 40 mm Hg, only a
with each other. minimal change in pH occurs. Thus, this buffer resists
changes in pH.
[H+] + HCO3−]
k = ________________ Protein Buffer System. The protein buffer system
[CO2] + [H2CO3]
(aqueous) acts as a physiological buffer for the pH of body. The
more effective protein buffers consist of the immidazo-
The equation can be restated as follows: lium group because the pka is around 7. Because of
their protein structure, however, some of these buffers
[CO2] + [H2CO3]
(aqueous) have a pka as low as 5 and as high as 8, and their
pk = pH + log ________________
− [HCO3 ] physiological-buffering ability deteriorates quickly as
the pka deviates from 7. The pka of the protein buffers,
This equation can be rewritten using the Henderson– consisting of alpha amino groups, ranges from above 7
Hasselbalch equation to yield to greater than 10. Only the buffers with a pka near or
below 8 have physiological-buffering capabilities.
[HCO3−]
pH = pka + log ________________ [protein−]
[CO2] + [H2CO3] pH = pka + log __________
(aqueous) [protein]
The concentrations of both CO2 and H2CO3 are When an acid (H+ ions) is added, the following
easily obtained from the PCO2 measurement reaction occurs:
multiplied by 0.03 at 38°. The pka under these H+ + protein− ↔ HProtein
conditions is 6.1. Substituting these values into the
equation results in the following:
Phosphate Buffer System. The phosphate buffer
[HCO3−] system, which consists of the dihydrogenphosphate
pH = 6.1 + log _____________
0.03 × [PCO2] (H2PO4) and monohydrogenphosphate (HPO42–) ions,
has a pka of 6.8. In addition, many organic phosphate
In a normal individual, the average HCO3– concen- compounds, such as adenosine monophosphate and
tration is approximately 24 mmol/L, and the PCO2 is nucleoside phosphate, have pka values between 6.5 and
40 mm Hg, resulting in the following pH: 7.5 and thus readily function as buffers in a physiologi-
24mEq/L
cal system. The following equations can be written:
pH = 6.1 + log ____________________________________
0.03 (conversion constant) × 40 mm Hg H2PO4− ↔ HPO42− + H+
24
= 6.1 + log ___
1.2 H2PO42−
pH = pka + log _________
= 6.1 + log 20 HPO42–
= 6.1 + 1.30 = 7.40

Hemoglobin Buffer System. The hemoglobin buffer
The PCO2 is maintained at approximately 40 mm Hg system consists of two buffering systems: nonoxygen-
by the lungs’ regulating the loss of CO2. ated and oxygenated hemoglobin. The oxygenated
The continuous internal respiration of tissue hemoglobin buffer system differs from the nonoxygen-
cells consumes O2 and produces CO2. The CO2 ated type due to the difference in the pka value. In these
reacts with water to produce hydrogen ions (H+). two systems, the weak acids consist of the nonoxygen-
These acids need to be buffered to maintain the ated (HHb) and oxygenated hemoglobin (HHbO2);
narrow range of pH in living organisms. When the conjugate bases are Hb⫺ and HbO2⫺. The nonoxy-
hydrogen ions are added to body fluids, the genated hemoglobin buffer pair can be symbolized as
following reaction occurs: follows:
H+ + HCO3− ↔ H2CO3 ↔ CO2 + H2O HHb ↔ H+ + Hb−

The oxygenated hemoglobin can be symbolized as blood. Another small portion reacts with water to
release hydrogen ions. Plasma protein buffers buffer
HHbO2 ↔ H+ + HbO2− this acid. Some carbon dioxide reacts, very slowly, with
the carbamino groups of proteins to form carbamino
The Isohydric Principle. The various fluid compart- compounds. Most of the carbon dioxide is transported
ments in a physiological system contain a variety of as the bicarbonate ion, formed when carbon dioxide
buffers that interact with each other to form a single pH. enters the red blood cells and reacts with water to form
For example, the plasma compartment is a homoge- carbonic acid. This reaction is very fast because of the
neous solution that contains several buffers, mainly the presence in the red blood cells of carbonic anhydrase,
bicarbonate buffer, the phosphate buffer, and a variety which rapidly catalyzes the formation of carbonic acid
of protein buffers. The plasma compartment is well and brings the reaction to a quick equilibrium. The
mixed because of rapid blood circulation. In the reaction quickly becomes 99.9% complete, forming
plasma compartment is a single hydrogen ion hydrogen and bicarbonate ions.
concentration, as determined by pH measurements, Most of the hydrogen ion generated in the red
that require various buffer pairs to be in equilibrium. blood cells reacts with deoxyhemoglobin. This
This balance is referred to as the isohydric principle process facilitates the release of oxygen from the
and is expressed as oxygenated hemoglobin. A small amount of carbon
dioxide remains dissolved, and some is carried by
[HA1] [HA2] [HA3] [HAn] hemoglobin in the form of carbamate (R-NHCO2−).
pH = pka1 ______
−
= pka2 ______
−]
= pka3 ______
−]
= pkan ______ The unionized form of the alpha-amino groups of
[A1 ] [A 2 [A 3 [An−]
hemoglobin can react reversibly with carbon dioxide.
The released oxygen from hemoglobin in the red
blood cells is transported to the tissue cells. This
How Acids, Bases, and Buffers process of exchanging oxygen and removing carbon
dioxide occurs normally without changing the
Affect Respiration hydrogen ion concentrations in the various compart-
The intracellular pH and the fluid pH are held at a ments. The overall process is known as the isohydric
steady concentration mainly because of the various shift because the pH remains constant.
buffers in these compartments. The interactions of These reactions in the red blood cells form a
acids, bases, and buffers are key to understanding how bicarbonate ion, which diffuses rapidly out of the red
respiration works. blood cell into the plasma compartment. Since there is
a substantial loss of anions as the bicarbonate ions
leave the red blood cells, chloride ions enter the red
TRANSPORT OF CARBON DIOXIDE TO THE ALVEOLI
bloods cells to maintain electrochemical balance. The
Respiration is a continuous interchange of oxygen and exchange of chloride and bicarbonate ions across the
carbon dioxide between a living organism and its red blood cell membrane is called the chloride shift. The
environment. Tissue cells continuously require oxygen reactions involved in the isohydric and chloride shifts
for their metabolic processes, which form carbon are illustrated in Figure 4-7.
dioxide that must be continuously eliminated. At the lungs, the reverse process occurs. The
Respiration has two components: external and internal. binding of oxygen to hemoglobin releases hydrogen
External respiration is the exchange of oxygen and ions from the hemoglobin. The reaction of hydrogen
carbon dioxide in the lungs between blood and
alveolar air. Internal respiration is the exchange of
these gases at the tissue level.
Oxygen is carried from the lungs to the tissue by PLASMA RED BLOOD CELL PLASMA
the blood. Normally, about 97–98% of the oxygen is carbonic
CO2 CO2 + H2O H CO HCO3– HCO3–
carried in reversible combination by the hemoglobin anhydrase 2
(Hb) molecule. This relationship can be presented as
H+ + Hb– HbH
Hb (deoxygenated) + O2 ↔ HbO2 (oxygenated) H+ + Hb– HbH
The carbon dioxide produced by the tissue’s H H

metabolic processes enters the interstitial and plasma CO2 CO2 + HbNH HbNCOO–
compartments. In the plasma compartment, a small
portion of the carbon dioxide remains dissolved in the FIGURE 4-7 Carbon dioxide reactions in the red blood cell.
ions with the bicarbonate ions results in the formation because they are present in small amounts and transient
of carbon dioxide, which is released by the lungs. These in nature. When present in small quantities, they are
processes are aided by the Haldane effect (the binding usually metabolized to carbon dioxide and water. For
of oxygen facilitates the displacement of carbon example, lactic acid accumulation due to exercise and
dioxide). The more acidic oxyhemoglobin has a beta-hydroxybutyric and acetic acids present after
reduced capacity to form carbamino hemoglobin; the fasting are transient because they are metabolized to
facilitation of carbonic anhydrase in the presence of carbon dioxide and water. When these acids are present
carbonic acid forms carbon dioxide. Maintaining the in very large amounts, however, perhaps as a result of
PCO2 at approximately 40 mm Hg keeps the bicarbon- diabetes or other pathological conditions, the kidney
ate ion and pH at a steady level. must eliminate them. The major noncarbonic acids
In a typical individual at rest, the bicarbonate ion (sulfuric and phosphoric) are eliminated by the kidney
concentrations in arterial and venous blood are approx- in amounts of 50–150 mmol per day.
imately 24.0 and 25.1 mmol/L, respectively, resulting in
a difference of approximately 1.1 mmol/L. Arterial
blood and venous blood differ by approximately REGULATION OF ALKALI IN THE BODY
0.15 mmol/L of dissolved carbon dioxide and In humans and other mammals, the major source of
0.5 mmol/L of carbamino carbon dioxide. Thus, alkali production is the formation of CO2 and H2O,
approximately 1.75 mmol/L of carbon dioxide is resulting in the bicarbonate ion. Often, increased
exchanged at each pass through the lungs at normal alkali is not directly the result of alkali production but
respiration. As the PCO2 increases, an almost linear rather results from the consumption of hydrogen ion
increase in alveolar ventilation occurs to remove the (usually in fruits and vegetables), increasing bicarbon-
increased carbon dioxide produced and to maintain ate ion concentration. Dietary habits that include the
normal pH (Figure 4-8). consumption of significant amounts of meat result in
the production of sulfuric and phosphoric acids,
which provide adequate amounts of hydrogen ions
PROCESSING OF NONCARBONIC ACIDS and maintain plasma bicarbonate levels around
In humans, the most common noncarbonic acids are 24 mmol/L. Thus, alkali is eliminated from the body
sulfuric and phosphoric acids, produced as a result of mainly as expired air in the alveoli. Excessive amounts
protein metabolism and the catabolism of phospholip- of carbonate ions must then be excreted by the
ids. Other noncarbonic acids produced in humans are kidneys, resulting in urine having an alkaline pH.
beta-hydroxybutyric acid, acetacetic acid, lactic acid, and
pyruvic acid. In addition, a variety of foods may contain
organic acids. The acids other than sulfuric and phos- Disturbance of the
phoric are of little consequence in the normal person
Acid–Base Balance
Metabolic changes, as well as many pathological condi-
ALVEOLAR VENTILATION (liters/minute: LPM)
tions, result in changes in electrolyte balance and acid–

10 base disturbances that can be identified and monitored by
examining extracellular fluids such as blood.6,7 Common
measurements include electrolyte, pH, PCO2, bicarbon-
ate, and total carbon dioxide. Theoretically, it should be
8
relatively easy to characterize disturbances in acid–base
status as either acidosis or alkalosis, which can be further
differentiated into those having respiratory causes and
6 those having metabolic causes.
• Respiratory acidosis is caused by an increase in
carbonic acid relative to bicarbonate.
4 • Respiratory alkalosis is characterized by a
decrease in carbonic acid with no change in

bicarbonate.
• Metabolic acidosis is characterized by a decrease in
2
100 80 60 40 20 bicarbonate without any significant change in
PCO2 (mm Hg)
carbonic acid.
• Metabolic alkalosis is an increase in bicarbonate
FIGURE 4-8 PCO2 removal with increasing alveolar ventilation. without a significant change in carbonic acid.
This theoretical simplicity is complicated by impaired respiration as a result of diseases such as

various compensatory mechanisms. For example, emphysema, asthma, pneumonia, chronic bronchitis,
compensation can occur by altering the carbon congestive heart failure, and hypoxia. Another cause is
dioxide concentration through hyperventilation depression of the respiratory center in the medulla, as a
(eliminating more carbon dioxide) or through result of the administration of anesthesia or the use of
hypoventilation (retaining more carbon dioxide). narcotics or sedatives. Exposure to sedatives and
Also possible is renal compensation by either retain- hypoxia can also cause decreased ventilation, resulting
ing more bicarbonate ion or increasing its elimina- in respiratory acidosis.
tion. In addition to simple causes of any of these An increase in carbonic acid results in a variety of
conditions, mixed causes can exist. compensatory mechanisms. In blood, an increase
in carbonic acid is initially and immediately buffered
by both the hemoglobin and protein buffer systems,
RESPIRATORY ACIDOSIS resulting in a slight increase in bicarbonate ion. Renal
Respiratory acidosis is caused by an increase in compensation, on the other hand, requires more
carbon dioxide retention, resulting in an increase in time. The resulting rise of PCO2 in respiratory acido-
carbonic acid and in PCO2 (Figure 4-9). Respiratory sis causes increases in bicarbonate ion reabsorption
acidosis is caused by a variety of conditions, including and ammonia formation by the kidney. The increase
Respiratory Acidosis
(Excess of carbonic acid in the extracellular fluid)
Lungs Kidneys Compensate
HCO3
CO2
Lungs are affected: insufficient gas Urine is acid. Kidneys conserve

exchange and/or ventilation. High base (bicarbonate) and excrete
PaCO2 causes a reflexive attempt to acid.
increase ventilation.
Treatment: Remove the cause. Administer an IV alkali solution. Deep breathing

exercise or use of a ventilator.
Respiratory Alkalosis
(Deficit of carbonic acid in the extracellular fluid due to hyperventilation)
Lungs Kidney
CO2
HCO3
Ventilation is affected. Treatment would be Urine is alkaline. Kidneys excrete

recommended. base (bicarbonate) and retain acid.
Treatment: Remove the cause. Rebreathe expired air, e.g., CO2 , from a paper bag.
Antianxiety drugs, e.g., Valium (diazepam), Ativan (lorazepam).
FIGURE 4-9 Body’s defense action and treatment for respiratory acidosis and respiratory alkalosis.
Best Practice CASE STUDY 4-1

Respiratory Acidosis A 54-year-old male patient, C. S., was admitted
The renal response to respiratory acidosis is a to the emergency room (ER) exhibiting speech
slow process, requiring several days. and gait disorders, irritability, and mental
confusion. A chemistry profile, including electro-
lytes, was performed. The chemistry profile was
essentially normal with the exception of glucose
(47 mg/dL; normal range 70–110 mg/dL) and a
total CO2 concentration of 51 mmol/L (normal
in bicarbonate retention is directly related to range 22–32 mmol/L). The ER physician subse-
PCO2 but not to pH. As a result, in the early stages of quently requested a blood gas determination,
respiratory acidosis, significant increases in arterial which yielded the following results:
PCO2 can be expected. Once renal compensation is
fully developed, it becomes more efficient than the PO2 ⫽ 65 mm Hg
initial rapid response of the buffer system. Once full
compensation has occurred, the increased resorption PCO2 ⫽ 71 mm Hg
of HCO3– reduces the extracellular H+ concentration pH ⫽ 7.18
to normal or near-normal blood pH.
In uncomplicated respiratory acidosis, laboratory HCO3⫺ ⫽ 22 mEq/L
findings consist of:
The ER physician concluded that the patient
• Decreases in blood pH. was suffering from uncompensated respiratory
• Increases in both the bicarbonate ion and acidosis as a result of impaired respiratory drive
dissolved bicarbonate. caused by a metabolic condition (hypoglycemia).
• A blood pH of less than 7.35. Rationale for diagnosis: Since there were no
• An increase of the bicarbonate ion to around known causes of overproduction of CO2, eleva-
30 mmol/L. tions of PCO2 are the result of defects in PCO2
• An increase of dissolved carbon dioxide to excretion. The low glucose level, along with the
2 mmol/L. Since most laboratories measure total absence of airway obstructions or impaired
carbon dioxide (both dissolved and the bicar- respiratory mechanics, suggested an impaired
bonate ion), results of close to 40 mmol/L may respiratory drive caused by hypoglycemia.
be obtained.
• Decreases in plasma chloride. Questions
• Increases in potassium. 1. What compensatory mechanism is likely to
occur in this patient?
2. What is the likely compensatory mechanism
RESPIRATORY ALKALOSIS
in a patient suffering from respiratory
An excessively increased rate of carbon dioxide loss acidosis when the defect is not in the
resulting in a reduced PCO2 along with an increased respiratory center?
pH results in respiratory alkalosis. (See Figure 4-9.)
The overall condition of hyperventilation can be
voluntary or the result of disease or drug consump-
tion. Examples of drug-induced hyperventilation are
early stages of salicylate poisoning, as well as the Initially, much of the lost acid is replenished by
effects of analeptic (central nervious system stimu- ions from extracellular fluids, along with a shift of
lant) drugs or hormones such as progesterone and sodium and potassium into the intracellular fluid.
catecholamines (sympathomimetic “fight-or-flight” Some acid is also supplied by an increased production
hormones). Conditions such as trauma to the central of lactic acid, probably due to the decreased availability
nervous system due to cerebral hemorrhage may also of oxygen. Renal compensation during respiratory
result in hyperventilation. Hyperventilation may also alkalosis is opposite to what occurs during respiratory
occur with no apparent cause, a condition known as acidosis. Instead of bicarbonate ions being retained, a
hyperventilation syndrome. Finally, respiratory alkalo- larger-than-normal amount is being excreted, and the
sis can be induced experimentally by deliberate amount of acid (hydrogen ions) in the urine signifi-
hyperventilation. cantly decreases.
Laboratory findings in respiratory alkalosis include.

• Increased lactic acid levels.
Best Practice
• Significantly reduced bicarbonate ions and
dissolved carbon dioxide. Respiratory Alkalosis
• Dissolved carbon dioxide that is generally less Respiratory hyperventilation is a compensatory
than 50% of normal. response to metabolic acidosis. Compensation for
• Total carbon dioxide analysis (the sum of respiratory alkalosis consists initially of buffering
dissolved carbon dioxide and bicarbonate ions) by erythrocytes and tissues. Subsequently, renal
of less than 20 mmol/L. buffering becomes a major factor if hyperventila-
• Lowered concentrations of both sodium and tion persists for several days.
potassium.
production of acids, increased transfer of hydrogen

METABOLIC ACIDOSIS ion from intracellular to extracellular fluid, the
Metabolic acidosis is the result of increased hydro- ingestion or infusion of organic acids into the blood,
gen ion concentration (a decrease in blood pH) kidney failure resulting in the reduced excretion of
(Figure 4-10). It can occur as the result of excessive acid, and excessive loss of bicarbonate as the result
of diarrhea and loss of duodenal fluid.
Metabolic Acidosis
(Deficit of bicarbonate or excess acid in the extracellular fluid)
Lungs Kidney
HCO3
CO2
Lungs "blow off" acid. Respirations Urine is acid. Kidneys conserve

are increased. bicarbonate ions and excrete acid.
Treatment: Remove the cause. Administer an IV alkali solution, e.g., sodium bicarbonate
or sodium lactate. Restore water, electrolytes, and nutrients.
Metabolic Alkalosis
(Excess of bicarbonate in the extracellular fluid)
Lungs Kidney
CO2
HCO3
Breathing is suppressed. Urine is alkaline. Kidneys excrete

bicarbonate ions, and retain

hydrogen ions.
Treatment: Remove the cause. Administer an IV solution of chloride, e.g., sodium chloride.
Replace potassium deficit.
FIGURE 4-10 The body’s defense action and treatment for metabolic acidosis and metabolic alkalosis.
A common cause of metabolic acidosis is diabetic

ketoacidosis. Excessive mobilization of triglyceride results CASE STUDY 4-2
in the excessive formation of beta-hydroxybutyric and
acetoacetic acid. The resulting severe metabolic acidosis can G. R., a 27-year-old female, was admitted to the
lead to coma and death if the patient is not treated with emergency room (ER). She was in a state of
insulin. Before the availability of insulin, diabetic ketoaci- hysteria, had a severe headache, and was hyperven-
dosis was a common cause of death in juvenile diabetics. tilating. The ER physician requested a chemistry
Milder forms of metabolic acidosis can also be profile including electrolytes, a urine toxicology
observed in cases of severe starvation, such as anorexia, screen, and blood salicylate level and blood gas
in which ketoacids are produced in excessive amounts studies. The chemistry profile was essentially
to meet the individual’s energy needs. normal. The electrolyte studies and blood gas
Severe hypoxia can lead to significant increases studies indicated significant depletion of total
in lactic acid, causing metabolic acidosis. Oxygen carbon dioxide (16 mmol/L; normal 22–32 mmol/L),
deprivation of tissue results in a significant increase a decreased P CO2 of 29 mm Hg, a pH of 7.50, a
in the blood lactate/pyruvate ratio. Hypoxia can be PO2 of 99 mm Hg, and HCO3– of 18 mEq/L. The
the result of pulmonary insufficiency or oxygen urine toxicology screen was negative, but the blood
deprivation, initiating a chain of reactions that can salicylate level was 450 mg/L.
culminate in coma and death. Increases in lactic acid The ER physician concluded that the patient
can be the result of the patient’s receiving large doses most likely was suffering from respiratory alkalosis
of drugs such as phenformin and streptozotocin. brought on by hysteria and an overdose of salicylate.
The ingestion of antifreeze (ethylene glycol) or Rationale for diagnosis: A salicylate level of
methyl alcohol can cause metabolic acidosis. Ethylene greater than 200 mg/L is uncommon. Salicylate
glycol is metabolized to glycolic and oxalic acid, and concentrations that exceed 300 mg/L are associ-
methyl alcohol results in the formation of formalde- ated with severe headache and hyperventilation.
hyde and formic acid. Salicylate and a variety of other drugs stimulate the
The chronic ingestion of high doses of salicylic acid respiratory center, causing an excessive loss of
can result in salicylate intoxication, resulting in the carbon dioxide. The resulting uncompensated loss
formation of excessive organic acids. of the bicarbonate ions results in an alkaline pH.
The bicarbonate buffer system, because of its ample
supply of bicarbonate ion, is initially involved in Questions
resisting change in pH as a result of metabolic acidosis. 1. The hyperventilation in this case resulted in
Laboratory findings vary with the cause and a significant decrease in the blood
severity of metabolic acidosis. In general, they are: PCO2 level. As expected, this decrease
• A significant decrease of both the bicarbonate significantly alters the 20:1 ratio of HCO3–/
ion and dissolved carbon dioxide. CO2. What compensatory system will
• Significantly increased organic acids, regardless attempt to reestablish this 20:1 ratio?
of the cause of metabolic acidosis. 2. Subnormal levels of PCO2 can result in
• In diabetic ketoacidosis, large reductions in respiratory alkalosis. Discuss a mechanism
plasma sodium and chloride. for this occurrence.
• Minimal reductions in sodium and chloride due
to renal causes.
Best Practice Best Practice

Laboratory Tests Metabolic Acidosis
Many conditions, such as metabolic acidosis Compensatory mechanisms in metabolic acidosis
caused by diabetic ketoacidosis and chronic consist of both respiratory and renal mecha-
renal diseases that develop over a prolonged nisms. In respiratory compensation, both the rate
period, will alter classic laboratory results. Labora- of ventilation and the tidal volume are increased.
tory tests that determine the severity of diabetes The respiratory response to metabolic acidosis is
and kidney diseases must be considered. Blood very rapid, occurring within minutes. Renal com-
urea nitrogen (BUN), creatinine, and glucose pensatory mechanisms are slower, taking place
levels provide important clinical information. over a period of hours and days.
CASE STUDY 4-3

S. C., a 13-year-old female student who was as a result of type I diabetes. Upon consultation
complaining that she was ill, was transferred by with the pediatric endocrinologist, the patient
ambulance from her junior high school to the was admitted, and insulin administration was
emergency room (ER). The patient stated that she initiated.
was feeling weak and was constantly thirsty. She Rationale for diagnosis: Diabetic ketoacidosis in
had been urinating frequently for the past few children is a common cause of metabolic acidosis.
weeks. A chemistry profile, including electrolytes, The very high blood glucose levels with urine
was performed. The chemistry profile revealed a ketones and a normal blood lactate level are
very high glucose level of 782 mg/dL (normal range consistent with this diagnosis. Diabetic ketoacidosis
70–110 mg/dL), along with a low total carbon results in large increases in ketoacid production,
dioxide concentration of 18 mmol/L (normal range which, if not treated, overwhelm the buffering
22–32 mmol/L) and an increased chloride concen- capacity. It is essential to administer insulin to
tration of 110 mmol/L (normal range 95–106 facilitate the use of glucose by the cells. Failure
mmol/L). The physician subsequently requested a to treat diabetic ketoacidosis could have fatal
urinalysis, a blood lactic acid determination, and consequences.
blood gas studies. The urinalysis was positive for
ketones, and the blood lactic acid level was a Questions
normal 1.1 mmol/L (normal range 0.6–2.2 mmol/L).
1. The primary cause of metabolic acidosis is the
The blood gases yielded the following results:
production of organic acids at a rate exceeding
that of their breakdown. Indicate possible
PO2 ⫽ 97 mm Hg
causes of metabolic acidosis besides diabetes
PCO2 ⫽ 24 mm Hg mellitus.
pH ⫽ 7.29 2. A patient who has been taking large
HCO3⫺ ⫽ 16 mEq/L doses of aspirin for a prolonged period
developed symptoms of metabolic acidosis.
The ER physician concluded that the patient What could be the cause of the patient’s
most likely was suffering from metabolic acidosis condition?
METABOLIC ALKALOSIS Laboratory findings in metabolic alkalosis include:

Metabolic alkalosis has a number of causes: • Increases in bicarbonate ions and dissolved
carbon dioxide.
• A decrease in hydrogen ion concentration due
• Decreases in chloride and potassium level.
to decreased noncarbonic acid or increased
bicarbonate ion or other conjugate base.
(See Figure 4-10.)
• The excessive loss of hydrochloric acid from the Best Practice
stomach after sustained vomiting.
• Certain types of external fistulas and gastric Metabolic Alkalosis
suction. Respiratory compensatory mechanisms in meta-
• Prolonged administration of diuretics, as well bolic alkalosis are not clear and occur mostly by
as the administration of excessive alkali and decreasing the resting tidal volume. Renal re-
therapies used to treat chronic pulmonary sponses include decreased sodium–hydrogen ion
insufficiency. exchange, formation of ammonia, and reabsorp-
• Excessive adrenal steroids, as in patients with tion of bicarbonate.
Cushing’s syndrome and hyperaldosteronism.
Acids are categorized as strong or weak, depending

CASE STUDY 4-4 on their degree of ionization. They are also further
divided into bicarbonic (carbonic) and noncarbonic
E. S., a 61-year-old female, was seen in the (fixed) acids. Fixed acids are eliminated daily by the
emergency room (ER). She was complaining of kidneys, but carbonic acids can permeate cell mem-
prolonged vomiting. A chemistry profile, includ- branes and affect cellular pH.
ing electrolytes, was performed. The chemistry Buffers are substances that resist changes in pH
results were essentially normal with the excep- when an acid or a base is added. Buffers are also
tion of chloride 82 mmol/L (normal range divided into two broad categories: bicarbonate and
95–106 mmol/L), potassium 3.2 mmol/L nonbicarbonate. The bicarbonate–carbonic acid pair
(normal range 3.5–4.5 mmol/L), and total is the most important buffer in plasma. The non-
carbon dioxide 38 mmol/L (normal range bicarbonate buffering systems include the phosphate,
22–32 mmol/L). The attending physician plasma protein, and hemoglobin buffer systems.
requested a blood gas determination that yielded Buffers are crucial for transporting carbon dioxide to
the following results: the alveoli during respiration.
The body closely regulates the acid–base balance,
PO2 ⫽ 98 mm Hg but several factors can disturb it. Disturbances in the
PCO2 ⫽ 38 mm Hg balance can be categorized as acidosis or alkalosis.
pH ⫽ 7.46 Each can be further categorized according to its cause:
Positive base excess respiratory or metabolic.
The respiratory system responds immediately to a
The ER physician concluded that the patient change in the acid–base status and becomes maximal
was suffering from metabolic alkalosis as the in 3–6 hours. In comparison, the renal response is slow
result of prolonged vomiting. and prolonged. The renal response is important
Rationale for diagnosis: Metabolic alkalosis because of its ability to conserve or increase acids or
is characterized by a decrease of chloride ion, bases depending on whether the patient is in acidosis
or chloride depletion. The patient’s prolonged or alkalosis.
vomiting resulted in the loss of fluid and a
greater Cl–/Na+ ratio than is normally present in
plasma. This condition caused the excessive Study Questions
reabsorption of HCO3–. Vomiting also resulted in REVIEW QUESTIONS
the excessive loss of acid. Prolonged diuretic use
may have further reduced the plasma potassium 1. A solution contains 180 mmol/L of hydrogen ions.
concentration. What is the pH of this solution?
2. What is the hydrogen ion concentration in milli-
Questions moles per liter of a solution with a pH of 7.2?
1. Hyperaldosteronism causes the kidney 3. To make 1000 mL of a 0.5-M acetate buffer solu-
secretion of K+ and H+ ions. How can tion of pH 4.6 at 25°C from glacial acetic acid and
hyperaldosteronism result in metabolic sodium acetate, how many millimoles of each
alkalosis? buffer pair is needed? The pka of acetic acid at
2. Diminished levels of extracellular potassium 25°C is 4.7.
can result in moving potassium ions from the 4. If the pH of a solution is 8.0, what is the approxi-
cells into the extracellular space. How could mate concentration of the OH−?
this shift result in metabolic alkalosis?
5. What is the HCO3− concentration of a plasma
sample with a pH of 7.4 and a PCO2 of 34 mm Hg?
Under these conditions, the pka is 6.1.
Summary
In a living system, acids are substances that can donate
electrons, and bases are substances that can receive 1. Respiratory acidosis may be caused by
electrons. The balance between acids and bases in body a. salicylate intoxication.
fluids, usually measured in terms of hydrogen ion b. vomiting.
concentration (pH), must be maintained for body c. pulmonary obstruction.
systems to function. d. sodium bicarbonate infusion.
2. The concentration of bicarbonate in blood can be c. hypoventilation.

determined from the measurement of pH and d. an excess of dissolved carbon dioxide.
PCO2 by the relationship 10. The Henderson–Hasselbalch equation can be used
a. pH = [HCO3−]/pka to calculate
b. pH = pka + log ([HCO3−]/[PCO2 3 0.03]) a. blood PCO2 only.
c. pH = PCO2/HCO3– b. blood CO2 only.
d. pH = PCO2/pka c. pka of buffers only.
3. Which of the following would provide the best d. blood PCO2, blood CO2, and pka of buffers.
information to evaluate a disturbed acid–base 11. The bicarbonate/carbonic acid ratio is calculated
balance? from the equation devised by
a. total PCO2 capacity and total H2CO3 a. Gilbert Lewis.
b. pH and total carbon dioxide b. Dmitry Mendeleyev.
c. pH and PCO2 c. Bronsted–Lowry.
d. total H2CO3 d. Henderson–Hasselbalch
4. In the tissues, most of the carbon dioxide that 12. Maintaining a normal pH at 7.4 in plasma requires
enters the erythrocytes is hydrated to form H2CO3, maintaining a
which dissociates to form H+ and HCO3−. The H+ a. 20:1 ratio of bicarbonate to dissolved carbon
thus produced is buffered by dioxide.
a. imidiazole groups of deoxygenated b. 10:1 ratio of bicarbonate to dissolved carbon
hemoglobin. dioxide.
b. histidine groups of carbonic anhydrase. c. 20:1 ratio of dissolved carbon dioxide to
c. carbamino groups of oxygenated hemoglobin. bicarbonate.
d. the phosphate buffer system. d. 10:1 ratio of dissolved carbon dioxide to
5. Metabolic acidosis, with an increased concentra- bicarbonate.
tion of acetoacetate, beta-hydroxybutyrate, may be 13. The chloride shift refers to
associated with a. an abnormally high concentration of plasma
a. renal tubular defects. chloride.
b. diabetes mellitus. b. the shift of plasma chloride to the red blood
c. ethanol consumption. cells.
d. diarrhea. c. an abnormally low concentration of plasma
6. An increase in the plasma bicarbonate concentra- chloride.
tion without a change in the dissolved CO2 will d. the irreversible binding of chloride ions with
result in the protein base.
a. no change in the acid–base balance. 14. The total CO2 is defined as the sum of
b. metabolic alkalosis. a. HCO3− + dissolved CO2.
c. metabolic acidosis. b. HCO3− − dissolved CO2.
d. respiratory alkalosis. c. PCO2 + carbamino compounds.
7. Respiratory acidosis is characterized by d. HCO3− + dissolved CO2 + carbamino
a. an excess of dissolved carbon dioxide. compounds.
b. an excess of bicarbonate. 15. Which is not a buffer system found in plasma?
c. an excess of total carbon dioxide. a. HPr/Prhr −
d. a reduction in disolved carbon dioxide. b. H2PO4−/HPO42−
8. The bicarbonate ion concentration can be calcu- c. bicarbonate buffer system
lated from the PCO2 and total carbon dioxide level d. HHbO2/HbO2−
using which equation?
a. total carbon dioxide − (0.03 × PCO2)
b. (total carbon dioxide + 0.03) × PCO2 CRITICAL-THINKING QUESTIONS
c. cannot be calculated from carbon dioxide and 1. Metabolic acidosis can occur because of uncon-
PCO2 values trolled diabetes mellitus and renal failure. Identify
d. 0.03 × (PCO2 − carbon dioxide) what causes metabolic acidosis in these conditions.
9. Respiratory alkalosis is characterized by 2. Explain the differences among acids, bases, and
a. a reduction in PCO2. buffers in a physiological environment and in a
b. an increase in PCO2. nonphysiological environment.
3. Explain how the body manages to eliminate the 6. Lippmann BJ. Fluid and electrolyte management.
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pairs in the body. Christenson RH, eds. Professional Practice in Clinical
Chemistry: A Review. Washington, DC: AACC Press;
5. Using the bicarbonate buffer system, determine the
1999.
pH of a plasma sample that has a PCO2 of 50 mm
Hg and a bicarbonate (HCO3−) concentration of
38 mmol/L. Assume that the value of the pka is 6.1. Suggested Readings
6. Differentiate between respiratory and metabolic Bennett JC, Carpenter CJ, Andriole TE, eds. Cecil
acidosis and between respiratory and metabolic Essential of Medicine. 8th ed. Philadelphia: WB
alkalosis. Saunders Co; 2010.
7. Provide specific causes for respiratory and meta- Brueckner PJ. Water, electrolyte, and hydrogen ion
bolic acidosis. disorders. In: Gornall AG, ed. Applied Biochemistry
of Clinical Disorders. 2nd ed. Philadelphia: JB
Lippincott Company; 1986:99–128.
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C12-A. Wayne, PA: National Committee of Electrolytes and blood gases. In: Burtis CA, Aswood
Laboratory Standards; 1994. ER, eds. Tietz Textbook of Clinical Chemistry. 3rd ed.
4. Heusel JW, Siggaard-Anderson O, Scott MG. Philadelphia: W.B. Saunders Co; 1999:1056–1092.
Physiology and disorders of water, electrolyte, and Siggaard-Anderson O. The Acid–Base Status of Blood.
acid–base metabolism. In: Burtis CA, Ashwood ER, 4th ed. Copenhagen: Munsgaard; Baltimore:
eds. Tietz Textbook of Clinical Chemistry. 4th ed. Williams & Wilkins; 1974.
Philadelphia: WB Saunders Co; 2005. Woolf CR. Respiratory disorders. In: Gornall AG, ed.
5. Scott MG, Heusel JW, LeGrys VA, Siggaard-Anderson Applied Biochemistry of Clinical Disorders. 2nd ed.
O. Electrolytes and blood gases. In: Burtis CA, Philadelphia: JB Lippincott Co; 1986:129–138.
Ashwood ER, eds. Tietz Textbook of Clinical Chemistry.
4th ed. Philadelphia: WB Saunders Co; 2005.
CHAPTER 5
Applied Microbiology
Janet Hudzicki and Stephen F. Wehrman
OBJECTIVES
• List the characteristics used to classify microorganisms.
• Describe disinfection and sterilization methods.
• Identify the beneficial roles of endogenous microflora.
• Describe the factors influencing bacterial growth.
• Identify human defenses against infectious diseases.
• Discuss infectious diseases of the respiratory system.
CHAPTER OUTLINE
Classification of Microorganisms Control of Microbial Growth
Staining Methods Sterilization and Disinfection
Gram Stain Physical Methods
Acid-Fast Stain Chemical Methods
Specialized Tests Antimicrobials
ELISA History
Specimen Collection Mechanisms
Suctioning Resistance
Bronchoscopy Classification
Culturing Microbial Pathogenicity
Human-Microbe Interactions Disease Types and Stages
Mucus Membranes Modes of Transmission
Normal Flora Epidemiology
Human Defense Mechanisms Important Respiratory Pathogens
Mucus Membranes Pneumonias
Cell-Mediated Response Influenza
The Humoral Immune Response Predisposition
101
KEY TERMS
antigen epidemic pathogenicity
antiseptic fomite resistant
bacteria fungi sterilization
disinfectant nosocomial infection vector
disinfection opportunistic virulence
endemic pandemic virus
endogenous pathogen
R
espiratory therapists frequently work with prokaryotes from other microorganisms is their lack of
patients with lung infections. Pneumonia, a nuclear membrane and organelles such as mitochron-
tuberculosis, AIDS, secretion management, dria. In other words, they are very simple organisms.
and ventilator care are just a few of the Scientists have described about 3000 species of bacte-
situations in which they are called on to apply their ria, but this number probably represents less than 1%
knowledge of microbiology and infection control. In of the total types of bacteria. Bacteria are classified and
addition, between 5% and 10% of all patients who identified according to nine characteristics: morphol-
enter a hospital acquire an infection during their stays. ogy, staining, motility, atmospheric requirements,
Up to 40% of these hospital-acquired infections nutritional requirements, metabolic activities, pathoge-
(formerly known as nosocomial infections) involve nicity, growth, and genetic composition.
the respiratory system. The sizes, shapes, and cell arrangements (morphol-
This chapter reviews how microorganisms are ogy) of bacteria are easily observed under an ordinary
classified and explains the relationship between these light microscope. The three basic shapes are cocci
organisms and health or disease. Methods for prevent- (spherical), bacilli (rod-shaped), and spirochete and
ing and treating infection, including the proper clean- spirillum (curved or spiral-shaped). Treponema pallidum
ing and disposal of equipment, maintaining host is spiral shaped. A short, plump, gently curved rod is a
defenses, and pharmacologic and therapeutic interven- Vibrio. In addition to shape, the arrangement of bacilli
tions, are presented. A strong foundation in microbiol- may help with identification. For example, Streptococci
ogy will provide you with the skills needed to protect are round bacteria arranged in chainlike groups.
yourself and your patients. Staphylococci occur in clusters. Corynebacterium diphthe-
riae cells stack up next to each other like a fence or
palisade. Figure 5-1 illustrates these shapes.
Classification of Microorganisms
Taxonomy, or the science of classifying living things,
recognizes five kingdoms: Plantae (plants), Animalia Staining Methods
(animals), Myceteae (fungi), Protista (microscopic Various staining methods are used to identify
algae and protozoans), and Prokaryotae (bacteria). organisms.
Each kingdom is subdivided into phyla, which are
further divided into classes, orders, families, and finally
genera and species. To identify the species, each GRAM STAIN
organism is given two names: the genus name and the The Gram stain uses crystal violet (purple) as the
species name, usually a descriptive adjective or noun. primary stain and safranin (pink) as the counterstain.
Human beings, for example, are known as Homo
(genus name) sapiens (species name); the bacterium
that causes syphilis is Treponema pallidum.
Viruses are not included in the five-kingdom
Best Practice
classification scheme. They are noncellular particles
that do not exhibit most of the life processes of cells Scientific Nomenclature
and that are unable to function independently of a The genus name is always capitalized, and the
host cell. They basically consist of a protein capsid species name is always lowercased. Both are
(outer shell) and nucleic acid. always in italics: for example, Corynebacterium
Bacteria make up the kingdom known as Pro- [genus] diphtheriae [species].
karyotae. An important characteristic that distinguishes
CHAPTER 5 ■ Applied Microbiology 103
Cocci Bacilli
Spirilla
Diplococci Streptococci
Coccobacilli
Streptobacilli
Staphylococci
FIGURE 5-1 Various shapes of bacteria.
Figure 5-2 illustrates the Gram stain procedure. Organ- Legionella pneumophila are gram-negative pulmonary
isms that retain the primary stain throughout the pathogens, or disease-producing organisms.
fixing, decolorizing, and counterstaining steps are
considered gram-positive (purple). Streptococcus
pneumoniae is a gram-positive organism that is seen in ACID-FAST STAIN
pulmonary infections. Bacteria that do not retain the To identify bacteria that do not consistently take up the
primary stain are identified as gram-negative (pink). dyes used in the Gram stain, the acid-fast stain is
Klebsiella pneumoniae, Pseudomonas aeruginosa, and another technique that may be useful. The genus
STEP TIME PROCEDURE RESULT
1 one minute Primary stain: Apply crystal All bacteria stain purple
violet stain (purple)
Rinse slide
2 one minute Mordant: Apply Gram’s iodine All bacteria remain purple
Rinse slide
3 three to five seconds Decolorize: Apply alcohol Purple stain is removed from
Gram-negative cells
Rinse slide
4 one minute Counterstain: Apply safranin Gram-negative cells appear pink-red;

stain (red) Gram-positive cells appear purple
Rinse slide
FIGURE 5-2 Steps in the Gram stain procedure.

Mycobacterium, whose members cause tuberculosis and

Hansen’s disease (leprosy), are commonly identified by Best Practice
this method.
Sputum Collection
SPECIALIZED TESTS Sputum may be obtained by allowing the patient
Many specialized tests are used to identify specific to spit the coughed-up material into a wide-
organisms. Fluorescent antibody techniques can be used to mouthed sterile bottle, by suctioning the airway,
detect pathogenic organisms directly in a patient’s or via bronchoscopy. A possible problem with
specimen. The dye-antibody complex will adhere to the expectorated sputum is oral contamination of the
organism in the specimen and can be viewed under an sputum with saliva containing epithelial cells.
ultraviolet microscope. This test is often used to make The laboratory personnel will discard a specimen
a positive identification of Legionella pneumophila, containing numerous epithelial cells. Directing
Bordetella pertussis, rabies virus, and many other patho- the patient to remove dentures and to thoroughly
gens. Fluorescent techniques can also be used to detect rinse or gargle with water before trying to pro-
antibodies in the patient’s serum. duce the specimen may reduce oral contamina-
tion. Special attention to safety should be
given when collecting specimens for suspected
ELISA tuberculosis.
Enzyme-linked immunosorbent assays (ELISA) are sensi-
tive immunochemical techniques that use an enzyme-
antibody-antigen combination placed in a test well. BRONCHOSCOPY
When a substrate for the enzyme is added, a color Bronchoscopy is the best method for collecting speci-
change develops if the antibodies or antigens are mens directly from the lung. Unfortunately, it is also
present. the most expensive and invasive collection technique.
It should be reserved for obtaining anaerobic speci-
mens for:
Specimen Collection
• Cytology (the study of cells, such as for the
Respiratory therapists are often called on to collect and diagnosis of cancer).
handle sputum specimens that are to be examined for • Diagnosis of Pneumocystis jiroveci (also known as
the presence of microorganisms. Proper techniques are Pneumocystis carinii) pneumonia.
essential to obtaining valid results. General guidelines • Bacterial, fungal, and viral pathogens when
should be followed for all specimen collection: simpler methods have failed.
• Specimens should be collected in a sterile The collected specimen is processed in the labora-
manner. tory. The Gram stain technique is the usual first step in
• Specimens should be collected before antimicro- evaluating sputum. The Gram stain reaction (positive or
bial therapy is started. negative), the shape of the bacteria present (rod, sphere,
• Specimens should be protected from heat and spiral, or curved), groupings (pairs, chains, or clusters),
cold and delivered promptly to the laboratory. and the presence of spores are all noted. This informa-
• Specimens should be properly sealed in a tion helps provide a presumptive diagnosis. For exam-
plastic bag to avoid exposing other health care ple, a patient may present with a cough, fever, and
practitioners. abnormal chest radiography typical of pneumonia.
• Containers must be properly labeled to identify Analysis of the sputum reveals gram-positive diplococci.
the patient, time of collection, date, source of These findings are typical of Streptococcus pneumoniae, a
specimen, and requested tests. common organism responsible for community-
• Specimen collection should be performed with acquired pneumonia. On the basis of this information,
care and tact to avoid harming the patient or the physician can initiate a course of antimicrobials
causing undue discomfort or embarrassment. appropriate to the organism and site of infection.
SUCTIONING
Specimens are obtained via suctioning with a sputum
Culturing
or Luken’s trap. The technique is simple but requires Simple biochemical tests may be performed to further
the same safety precautions for the patient and practi- identify the genus and species of the organism. A
tioner as standard suctioning procedures. definite diagnosis is made only after the organism has
been cultured, or grown, on a special medium. The good example. This opportunistic organism may
surface of an agar plate is inoculated with the patho- become pathogenic if competing flora are eliminated
gen, which is allowed to reproduce. Culturing may by antimicrobials or if the immune response of the
take several days or longer, depending on the type host is impaired by HIV infection. Normal flora
of organism. may also result in an infection if they migrate to a
Once the culture has grown, sensitivity (or antimi- normally sterile organ system.
crobial susceptibility) testing is performed. Small paper Humans benefit from their relationship with
disks are impregnated with various antimicrobials and normal flora. For example, nutrients such as vitamins K,
placed on the culture to test whether the organism is B12, and pantothenic acid are obtained from the
susceptible or resistant to the battery of antimicrobials. secretions of the coliform bacteria. These resident
Susceptibility testing is very important when dealing organisms also appear to stimulate the immune
with organisms that have become resistant (i.e., that system, producing a more rapid, powerful response to
do not respond) to standard antimicrobials. The foreign invaders. Resident microorganisms also com-
process of making a definitive identification of the pete with invading organisms for nutrients, thereby
organism and conducting susceptibility testing may reducing the likelihood of harmful infection by the
take several days. invaders.
Human-Microbe Interactions Human Defense Mechanisms

Microorganisms that are found in or on the body of Normal, healthy individuals have specific and general
normal individuals are referred to as endogenous defenses that constantly safeguard against microbial
microflora (also called normal, or resident, flora). These infection; the disruption or derangement of these
microorganisms include bacteria, fungi, viruses, and protective systems allows pathogens to gain a foothold for
protozoa. After birth, both harmless and helpful infectious disease. Our immune system defenses consist
organisms take up residence on the skin, in body of two major arms: the innate and the adaptive arms.
openings, on mucus membranes, and in the gastroin-
• The innate arm includes our mechanical barriers
testinal and genitourinary tracts. Microorganisms that
(skin, mucus membranes), specific chemical
are not normally found in or on the body are called
compounds (complement, proteins that assist in
exogenous or transient flora.
the destruction of foreign particles), and the cells
involved in phagocytosis (engulfing of foreign
MUCUS MEMBRANES bodies).
The mucus membranes provide a warm, moist • The adaptive arm has two branches: the cell-
environment that is particularly suitable for the growth mediated and the humoral.
of organisms. In contrast, blood, lymph, spinal fluid, The cell-mediated branch is made up of the
and most internal organs, including the lungs, are responses by different types of white blood cells
normally free of microorganisms. In addition to toward organisms that have invaded human
normal resident organisms, transient microflora may tissues or that have been phagocytized by white
take up temporary residence in the body or on the blood cells.
body surface. These microbes are usually temporary for The humoral branch is responsible for the
many reasons: They may be washed away during production of soluble antibodies, which includes
bathing; they may be unable to compete with resident the short-lived IgM class of antibodies and the
organisms and fail to survive; or they may be flushed long-lived IgG antibodies. Antibodies are
out by secretions. formed in response to the presence of antigens
(substances such as pollen and bacteria).
Although described as separate parts of the
NORMAL FLORA immune system, the humoral and cell-mediated
When the number of normal resident organisms is systems are intricately connected in the fight
reduced, such as by the administration of broad- against infectious disease.
spectrum antimicrobials, the delicate balance of
resident flora organisms may be disrupted, allowing a
normally nonpathogenic organism to cause an MUCUS MEMBRANES
opportunistic infection. Opportunists are microbes The orifices of the body are lined with mucus mem-
with the potential to cause disease when the branes that are designed to entrap invaders. Because
physiological state of the host is altered. Candida the respiratory system is constantly exposed to inhaled
albicans, a yeast that lives near many body orifices, is a particles, it has a number of defensive mechanisms.
The hairs, mucus membranes, and irregular shape

of the nose trap most of the inhaled debris. Mucus
lining the pharynx and large airways traps particles so
that the cilia can sweep them up and out of the system. Bacterium Cytoplasm Lysosomes
Refl exes such as sneezing and coughing also assist in
clearing particles. Microflora, phagocytic white blood
Ingestion Digestion
cells, and enzymes in secretions add to the general Formation of
protective functions. phagolysosome
Residual body
Phagosome
Excretion
CELL-MEDIATED RESPONSES
Cell-mediated responses involve cellular and chemical Adherence Undigested material
reactions to microbial invasion:
Plasma membrane of phagocyte
• Fever production.
• Cellular secretions (interferon, prostaglandins, FIGURE 5-3 The phagocytic process.
interleukins) (Prostaglandins are hormone-like
substances that have varied effects on organs and
tissues. They derive from natural fatty acids in
Neutrophil Eosinophil Basophil Macrophage
the body, reducing swelling and inflammation,
increasing or decreasing blood flow depending
on type.)
• Activation of blood proteins (complement),
phagocytosis, neutralization of toxins, and the
inflammatory response.
The fever that an ill person develops, for example, FIGURE 5-4 Cells of the immune system.
stimulates the white blood cells to increase their
response. The reduction of free iron in the plasma
helps to limit the production of bacterial toxins. Fever localize infection and prevent the spread of microbes
itself raises the body temperature above the preferred or toxins. Physiological reactions at the site of the
range of many bacterial strains, causing them to die off. inflammatory response are edema, redness, heat, pain,
A variety of cellular secretions are increased during and often pus formation. The inflammatory response
infection. starts with some type of injury. Injured cells (mast cells,
basophils, platelets) release powerful chemicals
• Interferons are small particles of protein that
(histamine, heparin, bradykinin) that increase capillary
enter cells and interfere with the protein synthe-
permeability, allowing blood and cells to enter the
sis necessary for the reproduction of pathoge-
affected area. Macrophages are attracted to the site.
netic viruses and bacteria. In the laboratory
Fluid and cells may accumulate to form an exudate. As
setting, human interferons are now being
the exudate becomes filled with dead leukocytes and
produced by bacteria containing recombinant
bacteria, it becomes thick and appears yellow or green;
DNA. This manufactured interferon is being
it is then referred to as pus. Figure 5-4 illustrates
used experimentally to treat viral infections,
various cells of the immune system.
cancers, and immunodeficiency diseases.
• Interleukins are also secreted during infections;
they serve to enhance the activation of THE HUMORAL IMMUNE RESPONSE
T-lymphocytes during the immune response.
The humoral immune response is the third line of
Phagocytosis is a process by which certain white defense against pathogens. Unlike our other body
blood cells surround and ingest foreign materials defenses, this response is usually specific in nature.
(Figure 5-3). Neutrophils are the most common and Lymphocytes produce antibodies that recognize, attach
efficient phagocytes. Eosinophils play an important to, inactivate, and destroy particular antigens. Antibod-
phagocytic role in allergic responses. Macrophages ies are found circulating throughout the blood, lymph,
wander through the bloodstream and are attracted and body secretions.
toward sites of infection. Immunity may be acquired naturally; for example,
Inflammation is a complex series of events trig- when you are initially exposed to a disease-producing
gered by irritation, injury, or microbial invasion. The organism, antibodies are produced that protect you in
inflammatory response occurs as the body attempts to the event of re-exposure. Immunity may also be
impaired immunity. The Centers for Disease Control

and Prevention (CDC) recommends a wide variety
of vaccines for all children before entering school:
diphtheria, pertussis, polio, tetanus, mumps,
hepatitis, and rubella. Although new vaccines are
constantly being developed, there has been little
success as yet in developing a vaccine for the common
cold because the infection is caused by a large variety
of viruses.
Antibodies. Antibodies belong to a class of proteins

known as immunoglobulins (abbreviated Ig), a group
of glycoproteins that participate in the immune
response. They are called antibodies because they are
generated in response to specific antigens. Five classes
of immunoglobulin are identified (Table 5-1).
Immunoglobulin E is of special interest to respira-
FIGURE 5-5 A negative-stained transmission electron tory therapists because it is most abundant in people
micrograph (TEM) showing the morphology of the swine with allergies and allergic forms of asthma. It is
flu virus. responsible for the immediate hypersensitivity seen
Courtesy of the Centers for Disease Control Public Health Image Library/ with skin testing and for the shock reaction of anaphy-
C. S. Goldsmith and A. Balish laxis. The allergic reaction occurs when IgE antibodies,
bound to basophils in the blood or mast cells in tissue,
acquired artificially through the administration of react to the presence of the allergen. The mast cells
vaccines. Vaccines are made from living or killed respond by releasing powerful chemical mediators such
pathogens or their toxins, and they play an important as histamine, prostaglandins, and leukotrienes. In
role in public health medicine, specifically in the asthma, the release of these mediators results in
prevention of serious illness. An important vaccine that bronchospasm and airway edema.
benefits respiratory therapists, the elderly, and patients
with chronic lung disease is the annual vaccine that is B Cells and T Cells. B cells and T cells are other
active against the A and B strains of the influenza virus important cells of the immune system. T cells (named
(Figure 5-5). Vaccination against the hepatitis B virus is for the thymus gland) aid in the control of antibody
recommended for all health care workers who may be production and are involved in cell-mediated
exposed to blood or body fluids in the course of their responses. An HIV infection gradually destroys a
work. Vaccination against pneumococcal pneumonia is specific type of T cell, eventually resulting in a deficient
recommended for individuals over the age of 65 and immune system. B cells (named for bursa) migrate to
for those with a chronic illness such as congestive heart lymphoid tissue where they are responsible for the
failure, lung disease, or any condition associated with production of antibodies.
TABLE 5-1 Classes and characteristics of immunoglobulins

Ig Class Percentage in Serum Functions/Sites
IgA 10–15 Protects the mucus membranes; found in tears, saliva, and other secretions
IgD 0.2 Controls stimulation of B cells; found in blood and on lymphocytes
IgE 0.002 Causes allergic responses such as immediate hypersensitivity and anaphylaxis;
high proportion in secretions
IgG 80 Secondary immune response; long-lived antibodies provide protection upon
re-exposure to the pathogen; major systemic immunoglobulin; produces
antimicrobial antibodies; found in extracellular fluids and blood
IgM 5–10 Primary immune response; short-lived; indicates an acute infectious process;
produces antimicrobial and blood group (ABO) antibodies; bactericidal to
gram-negative bacteria; found in lymph, blood, and extracellular fluid
Control of Microbial Growth Best Practice

Important environmental factors that may affect the
growth of microorganisms are moisture, pH, tempera- Pasteurization
ture, gases, and the presence of neighboring organisms.
Virtually all organisms require water to survive. Since Pasteurization is used by many respiratory
the human body contains a high proportion of water, care departments for the disinfection of equip-
the inadequacy or failure of immune mechanisms ment. It is an efficient, cost-effective method
facilitates the growth of organisms. Although microbes that destroys most organisms except for spores.
can grow throughout a wide range of pH, most of the Although spore-formers such as Clostridium
medically important pathogens grow best at a pH species are pathogenic to humans, they are
around 7.0, similar to that of the human body. The obligate anaerobes and not found as contami-
same is true of temperature. Both pathogens and nants of respiratory care equipment. The inability
normal flora tend to thrive at body temperatures. of pasteurization to kill spores is therefore of
The gaseous environment is so specific and impor- minor concern in respiratory care departments.
tant for the survival and growth of organisms that In the batch process of pasteurization, equip-
special terms are used to designate these requirements. ment is immersed for 30 minutes in a water bath
Species that require oxygen are called obligate aerobes. at 63°C. Aseptic techniques must be carefully
Those that cannot survive in the presence of oxygen are followed to avoid recontamination of equipment
known as obligate anaerobes. Gas gangrene, caused by during drying and packaging.
infection with the obligate anaerobe Clostridium
perfringens, may be treated by placing the patient in a
hyperbaric chamber to increase the amount of oxygen
to a level that kills the organisms. Bacteria that can tape color change does not necessarily mean that an
adapt and live with or without oxygen are called item is actually sterile if it was not properly prepared
facultative organisms. for autoclaving. Autoclaves should also be tested
periodically, usually weekly, with biological indicators
such as cultures of Geobacillus (formerly Bacillus)
Sterilization and Disinfection stearothermophilus to ensure proper functioning. This
A variety of physical and chemical methods are used to method of sterilization works well for many metal and
achieve disinfection or sterilization of equipment in glass items, but it is not acceptable for rubber, plastics,
the hospital and home settings. Disinfection is the and equipment that would be damaged by high
inhibition or destruction of pathogens; sterilization, temperatures.
or asepsis, is the complete absence or destruction of all
microorganisms. Dry Heat. Dry heat can be used to sterilize materials
that do not tolerate moisture, such as powders and oils.
PHYSICAL METHODS Incineration, or burning, is a very effective way to
destroy contaminated disposable items. Although it is
The five physical methods of sterilization and disinfec-
important to know that refrigeration and freezing may
tion involve heat, pressure, radiation, sonic disruption,
slow the growth of bacteria, these processes do not kill
and filtration. Because heat is both efficient and
all organisms.
inexpensive, it is commonly used for disinfection and
sterilization. Boiling for a period of 10–30 minutes
Radiation. Radiation is another method used to kill
works well as a disinfection technique; however, some
microorganisms.
organisms, such as hepatitis viruses and spore-formers
such as the Clostridium, are relatively resistant. • Ultraviolet (UV) rays are useful in killing airborne
and surface bacteria. Ultraviolet lamps help
Autoclaving. An autoclave is a metal pressure cooker reduce the number of bacteria in the air, and so
that uses steam under pressure to achieve sterilization. these lamps may be found in nurseries, operat-
Steam at a pressure of 15 psi (pounds per square inch) ing rooms, and isolation rooms. Caution:
and at 121°C kills organisms on properly prepared and Prolonged, direct exposure to UV light is harm-
packaged equipment in about 20 minutes. Before ful to skin and eyes, and it must be avoided.
autoclaving, equipment must be correctly processed by • X-rays and gamma rays in certain wavelengths are
careful washing to remove debris. An indicator tape also useful in disinfection and sterilization.
that is used to seal each package changes color when Produced in special facilities, radiation is used
conditions for sterilization have been met. However, to prevent food spoilage and to sterilize
heat-sensitive equipment. Plastic articles such as the temperature; and the presence of blood, mucus,
endotracheal tubes, tubing, and syringes may be pus, or other debris. Most chemical agents are too
sterilized with gamma radiation because it harsh to use directly on human tissue. An antiseptic is
penetrates the prepackaged materials. a solution that can be used on the skin and that is com-
• In many areas of the world, food—including monly used to reduce the number of organisms present
meats, milk, and milk products—and consum- on the skin.
ables are sterilized by irradiation. The method is
so effective that refrigeration is not necessary for Alcohols and Hydrogen Peroxide. Alcohols (ethyl and
these products. isopropyl) are good skin antiseptics. Ethyl alcohol is the
most effective in a 70% solution; isopropyl alcohol
Ultrasonic Waves. Ultrasonic waves are useful for should be used in a 90% solution. Alcohols are
disinfecting delicate equipment. High-frequency commonly used to disinfect stethoscopes, oximeter
sound waves, passed through a water bath, mechani- probes, and the surfaces of some respiratory care
cally dislodge organic debris from instruments and equipment. Hydrogen peroxide is another useful skin
glassware. The equipment is then usually sterilized by disinfectant. Respiratory care personnel use hydrogen
another method. peroxide for the stoma sites during tracheostomy care.
Filtration. Filters have long been used to separate Disinfectants. Disinfectants are chemical agents that
bacteria and liquids. are used to clean the surfaces of equipment and counter-
tops and that are too harsh to use on skin. Phenols, such
• Filter masks can be worn to prevent the passage
as Lysol, are good examples of chemical disinfectants.
of microbes from the patient and to protect
Phenols are effective even in the presence of organic
health care workers from inhaling bacteria, but
material, but they may not kill all viruses. A weak
they must fit very tightly for adequate protection.
solution of sodium hypochlorite (bleach, 1:10 solution)
Unfortunately, most filters do not prevent the
has also been advocated for disinfecting areas where
passage of viruses.
blood has been spilled. Equipment or surface areas must
• High-efficiency particulate air (HEPA) filters are
be cleaned before hypochlorite disinfection because the
used in negative-pressure clinical devices,
presence of organic matter will inactivate the solution.
biological safety cabinets, and laminar flow
Also, bleach solutions can be corrosive and must be
hoods to protect health care workers from
used carefully to avoid harm to personnel or equipment.
contamination.
• Powered, air-purifying respirators may be used to
Ethylene Oxide and Glutaraldehydes. Two chemical
provide additional protection to practitioners in
agents that are often used to sterilize respiratory care
certain situations.
equipment in the hospital setting are ethylene oxide
(ETO) and glutaraldehydes.
CHEMICAL METHODS Ethylene oxide is a highly penetrating toxic gas.
Chemical methods are commonly used for both Ethylene oxide sterilization chambers are carefully
disinfection and sterilization (Table 5-2). The effective- controlled for temperature (50–56°C) and humidity
ness of chemical agents depends on many factors: the (30–70%) to ensure optimum conditions for sterilization.
concentration of the agent; the duration of exposure; The gas mixture contains 1000 mg ETO/L, with a
TABLE 5-2 Characteristics of chemical agents of sterilization and disinfection

Agent Mode of Action Advantages Disadvantages
Alcohols Denature proteins Easy to use, not toxic Concentration is important;
not effective against spores
Ethylene oxide Lethally disrupt cell Can be used for items Requires safety precautions;
(ETO) gas metabolism sensitive to heat carcinogenic and explosive
Glutaraldehydes Attack lipoproteins in Will kill all living material Toxic effect on human
bacteria cell membrane (sterilizing agent) mucus membranes
and cytoplasm and eyes
Phenolic compounds Coagulate proteins, Powerful bactericide at Toxic, strong odor
lyse cells proper concentrations

Ethylene Oxide Sterilization Disinfection in the Home
Once the sterilization process has been complet- When teaching families or caregivers to disinfect
ed, items must be aerated sufficiently to ensure respiratory care equipment in the home setting,
that all ETO is removed from them. Aeration consider cost, infection risk, the skills of
times vary according to the composition of the caregivers, and safety.
sterilized items and the method and temperature
of the mechanical aeration chamber. An IPPB
machine used for the treatment of a patient with
active tuberculosis is an example of respiratory • The equipment must then be rinsed well and
care equipment that should be gas sterilized. excess water drained to avoid diluting the
glutaraldehyde solution.
• Glutaraldehyde is toxic to human tissue; so
gloves and eye protection should be worn during
balance of carbon dioxide and nitrogen or other inert equipment processing.
gas to decrease flammability. • After the equipment has been soaked in the
Items are placed in the ETO chamber. They must glutaraldehyde solution for the proper length of
be dry to prevent the formation of toxic ethylene glycol time, it must be rinsed well to remove all of the
and packaged in a moisture-permeable package. Special chemical solution.
indicator tape is used to seal the package. As in auto- • Finally, the equipment must be air-dried,
claving, the indicator tape changes color when the reassembled, and packaged under sterile, or at
proper conditions are met. The effectiveness of the least aseptic, conditions.
sterilization process should also be checked with
indicator strips containing Bacillus subtilis organisms.
Glutaraldehydes are liquid sterilizing agents com-
monly used in health care and by respiratory care depart- Antimicrobials
ments. Bronchoscopes, resuscitation equipment, tubing, Despite careful disinfection and sterilization proce-
circuits, masks, and many other equipment items can be dures, some patients become infected with microorgan-
sterilized by this method. Glutaraldehydes are available in isms. A wide variety of chemotherapeutic agents,
alkaline and acidic forms. Cidex is an example of an known as antimicrobials, are used to treat infections.
alkaline product; Sonicide is an acidic solution. The goal of antimicrobial chemotherapeutics is to
selectively kill the desired organism without seriously
• Alkaline glutaraldehydes kill viruses, bacteria, and
harming the human host.
Mycobacterium species in about 10 minutes,
spores in 10 hours. The alkaline solution
remains active for approximately 2 weeks.
• Acid glutaraldehydes are bactericidal in 20 minutes, HISTORY
but they can be ready in about 5 minutes if the The era of modern chemotherapy began in 1909, when
solution is heated to 60°C. Spores may be killed Paul Ehrlich developed an arsenic compound for the
in 1 hour with the heated solution. Acid glutaral- treatment of syphilis. In 1928, Alexander Fleming
dehyde is considered effective for 28 days. found that a substance produced by the mold Penicil-
lium notatum inhibited the growth of Staphylococcus in
Glutaraldehydes are now available for home use
the laboratory (Figure 5-6). In 1935, Gerhard Domagk
and are recommended by the American Association for
discovered a red dye that killed Streptococcus in mice.
Respiratory Care for the disinfection of respiratory care
Further research showed that the dye was broken down
equipment in the home. Thoroughly washed home
in the body into the active agent sulfanilamide.
equipment can also be disinfected by soaking it for
During World War II, Sir Howard Florey and Ernst
30 minutes in a white vinegar solution (1:3 dilution).
Chain purified penicillin for use on humans. By 1942,
This method is simpler but may not kill all organisms.
the U.S. drug industry was producing penicillin in
Several factors must be considered when using
sufficient quantities for public use. However, not until
liquid sterilizing agents.
after World War II did medicine begin to build an
• Equipment must be washed carefully with soap arsenal of drugs that would effectively treat infections,
(or detergent) and water to remove protein- a technique that we now take for granted. Anti-infective
aceous material such as mucus or blood. drugs are usually called antibiotics, although this term
TABLE 5-3 Methods of antimicrobial action

of selected agents
Method Examples
Inhibition of cell wall Penicillins,
synthesis cephalosporins
Disruption of cell Amphotericin B,
membrane nystatin
Inhibition of nucleic acid Ciprofloxacin, rifampin,
synthesis pentamidine, zidovudine
(AZT)
Inhibition of protein Erythromycin,
synthesis tetracycline
FIGURE 5-6 Gram stain of staphylococci. Inhibition of metabolism Sulfonamides, ribavirin
Courtesy of the Centers for Disease Control Public Health Image Library/
Dr. Richard Facklam
food poisoning, and other diseases, is a resistant

specifically refers to substances produced by microor- organism frequently encountered in the health care
ganisms to kill other microorganisms. setting. Vancomycin, a very expensive and toxic
antimicrobial, must be used to treat MRSA. Because
vancomycin is now used frequently, there is great
MECHANISMS concern that the Staphylococcus species will become
Most antimicrobial drugs work by disrupting the resistant. Of the many theories as to why drug-
structure or metabolism of the pathogen in a way resistant organisms are increasing so rapidly, the
that does not affect human cells. Sulfonamides, for overuse of antimicrobials and their misuse by
example, kill bacteria because they are shaped like patients are commonly cited ones.
the molecule of para-aminobenzoic acid (PABA).
Bacteria convert PABA into folic acid, which is needed
to produce essential proteins. The attempt by bacteria CLASSIFICATION
to convert the sulfonamide into PABA fails, resulting in Antimicrobial agents can be classified by how they kill
their death. Humans are not harmed by the drug bacteria. Table 5-3 shows five general methods of
because we must obtain our folic acid from food and antimicrobial action, with accompanying examples. For
are not able to synthesize it. Penicillin, on the other the ways in which microbes overcome these methods,
hand, interferes with the synthesis of peptidoglycans see Chapter 38.
(chains of sugar and peptide) that make up the bacte-
rial cell wall. The bacterial cell is unable to generate a Antituberculosis Agents. Tuberculosis, caused by the
wall and dies. Because human cells do not have walls, bacterium Mycobacterium tuberculosis, is one of the most
penicillin does not damage them. prevalent and important infectious diseases. World-
wide, millions of new cases and millions of deaths are
reported each year. One problem in the control of
RESISTANCE tuberculosis is the development of drug-resistant
Frequently, a single antimicrobial drug is not adequate bacteria. Outbreaks of multi-drug-resistant tuberculosis
to kill all the pathogens. In cases of tuberculosis, for (MDR-TB) have been reported in most of the states.
example, three or more drugs are used in combination. The most common drugs used to fight tuberculosis are
The problem of drug-resistant bacteria, or so-called ethambutol, isoniazid, pyrazinamide, rifampin, and
superbugs, has become important in the treatment of streptomycin.
infectious disease. These organisms have mutated so
that either the antimicrobials that were once able to Antifungal and Antiprotozoan Agents. Fungal and
destroy them are no longer effective or larger and more protozoan pathogens are more difficult to eradicate
toxic doses must be given to kill the bacteria. (For ways than are bacteria because, unlike bacteria, fungi and
that superbugs emerge and spread, see Chapter 38.) protozoans are eukaryotic (i.e., they have a defined
Methicillin-resistant Staphylococcus aureus nucleus and organelles). Drugs that are used against
(MRSA), the causative agent of toxic shock syndrome, these organisms are more toxic to human cells than are
drugs used to kill bacteria. Amphotericin B and Illness is the most communicable to others in the
nystatin are examples of antifungal agents. Pentami- symptomatic stage, which is also the time when other,
dine is an antiprotozoan agent used to prevent and opportunistic, infections may strike because the body
treat Pneumocystis jiroveci pneumonia (PCP) in defenses are lowered. For example, a COPD patient
HIV-infected or immunodeficient patients. starts with a viral upper respiratory infection that
eventually leads to bacterial pneumonia. Although
Antiviral Agents. Effective antiviral drugs are difficult most people recover from their initial illness, some-
to create because viruses replicate inside host cells. times permanent damage occurs, such as paralysis
Acyclovir is used against herpes. Zidovudine (AZT) is following polio, brain damage following meningitis,
one of several agents developed to slow the progression or bronchiectasis following whooping cough.
of HIV infection. Ribavirin was developed for treatment
of respiratory syncytial virus (RSV) infections in fragile MODES OF TRANSMISSION
infants. Its effectiveness is now being questioned,
A susceptible person can be exposed to a pathogenic
and the use of RSV-immune globulin (RespiGam) or
organism by means of seven primary modes of
palivizumab (Synagis) monoclonal antibody prophy-
transmission:
laxis is recommended.
• Person-to-person contact via the skin
• Direct mucus membrane contact such as kissing
Microbial Pathogenicity or sexual intercourse
An infection occurs when a pathogenic microbe is able to • Airborne droplets of liquid or dust that contact
invade tissues in the body and multiply. Pathogenicity the skin, eyes, or lungs
is the ability of an organism to cause disease. The • Contamination of food or water by fecal
relative ability of a pathogen to invade, infect, and material, soil, or other impurities
cause damage or disease is called virulence. In other • Blood contamination from injections,
words, virulence is the strength of pathogenicity. Some transfusions, or invasive medical devices
pathogens are more virulent than others and thus are • Contact with vectors, such as the bites of
more likely to result in infection and disease. Infections insects—mosquitoes, ticks, or biting flies
that can be transmitted from one person to another, • Contact with inanimate objects that carry
such as Varicella (chickenpox) or HIV, are called a pathogen (fomites)
communicable diseases. Communicable diseases that are
easily transmitted from person to person, such as colds Diseases transmitted directly via the mucus
or influenza, are called contagious diseases. membranes include sexually transmitted diseases such
Infection occurs when pathogens are able to enter as herpes, syphilis, gonorrhea, and Chlamydia.
the host, attach, multiply, and cause damage to the Respiratory pathogens in particular are known to be
tissues. Clinical disease occurs when the body’s primary spread by contaminated dust particles or droplets of
defenses lose the battle with a pathogen. The disease moisture. Diseases that can be transmitted in this
may be a local infection, such as a boil, strep throat, or
tuberculosis. If the organism is not stopped at the local
level, a systemic infection may develop as the pathogen Best Practice
is spread throughout the bloodstream.
Disease Transmission
DISEASE TYPES AND STAGES Prevention
An acute disease has a rapid onset and usually a rapid
Many diseases are transmitted by direct contact
recovery. Influenza and measles are good examples. A
with organisms carried on the skin. The pathogen
chronic disease has a slow onset and a long duration.
is then transferred via the hands to the mouth,
Tuberculosis and Hansen’s disease (leprosy) are
nose, or eyes. In the hospital setting, hands
examples of chronic infectious diseases.
are frequently the means of transfer of colds,
Once a person has been exposed to a pathogen, the
influenza, and staphylococcal, streptococcal, and
course of an infectious disease progresses through four
gastrointestinal tract organisms. For this reason,
stages:
frequent and proper handwashing is the most
• An incubation period with no symptoms important infection control process in health
• A prodromal, or preacute, phase in which the care. See Chapter 38 for detailed discussions of
person feels unwell but has no symptoms this and other personnel and patient protection
• Acute illness with symptoms issues.
• Recovery, disability, or death
manner include colds, measles, mumps, and chickenpox, Endemic diseases are those that are constantly
to name a few. Legionnaire’s disease is spread through present in a population, usually involving only a few
contaminated air conditioning systems or shower heads. people. The number of infected individuals may
Fungal respiratory diseases such as histoplasmosis increase or decrease from year to year, but the disease
may be spread via dried bird or bat droppings or, in the never goes away completely. Endemic infections in
case of coccidioidomycosis, by dust from dried soil. the United States include streptococcal infections,
In the hospital or home setting, improperly cleaned influenza, tuberculosis, and plague. Plague (caused by
respiratory care equipment, especially aerosol genera- the bacterium Yersinia pestis) is endemic in rats,
tors, can transfer pathogens. prairie dogs, and squirrels in certain parts of the
Organisms can easily contaminate food and water United States. Periodically, humans become infected.
supplies. Human feces may get into the water from How many people are sick from an endemic disease at
outhouses, cesspools, and sewer line breaks; animal any one time depends on environment, behavior, the
contamination can occur from feedlots and processing reservoir or source of infection, and the number of
plants. Improper handling or storage may result in immune people.
contaminated food supplies. Botulism, Salmonella An epidemic occurs when a greater-than-normal
poisoning, typhoid fever, hepatitis A, and giardiasis are number of cases of an endemic disease occur in an
all diseases transmitted via food or water. Hanta virus area at a specific time. For example, a modern
respiratory disease is an example of disease spread by respiratory epidemic occurred in 1976 in Philadelphia,
the droppings of field mice. Pennsylvania. Many of the large number of members
Because blood is normally sterile, special methods of the American Legion who met for a convention
are usually required to cause the transmission of became severely ill and were hospitalized. Some
organisms directly into the bloodstream. A vector (an even died from severe lung infections. The causative
intermediate host) is needed to transmit the pathogen. organism was extremely difficult to isolate and grow.
Many vectors are arachnids (ticks) or insects (fleas, When it was finally identified, the bacterium was given
lice, flies, and mosquitoes). In most cases, the organ- the name Legionella pneumophila.
isms live in the vector itself. Fleas, for example, may Epidemics may also break out in communities
carry plague or typhus organisms. Mosquitoes transmit where the pathogen was not previously present.
malaria, yellow fever, and encephalitis. In the United Travelers can easily bring organisms into an area.
States, there is great concern over ticks, which are Natural disasters and poverty lead to epidemics when
known to transmit Rocky Mountain spotted fever and sanitation practices decline, resulting in food and water
Lyme disease. The vector merely transports the organ- contamination. Outbreaks of cholera, typhoid, giardiasis,
isms from one person to another in the blood. and dysentery result.
Pets and wild animals may serve as reservoirs of The CDC is responsible for monitoring potential
zoonoses, or animal infections that can be transmitted and actual epidemics in the United States.
to humans. Dogs, cats, skunks, and bats are well- When an epidemic reaches worldwide proportions,
known vectors for rabies. Turtles and chickens com- it is called a pandemic. Pandemics of the flu were
monly transmit Salmonella. Toxoplasmosis, a protozoan recorded in 1898, 1917, 1955, 1968, 1972, 1975, 1978,
disease that can cause birth defects, may be acquired by and 2009. Influenza pandemics are usually named after
contact with cat feces in litter boxes. the point of origin, such as the Hong Kong flu or the
Inanimate objects through which pathogens are London flu. The best-known pandemics in the world
transmitted are called fomites. Hospital instruments today are human immunodeficiency virus (HIV)
and equipment can be fomites. Needles, syringes, infection and acquired immunodeficiency syndrome
surgical devices, solutions, and blood-processing (AIDS). An important outcome of the AIDS pandemic
equipment such as kidney dialyzers are all possible is increased attention to sexually transmitted diseases
culprits. As an example, the suctioning procedure in in general and to methods of prevention in particular.
respiratory care has a high potential for mechanically
introducing organisms into a patient’s lungs. A good Important Respiratory Pathogens
way to decrease the risk of cross-contamination among
patients is to adopt single-use disposable equipment. Infection is a common cause of respiratory disease.
Microorganisms responsible for significant upper and
lower respiratory tract infections are viruses, bacteria,
Epidemiology fungi, and protozoans. Even given today’s effective
Epidemiology is the science that deals with the frequency antimicrobial therapies, pneumonia remains a
and distribution of diseases and factors leading to the significant cause of morbidity (disease) and mortality
spread of infection. Respiratory caregivers should be (death). As the scope of medical care has expanded,
familiar with the terms that epidemiologists use. the range of microorganisms being seen with both
alcoholism, ARDS, or diabetes, as well as persons

Age-Specific Competency undergoing cancer chemotherapy, immunosuppressive
therapy, or prolonged endotracheal intubation.
High-Risk Populations Common microorganisms causing infections in
Infants and children under age 7 are at particular compromised hosts are Staphylococcus aureus, gram-
risk of infectious disease because of immature negative bacilli such Pseudomonas aeruginosa and
immune systems. The elderly are also suscep- Klebsiella pneumoniae, and anaerobic bacteria such as
tible owing to failing immune function. Preven- Bacteroides. Aspergillus species are ubiquitous fungi that
tion and control efforts have their greatest effect can cause bronchopulmonary infection, fungus balls
when targeted toward these populations. (aspergilloma), or disseminated disease in compro-
mised hosts. Because of their impaired immunity,
patients with HIV infection or AIDS often are infected
with Pneumocystis jiroveci, an atypical fungus (some-
community- and hospital-acquired pneumonias
times classified as a protozoan) that can cause severe
has increased.
pneumonia. Mycobacterium tuberculosis is also often
the first infectious agent to appear in AIDS patients.
PNEUMONIAS Persons with AIDS may also have multi-drug-resistant
Pneumonias have many causes. forms of the infection and are also susceptible to a
noncommunicable type of tuberculosis caused by
• A high percentage of the pneumonias occurring in
Mycobacterium avium complex.
otherwise healthy individuals result from infection
with Streptococcus pneumoniae, Hemophilus influenzae,
Chlamydia pneumoniae, Mycoplasma pneumoniae, or
common viruses, such as influenza in adults. Summary
• Respiratory syncytial virus and parainfluenza Respiratory therapists work with many patients either
virus are causative microorganisms in infants who are susceptible to pulmonary infections or who
and children. have already developed pneumonia. An understanding
• Less common causes of pneumonias in normal of the types, identification, and management of
adults are Legionella pneumophila, group A pathogens capable of causing pulmonary disease can
beta-hemolytic Streptococcus, and Mycobacterium help practitioners minimize the occurrence and
tuberculosis. transmission of respiratory infections.
• Fungal infections, or mycoses, cause respiratory Organisms that can infect the lung include bacte-
disease, the particular agents being geographi- ria, viruses, fungi, and protozoa. Specific microorgan-
cally endemic. Histoplasma capsulatum is found isms are identified in the laboratory through a process
in the soil of the Mississippi valley. Coccidioides that may use Gram staining, acid-fast testing, enzyme-
immitis is a common fungus found in the arid linked immunosorbent assays, and cultures. Specimens
and semiarid areas of New Mexico, Utah, may be obtained by having the patient cough, by
California, Texas, and Arizona. suctioning, or by bronchoscopy. The specimens must
be carefully collected and handled to avoid contamina-
INFLUENZA tion and to provide accurate information.
Host defense mechanisms are the skin, the mucus
Exacerbations of chronic obstructive lung disease (COPD)
membranes, and cellular and chemical responses to
are often caused by infections with viral agents such
invasion. The immune response specifically generates
as influenza viruses. The most common bacterial
protective antibodies in response to antigen challenges.
organisms associated with pneumonia in chronic lung
Vaccines artificially stimulate antibody production to
patients are Streptocococcus pneumoniae, Hemophilus
protect people from disease.
influenzae, and recently Moraxella catarrhalis. Because the
Disinfection and sterilization may be accom-
airways of some COPD patients may be colonized with
plished by means of physical methods, such as heat,
these microbes, determining whether the symptoms of
pressure, radiation, sonic disruption, and filtration. The
exacerbation are related to their presence can be difficult.
autoclave is an example of a device that incorporates
both heat and pressure to sterilize medical items and
equipment. Disinfection using the process of pasteuri-
Predisposition zation is appropriate for many types of equipment
Especially susceptible to pneumonias from unusual used in respiratory care. Chemical agents may also be
organisms are individuals with compromised immune used for sterilization; ethylene oxide gas and gluteral-
systems, such as those with HIV infection or AIDS, dehyde solutions are two examples.
Antimicrobial drugs are key in the management of 4. Which of the following immunoglobulins is
infections. However, because many pathogens have associated with an allergic response in the body?
become drug-resistant as they mutate, the development a. IgA
of new agents is now of grave importance. b. IgD
Infections may be transmitted by skin or mucus c. IgE
membrane contact, by airborne droplets, by contami- d. IgG
nated food and water, by blood that has been contami- 5. To increase the effectiveness of acid glutaralde-
nated by vectors, or by contact with contaminated hydes, the respiratory therapist should do which of
inanimate objects. Thorough and frequent handwash- the following?
ing remains the most important procedure for limiting a. Mix it with another agent such as alcohol.
the transmission of infection. b. Heat the acid glutaraldehyde to 60°C.
c. Do not rinse the equipment after immersion in
Study Questions the acid glutaraldehyde.
d. Chill the acid glutaraldehyde to 0°C.
REVIEW QUESTIONS 6. How does the antimicrobial amphotericin kill
1. Name five of the nine characteristics used to bacteria?
classify or identify bacteria. a. inhibiting cell wall synthesis
b. inhibiting nucleic acid synthesis
2. List the five physical methods used for sterilization
c. inhibiting metabolism
and disinfection.
d. disrupting cell membrane
3. Name the three benefits that humans receive from
their endogenous flora.
4. List the environmental factors that affect the CRITICAL-THINKING QUESTIONS
growth of microorganisms. 1. With more and more immunosuppressed patients,
5. Name the three lines of defense that humans have what precautions should the respiratory therapist
against infection. take? How do these precautions affect the
6. List the four types microorganisms responsible for efficiency of the practitioner while performing
infectious diseases of the respiratory system. procedures?
2. More and more physicians are prescribing broad-
spectrum antibiomicrobials. What are some of the
MULTIPLE-CHOICE QUESTIONS hazards of this practice? What changes would you
1. Which of the following microorganisms does not recommend? How can respiratory therapists help
flourish in an oxygen environment? to change this practice?
a. Streptococcus pneumoniae 3. Mycobacterium tuberculosis and Staphylococcus are
b. Clostridium perfringens currently the most common drug-resistant micro-
c. Hemophilus influenzae organisms that a respiratory therapist must deal
d. Candida albicans with. What can respiratory therapists do to
2. Which of the following microorganisms is a part of decrease the likelihood that other pathogens will
endogenous flora that can become pathogenic, become drug resistant?
especially in the mouth and throat, if the immune
system is impaired by the use of inhaled steroids? Suggested Readings
a. Streptococcus pneumoniae
b. Clostridium perfringens Centers for Disease Control and Prevention, Hospital
c. Hemophilus influenzae Infections Program. Bloodborne Pathogens: Worker
d. Candida albicans Protection. http://www.cdc.gov/ncidod/hip/Blood/uni
Kacamarek RM. The Essentials of Respiratory Care. 4th ed.
3. Which of the following vaccines is not recom-
St. Louis: Mosby-Yearbook; 2005.
mended by the CDC for all children before
Winn Jr, W, Allen S, Janda W, Koneman E, Procop G,
entering school?
Schreckenberger P, Woods G. Koneman’s Color Atlas
a. hepatitis B
and Textbook of Diagnostic Microbiology. 6th ed.
b. diphtheria
Philadelphia: Lippincott Williams & Wilkins; 2006.
c. human papillomavirus
d. rubella
CHAPTER 6
Cardiopulmonary Anatomy and Physiology

Oliver J. Drumheller
OBJECTIVES
• Name the respiratory system’s structures and functions.
• Describe ventilation principles for the lung.
• Review pulmonary gas diffusion properties.
• Summarize the structure and functions of the circulatory system.
• Discuss the body’s oxygen transport mechanisms.
• Describe carbon dioxide transport and acid-base balance.
• State the effects of the renal system on the cardiopulmonary system.
• Summarize ventilation/perfusion relationships.
• Explain the principles of the control of ventilation.
• Describe the cardiopulmonary physiology of the fetus and newborn.
• List the effects of aging on the cardiopulmonary system.
• Summarize the effects of exercise and high-altitude and high-pressure environments on the cardiopulmonary system.
CHAPTER OUTLINE
Upper Airway: The Nose, Oral Cavity, and Pharynx Interstitium
Nose Pulmonary and Systemic Circulatory Systems
Oral Cavity Lymphatic System
Pharynx Neural Control of the Lungs
Lower Airways The Lungs
Larynx Mediastinum and Pleural Membranes
Tracheobronchial Tree Thorax
Cartilaginous Airways Diaphragm and Accessory Muscles of Ventilation
Noncartilaginous Airways Ventilation
Bronchial Cross-Sectional Area and Bronchial Pressure Differences Across the Lungs
Blood Supply Static Characteristics of the Lungs
Sites of Gas Exchange and the Alveolar Epithelium
(continues)
116
CHAPTER 6 ■ Cardiopulmonary Anatomy and Physiology 117
(continued)
Dynamic Characteristics of the Lungs Urine Concentration and Volume

Ventilatory Patterns Regulation of Electrolyte Concentration
Pulmonary Function Measurements Renal Failure
Lung Volumes Cardiopulmonary Problems due to
Lung Capacities Renal Failure
Diffusion of Pulmonary Gases Ventilation/Perfusion Relationships
Partial Pressures of Oxygen, Carbon Dioxide, Ventilation/Perfusion Ratio
and Water Vapor Effects of the Ventilation/Perfusion Ratio on
Ideal Alveolar Gas Equation Alveolar Gases
Diffusion of Oxygen and Carbon Dioxide Effects of the Ventilation/Perfusion Ratio on
End-Capillary Gases
Perfusion-Limited or Diffusion-Limited Oxygen
Respiratory Quotient/Respiratory
Cardiovascular System Exchange Ratio
Blood Effects of Respiratory Disorders on the Ventilation/
Heart Perfusion Ratio
Pulmonary and Systemic Vascular Systems Control of Ventilation
Blood Pressures in the Pulmonary and Systemic Respiratory Components of the
Vascular Systems Medulla Oblongata
Distribution of Pulmonary Blood Flow Pontine Respiratory Centers
Hemodynamic Measurements Monitoring Systems That Influence the
Oxygen Transport Medulla Oblongata
Oxygen Dissolved in Blood Plasma Reflexes That Influence Ventilation
Oxygen Bound with Hemoglobin Cardiopulmonary Physiology of the Fetus
Total Oxygen Content and the Newborn
Fetal Circulation, Fetal Lung Fluids, and Alveoli
Oxygen Dissociation Curve
at Birth
Factors That Shift the Oxygen Dissociation Curve
Birth and the First Breath
Oxygen Transport Studies
Circulatory Changes at Birth
Pulmonary Shunting and Venous Admixture
Control of Ventilation in the Newborn
Tissue Hypoxia Infant Reflexes
Cyanosis and Polycythemia Normal Newborn Clinical Values
Carbon Dioxide Effects of Aging on the Cardiopulmonary System
Carbon Dioxide Transport Influence of Aging on the Respiratory System
Carbon Dioxide Elimination at the Lungs Influence of Aging on the Cardiovascular
Carbon Dioxide Dissociation Curve System
Acid–Base Balance Effects of Exercise and of High-Altitude
The pH Scale and Buffer Systems and High-Pressure Environments on the
Respiratory Acid-Base Imbalances Cardiopulmonary System
Metabolic Acid-Base Imbalances Exercise
Base Excess or Deficit High Altitude
High-Pressure Environment
The Renal System and Its Effects on the
Cardiopulmonary System
The Kidneys
Urine Formation
KEY TERMS
alveolar-capillary membrane elastance respiratory zone
atelectasis epithelium stroke volume (SV)
automaticity Frank-Starling principle trachea
autonomic nervous system Haldane effect tracheobronchial tree
(ANS) lower airways upper airway
Bohr effect lung-thorax relationship Valsalva maneuver
cardiac output (CO) mucociliary escalator ventilation
compliance oxygen content ventricular afterload
conducting zone oxyhemoglobin ventricular preload
contractility pulmonary shunting vibrissae
diffusion pulmonary surfactant
T
he practice of respiratory care is based on NOSE
thorough preparation in normal cardiopul- The nose filters foreign materials to prevent them from
monary anatomy and physiology. Grounding entering the lower airways, and it humidifies (attaining
in these areas allows the respiratory therapist 100% relative humidity) and warms the inspired air
to compare, analyze in-depth, and diagnose abnormali- to body temperature (98°F; 37°C). The outer nose
ties brought about by disease processes, and it fosters consists of bone and cartilage (connective tissue). The
objective treatment planning and patient management. internal portion, the nasal cavity, is divided into two
The cardiopulmonary system brings atmospheric gas equal chambers by the nasal septum (Figure 6-2). Air
into the lungs, through successively smaller airways to the enters the nose through two external openings called
alveoli. There, the gases are brought into close contact the nares, or nostrils. The air passes through vestibules,
with pulmonary capillary blood (mixed venous blood) which contain coarse hairs, called vibrissae, that filter
from the pulmonary vascular system. Oxygen diffuses out foreign materials and are the respiratory system’s
from gas exchange units into the blood, as carbon dioxide first line of defense.
diffuses from the blood into the gas exchange units. The respiratory system has a complete epithelial
This chapter presents the structures and functions lining consisting of ciliated and nonciliated cells
of the cardiopulmonary system. Breathing and circula- (Figure 6-3). Mucus is transported from the lungs by
tion are regulated efficiently, and benefit and energy the ciliated cells toward the larynx for elimination by
expenditure are continually balanced to meet the swallowing or coughing.
body’s always-changing needs. General science prin- Turbinates, or conchae, are three bony projections
ciples are applied throughout the chapter to explain from the lateral walls of the nasal cavity (see Figure 6-1).
lung ventilation, gas diffusion, perfusion of blood, They divide the inhaled gas into different gas streams,
gas transportation, and cellular delivery mechanisms. thereby increasing the contact area between the inhaled
The wonders of the fetus and newborn, the effects of gas and the nasal epithelium. In the turbinates, the gas
aging, exercise, and high-altitude and high-pressure is warmed and humidified before it enters into the
environments are also described. lower airways.
The paranasal sinuses are air-filled cavities in the
cranium that communicate with the nasal cavity,
Upper Airway: The Nose, Oral produce mucus, and provide resonation for speech
Cavity, and Pharynx (Figure 6-4). The olfactory (smell receptors) region is
located near the superior and middle turbinates.
The respiratory system is divided into the upper airway
and the lower airways. The upper airway contains the
nose, oral cavity, and pharynx (Figure 6-1), and it: ORAL CAVITY
• Conducts air from the atmosphere to the lower The oral cavity (mouth) is primarily the beginning of
airways. the digestive system, but it also is an accessory respira-
• Prevents foreign objects from entering the tory passage that participates in speech and sometimes
tracheobronchial tree. in breathing. It extends from the teeth back to the
• Serves as sites for speech and smell. oropharynx (Figures 6-1 and 6-5). The tongue is
Olfactory region
Frontal sinus
Sphenoid sinus
Conchae (turbinates)
Superior Pharyngeal tonsil
Middle
Inferior
Eustachian tube
Vestibule (auditory tube)
Nares Nasopharynx
Hard palate
Soft palate
Oral cavity
Uvula
Tongue
Oropharynx
Vallecula epiglottica
Lingual tonsil
Hyoid bone
Epiglottis
Larynx
Laryngopharynx
Thyroid cartilage
Esophagus
Cricoid cartilage
Trachea
FIGURE 6-1 Structures of the upper airway.
Anterior cranial fossa

Frontal sinus
Cribriform plate
of ethmoid bone Frontal bone
Perpendicular plate
Nasal bone
of ethmoid bone
Sphenoid sinus Septal cartilage
Sphenoid bone
Nasal cartilage
Vomer
Nasopharynx Palatine process of

the maxilla
Lip
Uvula
Soft palate Palatine bone
FIGURE 6-2 The nose and parts of the nasal septum.
attached posteriorly (toward the back, dorsally) to the opening between the nasopharynx and oropharynx
hyoid bone and mandible. The roof of the mouth is (described next). It moves upward and backward
formed by the hard palate and soft palate. The soft during swallowing, sucking, blowing, and speech. The
palate projects backward and downward, ending in the palatine tonsils, located on each side of the oral cavity,
soft, fleshy structure called the uvula, which is respon- are lymphoid (or lymphatic) tissues with immunologi-
sible for the gag reflex. The soft palate closes the cal functions.
Sphenoid
Squamous cells
Ethmoid
Layer of reproducing
cells
Basement membrane
Frontal
Connective tissue
Stratified squamous epithelium
Cilia
Cell membrane
Maxillary
Goblet cell
Nucleus
Basement membrane
Pseudostratified columnar ciliated epithelium
FIGURE 6-4 A lateral view of the head showing the sinuses.

Nucleus
Basement membrane
Connective tissue
Hard palate
Simple cuboidal epithelium

Soft palate
Palatopharyngeal arch
Nucleus
Basement membrane
Palatoglossal arch
Connective tissue
Palatine tonsil
Simple squamous epithelium Uvula
FIGURE 6-3 Epithelial cell types of the respiratory system.
Oropharynx
PHARYNX
The inspired air passes from the nose and enters the
pharynx. The pharynx is divided into three parts: the
nasopharynx, the oropharynx, and the laryngopharynx
(see Figure 6-1). FIGURE 6-5 The oral cavity.
• The nasopharynx is posterior to the nasal cavity
and above the oral cavity. Lymphatic tissues,
called pharyngeal tonsils or adenoids, are in the • The laryngopharynx is between the base of the
posterior nasopharynx. The eustachian tube (also tongue and the entrance to the esophagus. The
called the auditory canal) connects the nasophar- epiglottis is directly anterior (toward the front,
ynx to the middle ear and functions to equalize ventral) to the laryngopharynx and covers the
pressure in the middle ear. glottis during swallowing.
• The oropharynx lies between the soft palate and
the base of the tongue. The lingual tonsil Lower Airways
(lymphatic tissue) is located at the root of the
tongue. The lower airways begin in the area below the larynx.
LARYNX cartilage, the epiglottis, and the cricoid cartilage. It also

The larynx, or voice box, located between the base of has three pairs of smaller cartilages: the arytenoid,
the tongue and the upper part of the trachea, serves corniculate, and cuneiform cartilages.
three functions. It: The thyroid cartilage, or Adam’s apple, is the largest
cartilage and covers the anterior part of the larynx
• Acts as a passage between the pharynx and the (see Figures 6-1 and 6-6); its superior border is
trachea. V-shaped (thyroid notch). The upper thyroid is
• Protects against aspiration (inhaling materials). suspended from the hyoid bone by the thyrohyoid
• Generates sounds for speech (phonation). membrane (Figure 6-6).
The larynx consists of cartilages that are held The epiglottis is a broad fibrocartilaginous structure
together by ligaments, membranes, and intrinsic and attached to the medial (toward midline of the body)
extrinsic muscles (Figure 6-6). The body of the larynx aspect of the thyroid cartilage and is connected to the
consists of three large unpaired cartilages: the thyroid tongue by mucus membrane. The epiglottis prevents
the aspiration of liquids and solids by covering the
Epiglottis larynx during swallowing.
Hyoid bone
The cricoid cartilage, located below the thyroid
cartilage, is ring-shaped and attached to the first
Thyrohyoid membrane
C-shaped tracheal cartilage. The arytenoid cartilages
Cuneiform cartilage
are three-sided, with their base resting on the cricoid
Corniculate cartilage cartilages’ superior surface; they are attached to the
Thyroid cartilage vocal cords.
Arytenoid cartilage The interior of the larynx is lined by a mucus
Vocal process membrane that forms the false vocal cords (having no
Cricothyroid ligament role in speech) and true vocal cords (producing speech)
(Figure 6-7). The vocal cords attach to the thyroid
Vocal ligament
cartilage and to the arytenoid cartilages, which loosen
Cricoid cartilage
or tighten the vocal cords. The glottis, the opening
Anterior view Trachea Posterior view
LARYNGEAL CARTILAGES
Tongue
Base of tongue
Epiglottis
Aryepiglottic fold Lingual tonsil

Cuneiform tubercle
Median glossoepiglottic fold
(cartilage)
Corniculate tubercle Epiglottis
(cartilage)
Vallecula epiglottica
Aryepiglottic
muscle Vocal folds
Oblique (true vocal cords)
arytenoid muscle Vestibular fold
Transverse (false vocal cord)
arytenoid muscle
Aryepiglottic fold
Thyroarytenoid
muscle Trachea
Lateral (glottis)
cricoarytenoid Cuneiform cartilage
muscle
Lateral view Posterior Posterior view Arytenoid cartilage
cricoarytenoid
muscle Corniculate cartilage
Cricoid
cartilage Esophagus
Cricothyroid muscle
(cut away)
INTRINSIC MUSCLES OF THE LARYNX
FIGURE 6-6 Cartilages and intrinsic muscles of the larynx. FIGURE 6-7 View of the vocal cords.
Mastoid process
Stylohyoid muscle
Mylohyoid muscle
(severed)
Digastric muscle
(posterior belly) Digastric muscle
(anterior belly)
Geniohyoid muscle
Thyrohyoid muscle
Hyoid bone
Omohyoid muscle
Stylopharyngeus muscle
Thyroid cartilage
Cricoid cartilage
Sternothyroid muscle Sternohyoid muscle

(partially severed)
Posterior Lateral (anterior) Transverse

cricoarytenoid cricoarytenoid arytenoid
muscles muscles muscles
I II III
Thyroarytenoid Cricothyroid
muscles muscles
B
IV V
FIGURE 6-8 (A) Extrinsic laryngeal muscles. (B) Intrinsic laryngeal muscles I–V.
between the vocal cords, is the narrowest point in the

adult larynx (Figure 6-7). The cricoid cartilage is the Thyroid cartilage
Cricoid cartilage
narrowest place in the newborn airway. Above the vocal
cords, the larynx is lined with nonciliated stratified
squamous epithelium; below the cords the covering is Tracheal cartilages
pseudostratified columnar epithelium. The muscula-
ture of the larynx consists of the extrinsic muscles
(Figure 6-8A) and intrinsic muscle groups (Figure Right main stem
bronchus Left main stem
6-8B), which control the vocal cords.
bronchus
The larynx has two primary ventilatory functions.
In quiet breathing (breathing at rest), the vocal cords
abduct (move apart) during inspiration and adduct
(move closer together) on expiration. The glottis is
always open to allow a free flow of air into and out
of the lungs. The Valsalva maneuver is the tight
closing of the larynx during exhalation, with an
increase in pressure in the lungs. It is while a person
is performing physical work such as lifting, cough-
ing, vomiting, and defecating. During scuba diving Carina
and flying, the use of the Valsalva maneuver can help
to equalize the pressures in the sinuses and ears,
which become unequal during environmental Bronchioles
pressure changes. FIGURE 6-9 Tracheobronchial tree.
TRACHEOBRONCHIAL TREE cross-sectional area inside the airways greatly

The tracheobronchial tree is a series of airways that increases. The large cross-sectional area promotes
begins at the trachea (the windpipe) and branches smooth (laminar) airflow (see Chapter 3). The small-
into the right and left bronchi, which in turn divide est and most numerous bronchioles, the respiratory
into progressively smaller, shorter, and more numer- bronchioles, connect to the alveoli. Together, the
ous airways (bronchioles) throughout the lungs respiratory bronchioles and the alveoli provide the
(Figure 6-9). These divisions are called airway sites for gas exchange.
generations (Table 6-1). Although at each division, There are two major types of airway: cartilaginous
the individual airways become smaller, the total and noncartilaginous. The cartilaginous airways’ only
TABLE 6-1 Major structures and corresponding generations of the tracheobronchial tree
再冎
Structures Generations
Trachea 0
Main stem bronchi 1
Lobar bronchi 2 Cartilaginous airways
Conducting zone Segmental bronchi 3
Subsegmental bronchi 4–9
Bronchioles
Terminal bronchioles
10–15
16–19
冎 Noncartilaginous airways
Respiratory zone* 再 Respiratory bronchioles

Alveolar ducts
Alveolar sacs
20–23
24–27
28
冎 Sites of gas exchange
Note: The precise number of generations between the subsegmental bronchi and the alveolar sacs is not known.
*These structures collectively are referred to as a primary lobule or lung parenchyma; they are also called terminal respiratory units and functional units.
function is to conduct air between the external environ- Sol layer Surface goblet cells
ment and the noncartilaginous airways. The noncarti- Gel layer
laginous airways serve to conduct air between the Mucus Cilia
cartilaginous airways and the sites of gas exchange. The blanket Basal
cell
number of airway divisions varies markedly within the Epithelium
Basement
lungs.1 Notice from Table 6-1 that the lung conduct- membrane
ing zone consists of both cartilaginous and noncarti- Lamina Smooth
laginous airways, starting at generation 0 (trachea) and propria
muscle
ending with generations 16 to 19 (terminal bronchi-
oles). The respiratory zone is the gas exchange area; it Cartilaginous
Submucosal
starts at generations 20 to 23 and ends in generation 28 gland
layer
(alveolar sacs). Parasympathetic
The tracheobronchial tree is made up of three nerve
layers: an epithelial lining, the lamina propria, and a FIGURE 6-11 Epithelial lining of the tracheobronchial tree.
cartilaginous layer (Figure 6-10). The epithelial lining
is primarily pseudostratified ciliated columnar epithe-
lium with numerous mucus glands interspersed, the trachea to the respiratory bronchioles, slowly
separated from the lamina propria by a basement decreasing in height and becoming cuboidal. Each cell
membrane (Figures 6-3 and 6-10). The basement has about 200 cilia, and each cilium is about 5–7 μm
membrane contains basal cells that replace the ciliated long. The cilia disappear in the respiratory bronchioles.
and mucus cells as needed (Figure 6-11). The pseu- The mucus blanket covers the epithelial lining
dostratified ciliated columnar epithelium extends from of the tracheobronchial tree (Figure 6-11). Mucus is
Terminal bronchiole
Bronchiole
Submucosal Cartilage
gland Smooth muscle
Pulmonary
artery
Lamina propria
Alveolus
Mast cells
Epithelium Parasympathetic
Basement
membrane nerve
Goblet cell
FIGURE 6-10 Histology of the tracheobronchial tree.

mostly water; the balance consists of glycoproteins, function for the tracheobronchial tree. Several factors
lipids, DNA, cellular debris, and foreign particles. slow the rate of mucociliary transport: cigarette smoke,
Mucus is produced by goblet cells and submucosal dehydration, positive pressure ventilation, endotra-
glands. Goblet cells, which are interspersed between cheal suctioning, high FIO2 delivery, hypoxia, air
the ciliated cells, are present down to and within pollutants, general anesthetics, parasympatholytic
the terminal bronchioles. The submucosal, or drugs, and certain disease states.
bronchial, glands, which produce most of the mucus The lamina propria is the submucosal layer
(100 mL per day), are located in the lamina propria. containing fibrous tissue that contains blood and
They are innervated by vagal parasympathetic nerve lymphatic vessels, branches of the vagus nerve, and two
fibers (tenth cranial nerve). Increased parasympathetic sets of smooth muscle that wrap clockwise and coun-
activity increases mucus production; increased sympa- terclockwise around the tracheobronchial tree down
thetic activity and dehydration both decrease mucus into the alveolar ducts. The peribronchial sheath covers
production. The submucosal glands are present to the the outer lamina propria.
terminal bronchiole level. Mast cells are found in the lamina propria, in
The mucus blanket has two distinct layers: (1) smooth muscles, intra-alveolar septa, and the submuco-
the sol layer, which is closest to the ciliated cells, and sal glands. Mast cells are important in the two major
(2) the more viscous gel layer, which is located nearest immune response mechanisms: cellular immunity and
to the surface of the lumen. The gel layer traps foreign humoral immunity. The cellular immune response (type
particles for removal from the airway. The cilia beat IV, or delayed) is a hypersensitivity response responsible
approximately 1300–1500 times per second through for tissue rejection in transplants. The humoral immune
the sol layer, projecting the mucus blanket toward the response involves circulating antibodies, which are
head at a rate of 21.5 mm per minute.1 At the larynx, immunoglobulins that defend against invading envi-
the mucus and entrapments are coughed into the ronmental antigens (e.g., pollen, animal dander). The
oropharynx for expectoration or swallowing. This IgE antibody is basic to the allergic response. The IgE
process, called the mucociliary transport mechanism, antibody-antigen reaction mechanism is shown in
or mucociliary escalator, is a valuable cleansing Figure 6-12. When a susceptible person is exposed to an
Antigen Peripheral IgE

lymphoid tissue Sensitized
A mast cell
Histamine
Heparin Smooth-muscle
contraction
SRS-A
Antigen
PAF
IgE interaction
B ECF-A
Leukotrienes
Asthma attack
FIGURE 6-12 Immunological mechanisms.

antigen, lymphatic tissues release specific IgE antibodies

that travel via the blood supply and attach to mast cell
Thyroid cartilage
receptors. Once the antibodies have attached, the
person is sensitive to that specific antigen, and contin- Cricoid cartilage
Peribronchial
ued re-exposure causes the antigen to be destroyed by sheath
chemical mediators of inflammation located on the
mast cell surface. However, this process also causes
the mast cell to break down, releasing chemicals Trachea
[histamine, heparin, slow-reacting substance of anaphy-

laxis (SRS-A), and eosinophil chemotactic factor of Cartilage
anaphylaxis (ECF-A)] into the blood. These chemical
mediators cause increased vascular permeability, smooth
muscle contraction, increased mucus secretion, and
Right Left
vasodilation with edema. This reaction can be very main stem main stem
dangerous and is found in allergic asthma, where the IgE bronchus bronchus
levels can be greatly elevated. During an asthma attack,
the person has airway narrowing due to bronchial
To upper
edema, bronchospasm, and increased mucus production lobe To upper
with plugging. The result is lung hyperinflation due to lobe
the trapping of air (air trapping). Together these effects
can dramatically increase the work of breathing. To middle
lobe
The cartilaginous layer is the outer layer of the
tracheobronchial tree. It progressively diminishes
decreases in thickness as the airways branch and
become smaller. The cartilage is absent in bronchioles.
To lower
lobe To lower
CARTILAGINOUS AIRWAYS lobe
The cartilaginous airways, part of the conducting zone, FIGURE 6-13 The cartilaginous airways.
conduct air. They consist of the trachea, main stem
bronchi, lobar bronchi, segmental bronchi, and
subsegmental bronchi (Figure 6-13). The adult trachea
is 11–13 cm long and 1.5–2.5 cm in diameter.2 The
trachea extends from the cricoid cartilage of the larynx NONCARTILAGINOUS AIRWAYS
to the second costal cartilage, where it divides, or The noncartilaginous airways, the bronchioles and
bifurcates, at the carina into the right and left main terminal bronchioles, complete the conducting
stem bronchi. The trachea gains support from 15–20 zone. The bronchioles are less than 1 mm in diam-
C-shaped cartilages that posteriorly share a fibroelastic eter and form generations 10 through 15. Because
membrane wall with the esophagus. they lack cartilage for support, they are less rigid
The main stem bronchi are the tracheobronchial than the cartilaginous airways and more susceptible
tree’s first generation. At birth, they form at relatively to alterations due to pressure differences or respira-
equal angles with the trachea. During development, the tory disease. Both conditions result in decreased
right becomes wider, more vertical, and shorter than the airway patency. Terminal bronchioles form genera-
left, with the angle of the left diverging at a greater tions 16 through 19 and are about 0.5 mm in diam-
angle.3 The two main stem bronchi divide into the right eter. The epithelium flattens into a cuboidal shape,
upper, middle, and lower lobar bronchi and into the with the cilia and mucus glands disappearing.
left upper and lower lobar bronchi. These second-gener- Terminal bronchioles have Clara cells with secretory
ation lobar bronchi divide further into segmental functions. Also, collateral ventilation occurs at
bronchi (third generation) that serve specific lung this level and is important in lung disease. Two types
locations, 10 on the right and 8 on left. The subsegmen- of collateral ventilation are canals of Lambert, small
tal bronchi form the fourth through the ninth genera- channels connecting a terminal bronchiole with
tions. They are approximately 1–4 mm in diameter and an adjacent alveolus, and pores of Kohn, small
have a connective tissue sheath and contain nerves, lym- channels connecting adjacent alveoli. The terminal
phatics, and bronchial arteries. The connective tissue bronchioles connect the conducting zone to the
disappears in airways less than 1 mm in diameter. respiratory zone.
Bronchial Cross-Sectional Area SITES OF GAS EXCHANGE AND THE

ALVEOLAR EPITHELIUM
and Bronchial Blood Supply The functional units of gas exchange, which are distal
The total cross-sectional area inside the tracheobron- to the terminal bronchioles (Figure 6-15A), include
chial tree increases from the trachea to the terminal generations 20 through 28. There are three genera-
bronchioles (conducting zone) and significantly tions of respiratory bronchioles with alveoli budding
increases beyond the terminal bronchioles owing from their walls and three generations of alveolar
to the increased number of branches of the ducts. The alveolar ducts are composed of alveoli
respiratory zone (Figure 6-14). Ventilation (the separated by septal walls containing smooth muscle
mechanical movement of air into and out of the fibers and ending in 15–20 alveolar sacs that look
lungs) occurs down to the terminal bronchioles like clusters of grapes. Most gas exchange takes
and requires the expenditure of energy (work of place at the alveolar-capillary membrane
breathing). Molecular movement (diffusion) (Figure 6-15B).
becomes the gas distribution mechanism in the The adult male has approximately 300 million
respiratory zone. alveoli, each between 75 and 300 μm in diameter,
The bronchial blood supply consists of the with 85–95% of these alveoli covered by small
bronchial arteries (systemic circulation) that arise from pulmonary capillaries. This interface provides a huge
the aorta. This bronchial supply is about 1% of the surface area for gas exchange of from 50 to 100 m2;
cardiac output (CO) and nourishes the tracheobron- 75 m2 is the average area.4 The primary lobule contains
chial tree as far as the terminal bronchioles. About the respiratory bronchioles, alveolar ducts, and
one-third of the bronchial venous blood returns to the alveolar clusters. It is also called the acinus,
right atrium (azygos, hemiazygos, intercostal veins), terminal respiratory unit, lung parenchyma, and
with the remaining two-thirds draining into the functional units.
pulmonary circulation via bronchopulmonary anasto- There are three types of alveolar cell: I, II, and III.
moses (bronchial, pleural, and Thebesian veins) and The alveolar epithelium comprises two principal cell
returning to the left atrium. This latter blood, being types: type I (squamous pneumocyte) and type II
low in oxygen, mixes with the newly oxygenated (granular pneumocyte) (Figure 6-16). The type I cells
pulmonary blood from the alveolar-capillary are broad and thin (0.1–0.5 μm thick); they form 95%
interface, creating what is termed venous admixture. of the alveolar surface and are the major gas exchange
sites. The type II cells are cuboidal; they have microvilli.
These cells produce pulmonary surfactant, which,
Conducting zone spread thinly on the alveolar type I cell’s surface,
Respiratory zone decreases surface tension and promotes alveolar
integrity. Pores of Kohn, which are small openings in
the interalveolar septa, allow air to move between
adjacent alveoli. They increase in number with lung
parenchyma diseases, and their size increases with
500
Total aging (Figure 6-15B). Alveolar macrophages, or type III
cross-sectional pneumocytes (alveolar cells), protect the lung by
area
removing bacteria and other foreign materials from
(cm 2 )
400 the primary lobule.
INTERSTITIUM
300
23 Alveolar-capillary clusters are supported and shaped
20
200 by the interstitium, which is a gel-like substance held
15
together by a network of collagen fibers (connective
100
10 tissue). Collagen limits alveolar distensibility, and,
5 Airway when overdistension occurs, pulmonary capillaries
generation
0 can be occluded, leading to collagen formation and
alveolar damage. The interstitium is a tight space
between the alveolar epithelium and the capillary
FIGURE 6-14 The cross-sectional area of the bronchial endothelium (gas exchange area) and a loose space
area. Note the major increase in total cross-sectional area that surrounds the bronchioles and acinus area, which
of the respiratory zone. contain lymph vessels and nerve fibers.
End of
Loose space
Terminal
bronchiole conduction
zone
Tight space
Respiratory Type l cell

bronchioles
Respiratory
zone
Alveolar
ducts
Alveolar Collagen fiber
sacs
Alveoli Capillary
Type ll cell
A
FIGURE 6-16 Alveolar structures and the interstitium.
PULMONARY AND SYSTEMIC

CIRCULATORY SYSTEMS
The body has two distinct circulation, or vascular,
systems: pulmonary and systemic.
Capillary
• The pulmonary vascular system is a low-pressure,
low-resistance (approximately one-tenth
of systemic system), short-distance system
that carries blood from the right ventricle
Pore of Kohn
throughout the lungs and returns it to the
left atrium.
• The systemic vascular system is a high-pressure,
high-resistance, large-distance system that
Type l cell carries blood from the left ventricle throughout
the body and returns the blood to the right
atrium.
Arteries and veins are defined by the direction in
which they carry blood, not by the contents of the
blood. Arteries carry blood away from the heart, and
veins carry blood toward the heart.
The pulmonary vascular system serves two

Macrophage
functions: It carries blood to and from the lungs for
gas exchange with alveoli, and it provides nutrition
for the structures distal to the terminal bronchiole
B Type ll cell
level (acinus). The pulmonary vasculature contains
FIGURE 6-15 (A) Anatomical structures distal to the arteries, arterioles, capillaries, venules, and veins—
terminal bronchioles, called the primary lobule, or acinus. the same structures as found in the systemic vascu-
(B) The alveolar-capillary network. lar system.
Superior
pulmonary
veins
Pulmonary
arteries
Left lung
hilum
Right lung
hilum
Aorta
Inferior
pulmonary
veins
FIGURE 6-17 The major pulmonary vessels.
Pulmonary arteries (PAs) receive deoxygenated Capillaries are an extension of the arteriole
blood from the right atrium and divide into right endothelial lining and form a network of vessels
and left branches (Figure 6-17). These branches pass around the alveoli. They are very thin (less than 0.1 μm),
through the hilum, where the main stem bronchi, have an external vessel diameter of about 10 μm, and
vessels, and nerves also enter the lung. The pulmonary are the site for gas exchange with their adjacent alveoli.
artery divides along the branchings of the tracheobron- The pulmonary capillary endothelium is selectively
chial tree. Arterial walls have three layers (tunica permeable to water, electrolytes, and sugars and is
intima, tunica media, tunica adventitia), making them involved in the distribution of biologically active
relatively stiff; stiffness is necessary for carrying blood substances.
under high pressure, as in the systemic vascular system Venules are very small veins that collect blood
(Figure 6-18). The middle layer is the thickest and from capillaries and empty into veins, which carry the
contains primarily connective tissue in large arteries blood back to the heart. Veins have three layers, like
and smooth muscle in medium and small arteries. arteries, but they differ by having thinner walls and
The outer layer is connective tissue with blood vessels less smooth muscle. In the systemic system, veins in
that serve all three layers. the lower extremities have one-way valves to assist
Arterioles supply the acinus region, and their walls blood flow back to the heart. Veins are called capaci-
also have three layers (endothelial, elastic, smooth tance vessels because they can collect large amounts of
muscle). Arterioles, called resistance vessels, use their blood with small pressure changes. The pulmonary
smooth muscle fibers for the distribution and regula- veins merge into two large veins exiting the lungs at
tion of blood. the hilum.
Blood
flow
Vein
Venule
Connective
tissue
Capillaries
Endothelium Muscle layer Collagen
(Tunica intima) Elastic layers (Tunica media) (Tunica adventitia)
Arteriole
Artery
FIGURE 6-18 The components of the major blood vessels.
LYMPHATIC SYSTEM and arteriolar smooth muscle tone of the lungs, cardiac
Lymphatic vessels are found throughout the lungs and muscle, and glands (Table 6-2). The ANS has two
branch along with the airways and blood vessels. They divisions:
remove excess fluid and protein molecules that leak • The sympathetic nervous system relaxes bronchial
from the capillaries. Lymph vessels end in lymph nodes, smooth muscle (bronchodilation), speeds up
which are collections of lymphatic tissue. The nodes act the heart rate, and raises blood pressure.
as filters to keep particles from entering the blood- • The parasympathetic nervous system constricts
stream, and they produce lymphocytes and monocytes bronchial smooth muscle (bronchospasm),
(Figure 6-19). There are more lymph vessels in the slows the heart rate, and increases intestinal
lower lung lobes, with more on the right lower lobe peristalsis and glandular activity.
than on the left lower lobe.
Smooth muscle tone is a reflection of the relative
NEURAL CONTROL OF THE LUNGS balance between the sympathetic and parasympathetic
The autonomic nervous system (ANS) regulates nervous systems. When the sympathetic nervous
involuntary vital functions and controls the bronchial system is activated, the neural transmitters release
Trachea Tracheal
lymph nodes
Superior
tracheobronchial
lymph nodes
Right bronchus Left bronchus
Pulmonary
lymph nodes
Inferior
tracheobronchial
lymph nodes
Bronchopulmonary
lymph nodes
FIGURE 6-19 Lymph nodes of the trachea and the right and left mainstem
bronchi.
epinephrine. They stimulate the beta 2 receptors in increasing mucus production (secretions). Refer to
bronchial smooth muscle, causing bronchodilation. Chapter 9 for a detailed description.
The alpha receptors in the arterioles’ smooth muscle
cause the pulmonary vascular system to constrict The Lungs
(vasoconstriction) and elevate blood pressure. When
the parasympathetic nervous system is activated, the The lungs extend from the level of the first rib at the
neural transmitter acetylcholine is released, causing apex (top) and are continuous to the base anteriorly
constriction of the bronchial smooth muscle and at the sixth rib (xiphoid process level) and posteriorly
TABLE 6-2 Effects of autonomic nervous system activity

Effector site Sympathetic Nervous System Parasympathetic Nervous System
Heart Increases rate Decreases rate
Increases strength of contraction Decreases strength of contraction
Bronchial smooth muscle Relaxes muscle Constricts muscle
Bronchial glands Decreases secretions Increases secretions
Salivary glands Decreases secretions Increases secretions
Stomach Decreases motility Increases motility
Intestines Decreases motility Increases motility
Eye Widens pupils Constricts pupils
Anterior view Posterior view
Clavicle Sternal notch Manubrium

Scapula
1
2
Body of 4
sternum
5 Inferior angle
of scapula
6
Xiphoid 7
process 8
FIGURE 6-20 Anatomical relationship of the lungs and thorax.
to the eleventh rib (two ribs below the scapula) relationship describes the lungs’ natural tendency to
(Figure 6-20). The lungs are shaped to fit into the collapse and the chest wall’s natural tendency to
chest (thorax) along with the heart and mediastinal expand, which creates a subatmospheric (negative
structures and to accommodate the convex diaphragm gauge) pressure in the pleural cavity.
(Figure 6-21A). At the mediastinal border is the hilum,
which allows the right and left main stem bronchi,
THORAX
blood and lymph vessels, and nerves to enter and exit
the lungs (Figure 6-21B). The thorax contains and protects the organs of the
The right lung is larger, heavier, and shorter than cardiopulmonary system. The sternum forms the
the left lung and has three lobes (upper, middle, anterior chest border and is composed of the manu-
lower), which are divided by the oblique fissure brium, body, and xiphoid process. Twelve pairs of ribs
(between the upper and middle lobes) and the are directly attached posteriorly to the thoracic
horizontal fissure (middle and lower lobes). The left vertebrae and attached indirectly by costal cartilage
lung has two lobes, upper and lower, which are divided anteriorly to the sternum. Ribs 1 through 7 are true
by the oblique fissure. All of the lobes are subdivided ribs, directly attached to the sternum by their cartilage.
into bronchopulmonary segments (Figure 6-22). Ribs 8 through 10 are false ribs, and ribs 11 and 12 are
floating ribs (Figure 6-24). Between the ribs are 11
intercostal spaces, containing nerves, arteries, and veins
MEDIASTINUM AND PLEURAL MEMBRANES located below the lower rib border (Figure 6-25).
The mediastinum is the cavity between the lungs,
sternum (anteriorly), and the thoracic vertebrae DIAPHRAGM AND ACCESSORY MUSCLES
(posteriorly). It contains the trachea, heart, major OF VENTILATION
blood vessels (great vessels), nerves, esophagus, thymus
Breathing has two primary phases:
gland, and lymph nodes (Figure 6-23).
There are two pleural surfaces. The visceral pleura • Inspiration, which has active muscle use and
covers the lungs, and the parietal pleura covers the energy expenditure.
inside of the chest wall, the diaphragm, and the • Expiration, which in quiet breathing is a passive
mediastinal surfaces (Figure 6-23). The space between recoil of structures with minimal energy expen-
the two pleural surfaces, called the pleural cavity, diture. During increased activity levels, expira-
contains a small amount of serous fluid that allows tion becomes active with the use of accessory
smooth movement during breathing. The lung-thorax muscles.
Apex Trachea
Upper lobe
Upper lobe
Horizontal
fissure
Cardiac notch
Middle lobe
Oblique Oblique
fissure fissure
Lingula
Lower lobe Lower lobe
Base
A (Diaphragmatic surface)
Apex
Oblique
fissure
Upper lobe Upper lobe
Pulmonary
artery
Hilum
Bronchus Hilum
Pulmonary
veins
Horizontal Pulmonary
fissure ligament
Oblique Cardiac
Middle notch
fissure
lobe
Posterior
Anterior Anterior
border
margin margin
Base
(Diaphragmatic surface)
Right lung Left lung

Inferior
B border
FIGURE 6-21 (A) Anterior view of the lungs. (B) Medial view of the lungs.
The diaphragm is the major muscle of respiration. It cavities and is attached from the lumbar vertebrae, the
is made up of two dome-shaped muscles, the right and costal margin, and the xiphoid process. Passing
left hemidiaphragms, that merge into a central tendon. through the diaphragm are the esophagus, aorta,
The right hemidiaphragm is slightly higher in the nerves, and inferior vena cava. The primary motor
thoracic cavity than the left to allow room for the liver. innervation of the diaphragm is from the phrenic
The diaphragm separates the thoracic and abdominal nerves, which arise from cervical segments 3 through 5

Apical 1 Upper division
Posterior 2 Apical/Posterior 1&2
Anterior 3 Anterior 3
Middle lobe Lower division (lingular)

Lateral 4 Superior lingula 4
Medial 5 Inferior lingula 5

Superior 6 Superior 6
Medial basal 7 Anterior medial basal 7&8
Anterior basal 8 Lateral basal 9
Lateral basal 9 Posterior basal 10
Posterior basal 10
1 1 -2
2 3
Posterior
6 views
4 6
8
10 9 8 9 10
1 2
1
1 3 1-2
2
2 3 4 3
3 5 6
Lateral 4 4 Lateral
view 6 5 6
4 6 view
5
5 8 7 8
10 8 9 10
9 7
9 10 8
10 9
1-2
1
2 3
3 1
1-2
Anterior 2
4
view 4 5 3 Anterior
3 6 5 view
8 4 8
10
5 7 5
10 Medial
Medial 7-8
view 8 9 9 view
FIGURE 6-22 Lung segments.
(C 3–5), with the lower thoracic nerves also contribut- lungs. Expiration results when the diaphragm relaxes
ing to motor innervation. and returns to its dome shape, thereby increasing
When the diaphragm is stimulated, it contracts. pulmonary pressures and causing gas to flow from
The contraction moves the diaphragm downward and the lungs.
the lower ribs outward. This movement increases the For normal ventilation, a healthy person can
thoracic volume, decreases the intrapleural and manage ventilation using the diaphragm alone. The
intra-alveolar pressures in the thorax, and, with a accessory muscles of inspiration and expiration are
patent (open) airway, allows gas to flow into the activated to assist the diaphragm when increased
Hilum
Trachea Parietal
pleura
Visceral
Lung pleura
Pleural
cavity
Rib
Mediastinum
Diaphragm
FIGURE 6-23 Major structures around the lungs.
Anterior view Posterior view
Sternal Clavicle 1st thoracic

notch vertebra
1
2
1
3
2
4
3 5
Manubrium Scapula
6
sterni
4 7
Body of Inferior
5
sternum 8 angle of
6 scapula
9
Xiphoid 7
process 10
8
11
9
10 12
11 © Delmar/Cengage Learning
12
Costal 1st lumbar

Costal vertebra
angle 12th thoracic
margin
vertebra
FIGURE 6-24 The thorax.
ventilation is needed, such as during exercise and in • Trapezius muscles (elevate the thoracic cage).
chronic obstructive pulmonary disease (COPD) and • External intercostals (increase both lateral and
other disease states. The accessory muscles of inspiration anterioposterior diameters of the thorax).
generally work to expand the thorax. They include:
The accessory muscles of expiration generally work to
contract the thorax and help to overcome increased
• The scalenes (elevate the first and second ribs).
airway resistance. They include the:
• Sternocleidomastoids (increase the anterioposte-
rior diameter of the chest). • Rectus abdominis.
• Pectoralis major muscles (increase the anterio- • External abdominis oblique.
posterior diameter of the chest). • Internal abdominis oblique.
Spotlight
Rib On
Boyle’s Law
Normal breathing is an application of Boyle’s law,
which states that volume is inversely related to
Vein pressure. The body plethysmograph, used to test
pulmonary function and to measure total thoracic
gas volume, is an application of Boyle’s law.
Artery
Nerve
alveolar distending pressure, is the difference between
Palv and pleural pressure (Ppl). Transthoracic pressure
Internal (Ptt) is the difference between Palv and body surface
intercostal
muscles
pressure (Pbs). Gas flows through the airways because
of these pressure differences.
Role of the Diaphragm in Ventilation. The contrac-

External
tion of the diaphragm moves it downward, increasing
intercostal the thoracic volume and decreasing the intrapleural
muscles and intra-alveolar pressures. Gas flows through the
tracheobronchial tree to the alveoli, from the higher PB

to the lower Palv until these pressures equalize at
end-inspiration. During expiration, the diaphragm
relaxes and moves upward, decreasing thoracic volume
and increasing intrapleural and intra-alveolar pressures.
FIGURE 6-25 The intercostal space. Gas flows from the lungs until the pressures equalize
at end-expiration. The intrapleural pressure is always
less than barometric pressure in normal breathing
• Transversus abdominis (all four act to push the (Figure 6-26).
diaphragm into the thoracic cage). The normal movement of the diaphragm is about
• Internal intercostals (decrease lateral and anterio- 1.5 cm at rest, with a normal intrapleural pressure drop
posterior diameters and decrease lung volume). of 3 to 6 cm H2O. During a deep inspiration, the
diaphragm moves 6–10 cm, with intrapleural pressures
dropping as low as 50 cm H2O (subatmospheric, or
Ventilation negative). For a forced expiration, intrapleural pressure
Ventilation is the bulk movement of air into and out of can reach 70 to 100 cm H2O above (positive)
the lungs. It is responsible for the exchange of oxygen atmospheric pressure.
and carbon dioxide between the alveoli and pulmonary
capillary blood. The four characteristics describing
ventilation are pressure differences, static lung charac- STATIC CHARACTERISTICS OF THE LUNGS
teristics, dynamic lung characteristics, and ventilatory Static refers to matter at rest and to forces in equilib-
patterns. rium. After a normal expiration, the amount of air in
the lungs, the functional residual capacity (FRC), reflects
lung-thorax equilibrium. The two static forces causing
PRESSURE DIFFERENCES ACROSS THE LUNGS an expanded lung to inwardly recoil are the lungs’
Driving pressure is the difference between two points in elastic properties and the surface tension of the alveolar
a tube and is responsible for fluid movement through a fluid lining layer.
tube. Fluids consist of gases and liquids. Barometric
pressure (PB) is the atmospheric pressure at the mouth Elastic Properties of the Lungs. Compliance is the
and is normally 760 mm Hg at sea level. Transairway volume (in liters, L) change per unit of pressure (cm H2O)
pressure (Pta) is the pressure difference between the change. Compliance of the lung (CL) is expressed as
mouth (Pm), or airway pressure, and the alveolar liters per centimeter H2O change and provides the
pressure (Palv). Transpulmonary pressure (Ptp), or amount of volume attained for each pressure unit
Normal Inspiration and Expiration
Inspiration End-Inspiration
Intra-alveolar Gas No Gas Intra-alveolar

pressure below Flow Flow pressure in
atmospheric equilibrium
pressure with atmospheric
pressure
Intrapleural 0
pressure Intrapleural
progressively pressure holds
decreases at a level below
that at rest
Diaphragm
progressively Downward
moves downward movement of
diaphragm stops
Expiration End-Expiration
Intra-alveolar Gas No Gas Intra-alveolar

pressure above Flow Flow pressure in
atmospheric equilibrium
pressure with atmospheric
0
+ pressure
Intrapleural
pressure Intrapleural
progressively pressure holds
increases at resting level
Diaphragm Upward
progressively movement of
moves upward diaphragm stops
FIGURE 6-26 Diaphragm movement and pressure changes in the lungs during inspira-
tion and expiration.
applied, either negative or positive. Normal lung ance, and the two characteristics are inversely related.
compliance is 500 mL/5 cm H2O 100 mL/cm H2O, When a rubber band is stretched and then allowed to
or 0.1 L/cm H2O.5 The chest wall normally exerts a relax, it returns to its original dimensions, as does the
small static effect (chest wall compliance, or CCW) that lung during quiet expiration. When the lungs collapse,
is increased in some diseases affecting the thorax. elastance is increased.
Elastance is the lung’s attempting to return to its
original size and shape when force (pressure) is not Surface Tension, Pulmonary Surfactant, and Effects
being applied. Elastance is the reciprocal of compli- on Lung Expansion. Surface tension is the molecular,
cohesive force at the liquid-gas interface in the alveoli,
which, if left unchecked, would cause the alveoli to
Spotlight collapse.
On LaPlace’s law describes the effect of distending
pressure on a liquid bubble and is modified for use
Compliance with alveoli that have one liquid-gas interface.
Static compliance is measured without airflow. • The distending pressure of a liquid sphere (alveoli)
Dynamic compliance is measured using peak is directly proportional to the liquid’s surface
inspiratory pressure, which includes the effects tension and inversely proportional to the sphere’s
of airflow through the tracheobronchial tree radius. Distending pressure varies inversely with
(airway resistance). See Figure 6-27 for an the radius of the alveoli (Figure 6-28).
illustration of lung volume-pressure changes due • Critical opening pressure is the high pressure
to differences in compliance. needed to initially open a bubble by overcoming
its cohesive force, such as blowing up a balloon.
6
Increased Compliance
5
4 Normal Compliance
Volume 3
Change Decreased Compliance
(L)
2
0 5 10 15 20 25 30 35 40 45
Pressure (cm H2O)
FIGURE 6-27 Lung compliance and volume-pressure curves.
4 ST
P=
r
ST = 10 dynes/cm ST = 20 dynes/cm
Bubble A Bubble B
Distending Pressure Distending Pressure
A 5 cm H2O 10 cm H2O
4 ST
P=
r
r = 1 cm
r = 2 cm
Bubble A Bubble B
Distending Pressure Distending Pressure
B 5 cm H2O 10 cm H2O
FIGURE 6-28 (A) The surface tension (st) of two bubbles of the same size and the
distending pressures (P) needed to maintain their size. (B) The distending pressure
needed to maintain the size of two bubbles of different sizes (r radius).
When this pressure is reached, the volume Airway Resistance. Airway resistance (Raw) is the
rapidly increases with small, incremental pressure difference between the mouth and the alveoli
pressure increases. (transairway), divided by the flow rate (L/s). The
• Critical closing pressure is the point at which the difference is derived from Poiseuille’s law. Resistance to
liquid cohesive forces exceed the distending airflow (friction) is created as gas molecules come into
pressure and the sphere collapses. contact with the inner surface of the airways. Normal
Raw is 0.5–2.5 cm H2O per liter per second.6 Gas
Fortunately, in the healthy lung the natural ten-
movement through airways can be laminar (stream-
dency of the smaller alveoli to collapse is prevented by
lined and smooth, found with low flow rates and low
an extraordinary substance, pulmonary surfactant.
pressure differences), turbulent (random and rough,
Pulmonary surfactant is a phospholipid, with a major
found with high flows and high pressure differences),
component being dipalmitoyl phosphatidyl choline. It
or transitional (tracheobronchial), a mixed condition
is produced by the alveolar type II cells and functions
found near airway branching.
to decrease alveolar surface tension in proportion to
the ratio of surfactant to alveolar surface area. In
alveolar size (volume) changes, surfactant is inversely Time Constants. A time constant is the time necessary
related to surface area. to inflate an alveolus to 60% of its potential filling
capacity and is a product of Raw and CL (Figure 6-29).
• When alveolar volume increases, the proportion Long time constants are found in lung regions with
of surfactant to surface area decreases and surface increased Raw or increased CL. Short time constants are
tension increases. found in regions with decreased Raw or decreased CL.
• When alveolar volume decreases, the proportion Filling and emptying of lung regions are important
increases, decreasing surface tension and main- components for normal breathing, and they become
taining alveolar integrity. more important in respiratory disease, its treatment,
Alveolar surface tension varies from 5 to 50 dynes and its management. If time constants vary signifi-
per centimeter. Atelectasis is the collapse of small cantly between alveoli and lung regions, so does
alveoli. Once collapsed, the alveolar walls with their ventilation.
liquid lining form a strong bond that resists re-
expansion. Pulmonary surfactant deficiency results Dynamic Compliance. Dynamic compliance is the
from clinical conditions that cause acidosis, hypoxia, change in lung volume divided by the change in
hyperoxia, atelectasis, and pulmonary vascular conges- transpulmonary pressure as measured by esophageal
tion and from prematurity of the lung. balloon. Dynamic compliance is measured during gas
flow and includes Raw, whereas static compliance is
measured without gas flow. Normally the two types of
DYNAMIC CHARACTERISTICS OF THE LUNGS compliance are equal, but with obstructed airways the
Dynamic refers to the movement of gas into and out of ratio of dynamic to static compliance falls as the
the lungs and to the related pressure changes. These breathing frequency rises. This fall in the ratio occurs
dynamic factors are Poiseuille’s law for flow and because the alveoli distal to the obstruction lack the
pressure and airway resistance. Poiseuille’s law time to fill because of the increased breathing rate
describes the relationship between gas flow and (frequency dependent).
pressure through tubes and, when applied to the lung,
gas flow through nonrigid airways. During a normal
inspiration, the intrapleural pressure decreases by 3 VENTILATORY PATTERNS
to 6 cm H2O, causing passive dilation of the airways The ventilatory pattern consists of the tidal volume
(increased length, increased diameter, and increased (VT), ventilatory rate (f ), and the ratio of inspiratory
volume). During expiration, passive constriction occurs time (I) to expiratory time (E) (I/E ratio). Tidal volume
(decreased length, decreased diameter, and decreased is the volume of air inspired and expired in one normal
volume). The application of this law shows that gas breath and is equal to 3–4 mL/lb (7–9 mL/kg) of ideal
flow varies to the fourth power of the radius (r 4). If the body weight. The normal ventilatory rate (f) for an
airway radius is decreased by one-half, the airway adult is about 12–20 breaths per minute.6 The normal
pressure must be increased 16-fold to keep the flow I/E ratio is 1:2, with inspiration being active and
constant. In normal breathing, this relation is not a shorter and expiration passive and longer, including a
problem. In respiratory disease states, however, bron- brief pause before the next inspiration. At a ventilation
chial narrowing results in decreased flows and rate of 20, which is 3 seconds per respiratory cycle, a
increased pressures, resulting in an increased energy normal 1:2 I/E ratio equals 1 second for inspiration
cost of breathing (work of breathing). and 2 seconds for expiration.
Identical Raw and CL. Thus Time Constants Are Equal
CL = 1 A
Units A & B
Volume Change
A Raw = 1
Vol. = 1
CL = 1
Inflation Time (seconds) B
Raw = 1
1 2 3 4 Vol. = 1
Identical Raw, But Unit B Is 1/2 as Compliant as Unit A
CL = 1 B
Unit A
Volume Change
A Raw = 1
Unit B
Vol. = 1
B CL = 1/2
Inflation Time (seconds) Raw = 1
1 2 3 4 Vol. = 1/2 That of Unit "A"
Identical CL, But Unit B Has Twice the Resistance as Unit A
Unit A CL = 1 C
Raw = 1
Volume Change
Unit B A
Vol. = 1
CL = 1
Inflation Time (seconds) B
Raw = 2
Vol. = 1 But Takes Twice
1 2 3 4 as Long as "A" to Inflate
FIGURE 6-29 Time constants.
Minute Ventilation. Minute ventilation, V E, is the total Dead Space. Dead space ventilation (V D) is the
volume of gas exhaled (or inhaled) per minute and is volume of gas in the lungs that does not participate in
computed as V T f. A normal adult value is 500 mL gas exchange. The three types of dead space are ana-
12 f 6000 mL (6.0 L). tomic, alveolar, and physiologic.
Alveolar Ventilation. Alveolar ventilation (V A) is the

• Anatomic dead space (VDanat) is the volume of gas
in the conducting airways and normally equals
volume of inspired gas that reaches the alveoli and
1 mL/lb of ideal body weight. For example, a 150-lb
that is available for gas exchange with pulmonary
capillary blood. Minute alveolar ventilation, V A, is the
person has 150 mL of VDanat. The gas that enters the
alveoli is a combination of VDanat and atmospheric
volume of fresh gas entering the alveoli each minute
(fresh) gas. The fresh gas has to pass through the
and is computed as tidal volume minus dead space
(V D) f:
VDanat to reach the alveoli (Figure 6-30).
• Alveolar dead space is the dead space that occurs
V A (VT VD) f
when an alveolus is ventilated but not perfused
with pulmonary capillary blood and therefore is
(500 mL 150 mL) 12 not involved in gas exchange (as in pulmonary
350 mL 12 4200 mL (4.2L) emboli).
150 150
mL mL Fresh Gas
150 150
(VT)
mL mL
150 150 Non-Fresh Gas

mL mL
(VD) 150 150 150

mL mL mL
150
Fresh Gas
mL
150
mL
Non-Fresh Gas 150
mL
Pre-Inspiration End-Inspiration End-Expiration

A B C
FIGURE 6-30 Relationship of alveolar ventilation and dead space.
• Physiologic dead space is the total dead space tance increases, ventilatory rate usually decreases and
and is the sum of anatomic plus alveolar dead tidal volume increases, producing a slower and deeper
space. pattern that allows more time for exhalation.
Recognition of ventilatory patterns is important for
respiratory care practice.
Regional Differences in Normal Lung Ventilation.
For the normal individual, there is an intrapleural • Eupnea is normal, spontaneous breathing.
pressure difference (gradient) from the lung apex (top) • Apnea is the complete lack of spontaneous
to the lung base (bottom). The lungs are suspended breathing.
from the hilum and are gravity dependent. The lung • Hyperpnea is an increased volume of breathing,
bases weigh more than the apexes because of gravity with or without an increased ventilatory rate.
and greater perfusion. This difference results in nega- • Hyperventilation is any breathing pattern that
tive intrapleural pressures of 7 to 10 cm H2O at the results in a decreased arterial blood partial
apex and 2 to 3 at the base (Figure 6-31). Alveoli pressure of carbon dioxide (PaCO2).
respond to these intrapleural pressure differences and • Hypoventilation is any breathing pattern
are larger at the apex. The alveoli at the base are smaller that results in an increased arterial blood PaCO2.
but more compliant. In the upright lung, ventilation is • Tachypnea is a rapid rate of breathing.
favored at the lung bases, where the alveoli have a • Dyspnea is difficulty in breathing, of which the
greater potential to expand and have an increased ratio individual is aware (subjective).
of surfactant to surface area. This relation is important
when ventilation/perfusion matching is considered.
Spotlight
Effect of Airway Resistance and Lung Compliance On
on Ventilatory Patterns. The ventilatory pattern
adopted by an individual is based on minimum work Breathing Pattern
requirements rather than on efficiency. Normally, Breathing pattern can dramatically affect alveolar
about 5% of an individual’s total energy expenditure ventilation (Table 6-3). An increased depth of
(5% of the oxygen uptake) is used for breathing. breathing is far more effective in increasing total
When lung compliance decreases, the ventilatory rate alveolar ventilation than an equivalent increase
increases, and the tidal volume decreases, producing a in breathing rate.
rapid, shallow breathing pattern. When airway resis-
Airway
Pressure
Intrapleural
%
Pressure
100
–7 to –10
90
80
0
0 70
Alveolar Volume
Pressure
Gradient 60
50
0
40
–2 to –3 30
20
0
10
–10 0 10 20 30
Intrapleural
Pressure (cm H2O)
FIGURE 6-31 The intrapleural pressure gradient in the upright position.
Pulmonary Function • Expiratory reserve volume (ERV) is the maximum

volume of air that can be exhaled after normal
Measurements tidal volume expiration.
Pulmonary function measurements are an important • Residual volume (RV) is the amount of air remain-
application of assessing respiratory physiology. These ing in the lungs after a maximal expiration.
include testing for lung volumes and capacities, flow
rates, oxygen diffusion capacity, pulmonary mechanics,
arterial blood gases and pH, and more specialized LUNG CAPACITIES
measurements, such as distribution of ventilation and Lung capacities are combinations of two or more lung
blood flow. volumes or capacities (Figure 6-32).
• Vital capacity (VC) is the volume of air that
LUNG VOLUMES can be exhaled after a maximal inspiration
(IRV VT ERV), or the amount of air that
The total amount of air the lungs can hold is divided
can be inhaled after a maximum exhalation.
into four distinct lung volumes (Figure 6-32).
• Inspiratory capacity (IC) is the volume of air
• Tidal volume (VT) is the amount of air that moves that can be inhaled after a normal expiration
into and out of the lungs in one normal breath. (VT IRV).
• Inspiratory reserve volume (IRV) is the maximum • Functional residual capacity (FRC) is the volume of
amount of air that can be inhaled after a normal air remaining in the lungs after a normal expira-
tidal volume inspiration. tion (ERV RV) and is called the resting level.
TABLE 6-3 Effect of breathing depth and frequency on alveolar ventilation

Breathing Total Minute Total Dead Space Alveolar
Breathing
. Frequency Ventilation Ventilation Ventilation
Subject Depth (V T) (mL) (breaths/min) (mL/min) (mL/min) (mL/min)
A 150 40 6000 150 40 6000 0
B 500 12 6000 150 12 1800 4200
C 1000 6 6000 150 6 9000 5100
(VC) (IC) (TLC)
Inspiratory
Inspiratory
Reserve Volume
Capacity
Vital Capacity
(IRV)
Total Lung Capacity

Tidal Volume (V T)
Expiratory (FRC)
Reserve Volume
Functional
(ERV)
Capacity
Residual
Residual
Volume
(RV)
FIGURE 6-32 Normal lung volumes and capacities.
• Total lung capacity (TLC) is the maximum amount

of air that the lungs can hold (IC FRC). Spotlight
• The ratio of residual volume to total lung On
capacity (RV/TLC 100) is the percentage of the
TLC occupied by the RV. Patient Assessment
Normal lung volumes and capacities are listed in Patient assessment is based on observing signs
Table 6-4. and symptoms, interviewing the patient for
Measurements of pulmonary function, lung detail and clarity, and performing a physical
volumes, and lung capacities are important for patient assessment. The physical assessment includes
assessment and treatment. Pulmonary function testing chest examination, palpation, percussion,
(see Chapter 17) is an important assessment and is auscultation of the lungs, and review of pulmo-
used to identify the two primary types of lung disorder: nary function study results. Comparison of the
obstructive (decreased expiratory flow rates) and clinical findings with normal functions and
restrictive (decreased volumes). In an obstructive lung values allows setting initial patient care plans
disorder, RV, FRC, and RV/TLC are increased, and the and the trending of information for long-range
VC, IC, IRV, and ERV are decreased. In a restrictive lung patient management.
disorder, the VC, IC, RV, FRC, VT, and TLC are all
TABLE 6-4 Approximate lung volumes and capacities in the average normal subject
between 20 and 30 years of age
Male Female
Approximate Approximate
Measurement mL Percentage of TLC mL Percentage of TLC
Tidal volume (VT) 500 8–10 400–500 8–10
Inspiratory reserve volume (IRV) 3100 50 1900 30
Expiratory reserve volume (ERV) 1200 20 800 20
Residual volume (RV) 1200 20 1000 25
Vital capacity (VC) 4800 80 3200 75
Inspiratory capacity (IC) 3600 60 2400 60
Functional residual capacity (FRC) 2400 40 1800 40
Total lung capacity (TLC) 6000 4200
Residual volume total lung capacity 6000 20 4200 25
ratio (RV/TLC 100)
decreased. Individuals may also have both types of TABLE 6-5 Gases that compose the
disorder (mixed disorder). barometric pressure
Partial
Diffusion of Pulmonary Gases Percentage of Pressure
Gas Atmosphere (mm Hg)
Diffusion is the movement of gas molecules from an
area of relatively high concentration to an area of low Nitrogen (N2) 78.08 593
concentration. Each gas moves according to its own Oxygen (O2) 20.95 159
partial pressure gradients and continues until equilib- Argon (Ar) 0.93 7
rium is achieved. Oxygen and carbon dioxide are the
Carbon dioxide (CO2) 0.03 0.2
two pulmonary gases that diffuse across the alveolar-
capillary membrane (Figure 6-33). Refer to the gas laws
in Chapter 3.
oxygen diffuses into the alveoli, it is diluted with
carbon dioxide (which diffuses from capillaries) and
PARTIAL PRESSURES OF OXYGEN, CARBON water vapor, both of which are higher than atmo-
DIOXIDE, AND WATER VAPOR spheric pressure levels. Water existing as a gas (water
vapor) exerts a partial pressure (pH2O) of 47 mm Hg
The weight of the atmospheric gases on the earth’s
in the alveoli; that value represents 100% saturation at
surface is the barometric pressure (PB), or atmospheric
37°C (body temperature). This water vapor weighs 44
pressure. The normal value at sea level is 760 mm Hg.
mg/L. The balance of the atmosphere is composed of
Barometric pressure decreases as elevation increases
nitrogen (78%) and trace gases that are considered
(when you are, say, climbing a mountain) and
physiologically inactive.
increases below the water’s surface (diving). The
percentage concentration of the atmospheric gases
remains constant at high and low elevations IDEAL ALVEOLAR GAS EQUATION
(Table 6-5). The alveolar oxygen partial pressure, or tension, is
The partial pressures (P) of gases in an atmosphere computed for clinical use. The ideal alveolar gas
are defined by Dalton’s law of partial pressures. Table equation for a normal individual breathing room air
6-6 displays the partial pressures of gases in the air, (room air has an oxygen concentration of 0.21, or
alveoli, and blood. Note that the partial pressures of 21%) is:
oxygen (159 vs. 100) and of carbon dioxide (0.2 vs. 40)
are quite different in the atmosphere and alveoli. As PAO2 FIO2 (PB PH2O) PQCO2 (1/R)
0.21 (760 47) (40 1.25)
Capillary
basement
Capillary (0.21 713) 50
Alveolar membrane
endothelium
epithelium 150 50
100 mm Hg
Alveolar Erythrocyte
basement membrane
where PAO2 is the partial pressure of oxygen in the
membrane
alveoli, PB is barometric pressure, PH2O is water vapor
Intracellular pressure, FIO2 is the fractional concentration of
O2 erythrocyte inspired oxygen, and PaCO2 is the partial pressure of
fluid
CO2 arterial carbon dioxide.7 The factor 1.25 (R) represents
Fluid layer
variations in the FIO2 in the calculation of the respira-
(with pulmonary tory exchange ratio (RR). The normal RR is 0.8 and is
surfactant) the comparison of 200 mL CO2/minute diffusing into
the alveoli divided by 250 mL O2/minute diffusing
Alveolus
into the capillaries (oxygen uptake). The detailed
Capillary
equation uses 1/R, which equals 1 0.8, resulting
in 1.25.
Interstitial Plasma DIFFUSION OF OXYGEN AND CARBON DIOXIDE

space
Gas diffuses through the thin (0.36–2.5-μm) alveolar-
ALVEOLAR-CAPILLARY MEMBRANE
capillary membrane, which has nine layers, as listed
FIGURE 6-33 The alveolar-capillary membrane. in Figure 6-33. In a healthy person, mixed venous
TABLE 6-6 Partial pressure (mm Hg) of gases in the air, alveoli, and blood at standard
pressure and temperature
Gas Dry Air Alveolar Gas Arterial Blood Venous Blood
PO2 159.0 100.0 95.0 40.0
PCO2 0.2 40.0 40.0 46.0
PH2O (water vapor) 0.0 47.0 47.0 47.0
PN2 (and other gases in minute quantities) 600.8 573.0 573.0 573.0
Total 760.0 760.0 755.0 706.0
capillary blood (returned from the body) has a PaCO2 of 40 mm Hg and 100 mm Hg for carbon dioxide
of 46 mm Hg and PVO2 of 40 mm Hg (PVO2 is venous and oxygen, respectively (Figure 6-34). The pressure
oxygen). This mixed venous blood flows past alveoli gradients are 6 mm Hg for PCO2 (46 40) and
and, within 0.25 second, via diffusion achieves values 60 mm Hg for PO2 (100 40).1
PAO2 = 100 mm Hg
Alveolus
PACO2 = 40 mm Hg
O2
Nonoxygenated Reoxygenated
Blood Blood
PvO2 = 40 mm Hg PaO2 = 100 mm Hg

PvCO2 = 46 mm Hg PaCO2 = 40 mm Hg
CO2
O2 and CO2
Diffusion Blood Flow
Capillary
100
80
PO2 mm Hg
60
40
50
PCO2 mm Hg
45
40
0
0 0.25 0.50 0.75
Blood Enters Transit Time in Capillary Blood Exits

Capillary (Sec) Capillary
FIGURE 6-34 Alveolar-capillary gas exchange.

The average total time for blood to perfuse an from the body, and to carry substances such as hor-
alveolus is about 0.75 second, which leaves about a mones from one part of the body to another.
quarter of a second in reserve to meet increased gas
exchange needs, such as during exercise or stress.
With lung disease (fibrosis, pulmonary edema), the BLOOD
diffusion transit time may be lengthened, and gas Blood consists of 55% fluid (plasma) and 45% blood
equilibration may not be achieved (see Chapter 3). cells.8 Serum is plasma without the factors involved
Basically, three situations decrease diffusion across the with clotting. The blood contains specialized cells:
alveolar-capillary membrane: (1) decreased alveolar erythrocytes (red blood cells, RBCs), leukocytes (white
surface area, (2) decreased PIO2 or PAO2, and (3) blood cells, WBCs), and thrombocytes (platelets).
increased alveolar-capillary thickness. The administra- The erythrocytes (RBCs) contain hemoglobin, which
tion of increased amounts of inhaled oxygen can is a major carrier of oxygen and carbon dioxide. Red
improve diffusion of oxygen by increasing the PAO2. blood cells are made in the red bone marrow. The
comparison of RBCs to total blood volume is called
hematocrit, a viscosity measurement. Normal values are
PERFUSION-LIMITED OR DIFFUSION-LIMITED 45% for males and 42% for females.
OXYGEN Leukocytes (WBCs) function to protect the body
Perfusion-limited gas flow is the transfer of oxygen across from invaders, such as foreign bodies and bacteria,
the alveolar wall as a function of the amount of blood and include the polymorphonuclear granulocytes
flow (perfusion) past the alveoli. Once equilibrium is (neutrophils, eosinophils, basophils) and mononuclear
reached, diffusion stops and resumes only when new cells (monocytes, lymphocytes). The differential count is
perfusion occurs. Diffusion-limited gas flow is the the number of each type of WBC in 100 WBCs. Neutro-
movement of gas across the alveolar wall as a function phils and monocytes destroy bacteria; eosinophils
of the alveolar-capillary membrane integrity (diffusion become elevated in an allergic reaction; and lympho-
characteristics). Carbon monoxide (CO) is used to cytes produce antibodies that respond to antigens
evaluate the lung’s diffusing capacity (normal capacity (invaders).
is 25 mL/minute/mm Hg). As CO moves through the Platelets are cell fragments that cause blood clotting
alveolar-capillary membrane and enters the red blood at trauma sites, stimulate smooth muscle contraction,
cell, it rapidly attaches chemically to hemoglobin (210 and reduce blood flow (perfusion).
times faster than oxygen). Affinity is the natural
attraction and measure of binding strength for oxygen
and carbon monoxide to combine with hemoglobin. HEART
Once oxygen chemically combines with hemoglobin, The heart is a muscular pump with four hollow cham-
the combined oxyhemoglobin no longer exerts a bers, valves, circulation, and an electrical conductive
partial pressure. system (Figure 6-35). The two upper chambers, called
When oxygen diffuses across the alveolar wall and atria (right, left), are separated by a muscular interatrial
dissolves in blood plasma as PO2, it enters the red septum, or wall. The two lower chambers, or ventricles
blood cell, combining chemically with hemoglobin. (right, left), are separated by the interventricular septum.
Hemoglobin quickly becomes saturated, oxygen stops The right atrium and right ventricle act as a single
entering the red blood cell, and the plasma PO2 rises. pump for sending underoxgenated blood to the lungs
Under normal circumstances, the diffusion of oxygen (pulmonary circulation); the left atrium and left
is perfusion limited. When an individual has a ventricle work together circulating oxygenated blood to
decreased cardiac output or anemia (decreased hemo- the body (systemic circulation).
globin), the perfusion limitation may become signifi-
cant. Under certain abnormal conditions, however, Blood Flow Through the Heart. Venous blood (low
oxygen transfer may become diffusion limited (as in oxygen, high carbon dioxide) returning from the
pulmonary edema). body enters the right atrium from the superior vena
cava and inferior vena cava and passes through the
tricuspid (three-leaved) valve into the right ventricle
Cardiovascular System (Figure 6-35). The tricuspid is a one-way valve stabi-
The cardiovascular (circulatory) system consists of the lized by the chordae tendineae, which are attached to
blood, the heart (cardio), and the blood vessels the ventricle by the papillary muscles. This arrange-
(vascular system). Its primary functions are to carry ment prevents the valve from opening back into the
oxygen and nutrients to all body cells, to collect and atrium, thereby preventing regurgitation of blood back
remove metabolic waste products and carbon dioxide into the atrium. When the ventricles contract, the
Right pulmonary artery Aorta (to general

(carries deoxygenated blood) circulation)
Superior vena cava

Pulmonary trunk
To upper part of body
Left pulmonary
artery
Pulmonary veins
Pulmonary veins
(carries oxygenated
Pulmonary semilunar valve
blood)
Right atrium
Left atrium
Pericardium
Tricuspid valve Mitral (bicuspid) valve
Right ventricle Aortic semilunar valve
Endocardium
Left ventricle
Inferior vena cava Myocardium
Endocardium
Septum
FIGURE 6-35 Blood flow through the heart.
tricuspid valve closes, and blood is sent through the arteries cover the heart much as your fingers do when
pulmonary valve to the pulmonary artery and the lungs for gripping a baseball.
oxygenation.
The blood returns from the lungs via the pulmo- The Heart Conducting System. The cardiac muscle
nary veins and enters the left atrium before it goes has a special property, automaticity, or autorhyth-
through the mitral (bicuspid) valve to the left ventricle. micity, that enables it to initiate its own beat without
The mitral valve is stabilized the same way as the outside stimulation. The heart’s conducting system
tricuspid and prevents blood regurgitation back to the includes the sinoatrial (SA) node, atrioventricular
left atrium. When the left ventricle contracts, blood (AV) node, bundle of His, right and left bundle
passes through the aortic valve and enters the aorta, the branches, and Purkinje fibers (Figure 6-36). The SA
largest artery for distribution throughout the body. node (pacemaker) in the right upper part of the right
Both the pulmonary and aortic valves are one-way atrium sends an electrical impulse through the atrial
valves. muscles, resulting in simultaneous atrial contraction
The atria contract slightly to increase emptying. and blood flow to the ventricles. The AV node, located
However, when the ventricles contract (to eject blood) in the lower right atrium, receives the impulse and
and then relax, they create a pressure drop inside the sends it to the ventricles via the bundle of His. The
chamber that sucks most of the blood from the atria bundle of His then divides into the right and left
for efficient ventricular filling. The left ventricle’s wall is bundle branches, and they further divide into the
thicker than the right ventricle’s because it must pump Purkinje fibers, which stimulate the ventricles to
against a higher resistance (aorta, arteries) and through contract simultaneously. The autonomic nervous
the larger, whole body system. system also controls cardiac activity levels and con-
tractions to meet always-changing bodily require-
The Heart Blood Supply. The heart receives systemic ments. The cardiac centers of the medulla oblongata
blood directly from the aorta through the left and right control cardiac acceleration (sympathetic) and
coronary arteries. These arteries are the first two branches inhibition (parasympathetic) to meet varying needs.
off the aorta. The left coronary artery divides into the Depolarization and repolarization of cardiac muscle
circumflex and anterior descending branches. About can be recorded by chest electrodes. The resultant
5% of resting cardiac output passes through the measurement is called an electrocardiogram (see
coronary arteries to serve the heart. The coronary Chapter 19).
Superior vena cava
Sinoatrial node
(pacemaker)
Left atrium
Right atrium Atrioventricular bundle

(Bundle of His)
Atrioventricular
junction
Bundle branches Purkinje

fibers
Purkinje fibers
Interventricular septum
FIGURE 6-36 The conduction system of the heart.
PULMONARY AND SYSTEMIC VASCULAR SYSTEMS

The overall vascular system is divided into two subdivi-
sions: the pulmonary vascular system (pulmonary
artery to left atrium) and the systemic vascular system Normal Heart Rates
(aorta to right atrium). The normal heart rate is 60–100 beats per min-
Vascular structures become progressively smaller ute (bpm) for adults. It is affected by exercise,
from arteries to arterioles to capillaries, and then altitude, and disease states. The normal infant
increase in size from capillaries to venules to veins heart rate ranges from 100–190 bpm and aver-
(Figure 6-37). Arteries carry blood away from the heart, ages 140 bpm.
can handle high systemic pressures, and divide into
smaller arterioles that help regulate blood pressure.
Small arterioles divide into thin-walled capillaries that
allow gases, nutrients, and wastes to move through tracted state called vasomotor tone. Blood flow through
them. In the pulmonary capillaries, gases move arteries is also affected by arterial baroreceptors (pres-
between the air and the blood (external respiration); in sure receptors), by blood volume, and by the large veins
the systemic capillaries, gases move between the blood through changes in intrathoracic and abdominal
and tissues (internal respiration). Venules collect the pressures.
capillary blood and empty into veins. Veins carry blood
toward the heart. They can hold large amounts of The Baroreceptor Reflex. Baroreceptors, or pressorecep-
blood (about 60% of the body’s blood volume) at tors, located in the carotid arteries and aorta, contain
small pressure changes (Figure 6-38). nerve endings that sense the stretching of their walls.
They respond by reflex action to maintain the most
Neural Control of the Vascular System. The blood efficient and effective heart rate, force of cardiac
vessels—primarily the arteries, arterioles, and, to a lesser contraction, arterial and venous constriction, and
extent, the veins—continuously receive sympathetic arterial blood pressure. When they sense decreased
impulses from the vasomotor center in the medulla blood pressure, with a related decrease in stretch, the
oblongata. These impulses result in a moderate con- baroreceptors increase impulses to the medulla, which
Capillaries of lungs
Aorta
Pulmonary trunk
Superior vena cava
Right atrium
Left atrium
Right ventricle Left ventricle
Inferior vena cava
Capillaries of head, neck, upper extremities,

stomach, gastrointestinal tract, liver, pelvis,
and lower extremities
FIGURE 6-37 Vascular structures.
increases sympathetic impulses. The result is height- • Intravascular (intraluminal), the actual pressure
ened arterial blood pressure. The opposite occurs when inside the vessel.
an increased arterial blood pressure is sensed. • Transmural, the difference between intravascu-
lar pressure and the pressure external to that
BLOOD PRESSURES IN THE PULMONARY vessel.
AND SYSTEMIC VASCULAR SYSTEMS • Driving pressure, the difference in pressure at one
point in a vessel and the pressure at any other
Three pressures are used for studying blood flow
point downstream in the same vessel.
(perfusion):
Systemic Circulation
Arteries Arterioles Capillaries Venules Veins

120/80 80/30 30/10 10/5 5/0
mm Hg mm Hg mm Hg mm Hg mm Hg
Blood flow
120 Systolic
110
Systemic 100
Circulation 90
80
70 Diastolic
60
50
40 Systolic
30
Pulmonary 20
Circulation 10 Diastolic
5
0
Blood flow
Arteries Arterioles Capillaries Venules Veins
30/20 20/12 12/8 8/5 5/0
mm Hg mm Hg mm Hg mm Hg mm Hg
Pulmonary Circulation
FIGURE 6-38 Blood pressures in the circulatory system.
The Cardiac Cycle and Effect on Blood Pressure. A surge of blood runs through the vessels as dia-
When the ventricles contract (systole) and eject blood stolic goes to systolic and then back again. This surge
to the arteries, the blood pressure in the arteries rises creates a waveform that is measured and used for
to its highest level; this point is called the systolic monitoring a person’s cardiovascular status. In addition,
pressure. When the ventricles relax (diastole), the the surge of blood can be felt peripherally as the pulse, or
arterial blood pressure drops to its resting level; this heart, rate. See Figure 6-40 for sites to measure pulse rate.
point is called the diastolic pressure (Figure 6-38).
The systemic system is a high-pressure system, The Blood Volume and Effect on Blood Pressure.
serving the body with a 120 mm Hg systolic pressure The cardiac output (CO) is the amount of blood ejected
and an 80 mm Hg diastolic pressure (Figure 6-39). by each ventricle each minute. It is measured by
The pulmonary system is a low-pressure, large-volume, multiplying the heart rate (HR, beats per minute) by
short-distance system with a blood pressure of the stroke volume (SV, volume of blood ejected by
25 mm Hg systolic and 8 mm Hg diastolic. In general each ventricular contraction).
terms, the systemic system has a driving pressure about
CO HR SV
10 times higher than that of the pulmonary system.
The mean (average) pressures are 15 mm Hg in the The normal cardiac output is about 5040 mL/
pulmonary artery and 5 mm Hg in the left atrium; minute (pulse rate of 72 stroke volume of 70 mL).
together, they equal a driving pressure of 10 mm Hg Normally, cardiac output increases with an increase in
(15 5 10). For the systemic system, the mean either stroke volume or pulse rate, and it decreases with
aortic pressure is about 100 mm Hg and the mean a decrease in stroke volume or pulse rate. The adult
pressure in the right atrium is 2 mm Hg; together, they total blood volume is typically about 5 L, with 75% of
equal a driving pressure of 98 mm Hg (100 2 98). the blood in the systemic system, 15% in the heart, and
Upper body
Temporal •
Facial
•
•
10
30
Carotid
Arterial
Lung
Brachial
120/80 •
12
Venous mean 15 Radial
• • Femoral
5 10
Arterial
25/8
2
• Popliteal
8
120/0
Venous
25/0
Posterior
Right heart tibial
10 Left heart
Dorsalis pedis •
30 •
Lower body FIGURE 6-40 Major sites where an arterial pulse

can be measured.
FIGURE 6-39 Mean intraluminal blood pressures (mm Hg).
Gravity. Gravity pulls most of the blood to the lower

Best Practice half of the lungs. The lungs are about 30 cm high; the
pulmonary blood pressure must overcome this height
Clinical Use of Systemic Pulses to deliver blood to the lung apex. The effect of gravity
is lessened when the person is supine (lying on the
Systemic pulses are valuable for basic assess-
back) and the distance is shorter.
ments during therapy, during cardiopulmonary
See Figure 6-41 for a description of the three-zone
resuscitation, and for drawing arterial blood
model of lung perfusion, showing the effects of gravity
for sampling. The sites are also easy to locate
and alveolar pressures on the distribution of pulmo-
quickly. Practice finding the sites shown in
nary blood flow.
Figure 6-40.
Note:
• Zone 1 is nongravity dependent and has the least
10% in the pulmonary system. The pulmonary capil- blood flow.
lary bed contains about 75 mL of blood but has a • Zone 2 has progressively increased blood flow
capacity of up to 200 mL for use in exercise. moving down the lung toward zone 3.
• Zone 3 is gravity dependent and enjoys almost
universal blood flow throughout.
DISTRIBUTION OF PULMONARY BLOOD FLOW
Blood flow progressively decreases from the lung base Cardiac Output. Stroke volume is an important
(bottom) to the lung apex (top). The factors affecting component of cardiac output. Three factors determine
blood distribution are (1) gravity, (2) cardiac output, stoke volume: ventricular preload, myocardial contrac-
and (3) pulmonary vascular resistance. tility, and ventricular afterload.
Lung
PA>Pa>PV
Zone 1
+2 +2
+2
0 3 2 1
4
5
5
Pressure (cm H2O)
+2 +2 Pa>PA>PV
10 10 +2
Zone 2
Pulmonary
15 Artery 15 14 1 0 8 5 4 2
20 20
+2 +2 +2
25 25 Pa>PV>PA
Zone 3
30 25 20 15 10
30
Column
0 1 2 3 4 5
of Water
Blood Flow
(L/min)
Arteries Capillaries Veins
FIGURE 6-41 The three-zone model of lung perfusion. Pressures are expressed as cm H2O.
• Ventricular preload is the amount the ventricle See Chapter 19 for factors that affect preload, contrac-
is stretched with blood (diastole) before the next tility, and afterload.
contraction. In general, the more stretched the
myocardial muscle fibers are (i.e., the higher the Vascular Resistance. Vascular resistance is found by
preload), the higher the stroke volume and dividing the mean blood pressure by the cardiac
cardiac output will be. This relationship between output. In general, when vascular resistance increases,
ventricular stretching and cardiac output is blood pressure and afterload increase as a result. The
described by the Frank-Starling principle: opposite is also correct. Both active and passive mecha-
more in, more out. nisms affect vascular resistance. Active mechanisms are:
• Myocardial contractility is the force produced
by the myocardial muscle fibers as they shorten. • Decreased alveolar oxygen levels.
When contractility increases (called positive • Increased PCO2.
inotropism), cardiac output increases. When • Lowered pH (more acidic blood).
contractility decreases (called negative inotro- • Pharmacologic stimulation.
pism), cardiac output falls. • Pathologic conditions, such as pulmonary edema.
• Ventricular afterload is the force the ventricles Passive mechanisms are:
must produce to eject blood. It is affected by
blood volume and viscosity, peripheral vascular • Pulmonary arterial pressure changes.
resistance, and the total vascular cross-sectional • Left atrial pressure changes.
area being served (including the valve area). • Lung volume changes.
The arterial blood pressure is a very good • Alveolar pressure effects on vessel size
measure of ventricular afterload because blood (transmural pressure).
pressure equals cardiac output times vascular • Intrapleural pressure effects on large arteries
resistance. and veins.
Vascular resistance is also affected by blood volume plasma and is measured as PO2 (partial pressure of
changes (increased blood volume, vascular resistance oxygen). A PO2 of 1 mm Hg equals 0.003 mL of
decreases) and by blood viscosity changes (viscosity dissolved oxygen.4 For a normal person with a PO2
increases are reflected by higher-than-normal hemato- of 100 mm Hg, the dissolved volume of oxygen is
crit and vascular resistances). 0.3 mL per 100 mL of blood, or 0.3% volume
(100 0.003 0.3). This is a very small, but
important, amount of the total oxygen content.
Hemodynamic Measurements
Hemodynamic data can be obtained either directly or
indirectly. Table 6-7 lists hemodynamic values directly OXYGEN BOUND WITH HEMOGLOBIN
obtained by pulmonary artery catheter. Table 6-8 lists Most of the oxygen that enters the blood moves rapidly
computed hemodynamic values. (Refer to Chapters 12 through the plasma as dissolved oxygen and enters the
and 19.) RBCs, where it chemically binds to hemoglobin (Hb).
Hemoglobin is a specialized molecule made up of four
heme (iron) groups and four protein chains (amino
Oxygen Transport acids) that constitute the globin portion. At the center
Oxygen transport is important in the study of pulmo- of the heme group, oxygen combines in a reversible
nary physiology, especially for the interpretation of reaction with the iron molecule, forming oxyhemoglobin
arterial and mixed venous blood gas values. Oxygen is (O2Hb). Hemoglobin also transports carbon dioxide
carried in the blood in two ways: dissolved and chemi- gas by combining chemically; the resulting compound
cally bound to hemoglobin (Hb). is known as reduced hemoglobin (Rhb, Hbr, or HbR), or
deoxygenated hemoglobin.
The normal hemoglobin value for males is
OXYGEN DISSOLVED IN BLOOD PLASMA
15 g/100 mL blood; the normal value for females is
Oxygen that diffuses from the alveoli across the 14 g/dL blood. The average hemoglobin value for
alveolar-capillary membrane dissolves in the blood infants is 14–20 g/dL.
Hemoglobin makes up about 33% of the RBCs’
TABLE 6-7 Hemodynamic values directly total weight and carries the vast majority of oxygen.
measured (pulmonary artery catheter) One gram of hemoglobin can carry 1.34 mL of oxygen.
Therefore, the total oxygen that is chemically combined
Normal with hemoglobin is 20.1 mL O2/dL blood: 15 g Hb
Hemodynamic Value Abbreviation Range 1.34 mL oxygen 100% (full) saturation. Normally
Central venous pressure CVP 0–8 mm Hg about 3% of the hemoglobin is deoxygenated; so the
Right atrial pressure RAP 0–8 mm Hg true value is about 19.5 mL/dL (20.1 0.97 19.5).
Mean pulmonary artery PA 9–18 mm Hg
Pulmonary capillary PCWP 4–12 mm Hg TOTAL OXYGEN CONTENT
wedge pressure (also PAW Total oxygen content is calculated by adding the
called pulmonary artery
PAO values for dissolved and combined oxygen (0.3
wedge; pulmonary
19.5 19.8 mL O2/dL blood). Total oxygen content can
artery occlusion)
be calculated for arterial blood (CaO2), mixed venous
Cardiac output CO 4–8 Lpm blood (CvO2), and pulmonary capillary blood (CcO2).
TABLE 6-8 Computed hemodynamic values

Hemodynamic Value Abbreviation Normal Range
Stroke volume SV 60–130 mL
Stroke volume index SVI 30–65 mL/beat/m2
Cardiac index CI 2.5–4.2 L/min/m2
Right ventricular stroke work index RVSWI 7–12 g-m/m2
Left ventricular resistance LVSWI 40–60 g-m/m2
Pulmonary vascular resistance PVR 20–120 dynes s cm5
Systemic vascular resistance SVR 800–1500 dynes s cm5
slope flattens, showing a small 7% gain in hemoglobin

Spotlight O2 saturation. Increases above 100 mm Hg in PaO2
On offer little increase in SO2 because the hemoglobin is
almost fully saturated.
Oxygen Dissociation Curve
On the steep part of the oxygen dissociation
curve, small changes in PaO2 result in large FACTORS THAT SHIFT THE OXYGEN
changes in SaO2. The reverse is true on the flat DISSOCIATION CURVE
upper part of the curve. The oxygen dissociation curve shows a rapid loading of
oxygen at the lung and a rapid unloading of oxygen at
the cellular level. In the presence of elevated carbon
dioxide levels, hemoglobin tends to release oxygen; this
These calculations allow the objective study of pulmo- phenomenon is called the Bohr effect. Changes in
nary physiology and serve as a basis for patient care. hemoglobin’s affinity for binding oxygen—whether
induced by carbon dioxide, pH, or temperature
alterations—are rapid, resulting in enhanced oxygen
OXYGEN DISSOCIATION CURVE uptake at the lung and its release at the systemic tissues.
The oxygen dissociation curve (also called the oxyhemoglo- Consider that venous blood returning to the right
bin dissociation curve) is S-shaped, reflecting the nonlin- atrium has low oxygen and high carbon dioxide levels.
ear relationship between dissolved oxygen and oxygen At the alveolar-capillary (A-C) surface, carbon dioxide
chemically bound to hemoglobin (% O2Hb or SO2). diffuses rapidly from the plasma into the alveoli. This
Figure 6-42 shows this relationship, with PaO2 on the drop in PCO2 causes hemoglobin to release carbon
horizontal and the SO2 on the vertical. In addition, the dioxide into the plasma and drives carbon dioxide
corresponding oxygen content is listed on the right side diffusion into the alveoli for equilibration. Also at the
of the figure. The part of the curve from a PaO2 of 10 to A-C level, oxygen diffuses from the alveoli into the
60 mm Hg is vertically steep, reflecting the rapid plasma and dissolves as PaO2. The hemoglobin can then
uptake of oxygen by hemoglobin at the lung. Note take up oxygen rapidly to replace the carbon dioxide
that, at a PaO2 of 60 mm Hg, the hemoglobin is about that has vacated the hemoglobin chemical-bonding
90% saturated. From a PaO2 of 60 to 100 mm Hg, the sites and raises the SO2. The differences in arterial and
Dissolved O2
100 (Total O2) 20
90 18
80 16
O2 Content mL/ 100 mL (vol%)
70 14
% Hb Saturation
60 12
O2 Combined with Hb
50 10
40 8
30 6
20 4
Dissolved O2
10 2
0 0
10 20 30 40 50 60 70 80 90 100
PO2 (mm Hg)
Normal PO2
FIGURE 6-42 The oxygen dissociation curve.

100 20
Left Shift
90 18
80 16
O2 Content mL/ 100 mL (vol%)

70 14
Right Shift
% Hb Saturation
60 12
P
50
50 10
40 8
30 6
20 4
10 2
0 0
10 20 30 40 50 60 70 80 90 100
PO2 (mm Hg)
27
FIGURE 6-43 Factors that shift the oxygen dissociation curve to the right
and left.
venous values are a reflection of tissue oxygen use and Where QT is total cardiac output, CaO2 is arterial
carbon dioxide production by the body. oxygen content, and the factor of 10 is needed to
Factors that affect the oxygen dissociation curve are convert from CaO2 to milliliters of oxygen per liter. The
pH, temperature, carbon dioxide, 2,3-diphosphoglycate difference between the arterial and venous oxygen
(2,3 DPG), fetal hemoglobin (HbF), and carbon contents (CA-VO2) is simply the arterial oxygen content
monoxide combined with Hb (carboxyhemoglobin, minus the venous oxygen content (vol%). Oxygen
COHb). These factors affect hemoglobin in two ways: consumption (oxygen uptake, VO2) is the amount
They either cause it to hold on to oxygen more tightly of oxygen extracted from the blood by the cells in
(shift the curve to the left) or release oxygen more 1 minute. It is calculated by the equation
V O2 Q
easily (shift the curve to the right). A left shift has a
higher %Hb saturation but oxygen available to unload T (CA-VO2 10)
at the cells because of increased affinity of the hemo- The oxygen concentration ratio is the arterial-venous
globin for oxygen. A right shift has a lower %Hb oxygen content difference divided by the arterial
saturation and decreased affinity for oxygen and oxygen content:
therefore less oxygen for release to the cells. Figure 6-43
C(a-v)O2
summarizes these factors and their effects. Clinically, O2 extraction _______
these must be considered in the interpretation of CaO2
arterial blood gas and acid-base values. Mixed venous oxygen saturation is the measurement
of blood from the pulmonary artery, sampled from
an indwelling catheter. In addition, the volume of
OXYGEN TRANSPORT STUDIES
pulmonary blood flow (Q) is calculated by:
Arterial, mixed venous, and capillary oxygen contents
are good indicators of cardiopulmonary function. The VO2
____________
Q
total oxygen content for delivery (DO2) can be calcu- CaO2 CvO2
lated by the equation
where cardiac output through the lungs equals the
DO Q (C O 10) volume of oxygen uptake per minute divided by the
2 T a 2
arterial-mixed venous oxygen content difference. The nisms. In a true shunt, also called absolute shunt, no gas
normal saturation of mixed venous blood is 75% with is exchanged, and the deoxygenated blood enters the
a PvO2 of 40 mm Hg. Refer to Chapters 12 and 19. left heart. Types of true shunt are anatomic and
capillary.
Pulmonary Shunting • Anatomic shunt occurs when blood passes from
the right side of the heart to the left without
and Venous Admixture entering the pulmonary vasculature. Normally,
Pulmonary shunting is the part of cardiac output this is about 2% to 5% of the blood; it is blood
that enters the left side of the heart without having that drains via the bronchial, pleural, and
exchanged gases with alveoli (Figure 6-44). True Thebesian veins, emptying into the pulmonary
shunting and shuntlike effect are two shunt mecha- venous system. Common pathologic causes of
Normal Alveolar-Capillary Unit Anatomic Shunt
Pulmonary Oxygenated
Capillary Blood
Ventilated Oxygenated Ventilated
Blood Alveolus
Alveolus
Pulmonary
Capillary Anatomic Non-Reoxygenated
Shunt Blood
Types of Capillary Shunts
Non-oxygenated
Pulmonary Consolidated
Blood
Capillary or
olu d
ve se
Fluid-Filled
s
Al llap
Alveolus
Co
Types of Shunt-Like Effects
Obstruction
Non-oxygenated
Alveolus Blood
Alveolus
with
Pulmonary with a
Decreased
Capillary Diffusion
Ventilation
Defect
FIGURE 6-44 Pulmonary shunting.

anatomic shunting are congenital heart disease, Tissue Hypoxia

intrapulmonary fistula, and vascular lung
tumors. Tissue hypoxia is a decreased amount of oxygen avail-
• Capillary shunting is blood passing through the able in the tissues. The four main types of hypoxia are
pulmonary capillaries without having exchanged hypoxic hypoxia, anemic hypoxia, circulatory hypoxia,
gases with alveoli. The causes are atelectasis and histotoxic hypoxia.
(alveolar collapse), liquid in the alveoli, and • Hypoxic hypoxia is also called hypoxemia because of
alveolar consolidation. the low oxygen concentration in the blood (low
The physiological shunt is the total of anatomic and PaO2). Hypoxemia results from (1) pulmonary
capillary shunts. These types of shunts do not respond shunting; (2) low alveolar PO2 (PAO2) due to
to (i.e., they are refractory to) oxygen therapy. hypoventilation, ascent to altitude, or breathing
Shuntlike effect occurs when pulmonary perfusion gases lower than 21% oxygen; (3) diffusion
is more than alveolar ventilation. The causes are impairment due to fibrosis or alveolar edema; and
(4) ventilation/perfusion mismatches (V /Q ratio).
hypoventilation, uneven distribution of ventilation,
and alveolar-capillary diffusion defects. Shuntlike effect • Anemic hypoxia is a low oxygen-carrying capacity
responds positively to oxygen therapy. due to either a low hemoglobin amount
Venous admixture (Figure 6-45) results when or abnormal hemoglobin, such as carbon
shunted deoxygenated blood mixes with freshly monoxide poisoning. The PO2 may be normal in
oxygenated blood distal to alveoli. This blood with this form of hypoxia.
differing oxygen levels mixes and equilibrates down- • Circulatory hypoxia is characterized by a decreased
stream, and it is measured via an arterial blood amount of blood reaching the tissues, with the
sample. amount of oxygen available being inadequate for
The amount of intrapulmonary shunting is calcu- cellular needs.
lated by the classic shunt equation: • Histotoxic hypoxia occurs when the cells cannot use
oxygen; the classic cause is cyanide poisoning.

CcO2 CaO2
Qs ____________
___
CcO2 CvO2
Qt Cyanosis and Polycythemia
where QS is the cardiac output that is shunt, QT is the Cyanosis is an observed discoloration, or blueness, of
total cardiac output, and CcO2, CaO2, and CvO2 are the the lips, nailbeds, and mucus membranes. This is a
oxygen contents of capillary, arterial, and mixed venous variable sign and only a gross indicator of hypoxemia.
blood, respectively. The amount of pulmonary shunt- Therefore, arterial blood gases should be used for a
ing is significant for patient care planning. definitive diagnosis of low oxygen levels.
Venous Blood Airways

Pv–O mm Hg
2
In Equilibrium
Pv–O mm Hg
2
Ventilated
Consolidated
Alveolus
Alveolus
PAO = 100 mm Hg
2 PA O = 40 mm Hg
2
Shunted
Venous Blood
PO = 100 mm Hg
2 PO = 40 mm Hg
2
Venous Admixture
(PO reduced to about 85 mm Hg)
2
FIGURE 6-45 Venous admixture.

Polycythemia is an increased amount of circulating In the red blood cells, carbon dioxide is trans-
red blood cells (RBCs) (see Chapters 15 and 19). ported as:
Secondary polycythemia occurs when the kidneys
• Dissolved CO2 (about 5% of total).
release erythropoietin owing to chronic hypoxemia,
• Carbamino-Hb, combined with hemoglobin,
which stimulates an increase in RBC production.
which enhances oxygen release to the tissues
The resultant increase in hemoglobin and hematocrit
(21% of total).
(increased blood thickness) also increases oxygen-
• Bicarbonate (approximately 63% of total).
carrying ability. However, this increased hematocrit
produces cor pulmonale, which is an increase in right The vast majority of carbon dioxide that enters the
ventricular size secondary to pulmonary disease. RBCs is converted to bicarbonate via hydrolysis. The
reaction is speeded up by carbonic anhydrase (CA), an
enzyme in the RBCs. Because of this rapid production,
Carbon Dioxide HCO3 diffuses from the RBCs into the plasma and, to
Carbon dioxide must be transported from the tissues to maintain intracellular electrical neutrality, is replaced
the lungs for elimination. by chloride (Cl). This process is called the chloride
shift, or Hamburger phenomenon.
CARBON DIOXIDE TRANSPORT
Carbon dioxide (CO2) study is important for evaluat- CARBON DIOXIDE ELIMINATION AT THE LUNGS
ing pulmonary physiology and acid-base balance When mixed venous blood enters the pulmonary
and for interpreting arterial blood gas analyses. At rest, capillaries, carbon dioxide is released to diffuse into
an adult produces 200 mL of carbon dioxide per the alveoli until equilibration is reached. This is the
minute and takes up 250 mL of oxygen per minute. reverse of activities at the tissue level, where carbon
The carbon dioxide is carried from the tissues, where it dioxide diffuses into the plasma.
is a waste product of metabolism, to the lungs by six
methods: three in the plasma and three in the RBCs CARBON DIOXIDE DISSOCIATION CURVE
(Table 6-9).
The carbon dioxide dissociation curve is linear, unlike
In plasma, carbon dioxide is transported as:
the oxygen dissociation curve. For any PCO2, there is a
• Carbamino compound, bound to protein (about direct relationship between dissolved carbon dioxide
1% of total). and the total CO2 in the blood. The effect of changes in
• Bicarbonate (HCO3), through slow but reversible oxyhemoglobin saturation on the relationship of
hydrolysis (about 5% of total). carbon dioxide content to PCO2 is called the Haldane
• Dissolved CO2, measured as PCO2 in arterial effect. In the tissues, the unloading of oxygen from
blood gas (about 5% of total). hemoglobin enhances its ability to take up carbon
dioxide. The reverse occurs at the lung, where oxygen
uptake enhances carbon dioxide unloading.
TABLE 6-9 Carbon dioxide transport
mechanisms
Approximate
Acid–Base Balance
Approximate Quantity of Terminology is important in the study of acid-base
Percentage Total CO2 balance. Electrolytes are charged ions that conduct
Carbon Dioxide of Total CO2 Transported a current in solution. Buffers are substances that
Transport Transported to Lungs
Mechanism to Lungs (mL/min)
In plasma:
Spotlight
Carbamino compound 1 2
On
Bicarbonate 5 10 Conversion of CO2 Pressure to
Dissolved CO2 5 10 Millequivalents per Liter
In red blood cells: The PCO2 is a pressure measurement that can be
Dissolved CO2 5 10 converted to millequivalents per liter by multiply-
Carbamino-Hb 21 42 ing PCO2 by 0.03. The normal value calculation
for acid-base balance is:4
Bicarbonate 63 126
PCO2 40 mmHg 0.03 1.2 mEq/L H2CO3
Total 100 200
neutralize acids and bases, preventing wide swings in TABLE 6-10 Normal blood gas value ranges
pH. Acids dissociate (divide out) into hydrogen ions
(H) in a solution. Bases react with water to form Blood
hydroxide ions (OH) in a solution. A dissociation Gas
constant is the equilibration between the molecular Value Arterial Venous
form and its ions, represented by the letter k in calcula- pH 7.35–7.45 7.30–7.40
tions of pH (see Chapter 4). PCO2 35–45 mm Hg (PaCO2) 42–48 mm Hg (PvCO2)
HCO3 22–28 mEq/L 24–30 mEq/L
THE pH SCALE AND BUFFER SYSTEMS PO2 80–100 mm Hg (PaO2) 35–45 mm Hg (PvO2)
The pH is defined as the negative logarithm (base 10)
of the hydrogen ion concentration. A pH of 7.0 is
neutral. The normal range for human arterial blood is Thus, the normal pH of 7.4 results from the 20:1
7.35–7.45. When there is an increase in acid, the pH bicarbonate/PCO2 ratio. See Table 6-10 for normal
number decreases (7.40). Acids donate H to solu- acid-base values.
tion, causing an increase in acidity and a drop in pH.
When base increases, less acid is available, and the pH RESPIRATORY ACID-BASE IMBALANCES
rises ( 7.45). Bases accept H and raise the pH value.
Respiratory changes brought on by acid-base imbal-
The pH is maintained by means of the balance between
ances are reflected in arterial blood gas sampling. For
buffer systems and the respiratory system’s ability to
example, if ventilation slows or stops, PCO2 rises in
eliminate carbon dioxide.
the plasma, increasing H levels and lowering the pH.
The Henderson-Hasselbalch (H-H) equation uses
This condition is called respiratory acidemia (increased
the bicarbonate–carbon dioxide relationship to arrive
acid due to respiratory causes). If ventilation
at the pH value:
increases, a rapid decrease in PCO2 causes a respiratory
HCO alkalemia (increased base). Respiratory system
pH pk log ______3
CO2 changes can bring on rapid changes in pH values
Where pk is the dissociation constant of the acid (see Chapters 4 and 15).
portion of the buffer combination.
Normally, the pk is 6.1. With an HCO3 value of METABOLIC ACID-BASE IMBALANCES
24 mEq/L and a PCO2 of 1.2 mEq/L (PCO2 of Disturbances due to metabolic conditions can lead to
40 mm Hg 0.03), the equation yields a pH value of 7.4: metabolic acidemia. Examples are:
24 mEq/L
pH 6.1 log __________ • Lactic acidemia, resulting from inadequate tissue
1.2 mEq/L oxygenation, anaerobic metabolism, and the
6.1 log 20:1 production of lactic acid that accumulates in the
plasma.
6.1 1.3
• Ketoacidemia in the diabetic patient, caused by
pH 7.4 low insulin levels.
• Renal failure, in which H accumulate in the
plasma.
Spotlight
On Metabolic alkalemia is caused by the elevation of other
bases in the plasma. The causes are:
Bicarbonate: Carbon Dioxide • Hypokalemia [decreased potassium (K)]
Ratio for pH resulting in the kidney’s excreting increased
amounts of H.
In the plasma, the ratio of HCO3 to P CO2,
• Gastric suction, rapidly removing acidic stomach
in millequivalents per liter, is 24:1.2. This is
contents.
reduced to a 20:1 ratio, with bicarbonate
• Excessive administration of bicarbonate during
20 times greater than carbonic acid (CO2). This
cardiopulmonary resuscitation.
20:1 ratio is a balance point for maintaining a
normal pH (7.35–7.45). When the ratio is The body will compensate for disorders by attempt-
greater than 20:1, the blood is more alkaline ing to bring acid-base imbalances back into balance.
(less acidic); when the ratio is less than 20:1, The buffer system controlled by the kidneys compen-
the blood is more acidic. sates for respiratory disorders. The respiratory system
compensates for metabolic disorders (Table 6-11). In
TABLE 6-11 Acid-base conditions and compensations

pH P CO2 HCO3– Compensation*
Normal 7.40 40 24 Unchanged
Respiratory acidemia Decreased Increased Unchanged Primarily kidneys
Respiratory alkalemia Increased Decreased Unchanged Primarily kidneys
Metabolic acidemia Decreased Unchanged Decreased Respiratory system
Metabolic alkalemia Increased Unchanged Increased Respiratory system†
*Compensation is always less than complete, with the pH moving toward normal without reaching a normal value.
†Respiratory compensation for metabolic alkalemia entails slowing breathing to increase PCO levels. This mechanism is very limited because the respiratory
2
control centers increase breathing to overcome this action.
addition, often mixed disturbances require in-depth • In tubular secretion, the opposite of tubular
analysis. See Chapter 15 for a detailed discussion. reabsorption, hydrogen ions and potassium
enter the urine. Secretion regulates the blood
BASE EXCESS OR DEFICIT levels of these substances, as well as the amount
and composition of urine. The total normal
The base excess or deficit is reported in millequivalents volume of urine excreted daily is about 1500 mL
per liter of base above or below the normal buffer base per day.9 This volume is reduced in hypotension
level. Use of a nomogram or software application (low blood pressure).
reveals the amount of base excess or deficit and may
lead to corrective treatment (see Chapter 15).
URINE CONCENTRATION AND VOLUME
The concentration and volume of urine are controlled
The Renal System and Its Effects to produce either a concentrated or a diluted urine.
on the Cardiopulmonary System The countercurrent mechanism controls water reab-
The kidneys are an important component of the body’s sorption in the distal tubules and collecting ducts.
acid-base regulatory system. Selective permeability of the collecting ducts is regu-
lated by antidiuretic hormone (ADH). When blood
volume and pressure increase, ADH production is
THE KIDNEYS inhibited, increasing urine volume and decreasing the
The kidneys are located against the posterior wall in the concentration (dilute). When dehydration occurs,
abdominal cavity. The blood composition is determined ADH production is stimulated and fluids are retained,
by the kidneys, through filtration and reabsorption of urine volume decreases, and urine concentration
substances necessary to maintain normal body fluids. increases. Normal blood volume is maintained at
The nephron is the functional unit of the kidneys, with about 5 L.
perfusion through blood vessels including arteries,
capillaries, and veins.
REGULATION OF ELECTROLYTE
CONCENTRATION
URINE FORMATION
Important ions regulated by the kidney are sodium,
Urine is formed by glomerular filtration, tubular potassium, calcium, magnesium, and phosphate.
reabsorption, and tubular secretion. Sodium produces the majority of osmotic pressure and
regulates the amount of water in the body. Potassium is
• Glomerular filtration occurs because of hydrostatic essential for normal nerve and muscle function.
pressure, which forces water and electrolytes out Aldosterone stimulates potassium transport into the
of the glomerular capillaries. Osmosis opposes urine. The other electrolytes are regulated to maintain
hydrostatic pressure and attracts water into the normal body function. The kidney also plays a major
blood vessel. role in acid-base balance, primarily by regulating
• Although tubular reabsorption occurs throughout hydrogen ions through excretion and by the reabsorp-
all of the renal tubules, most of it occurs in the tion of bicarbonate.
proximal convoluted tubule. Leaving the tubule
are water, sodium, and glucose, with about 99%
of glucose and amino acids reabsorbed. Approxi- RENAL FAILURE
mately 50% of urea is reabsorbed, according to Renal failure is a life-threatening condition caused by
the body’s needs. congenital disorders, infections, obstructive disorders,
V
Spotlight Q
Ratio ~ 4:5 = 0.8
On
Mechanical Ventilation as a
Cause of Renal Failure Alveolus
The use of positive pressure ventilation (pressure
above atmospheric) is a life-supportive therapy, Alveolar
but the higher pressures stimulate ADH produc- Ventilation ~ 4 L/min
tion. The results are decreased urine formation (V)
and decreased urine elimination.
inflammation and immune responses, and neoplasms

(new growths). Monitoring intake and output of fluids
is a basic method to monitor renal function. Perfusion ~ 5 L/min
(Q)
CARDIOPULMONARY PROBLEMS DUE

TO RENAL FAILURE Pulmonary
Capillary
Renal failure affects acid-base balance and the cardio-
FIGURE 6-46 The ventilation/perfusion ratio.
pulmonary system. It can result in:
• Hypertension (increased blood pressure) and
edema formation.
• Metabolic acidosis due to retention of hydrogen
ions and potassium ions.
• Electrolyte imbalances.
Increase
• Anemia (decreased hemoglobin) due to reduced
V/Q Ratio
erythropoietin production. (0.8)
• Bleeding and cardiovasculature disorders.
Decrease
Ventilation/Perfusion
Relationships
The interaction and effectiveness of the heart and lungs
can be examined by determining the ventilation/
perfusion ratio.
VENTILATION/PERFUSION RATIO V/Q

The matching of alveolar ventilation and pulmonary Bl
L/ min Increases
oo
capillary perfusion is vital for life. Normally, alveolar dF
low
ventilation is about 4 L/min, and pulmonary capillary
blood flow (perfusion) is about 5 Lpm (Figure 6-46).
Ventila Ventila
The result is a ventilation/perfusion ratio of 4:5, or 0.8. ti on tion
Actually, this overall V /Q
reflects the sum of numerous Bl
oo
V/Q
dF
regional V/Q ratios.5 For example, the alveoli in the low
lung apex receive moderate ventilation but little

perfusion; they have a V /Q ratio greater than 0.8. The
opposite is true for the lung bases, where ventilation is V/Q Ratio Increases
increased but perfusion is greatly decreased. The result Lung Lung
at the bases is a V /Q
of less than 0.8. The V /Q
ratio Base Apex
progressively decreases from the apex to the base of the FIGURE 6-47 The ventilation/perfusion ratio in the upright
upright lung (Figure 6-47). lung.
The respiratory exchange ratio (REQ) measures

Spotlight external pulmonary gas exchange between the alveoli
On and the atmosphere per minute. The normal value is
also 0.8.
Ventilation/Perfusion
Considerations EFFECTS OF RESPIRATORY DISORDERS
The following relationships are for the normal, ON THE VENTILATION/PERFUSION RATIO
Increased V /Q
upright person: ratios result from disorders characterized
• There is more ventilation in the lung bases by ventilation that is greater than perfusion (increased
than in the apexes. PAO2s, decreased PACO2s). This condition is called
• There is more perfusion in the bases than in deadspace, or wasted, ventilation. Disorders that cause
the apexes. increased deadspace are pulmonary emboli, obstruc-
• There is more ventilation than perfusion in the tions of the pulmonary artery, increased pressure on
apexes. the pulmonary blood vessels (pneumothorax, tumors),
• There is more perfusion than ventilation in the decreased cardiac output, and destruction of pulmo-
bases. nary vessels (emphysema).
Decreased V /Q
ratios reflect perfusion in excess of
ventilation and an increased shunting of blood. These
ratios result from obstructive lung diseases (asthma,
bronchitis, emphysema), restrictive lung diseases
EFFECTS OF THE VENTILATION/PERFUSION (fibrosis, pneumonia, neuromuscular), and alveolar
RATIO ON ALVEOLAR GASES hypoventilation.
Changing V /Q ratios also alter alveolar gas composition
for both PAO2 and PACO2 and for arterial values as well.
For PAO2, the value is determined by the amount of Control of Ventilation
oxygen entering the alveoli and the oxygen removal by Breathing is controlled automatically by neurons in the
capillary perfusion. For PACO2, the value depends on medulla oblongata and the pons of the brain and
the amount of carbon dioxide entering the alveoli and voluntarily, from the cerebral cortex, which allows
on the amount removed by ventilation. Increased V /Q
specialized functions such as talking, coughing, and
ratios reflect ventilation greater than perfusion. This sniffing. Respiration is rhythmic and coordinated to
leads to higher PAO2s and lower PACO2s. Decreased V /Q
meet changing ventilatory needs and to satisfy varying
ratios reflect perfusion greater than ventilation, with metabolic demands, ranging from sleep to extreme
lower PAO2s and higher PACO2s. Note that the alveolar exercise.
air equation can calculate an estimate for use clinically.
RESPIRATORY COMPONENTS OF THE
EFFECTS OF THE VENTILATION/PERFUSION MEDULLA OBLONGATA
RATIO ON END-CAPILLARY GASES Two groups of respiratory neurons in the medulla
As the V /Q
ratio progressively decreases from the apex
oblongata are believed to coordinate the intrinsic
to the base, the capillary values decrease for oxygen and rhythmicity of breathing. The dorsal (back, posterior)
increase for carbon dioxide, paralleling the changes in respiratory group and the ventral (belly, anterior)
PAO2 and PACO2. The pulmonary veins contain blood respiratory group.
that has been mixed from all pulmonary regions.
RESPIRATORY QUOTIENT/RESPIRATORY Spotlight

EXCHANGE RATIO On
The respiratory quotient (RQ) reflects internal tissue gas Sighing and Coughing
exchange (internal respiration). At rest, the tissues use
about 250 mL of oxygen and produce about 200 mL of An effective and inexpensive method to help
carbon dioxide as waste. The RQ is calculated by: patients’ breathing is to have them take a deep
breath and cough. This action stretches the lungs
200 mL CO2/min and helps eliminate excess mucus. The deep
RQ ________________ breath is similar to a normal, periodic sigh,
250 mL O2/min
which also stimulates surfactant production.
The normal RQ 0.8.
Dorsal Respiratory Group. The dorsal respiratory group Normally, the apneustic center receives suppressing
(DRG) contains primarily inspiratory neurons that are signals that allow expiration.
responsible for the basic rhythm of ventilation. The
• These signals are from the pneumotaxic center and
DRG receives input from the body, evaluates and
the Hering-Breuer inflation reflex. The pneumo-
prioritizes the signals, and responds via impulses
taxic center is in the upper third of the pons
(1–2 seconds each in duration) that stimulate the
and functions to interrupt the apneustic center,
inspiratory respiratory muscles (diaphragm). During
promoting rhythmic breathing patterns. These
expiration, the lungs recoil naturally and without
impulses also stimulate shallower, more rapid
DRG input.
breaths.
Ventral Respiratory Group. The ventral respiratory group The medullary respiratory centers can be depressed
(VRG) has both inspiratory and expiratory neurons, by conditions such as decreased blood flow due to
and, in quiet breathing, they are both inactive. During increased pressure, acute poliomyelitis, and drugs that
heavy exercise or stress, however, the expiratory neurons depress the central nervous system (CNS).
stimulate the expiratory muscles (abdominal) to
become active. The inspiratory neurons also send
impulses that stimulate the accessory muscles of MONITORING SYSTEMS THAT INFLUENCE
inspiration (sternocleidomastoids). THE MEDULLA OBLONGATA
The DRG and VRG of the medulla oblongata receive
monitoring system input from the body, primarily
PONTINE RESPIRATORY CENTERS from central chemoreceptors and peripheral
The pontine respiratory centers contain the apneustic chemoreceptors.
and pneumotaxic centers, whose basic functions seem The central chemoreceptors, located bilaterally and
to modify the rhythmicity of breathing (Figure 6-48). ventrally, monitor the H concentration in the cerebral
The apneustic center, in the middle to lower pons, spinal fluid (CSF). Hydrogen ions are the strongest
sends signals continuously to promote a prolonged, stimulus to both the DRG and VRG neurons. The
unrestrained inspiration called apneustic breathing. central chemoreceptors regulate breathing via the
Cerebrum
PNC
Pons
APC
DRG
CC CC
Medulla oblongata
VRG
FIGURE 6-48 The respiratory centers in the brain stem: PNC, pneumotoxic center;
APC, apneustic center; DRG, dorsal respiratory group; CC, central chemoreceptors;
VRG, ventral respiratory group
indirect effects of carbon dioxide on the CSF pH level. send inhibitory impulses to the medulla oblongata to
The basic mechanism is: stop inspiration.
1. CO2 diffuses from the arterial blood through the • The deflation reflex becomes activated when the
semipermeable blood-brain barrier into the CSF. lungs are deflated.
2. CO2 combines with water to form carbonic • The irritant reflex, when stimulated by noxious
acid, which dissociates into hydrogen ion and gases, produces an increase in breathing rate,
bicarbonate. cough, and bronchoconstriction (spasm).
3. Because the CSF has minimal buffering (low • Juxtapulmonary-capillary receptors (J-receptors)
HCO3, low protein levels), the pH rapidly in the alveolar-capillary interstitium, when
decreases in the CSF. stimulated, cause a rapid-shallow breathing
4. The elevated H stimulates the central chemore- response.
ceptors, which send signals to increase alveolar • The dive reflex follows sudden immersion in
ventilation. cold water, resulting in apnea.
5. The increased ventilation reduces the arterial • Sudden pain results in apnea followed by
CO2, reversing the stimulation process. tachypnea.
• Irritation to or pressure applied to the pharynx or
The result is decreased alveolar ventilation. The blood- larynx causes a brief apnea followed by coughing.
brain barrier is basically impermeable to H and
HCO3 ions.
The peripheral chemoreceptors are specialized oxygen- Cardiopulmonary Physiology
sensitive cells in the carotid arteries (carotid bodies) of the Fetus and the Newborn
and in the aortic arch (aortic bodies). The carotid
bodies are in close contact with arterial blood and play Adult anatomy and physiology differ markedly from
a greater role in ventilation than do the aortic bodies. those of the fetus and newborn. The development of
When a low PaO2 is sensed, afferent signals are sent via the lungs is commonly divided into four periods
the ninth cranial nerve (glossopharyngeal) from the (see Chapter 29): the embryonic period, the pseudo-
carotid bodies and via the tenth cranial nerve (vagus) glandular period, the canalicular period, and the
from the aortic bodies. Efferent signals are sent to terminal sac. Sometimes a fifth period, the alveolar
increase ventilation and elevate oxygen levels. The period, is considered to last from the 36th week of
peripheral chemoreceptors become active at a PaO2 of gestation onward.10
approximately 60 mm Hg and then fully stimulated The placenta is the life support system from
with further drops in oxygen. However, they are the mother to the fetus. It appears at the point of
suppressed at PaO2s below 30 mm Hg. fertilization and transfers oxygen and nutrients from
In certain disease states (e.g., emphysema), the the mother to the fetus and eliminates wastes from
peripheral chemoreceptor drive to breathe may play fetal circulation. The placental segments, called cotyle-
a major role in ventilation. Patients with chronically dons, provide the interface between maternal and fetal
high carbon dioxide levels may have their normal circulation. Deoxygenated blood is carried from the
drive to breathe suppressed and have to rely on their fetus to the placenta by two umbilical arteries, both
peripheral drive mechanism. Careful administration wrapped around the umbilical vein. Oxygen transfers
and monitoring of oxygen therapy are encouraged to from maternal to fetal blood because of the pressure
avoid oxygen-induced hypoventilation. The periph- gradient, the higher hemoglobin concentration in fetal
eral chemoreceptors are stimulated by decreased blood, and the greater affinity of fetal hemoglobin for
blood pH, hypoperfusion, increased temperature, oxygen. Carbon dioxide and wastes move from fetal to
nicotine (from smoking), and the direct influence maternal blood at this time.
of carbon dioxide. Peripheral chemoreceptors There are great differences between maternal and
stimulate peripheral vasoconstriction, increased fetal blood values owing to maternal shunts and
pulmonary vascular resistance, systemic arterial placental metabolism. Normal values for fetal blood
hypertension, tachycardia, and increased left are PO2 20 mm Hg and PCO2 55 mm Hg, whereas for
ventricular performance. maternal blood they are PO2 80–100 mm Hg and
PCO2 33 mm Hg.
REFLEXES THAT INFLUENCE VENTILATION

FETAL CIRCULATION, FETAL LUNG FLUIDS,
Refl exes also affect ventilation. AND ALVEOLI AT BIRTH
The Hering-Breuer reflex is a protective mecha-
Fetal circulation is depicted in Figure 6-49.
nism that prevents excessive lung inflation. Stretch
receptors become excited when the bronchi and • The umbilical vein carries oxygenated blood and
bronchioles are stretched during inhalation and then nutrients from the placenta to the fetus.
Aortic Arch
Pulmonary Arch
Superior Vena Cava
Ductus
Ascending Aorta Arteriosus
Right Atrium Left Atrium
Foramen Ovale
Left Ventricle
Ductus Venosus
Liver
Right Ventricle
Aorta
Umbilical Vein
Umbilical Cord
Inferior Vena Cava

To Mother
Common Iliac Arteries

From Mother
Fetal Umbilicus
Umbilical Arteries Oxygenated Blood

from the Placenta
Deoxygenated Blood
Placenta
Mixture of Oxygenated/
Deoxygenated Blood
Internal Iliac
Arteries
External Iliac
Arteries
FIGURE 6-49 Fetal circulation.
• Half of this blood enters the liver, and the other • Most of the right atrial blood passes through
half flows through the ductus venosus into the the foramen ovale into the left atrium, where it
inferior vena cava (IVC), mixing with deoxygen- mixes with deoxygenated blood from the
ated blood from the lower extremities. pulmonary veins.
• The blood travels via the IVC into the right • The left atrial blood passes next into the
atrium and mixes with deoxygenated blood from left ventricle and is pumped to the heart and
the superior vena cava (SVC). brain.
• The balance of blood in the right atrium flows

into the right ventricle and is pumped into the Age-Specific Competency
pulmonary artery.
• About 85% of this blood bypasses the lungs and The First Breath
goes directly through the ductus arteriosis into The first air breath requires the infant to
the aorta. The balance (15%) passes through the generate negative intrapleural pressures of from
lungs and returns to the left atrium via the 40–80 cm H2O. These large pressures are
pulmonary veins. The resultant PaO2 in the needed to overcome lung resistance, primarily
descending aorta is about 20 mm Hg. due to viscous fluid in the lungs. This is similar
• Downstream, the blood passes into the internal to the effort needed to inflate an empty balloon.
illiac arteries and returns to the placenta. On the first and subsequent breaths, the residual
After birth, the structures of fetal circulation become volume and functional residual capacity are
unnecessary and change to prepare for postuterine life. established. The average values for newborn
At birth, the lungs are partially filled with liquid, lung compliance and airway resistance are
roughly equal to the residual volume, produced by 0.005 L/cm H2O and 30 cm H2O, respectively.
the alveolar cells during development. This fluid is
removed from the lungs in the first 24 hours by three
mechanisms:
the ductus arteriosus to constrict. Failure of alveolar
• Squeezing of the chest during birth. expansion and increased oxygen levels keeps the ductus
• Absorption by pulmonary capillaries. open,11 contributing to the production of persistent
• Absorption by the lymphatic system. pulmonary hypertension of the newborn (PPHN).
There are approximately 24 million alveoli at The major cause of PPHN is continuing pulmonary
birth, increasing to more than 10 times that number in hypertension.
the normal adult. Alveoli continue to increase in
number until 12 years of age; therefore, respiratory CONTROL OF VENTILATION IN THE NEWBORN
problems in childhood can significantly affect adult
lungs. The central and peripheral chemoreceptors are
active in stimulating the first breath. The peripheral
chemoreceptors respond to hypoxemia by stimulat-
BIRTH AND THE FIRST BREATH ing a transient increase, followed by a decrease in
After birth, rapid changes take place: The placenta stops ventilation, which is stronger in the full-term
functioning, the lungs open and begin breathing air, newborn. The central chemoreceptors respond
and features of adult circulation begin. The first breath to elevated carbon dioxide levels similarly to the
marks the dramatic change from placental life support adult response.
with liquid-filled lungs to newborn air breathing.
Stimulation for taking the first breath is partly from INFANT REFLEXES
placental failure, with decreasing PO2s and increasing
PCO2s and pH, and from the sudden exposure to a Several reflexes assist the newborn’s breathing.
noisy, bright, colder environment. In response to these • In the trigeminal reflex, the cooling of the face
stimuli, the newborn inhales. results in a decrease in heart and respiratory
rates.
• The irritant reflex causes slowing of respiration
CIRCULATORY CHANGES AT BIRTH in the preterm infant but hyperventilation in the
As the first breath is taken, pulmonary vascular resistance full-term infant.
(PVR) decreases dramatically for two reasons: the rapid • The head paradoxical reflex, which is a deep
increase in alveolar PO2, offsetting the fetal circula- inspiration (sigh), results in increased lung
tion’s hypoxic vasoconstriction, and the mechanical volume, improved lung compliance, and the
increase in size of the pulmonary vessels, reducing prevention of atelectasis.
resistance to perfusion. As the PVR drops, more blood
passes from the right atrium to the right ventricle and
more is returned to the left atrium. The volume and NORMAL NEWBORN CLINICAL VALUES
pressure in the left atrium increase, and the flap of the The normal values for lung volumes and capacities and
foramen ovale closes functionally. In addition, the fall vital signs of newborns are listed in Table 6-12. The
in right atrial pressure assists closure of the foramen normal values for newborns’ blood gas values are
ovale. In the next few minutes, the elevated PO2 causes shown in Figure 6-50.
7.40
Lung Prematurity
pH
Infants born before the 28th week of gestation 7.30
are at risk because of their immature lungs.

Surfactant production is necessary in large 7.20
enough amounts to maintain alveolar stability 60
(mm Hg)
PaCO2
for air breathing. Treatments for lung prematu- 50
rity include continuous positive airway pressure
40
(CPAP) and surfactant administration. Support-
30
ing the infant until the lungs grow and mature
24
(mEq/L)
has been successful.
HCO3
22
20
95
TABLE 6-12 Approximate lung volume and
85
capacity and vital sign values of the
(mm Hg)
PaO2
75
normal full-term newborn
65
Lung Volumes 55
Tidal volume (VT) 15 mL
1/2 1 2 3 4 24 48 72
Residual volume (VR) 40 mL Age in Hours
Expiratory reserve volume (VER) 40 mL
Inspiratory reserve volume (VIR) 60 mL
FIGURE 6-50 Average infant blood gas values during the first
Lung Capacities 72 hours after birth.
Vital capacity (VC) 115 mL
• Exercise tolerance is reduced, owing to decreased
Functional residual capacity (FRC) 80 mL
cardiac output.
Inspiratory capacity (IC) 75 mL • Diffusing capacity is decreased. Alveolar dead
Total lung capacity (TLC) 155 mL space is increased.
Vital Signs • Pressure differences between alveolar and arterial
oxygen become greater.
Respiratory rate (RR) 35–50 breaths/min
• Hemoglobin is decreased (anemia).
Heart rate (HR) 130–150 bpm • Ventilatory responses to carbon dioxide and
oxygen are decreased.
In addition, environmental factors (occupation,
Effects of Aging on the smoking, trauma) and chronic pulmonary disease
result in further decreases in function.
Cardiopulmonary System
Like changes associated with aging from newborn to INFLUENCE OF AGING ON THE
adult, other changes accompany aging during adult- CARDIOVASCULAR SYSTEM
hood and into senior years.
Normal aging results in the following changes in the
cardiovascular system.
INFLUENCE OF AGING ON THE
RESPIRATORY SYSTEM • Cardiac output decreases, primarily because of
decreased stroke volume.
Aging is a normal process, and with it comes numerous
• The maximal heart rate decreases.
normal changes.
• Fatty deposits and fibrosis form in the heart
• The chest wall becomes stiffer, and the respira- chambers.
tory rate slightly increases. • Fatty deposits (plaques) form on the arterial
• The residual volume rises slightly. The forced walls, leading to atherosclerosis and increased
vital capacity drops 21–25 mL per year after the blood pressure.
30th year. • Peripheral vascular resistance increases.
Effects of Exercise and of 3500 mL per minute for an untrained person and to
over 5000 mL per minute for the trained athlete.
High-Altitude and High- During exercise, PAO2 remains constant. The same
Pressure Environments on the is true for PACO2 and pH, until they increase during
heavy exercise. Oxygen diffusion capacity increases
Cardiopulmonary System linearly during exercise because of increased alveolar-
The cardiopulmonary system is challenged to respond capillary surface area and increased cardiac output. The
and adapt to various stressors. alveolar-arterial oxygen difference remains constant up
to about 40% of maximal levels, and then widens to a
EXERCISE value close to 33 mm Hg for distance runners.
During exercise, the cardiopulmonary system is stressed Circulation. The circulatory system and muscles are
to meet the body’s increased needs for oxygen delivery equally important for determining exercise limits.
and carbon dioxide elimination. When the cardiopul- Muscles are supplied with:
monary system is unable to provide enough oxygen for
the working muscles, the body changes from aerobic • Appropriate blood flow by increased sympathetic
(with oxygen) to anaerobic (without oxygen) metabo- impulses, which stimulate the heart to increase
lism. This point is called the anaerobic threshold. its rate and contractile strength and to dilate the
working muscles to increase perfusion.
Ventilation. Alveolar ventilation is increased in exercise • Increased cardiac output via heightened stroke
to maintain normal oxygen and carbon dioxide levels volume (Frank-Starling mechanism) and
in the body. The increased ventilation is probably a increased heart rate.
result of impulses sent from the cerebral cortex to the • Increased arterial blood pressure, with the
exercising muscles and the medulla oblongata, signals systolic pressure rising 20–80 mm Hg.
from proprioreceptors in the muscles and joints to the
The maximal heart rate is calculated as
respiratory centers of the medulla, and the increase in
body temperature. At rest, minute volume is about 6 L, 220 age (in years)
but it can increase to about 120 L during heavy exer-
This calculation is used for setting exercise and
cise.4 The increase in alveolar ventilation is due primar-
rehabilitation limits.
ily to an increased depth (tidal volume). Alveolar
As oxygen consumption and cardiac output
ventilation increases at the start of exercise, followed by
increase, the systolic and diastolic blood pressures also
a gradual increase and stabilization.
rise in the pulmonary vasculature. Oxygen uptake is
When exercise ends, alveolar ventilation drops
increased because of distension of the pulmonary
(Figure 6-51). Cardiac output, not alveolar ventilation,
capillaries and the recruitment and opening of closed
is the major factor limiting aerobic performance.
pulmonary vessels, allowing perfusion.
Oxygen consumption has a linear relationship with
alveolar ventilation. At rest, oxygen consumption is 250
Muscle Work, Oxygen Consumption, and Cardiac
mL per minute. During exercise, this value rises to about
Output Interrelationships. Increased muscle work
results in increased oxygen consumption, increased
perfusion in working muscles, greater venous return,
and heightened cardiac output. Maximal cardiac
outputs range from about 25 to 40 L/min.
The Training Influence. The trained athlete develops

Ventilation (L/ min)
an increased heart chamber size and increased pump-

Increasing
ing action. At rest, the cardiac outputs of athletes and

B nonathletes are similar, but the athlete achieves it by
having a higher stroke volume and lower heart rate.
After exercise, the time the body needs to rest before
A
continuing exercise is called the recovery period.
Rest Exercise Recovery Body Temperature–Cutaneous Blood Flow

Relationship. Heat is produced during exercise,
and the body temperature may rise above normal.
FIGURE 6-51 Relationship of exercise and ventilation: Sweating allows heat to dissipate, and as much as
(A) onset of exercise warm up. (B) end of exercise 5–10 lb of fluid may be lost. When liquid levels are
cool down. inadequate before exercise or are not replaced after
it, the body may experience heat stroke. This is a carbon dioxide is greater than capillary carbon dioxide.
serious condition; symptoms include copious sweating, At this point, carbon dioxide diffuses from alveoli into
followed by no sweating, cramps, weakness, dizziness, capillaries (the reverse directional movement of carbon
confusion, and circulatory collapse. Before exercising, dioxide). At the point during descent at which capillary
drink liquids (water), and then drink periodically oxygen is greater than alveolar oxygen, oxygen reverses
during exercise. After exercise, take some time to cool its movement, going from capillaries to alveoli.
down, stretch, and drink water to replace lost fluids. During a deep dive, gases in the blood move into the
tissues. When the diver ascends back toward the surface,
HIGH ALTITUDE the pressure around the body is reduced (decompres-
sion). When ascent is done slowly, gases gradually move
Atmospheric pressure decreases with ascent to altitude. At
back into the blood for transport. At a rapid rate of
18,000 feet, the PB is one-half of that at sea level (380
ascent, however, the gases are released as bubbles; the
mm Hg). When an individual from a low altitude spends
bubbles then become trapped in the tissues causing
time at a high altitude, the body develops compensa-
decompression sickness, or the bends. These bubbles become
tions, known collectively as acclimatization. Major
trapped in tissues producing the signs and symptoms of
cardiopulmonary acclimatization responses include:
the bends that include joint pain, chest pain, paralysis
• Increased alveolar ventilation via peripheral and circulatory failure that can result in death. Treatment
chemoreceptor stimulation. for this life-threatening disorder is hyperbaric medicine
• Secondary polycythemia, increased RBC produc- (see Chapter 20), which reduces bubble size and resolu-
tion due to low oxygen levels. tion and increases tissue oxygenation.
• Development of respiratory alkalemia, due to
the increased alveolar ventilation and carbon
dioxide elimination. Summary
• Increased oxygen diffusion capacity in native
The cardiopulmonary system brings atmospheric gas
high dwellers, due to increased lung size.
into the lungs, through successively smaller airways, to
• Increased alveolar-arterial oxygen difference.
the alveoli. In the alveoli, these gases are brought into
• Improved ventilation/perfusion ratio.
close contact with pulmonary capillary blood from the
• Increased cardiac output for nonacclimatized
pulmonary vascular system, and oxygen rapidly moves
individuals.
into the blood and carbon dioxide out of it.
• Increased pulmonary hypertension as a result of
Breathing and circulation are controlled efficiently,
hypoxic vasoconstriction.
balancing benefit and energy expenditure to meet
Other changes found at high altitude are poor the body’s always-changing needs. General science
sleep, increased myoglobin in skeletal muscles, acute principles clarify lung ventilation, gas diffusion, the
mountain sickness, high-altitude pulmonary edema, perfusion of blood, gas transportation, and cellular-
high-altitude cerebral edema, and chronic mountain delivery mechanisms.
sickness. Seeking medical advice before ascending to The fetus and newborn have different lung
high elevations is recommended. function and circulatory patterns than adults.
Aging, exercise, and high-altitude and high-pressure
HIGH-PRESSURE ENVIRONMENT environments all affect respiratory function.
Breathing in gases at higher-than-atmospheric pres-
sures affects the cardiopulmonary system. Scuba diving
is the most commonly experienced high-pressure
Study Questions
activity. Water is not compressible, and pressure REVIEW QUESTIONS
increases directly with depth. For every 33 feet of
descent below the water’s surface, an additional 1. What are the lung structures (airway generations)
atmosphere of pressure (760 cm H2O) is added. At a from the trachea to the gas exchange area?
depth of 33 feet, the total pressure exerted on the body 2. Name the tracheobronchial tree’s lining layer and
is 2 atmospheres; at 66 feet, 3 atmospheres; and so its functions.
forth. Subjected to these pressure increases, the lungs 3. Name the four characteristics that describe ventilation.
are compressed in size. The length of the dive is
4. What are the static and dynamic characteristics of
determined by the diver’s metabolic rate and gas
the lungs?
transport (oxygen and carbon dioxide). The feeling of
breathlessness (dyspnea) signals the need for ascent. 5. Trace one drop of blood as it flows through the
Interestingly, swallowing resets this feeling briefly. adult heart, starting in the right atrium.
The carbon dioxide–oxygen paradox occurs at 6. Name the components of the heart’s conducting
depth. As the diver goes deeper, at some point alveolar system.
7. Describe the lung-thorax relationship. 8. How do the central chemoreceptors regulate

8. Discuss the two ways that oxygen is carried in the breathing?
blood. a. by monitoring oxygen levels in the carotid arteries
b. by the indirect effects of carbon dioxide on the
9. Name the six ways carbon dioxide is carried in the
cerebral spinal fluid
blood.
c. directly from monitoring the medulla oblongata
10. Discuss exercise and at least three effects on breathing. d. via input from the aortic bodies
MULTIPLE-CHOICE QUESTIONS CRITICAL-THINKING QUESTIONS

1. What is the minute ventilation, in milliliters, for a 1. Using the four lung volumes and four lung capaci-
person with these values: respiratory rate (f) of 12, ties, list three different combinations that can
tidal volume of 600 mL, and dead space of 200 mL? describe vital capacity (VC).
a. 4800
2. A newborn infant with a PaO2 that remains below
b. 6000
normal will have what circulatory effects?
c. 7200
d. 9600 3. When a person who lives at sea level travels to a
mountainous area for a 2-week vacation, what
2. What is the average normal alveolar-capillary
changes occur?
surface area, in square meters, for gas exchange?
a. 50
b. 75
c. 100 References
d. 125 1. Murray JF. The Normal Lung. 2nd ed. Philadelphia:
3. Which blood cells contain hemoglobin? WB Saunders Co; 1986.
a. erythrocytes 2. Gorback MS. Chapter 29. In: Dantzker DR,
b. thrombocytes MacIntyre NR, Bakow ED. Comprehensive Respiratory
c. leukocytes Care. Philadelphia: WB Saunders Co; 1995.
d. platelets 3. Slonim NB, Hamilton LH. Respiratory Physiology.
4. What is the minute alveolar ventilation, in millili- 2nd ed. St. Louis: CV Mosby Co; 1971.
ters, for a person with these values: respiratory rate 4. West J. Respiratory Physiology: The Essentials. 8th ed.
(f) of 12, tidal volume of 600 mL, and dead space Baltimore: Lippincott Williams & Wilkins; 2008.
of 200 mL? 5. Levitzsky MG. Pulmonary Physiology. 7th ed. New
a. 4800 York: McGraw-Hill; 2007.
b. 6000 6. Oaks DF. Clinical Practitioners Pocket Guide to
c. 7200 Respiratory Care. 7th ed. Old Town, ME: Health
d. 9600 Educator Publications; 2008.
7. Ruppel GE. Manual of Pulmonary Function Testing.
5. The nephron is the functional unit of what organ?
9th ed. St. Louis: Mosby-Yearbook; 2008.
a. lung
8. Anthony C, Thibodeau G. Anthony’s Textbook of
b. heart
Anatomy and Physiology. 19th ed. St. Louis: CV
c. placenta
Mosby Co; 2009.
d. kidney
9. Mosby’s Medical, Nursing, and Allied Health Dictionary.
6. Which of these is/are part of a true shunt? 6th ed. St. Louis: Mosby-Yearbook; 2005.
I. physiological shunt 10. Volpe M. Control of morphologic development of
II. capillary shunt the lung. Neonatal Respir Dis. 1999;9:2.
III. anatomic shunt 11. Dantzker DR, MacIntyre NR, Bakow ED. Compre-
a. I only hensive Respiratory Care. Philadelphia: WB Saunders
b. II only Co; 1995.
c. I, II
d. I, II, III
7. What is the oxygen content (volume percentage) Suggested Reading
for these values: PaO2 90 mm Hg, Hb 14 g,
O2Sat 95%? Des Jardins T. Cardiopulmonary Anatomy and
a. 0.27 Physiology—Essentials for Respiratory Care. 5th ed.
b. 17.8 Clifton Park, NY: Delmar Cengage Learning; 2008.
c. 18.1
d. 19.0
CHAPTER 7
Cardiopulmonary Pharmacology
Kenneth A. Wyka
OBJECTIVES
• Differentiate between the three phases of pharmacology: pharmaceutical, pharmacokinetic, and pharmacodynamic.
• Differentiate between tolerance and tachyphylaxis.
• Define the terms “additive effect,” “cumulative effect,” and “synergy,” and explain the differences among
these actions.
• Describe the types of drugs commonly administered by aerosol route and their mechanism of action.
• Describe the indications for, contraindications for, side effects of, and adverse reactions of aerosol drugs.
• Identify brand names and dosages of aerosol drugs.
• Determine the dosage of drug to be administered by either weight or volume.
• Describe drugs used in the management of asthma and COPD.
• List indications for and dosages of drugs used in advanced cardiac life support.
• Determine appropriate therapeutic actions when given a patient case scenario.
CHAPTER OUTLINE Indications and Contraindications

for Bronchodilators
Principles of Pharmacology
Side Effects of and Adverse Reactions
Pharmaceutical Phase to Bronchodilators
Pharmacokinetic Phase Bronchodilator Dosage Guidelines
Pharmacodynamic Phase Bronchodilator Administration in Mechanically
Drug Actions and Interactions Ventilated Patients
Drug Calculations Anti-Asthmatic and Anti-Inflammatory Drugs
Concentration Calculations Indications and Contraindications for
Ratio Calculations Anti-inflammatory Drugs
Dilution Calculations Side Effects of and Adverse Reactions
to Corticosteroids
Bronchodilators
Mechanism of Action of Anti-Asthmatic Drugs
Sympathomimetic Bronchodilators
Indications for Anti-Asthmatic Drugs
Anticholinergic Bronchodilators
Asthma Relievers and Controllers
Xanthines
(continues)
171
(continued)
Drugs Used in the Management of COPD Surface Active Aerosols

Wetting Agents and Mucolytics Surfactant Replacement Therapy
Bland Aerosols Drying Agent (Ethyl Alcohol)
Mechanism of Action of Mucolytics Assessing the Effectiveness of Aerosol
Indications and Contraindications Medications
for Mucolytics Conscious Sedation
Side Effects of and Adverse Reactions Anesthesia Drugs
to Mucolytics
Advanced Cardiac Life Support Pharmacology
Dosage of Mucolytics
Intraosseous (IO) Administration of ACLS Drugs
Aerosol Antimicrobial Therapy Drugs for Control of Cardiac Rhythm and Rate
Indications for Aerosolized Drugs to Improve Cardiac Output and
Antimicrobial Drugs Blood Pressure
Disadvantages of Aerosol Other ACLS Drugs
Antimicrobial Therapy
KEY TERMS
adrenergic mediator antagonists potentiation
additive effect mucolytics synergy
antagonism pharmaceutical phase tachyphylaxis
anticholinergic pharmacodynamic phase therapeutic index (TI)
cumulative effect pharmacokinetic phase tolerance
P
harmacology is the study of drugs: their origin, PHARMACEUTICAL PHASE
nature, properties, and effects on living
The term pharmaceutical phase refers to the method
organisms. Respiratory therapists administer
by which a drug is delivered to the body (i.e., the route
drugs by aerosol and instillation. They also
of administration and drug form). Respiratory thera-
routinely participate in the care of patients with
pists commonly administer drugs in aerosol form by
complex metabolic and cardiovascular disorders,
inhalation. The aerosol may consist of droplets of a
including those requiring resuscitation. This chapter
liquid solution or a dry powder. Liquid solutions are
introduces the general concepts of pharmacology as
typically administered by small-volume nebulizer (SVN)
they are related to the care and support of patients with
or metered-dose inhaler (MDI). Few medications are
cardiopulmonary disorders. Specific information is
currently administered by dry powder inhaler (DPI); the
provided regarding the selection and administration of
ones that are designed for use with specific devices are
bronchoactive drugs and selected cardiovascular agents
marketed by the drug manufacturers.
used during advanced cardiac life support. This chapter
The administration of a drug by the aerosol route
is intended to be not a comprehensive pharmacology
offers several advantages:
source but rather an overview and introduction to
essential principles required for the practice of • Immediate onset of action at the desired site
respiratory care. • Reduced side effects from systemic absorption
• Ability to administer smaller doses of
potent drugs
Principles of Pharmacology • Ability of patients to self-administer medications
Drug action can be divided into three distinct To administer a drug by instillation, a bolus of drug is
phases: pharmaceutical, pharmacokinetic, and injected directly into the tracheobronchial tree via tube or
pharmacodynamic. catheter. This route is typically used for the administration
CHAPTER 7 ■ Cardiopulmonary Pharmacology 173
of wetting agents, mucolytics, surface-active agents (such oral (PO), and various routes of absorption
as surfactant replacement), and advanced cardiac life (subcutaneous, sublingual, transdermal, rectal). The
support (ACLS) drugs during cardiac resuscitation. onset of drug action is directly related to its route of
Other common routes of administration include administration, as shown in Table 7-1.
intravenous (IV), intra-arterial (IA), intramuscular (IM),
TABLE 7-1 Common routes of drug administration, their onset of action, clinical
indications, and examples
Route of Administration Onset of Action Clinical Indicators Examples of Clinical Uses
Intra-arterial (IA) < 1 minute Drug delivery to specific Anticancer drugs
target organ
Intravenous (IV) Within 1 minute Emergencies; long-term ACLS, nutrient solutions,
infusion hydration, antibiotics,
general anesthesia
Aerosol Within 1 minute Localized effect in Bronchoactive drugs in
respiratory tract; good respiratory care; convenient
systemic absorption of noninvasive method for
appropriate agents; self drugs such as insulin
administration
Instillation 1–2 minutes Useful when rapid onset is Instilled ACLS drugs;
required and no IV is mucolytics or
available; direct pulmonary wetting agents for
activity desired transtracheal oxygen
therapy (TTOT) or during
bronchosopy; surfactant
replacement
Sublingual Within minutes Rapid systemic absorption Nitroglycerin for angina
required without IV access pectoris
Transdermal (topical) 15–30 minutes Continuous low dosage, Nitroglycerin patches,
usually self-administered hormone patches, nicotine
patches, analgesic
ointments
Intramuscular (IM) 15–30 minutes Drugs that have poor oral Narcotics
absorption; when higher
serum levels are needed
more rapidly than by
oral route
Rectal 30 minutes When patient is unable to Antinausea medications
take oral medication or
does not tolerate PO route
Subcutaneous 30–45 minutes Drugs that have poor oral Insulin, local anesthetic by
absorption; when higher hypodermic injection
serum levels are needed
more rapidly than by oral
route but more slowly than
by IM
Oral (PO) 30–60 minutes Self-administered, Most medications,
convenient, immediate particularly over-the-counter
onset not required preparations
PHARMACOKINETIC PHASE over a period of time. (The higher enzyme levels

The pharmacokinetic phase is the time required produced metabolize the drug faster and so a
for drug absorption, drug action, drug distribution higher dose is needed to produce the effect. In
in the body, and the metabolization and excretion other words, the individual is becoming tolerant
of the drug. Drugs must pass through cell mem- to the drug.)
branes to reach the target tissue to exert their • Tachyphylaxis is the rapid development of drug
intended therapeutic effects. A fully ionized drug is tolerance.
not readily absorbed across lipid membranes. A • Cumulative effect, an exaggerated response
nonionized drug is generally lipid soluble and will and possibly toxic situation, occurs when doses
diffuse across cell membranes and into the blood- of the same drug are administered before
stream. For example, ipratropium bromide is a previous doses are inactivated and removed/
bronchodilator administered by aerosol that has few eliminated from the body. The effect is espe-
systemic effects because it is a fully ionized com- cially likely if the drug has a long half-life, that
pound. Lipid-soluble nonionized drugs such as is, the time required to metabolize 50% of the
general anesthetics are readily absorbed into the administered drug.
central nervous system, where they alter neurologi- • Additive effect, an exaggerated response, occurs
cal activity. when two or more drugs are administered with
The distribution of a drug administered by the the same effect on the body.
aerosol route depends on factors such as the • Synergy is the result when two or more drugs
person’s breathing pattern (tidal volume and produce an effect or response that neither could
respiratory rate) and the aerosol’s particle size. produce alone.
Although the intended site of action of inhaled • Potentiation is the result either when two
bronchoactive drugs is the lung, some medication is drugs produce an effect that is greater than
inevitably deposited in the pharynx and will be what they usually produce when given alone
swallowed. The portion of the drug that is deposited or when one drug enhances the effect of
in the lung has therapeutic effects. Systemic effects another drug.
are due to the absorption of the drug into the • Antagonism occurs when two drugs have
bloodstream through the gastrointestinal tract or the opposite effects.
pulmonary mucosa. • Therapeutic index (TI) is the ratio of the
lethal dose (LD50) to the effective dose (ED50).
The LD50 is the dose that would be lethal to
PHARMACODYNAMIC PHASE 50% of the test population, and the ED50 is the
The term pharmacodynamic phase refers to the dose that would be effective for 50% of the test
mechanism of action by which a drug causes its population.
therapeutic effect. In the following sections, drugs
administered by aerosol are described according to
their mechanism of action. For example, both adrener- Drug Calculations
gic and anticholinergic bronchodilators are used to
enhance bronchodilation, but their mechanisms of Respiratory therapists must develop problem-solving
action are different. skills when administering medications to their
patients. Drug calculations follow basic mathematical
principles. They include concentration calculations
Drug Actions and Interactions involving volume-to-weight and weight-to-volume
problems or dilution calculations using volumes and
When a drug is administered repeatedly or when concentrations.
combinations of drugs are administered, the patient
may experience a number of drug actions or effects.
Some of these may be beneficial, and others may result CONCENTRATION CALCULATIONS
in detrimental or harmful side effects. The major drug
The concentration of any drug is the percentage
actions and interactions are:
solution of the active ingredient. This percentage is
• Tolerance is the effect when increased amounts commonly found on the label or in the product
of a drug are needed to produce the desired information brochure. Respiratory therapists should
effect, possibly due in part to increased enzyme be familiar with the following common drug
levels related to enzymatic activity that develops calculations.
In the terminology of drug solutions, a 1% Here is another sample problem: How many milliliters
strength solution, by definition, means that 1 g of the of a 0.5% strength solution should be used to adminis-
drug (the solute) is dissolved in 100 cc (or 100 mL) ter 0.5 mg of a drug to a patient? A 0.5% solution
of a solvent. Most drugs, however, are expressed in contains 5 mg/mL. Therefore:
milligrams (mg), not in grams. Therefore, in the
setup of a drug problem, it is more appropriate to _____ 0.5 mg
5 mg _______
⫽
express the concentration as milligrams per millili- 1 mL x mL
ter (mg/mL). Then, for example, a 1% solution has 0.5 ⫽ 5x
1000 mg/100 mL (1 g ⫽ 1000 mg). Simplified, the
1% strength solution contains 10 mg/mL. The x ⫽ 0.1 mL
following expression is used in solving many drug
problems. DILUTION CALCULATIONS
mg ⫽ mL x% ⫻ 10 At times, an available drug is too strong for the
patient and must be diluted before it is adminis-
Here is a sample problem: How many milligrams tered. In these situations, a volume times concentra-
of drug are in 0.5 mL of a 2% strength solution? This tion expression is set up to determine the
problem may be set up and solved as follows: If a 1% appropriate amount of dilution. In most cases,
solution contains 10 mg/mL, a 2% solution will normal saline is used as the diluent. A dilution
contain 20 mg/mL. A simple mathematical calculation expression is as follows:
provides the answer:
volume 1 ⫻ concentration 1 ⫽ volume 2
20 mg ________
______ ⫽
x mg ⫻ concentration 2
1 mL 0.5 mL
where 1 represents the normal volume or concentra-
x mg ⫽ 20 ⫻ 0.5 tion, and 2 represents the volume or concentration
x ⫽ 10 mg needed.
For example, a respiratory therapist (RT) has a
This problem can also be solved logically: A 2% 10% strength solution but needs to administer 2.0 mL
solution containing 20 mg/mL has 10 mg/0.5 mL (half of a 2.5% strength solution. How much drug should
of the given amount). be used, and what dilution is needed? The problem
should be set up in the following manner:
RATIO CALCULATIONS volume 1 ⫻ concentration 1 ⫽ volume 2
A drug solution may be expressed as a ratio instead of ⫻ concentration 2
as a percentage. For instance, 1:100, 1:200, and 1:1000 x mL ⫻ 10% ⫽ 2 mL ⫻ 2.5%
are drug ratios often encountered; they all describe a
strength of solution. Mathematically: 10x ⫽ 5
• A 1:100 solution is a 1% solution x ⫽ 0.5 mL
(1/100 ⫻ 100 ⫽ 1%). To make 2.0 mL of a 2.5% strength solution, the RT
• A 1:200 solution is 0.5% strength. has to dilute 0.5 mL of the drug with 1.5 mL of
• A 1:1000 solution is 0.1% strength. normal saline.
With this knowledge, respiratory therapists can convert Here is another sample problem: How many
ratio and percentage strengths and solve most drug milliliters of a drug with a 3% strength solution
problems. should be used to administer 0.75 mL of a 1%
Here is a sample problem: How many milligrams strength solution? To solve, set up the problem as
of drug are in 0.1 mL of a 1:100 strength solution? A follows:
1:100 ratio solution is really a 1% strength solution
volume 1 ⫻ concentration 1 ⫽ volume 2
containing 10 mg/mL. Therefore:
⫻ concentration 2
10 mg _______
______ x mg
⫽ x mL ⫻ 3% ⫽ 0.75 mL ⫻ 1%
1 mL 0.1 mL
x mg ⫽ 10 ⫻ 0.1 3x ⫽ 0.75
x ⫽ 1.0 mg x ⫽ 0.25 mL
Age-Specific Competency Bronchial smooth muscle cell

Beta-2
Norepinephrine
When drugs are to be administered to infants receptor site
causes
or children, smaller amounts (in milligrams Sympathetic
ATP cAMP bronchodilation
or milliliters) are given on the basis of patient
age or weight. Five basic rules or formulas are
generally used:
1. Fried’s rule (for patients younger than 1 year
of age):
FIGURE 7-1 Sympathomimetic drugs stimulate
age in months cAMP.
pediatric dose ⫽ _____________ ⫻ adult dose
150
2. Clark’s rule (for patients older than 2 years
of age):
weight in pounds Bronchial smooth muscle cell

pediatric dose ⫽ ________________ ⫻ adult dose
150
Muscarinic
Acetylcholine
3. Young’s rule (for patients older than 2 years receptor site
of age): Parasympathetic
GTP cGMP bronchoconstriction
age in years
pediatric dose ⫽ ________________ ⫻ adult dose
age in years ⫹ 12
4. Cowling’s rule (for patients older than 2 years
A
of age):
age next birthday

pediatric dose ⫽ ________________ ⫻ adult dose Bronchial smooth muscle cell
24
Muscarinic
Acetylcholine
5. Body surface area (BSA) formula: receptor site

Parasympathetic
surface area of child (in mm2)
pediatric dose ⫽ ___________________________
1.7
⫻ adult dose
Anticholinergic blocks
B
To produce the prescribed 0.75 mL of the 1% strength FIGURE 7-2 (A) Effect of parasympathetic stimulation
solution, the RT dilutes 0.25 mL of the 3% strength in bronchial cells. (B) Anticholinergic drugs block
drug with 0.5 mL of normal saline. parasympathetic stimulation.
Bronchodilators
There are three commonly recognized mechanisms for
inducing bronchodilation.
Bronchial smooth muscle cell
• Beta-adrenergic, or sympathomimetic, drugs
Beta-2
directly stimulate the conversion of ATP to
Norepinephrine
receptor site
cyclic 3’5’-AMP via the enzyme adenyl cyclase causes
Sympathetic
(Figure 7-1). ATP cAMP dilation

• Anticholinergic drugs block the bronchocon-
blocks
stricting effects of the parasympathetic or phosphodiesterase
cholinergic system (Figure 7-2).
• Xanthines inhibit phosphodiesterase to prevent GMP no dilation
the conversion of cyclic 3’-5’-AMP into GMP
(Figure 7-3). FIGURE 7-3 Xanthines inhibit phosphodiesterase.
HO agonists are noncatecholamine in nature, but both
NH2 isoproterenol and racemic epinephrine (catechol-
amines) are still in use today.1
HO
Some of the noncatecholamine bronchodilators
OH are further classified as either resorcinols or saligenins
on the basis of their chemical structure and drug
FIGURE 7-4 Catecholamine bronchodilator chemical structure:
benzene ring (catechol nucleus) with placement of hydroxyl action specificity.
(OH) groups on the 3rd and 4th carbon sites of the ring, • Resorcinols (metaproterenol and terbutaline)
carbon side chain and terminal amino (NH2) group. have a shift in the hydroxyl (OH) group from
the 4th carbon site on the catechol nucleus to
SYMPATHOMIMETIC BRONCHODILATORS the 5th carbon site. This shift produces the
Sympathomimetic bronchodilators promote the relaxation resorcinol nucleus. COMT does not affect this
of bronchial smooth muscle by stimulating the intra- nucleus, resulting in a drug duration of action of
cellular production of cyclic 3’5’-AMP. They are also up to 6 hours.
referred to as adrenergic because they promote • Saligenins, on the other hand, have a modifica-
bronchodilation via the neurotransmitter norepineph- tion (OH group to CH2OH group) at the 3rd
rine, which is similar to epinephrine (adrenalinelike, carbon site. This produces the saligenin nucleus
thus the term “adrenergic”). that is also not affected by COMT and MAO.
The first sympathomimetic bronchodilators were Albuterol is classified as a saligenin bronchodi-
classified as catecholamines because they had a chemi- lator with a duration of action up to 6 hours.
cal structure that included a benzene ring (catechol An isomer of albuterol (levalbuterol, or
nucleus) and a carbon side chain with a terminal amino Xopenex) has a long duration of action with
(NH2) group (Figure 7-4). The length of this carbon reportedly fewer side effects. Another drug,
chain can vary and can impact the duration of action of Pirbuterol or Maxair, is very similar to albuterol
some bronchodilators, many of which are noncatechol- except it has a pyridine ring structure (N at the
amine in chemical structure.1 Bronchodilators with long 2nd carbon site) instead of the traditional
carbon chains have longer durations of action. benzene ring structure.
Enzyme breakdown or deactivation can also affect Another classification of bronchodilator is the
the duration of catecholamine bronchodilation action. prodrug variety. Bitolterol mesylate (Tornalate) is
Catechol-O-methyl transferase (COMT) is the enzyme converted in the body, via esterase hydrolysis, to the
responsible for the rapid breakdown of the ultrashort- active catecholamine, colterol. This agent also has a
acting bronchodilators such as isoproterenol, resulting in prolonged bronchodilator effect of up to 8 hours.
a very short duration of action. On the other hand, the However, Tornalate is no longer available in the
enzyme monoamine oxidase (MAO) works more slowly United States.
but also has an effect on deactivating catecholamine The most common long-acting beta-agonist (LABA)
bronchodilators. For example, isoetharine is affected more bronchodilators are formoterol (Foradil) and salmeterol
by MAO and less by COMT, and therefore it has a longer (Serevent). Formoterol is an analogue of catecholamine
duration of action (up to 3 hours) than isoproterenol. with very selective beta 2 activity. It has a duration of
Sympathetic system receptor sites include alpha, action of up to 12 hours, due in part to a lipid-soluble
beta-1, and beta 2. group on its structure that increases lipid solubility,
• Alpha receptor stimulation results in resulting in greater beta 2 receptor binding. Salmeterol
vasoconstriction. has enhanced beta 2 activity because of its chemical
• Beta-1 receptors are located only in the heart, structure, which includes a very long carbon side chain.
and stimulation results in increased heart rate. Its duration of action is also up to 12 hours.1
• Beta 2 receptors are located in the smooth
muscle of the bronchi and uterus, and stimula- ANTICHOLINERGIC BRONCHODILATORS
tion results in muscle dilation (relaxation).
Anticholinergic bronchodilators, also referred to as
Aerosol delivery of alpha agents is recommended parasympatholytics, promote bronchodilation by
for conditions associated with mucosal edema (e.g., blocking bronchoconstriction. Parasympathetic
croup, laryngeal trauma, postextubation laryngeal stimulation via the neurotransmitter acetylcholine
edema). Adrenergics are categorized as either catechol- induces bronchoconstriction; thus anticholinergic
amine (having mixed beta-1 and beta 2 effects or drugs block cholinergic-induced bronchoconstriction.
alpha, beta-1, and beta 2 effects) or noncatecholamine This category currently includes four agents: atropine,
(having strong beta 2 specificity). All newer beta ipratropium bromide (Atrovent), tiotropium bromide
(Spiriva), and glycopyrrolate. Of the four, atropine is Selection of an Adrenergic or Anticholinergic

not commonly delivered by aerosol. Bronchodilator. Adrenergic bronchodilators
Generally, anticholinergics have a longer onset generally have a more rapid onset of action than
than that of most beta-agonists but also have an anticholinergics because they directly stimulate the
extended duration of effectiveness. Anticholinergics are relaxation of bronchial smooth muscle cells. Anti-
useful in managing chronic airflow obstruction cholinergic agents have little application in the
associated with COPD but have limited usefulness in treatment of acute bronchospasm, such as asthma or
reversible airway diseases such as asthma.2 exercise-induced bronchospasm, but they have been
shown to be useful in the management of chronic
bronchospasm associated with COPD. Concurrent
XANTHINES
use of an anticholinergic drug with a beta-agonist has
Xanthines include caffeine, theobromine, and theophyl- also been shown to improve the effectiveness of each
line. Theophylline and its derivatives (aminophylline) drug. Combivent is such a combination (MDI
are delivered by IV and oral routes in the management formulation of albuterol and ipratropium bromide);
of chronic bronchospasm. Although xanthines are DuoNeb is a similar liquid formulation for aerosol-
rarely administered by aerosol, some COPD patients ization via a small-volume or hand-held nebulizer.
receive oral xanthines as part of their overall pharmaco- Assessing the response to bronchodilator therapy at
logic management. Within bronchial smooth muscle the point of care in terms of airflow, desired out-
cells, cyclic 3’5’-AMP is constantly degraded by the comes, patient monitoring, and presence of any side
enzyme phosphodiesterase; one of the bronchodilating effects is thoroughly reviewed in an American Asso-
mechanisms of xanthines is their inhibition of ciation for Respiratory Care (AARC) clinical practice
phosphodiesterase. guideline (CPG) published in 1995.4
Xanthines have numerous other effects, including
pulmonary vasodilation, cardiac stimulation, skeletal Contraindications for Bronchodilators. All broncho-
muscle stimulation (including enhanced diaphragmatic dilators, regardless of their mechanism of action or
contractility), central nervous system stimulation, and beta 2 specificity, have some cardiovascular side effects.
diuresis. Xanthines also have serious neurological and Respiratory therapists should always exercise caution
gastrointestinal side effects and must be kept within a when administering bronchodilators to patients who
narrow therapeutic range (10–15 μ/mL). have a history of cardiac disease or arrhythmias.
Xanthines also interact with a wide variety of
drugs, most notably many of the cardiovascular drugs
concurrently used in the complex management of SIDE EFFECTS OF AND ADVERSE REACTIONS
many pulmonary patients. Beta-blockers (e.g., TO BRONCHODILATORS
Inderal, Tenormin, Lopressor), calcium channel The most common side effects associated with inhaled
blockers (e.g., Procardia, Cardizem, Isoptin), bronchodilators are tachycardia, headache, nervous-
corticosteroids, and many antibiotics tend to increase ness, and nausea. Many patients experience tremors,
serum theophylline levels.3 which usually diminish with continued use. Although
the newer drugs are formulated for more targeted
beta 2 specificity, most patients still experience some
INDICATIONS AND CONTRAINDICATIONS
degree of increased heart rate and nervousness.
FOR BRONCHODILATORS
Headache is a commonly reported side effect, but it
The general clinical indication for the administration occurs almost as often in patients receiving a placebo.
of a bronchodilator is the presence of reversible Table 7-2 summarizes the side effects associated with
airway obstruction, usually manifested by the pres- currently used aerosol bronchodilators.
ence of wheezing. Selection of the appropriate
medication to treat wheezing depends on the cause of
the airway obstruction. Wheezing is a symptom of BRONCHODILATOR DOSAGE GUIDELINES
bronchoconstriction, which may be due to broncho- The standard dosages for aerosolized bronchodilators are
spasm, mucosal edema, or the presence of mucus. provided in Table 7-3. Recent clinical use of high-dose
Bronchospasm is best reversed by the use of adrener- and continuous nebulization of bronchodilators has
gic or anticholinergic agents. Other conditions been shown to be useful in the management of intrac-
respond better therapeutically to the use of an adren- table bronchospasm and status asthmaticus.
ergic agent with alpha properties such as racemic
epinephrine. An example is croup, manifested by High-Dose Bronchodilator Protocol. When a patient
laryngeal edema and bronchiolitis with associated presents in acute respiratory distress with diffuse
mucosal edema. wheezing, tachypnea, and a peak expiratory flow rate
TABLE 7-2 Classification, receptors, and common side effects of aerosol bronchodilators
Drug (Trade name) Type Receptors Side Effects
Albuterol (Proventil, Sympathomimetic Primarily beta 2 Mild tremors, headache,
Ventolin) insomnia, nervousness,
nausea
Albuterol and ipratropium Adrenergic, anticholinergic Adrenergic, primarily Mild tremors, headache,
(Combivent) beta 2; anticholinergic insomnia, nervousness,
blocks muscarine receptors nausea, dry mouth, cough
Bitolterol (Tornalate) Sympathomimetic Primarily beta 2 Mild tremors, headache,
insomnia, nervousness,
nausea
Epinephrine (Asthmahaler Catecholamine Strong alpha, beta-1, Profound tachycardia,
Bronitin Mist, Bronkaid sympathomimetic and beta 2 hypertension, palpitations,
Mist, Medihaler-Epi, vasoconstriction
Primatene Mist)
Glycopyrrolate (Robinul) Anticholinergic; Blocks muscarinic; Few, mild: dry mouth,
parasympatholytic receptors cough
Ipratropium bromide Anticholinergic, Blocks muscarinic Few, mild: dry mouth,
(Atrovent) parasympatholytic receptors cough
Isoetharine (Bronkosol) Catecholamine, Mild beta-1, primarily Tachycardia, palpitations,
sympathomimetic beta 2 nausea, headache
Isoproterenol (Isuprel) Catecholamine, Strong beta-1 and beta 2 Profound tachycardia,
sympathomimetic palpitations, nervousness
Metaproterenol (Alupent, Sympathomimetic Primarily beta 2 Mild tremors, headache,
Metaprel, Pirbuterol insomnia, nervousness,
(Tomalate) nausea
Racemic epinephrine Catecholamine, Alpha, beta-1, and beta 2 Mild tachycardia, shakiness,
(Micronefrin, Vaponefrin, sympathomimetic nausea, headache
Racepinephrine)
Salmeterol (Serevent) Sympathomimetic Primarily beta 2 Mild tremors, headache,
insomnia, nervousness,
nausea
Terbutaline (Brethair, Sympathomimetic Primarily beta 2 Mild tremors, headache,
Brethine, Bricanyl) insomnia, nervousness,
nausea
(PEF) less than 50% predicted, it may be appropriate to Ultrashort-, Short, and Long-Acting Adrenergic
administer a series of high-dose aerosol bronchodilator Bronchodilators. As noted in Table 7-3, certain
treatments with less than the usual time between bronchodilators have an ultrashort duration of
treatments. A typical approach could include adminis- effectiveness or action (1–2 hours). These drugs
tering up to three aerosol treatments at 20-minute include isoproterenol (Isuprel) and racemic epineph-
intervals with 1.0 mL albuterol (5.0 mg) and 1.0 mL rine (Micronefrin). Others are short-acting beta-
normal saline. agonists (SABA) with 4–6 hours of pharmacologic
action: albuterol (Proventil or Ventolin), levalbuterol
Continuous Bronchodilator Aerosol. Situations (Xopenex), and metaproterenol (Alupent or Metaprel).
such as status asthmaticus, refractory bronchospasm, Long-acting beta agonists (LABA), with up to 12 hours
or cystic fibrosis may indicate continuous aerosol of action, are salmeterol (Serevent), formoterol
by face mask or endotracheal tube. This dosage (Foradil), and arformoterol (Brovana).
typically delivers a solution that provides 2.0 mL/ Isoproterenol is rarely used today because of its
hour (10 mg), which is administered until the profound cardiovascular side effects and ultrashort
patient’s clinical condition improves. duration of action. However, it may be useful in
TABLE 7-3 Aerosol bronchodilator strengths, dosages, onsets, and durations of effectiveness
Onset
Drug Strength Dosage Frequency (minutes) Peak Duration
Albuterol 0.50% solution 0.50 mL tid, qid 1–5 30–60 minutes 3–6 hours
Albuterol MDI 90 μg/puff 2 puffs tid, qid 1–5 30–60 minutes 3–6 hours
Albuterol and MDI 18 μg/puff 2 puffs qid 15 1–2 hours 4–6 hours
ipratropium Ipratropium and
90 μg/puff
albuterol
Bitolterol 0.20% solution 1.25 mL tid 3–4 30–60 minutes 5–8 hours
Bitolterol MDI 0.37 mg/puff 2 puffs q 8 hours 3–4 30–60 minutes 5–8 hours
Epinephrine 1:100 (1.0%) 0.25–0.50 mL q 2–4 hours 1–3 15 minutes 60
minutes
Glycopyrrolate 0.20 mg/mL 2.50–5.0 mL tid, qid 15–30 1–2 hours 4–6 hours
Ipratropium 0.025% solution 1.0–2.0 mL q 4–6 hours 15 1–2 hours 4–6 hours
Ipratropium MDI 18 μg/puff 1–2 puffs qid 15 1–2 hours 4–6 hours
Isoetharine 1.0% solution 0.25–0.50 mL qid 1–3 15–60 minutes 1–3 hours
Isoproterenol 1:200 (0.50%) 0.25–0.50 mL qid 1–3 5–30 minutes 30–120

minutes
Metaproterenol 5.0% solution 0.50 mL tid, qid 1–5 30–60 minutes 3–4 hours
Metaproterenol MDI 0.65 mg/ 2–3 puffs q 4 hours 1–5 30–60 minutes 3–4 hours
puff
Pirbuterol MDI 0.20 mg/ 2 puffs q 4–6 hours 3–4 30–60 minutes 5 hours
puff
Racemic 2.25% solution 0.25–0.50 q 1–2 hours 1–3 15 minutes 30–60
epinephrine mL minutes
Salmeterol MDI 25 μg/puff 1–2 puffs bid (morning 20 3–5 hours 12 hours
and evening)
Terbutaline MDI 0.20 mg/ 2 puffs q 4–6 hours 5 30–60 minutes 3–6 hours
puff
selected clinical situations. Isoproterenol should not be (such as albuterol or levalbuterol) for use when an
given more often than every 4 hours, regardless of its acute attack occurs.
very short therapeutic effects.
Racemic epinephrine, however, may safely be
administered within 60 minutes of an initial treat- BRONCHODILATOR ADMINISTRATION IN
ment because it rapidly degrades and has few serious MECHANICALLY VENTILATED PATIENTS
side effects. Bronchodilators are routinely administered to patients
Salmeterol is intended for the long-term mainte- on ventilators. The American Association for Respiratory
nance and control of the chronic asthmatic. It does Care (AARC) has published a clinical practice guideline
not have a rapid onset (as compared with other (CPG) that recommends the selection of a device to
beta-agonists) and should not be used during an administer the bronchodilator, how to administer it, and
acute asthma attack. Asthmatics who use salmeterol how to evaluate the response to therapy.5 The CPG
should be instructed to carry a fast-acting beta-agonist recommends use of metered dose inhalers (MDIs),
small-volume nebulizers (SVNs), large-volume nebuliz- mucosa by activated T cells, mast cells, and eosino-
ers (LVNs), and ultrasonic nebulizers for delivery of phils. T cells and mast cells release cytokines, which
bronchodilators to mechanically ventilated patients. promote the production of IgE antibodies and the
However, it states that dry-powder inhalers (DPIs) are consequent increase in capillary permeability and
not be suitable for use, suggesting that clinical trials are mucosal edema.
necessary to validate their use. Central to the CPG The management of patients with asthma now
recommendations is that the tidal volume of an adult focuses on the inflammatory elements of the disease.
patient should be large enough to ensure that the drug Treatment includes anti-inflammatory drugs such as
will reach the small airways. The guideline suggests that corticosteroids and other controller drugs (e.g., mast
the tidal volume be greater than 500 mL for adults and cell inhibitors along with leukotriene inhibitors and
recommends the use of lower inspiratory flows or an antagonists).
inspiratory pause to improve the disposition of the
aerosol. Either method should be used only if it does
INDICATIONS AND CONTRAINDICATIONS
not compromise the patient and ensures that the
FOR ANTI-INFLAMMATORY DRUGS
patient’s inspiratory needs are met.
Humidifiers and metered-dose drugs can pose Inflammation is associated with increased capillary
extra problems for drug delivery to mechanically permeability, which leads to mucosal edema. Adminis-
ventilated patients. Humidified gas can lower aerosol tration of an alpha-adrenergic, such as racemic
delivery, but the hazards of ventilating a patient with epinephrine, is indicated if the mucosal edema is
dry gas are greater. The guideline recommends that associated with an inhalational injury (e.g., inhalation
the humidifier remain inline, although an increase in of smoke, fumes, or steam), trauma (e.g., intubation
aerosol dose may be necessary. The respiratory or extubation), or infectious process (e.g., croup,
therapist may find it difficult to accurately time the epiglottitis, bronchiolitis). In these situations, the
activation of the metered-dose device with the onset mucosal edema is not secondary to an allergic
of inspiration. The guideline recommends that the response; therefore, the vasoconstricting action of an
metered-dose device be fitted with a chamber that alpha-adrenergic drug is very effective. The dosage of
will hold the aerosol for the next inspiration. racemic epinephrine is noted in Table 7-3.
Last, the CPG recommends that an inline nebulizer Inflammation associated with a chronic
should be placed no farther than 30 cm from the inflammatory response such as asthma is controlled
proximal end of the endotracheal tube. The practitioner by corticosteroids. Inhaled corticosteroids (ICS)
should also place a filter on the expiratory limb of the provide the advantage of reducing systemic side
ventilator circuit to prevent aerosolized drug from effects associated with long-term corticosteroid use.
entering any flow-sensing device in the ventilator. The The primary indication for the use of ICS is to
nebulizer should never be left inline after the treatment control the inflammation associated with mild to
is over.5 The details of aerosol and humidity therapy moderate persistent asthma.7,8 Current drugs and
are covered in Chapter 21. drug administration guidelines for ICS are presented
in Table 7-4.
The presence of a systemic fungal infection, renal
Anti-Asthmatic and failure, or severe diabetes mellitus contraindicates the
Anti-Inflammatory Drugs use of corticosteroids.
Asthma affects an estimated 20 million Americans,

and asthma mortality continues at a rate of 5000 SIDE EFFECTS OF AND ADVERSE REACTIONS
deaths per year in the United States.6 The primary TO CORTICOSTEROIDS
clinical features of asthma are profound dyspnea The systemic side effects of ICS have been documented
and wheezing; thus, traditional therapy has long and are similar to those of the oral variety (predni-
concentrated on controlling the bronchospasm, sone). The general side effects associated with inhaled
typically with inhaled or oral beta-agonists. Current steroids include hoarseness, dry mouth, dysphonia,
asthma management addresses clinical manifesta- and cough. Inhaled steroids may suppress the normal
tions of the disease: bronchospasm, inflammation bacterial flora in the oropharynx and lead to fungal
with mucosal edema, and excessive airway secre- infections such as oral candidiasis or aspergillosis if the
tions. Although asthma may be triggered by intrin- patient does not routinely rinse the mouth after
sic or extrinsic causes, its primary manifestation is inhalation of the steroid.8
an acute inflammatory response, which is initiated Many asthmatics use multiple metered-dose
by the complement cascade. Asthmatics exhibit inhalers (MDIs) and/or dry powder inhalers (DPIs) for
airway inflammation with infiltration of the symptom control. In such cases, the patients have to be
TABLE 7-4 Aerosol corticosteroid dosages and onset of action

Drug Strength (μg/puff) Dosage Onset
Beclomethasone 42 Adults: 2 puffs, tid, qid; Usually within 24 hours
(Beclovent, Vanceril) children: 1-2 puffs,
tid, qid
Budesonide (Rhinocort, 200 Adults: 1–2 puffs, bid; Usually within 24 hours
Pulmicort) children: (>5 years old):
1 puff bid
Dexamethasone(Decadron 84 Adults: 3 puffs, tid, qid; Usually within 24 hours
Respihaler) children: 2 puffs, tid, qid
Flunisolide (Aerobid) 250 Adults and children: 2–3 days
2 puffs, bid
Fluticasone diproprionate 44 >12 years old, 2 puffs bid 2–3 days
(Flovent)*
Fluticasone diproprionate 110 >12 years old, 1–2 puffs 2–3 days
(Flovent)* bid
Fluticasone diproprionate 220 >12 years old, 1–2 puffs 2–3 days
(Flovent)* bid; maximum 880 μg/day
Triamcinilone (Azmacort) 100 Adults: 2 puffs, tid, qid; 1–3 days
children:1–2 puffs, tid, qid
*Fluticasone dosages vary according to concurrent dosages of bronchodilators and oral corticosteroids; adrenal suppression occurs in 10%–16% of patients
receiving 440 μg/day or more of fluticasone.
instructed in the proper sequence of medication three times as expensive as a bronchodilator); there-
administration to both optimize the therapeutic effects fore, patients may “save” their steroids or, if money is
and minimize adverse reactions. If multiple MDIs are an issue, discontinue them because they can rely on
used, the general sequence should be: symptomatic treatment with beta-agonists. This
practice is particularly troubling because corticoste-
1. Bronchodilator (e.g., albuterol).
roid use, even by aerosol, should be gradually tapered
2. Mast cell inhibitor (e.g., Intal or Tilade).
until finally discontinued by the physician. Patient
3. Corticosteroid (e.g., Azmacort, Flovent, Pulmicort).
education is a key component to the effective man-
Regardless of the number of MDIs used, the agement of asthma.
corticosteroid should be taken last and the mouth
thoroughly rinsed after inhalation. The most common
DPI used in the management of asthma is Advair, a MECHANISM OF ACTION OF
combination of the long-acting beta-agonist salme- ANTI-ASTHMATIC DRUGS
terol and the corticosteroid fluticasone. Patients Mediator antagonists are drugs that compete for a
simply use this DPI, followed by any other prescribed receptor site and prevent a subsequent response to a
MDI or DPI. Mouth rinsing after DPI use is also stimulus. Two types of mediator antagonists are used in
recommended. the management of asthma: mast cell inhibitors and
Patient noncompliance is a possible cause of leukotriene inhibitors. Mast cells are a component of
adverse effects or lack of effective asthma manage- the immune system that contain large quantities of
ment. Corticosteroids have no bronchodilating histamine. These cells degranulate when exposed to an
properties but must be continued in the absence of allergic or a nonallergic stimulus, releasing histamine
symptoms. Many asthmatics do not understand or do and other mediators of inflammation [leukotrienes,
not comply with treatment, which is intended to formerly known as slow-reacting substance of
reduce the need for fast-acting beta-agonists. Cortico- anaphylaxis (SRS-A), prostaglandins, bradykinin,
steroid MDIs are very expensive (some are two or and platelet-activating factor].
Mast cell Mast cell bronchoconstriction, mucus secretion, and chemotaxis
of other inflammatory mediators. This family of drugs
+ therefore prevents the leukotriene-stimulated inflam-
Histamine
Allergen
Histamine matory response.9
FIGURE 7-5 In the normal allergic response, ruptured mast

cells release histamine. INDICATIONS FOR ANTI ASTHMATIC DRUGS
Several anti-asthmatic drugs are indicated for the
prophylactic management of asthma. The leukotriene
Mast cell Mast cell inhibitors are taken orally (they are not available by
inhalation) and in tablet form two to four times a day.
+
Allergen Cromolyn sodium and nedocromil are not available in
Histamine Histamine oral forms and must be administered by aerosol
(small-volume nebulizer, dry powder inhaler, or
FIGURE 7-6 Cromolyn sodium and nedocromil stabilize
mast cells to prevent histamine release.
metered-dose inhaler). Patient compliance is also a
concern with this group of drugs because their action
is completely preventive and requires consistent
dosing to maintain appropriate serum levels for
These mediators cause bronchospasm and lead to therapeutic effect. Dosage guidelines for anti asthmatic
the cascade of other mediators and the inflammatory drugs are provided in Table 7-5.
response in the airway. Mast cell inhibitors (cromolyn
sodium and nedocromil) prevent the degranulation of
these cells and thus prevent the cascade of inflamma- ASTHMA RELIEVERS AND CONTROLLERS
tory events. Nedocromil has both mast cell inhibition The National Asthma Education and Prevention Pro-
and anti-inflammatory properties. Figure 7-5 illustrates gram (NAEPP) of the National Institutes of Health has
the normal allergic response, and Figure 7-6 illustrates established current guidelines distinguishing asthma
the mast cell inhibition by cromolyn sodium and medications as either relievers or controllers.6 Short-
nedocromil. acting beta agonist and anticholinergic bronchodilators
Leukotriene inhibitors either compete for leukotri- are categorized as relievers; other bronchodilators
ene receptors (e.g., zafirlukast and montelukast) or (long-acting beta agonists and xanthines) are catego-
inhibit the formation of leukotriene (e.g., zileuton). rized as controllers. Respiratory therapists must under-
Leukotrienes stimulate leukotriene receptors and cause stand the significance of this distinction when evaluating
TABLE 7-5 Anti-asthmatic drugs and dosages

Route of
Drug Classification Administration Strength Dosage Frequency
Cromolyn sodium Mast cell Aerosol metered- 0.80 mg/puff 2 puffs qid
(Intal) inhibitor dose inhaler (MDI)
Cromolyn sodium Mast cell Aerosol dry powder 20 mg/capsule 20 mg (1 capsule) qid
(Intal) inhibitor inhaler
Cromolyn sodium Mast cell Aerosol small- 20 mg/2 mL 20 mg qid
(Intal) inhibitor volume nebulizer
Montelukast Leukotriene Oral 5- and 10-mg 1 tablet qid
(Singulaire) inhibitor tablets
Nedocromil Mast cell Aerosol MDI 1.75 mg/puff 2 puffs qid
(Tilade) inhibitor
Zafirlukast Leukotriene Oral 20-mg tablet 1 tablet bid
(Assolate) inhibitor
Zileuton (Zyflo) Leukotriene Oral 600-mg tablet 1 tablet qid
inhibitor
TABLE 7-6 Asthma relievers and controllers Antibiotics administered orally are also used in manag-
ing these patients when bronchial infection and/or
Quick-Relief Long-Term pneumonia are present. Aerosolized antimicrobials are
Asthma Agents Asthma Controllers generally reserved for patients with either bronchiectasis
Short-acting Inhaled corticosteroids or cystic fibrosis.
inhaled beta 2 Mast cell inhibitors Finally, mention must be made about COPD
agonists (albuterol, patients with alpha-1 antitrypsin (AAT) deficiency and
metaproterenol, the use of Prolastin, or alpha-1 proteinase inhibitor
bitolterol, pirbuterol, (human). AAT deficiency is also known as genetic
terbutaline) emphysema because it is triggered by defective family
Inhaled anticholinergic Leukotriene antagonists genes, resulting in individuals’ having a congenital
(ipratropium) and inhibitors deficiency of alpha1-Pl in clinically demonstrable
Systemic corticosteroids Long-acting beta 2 agonists panacinar emphysema. This type of lung damage is
(e.g., salmeterol and oral similar to that caused by emphysema, but the clinical
sustained–release tablets symptoms occur earlier in life (usually between 35 and
such as terbutaline and 40 years of age).
albuterol) For patients with this deficiency, Prolastin is
indicated for chronic replacement therapy. It is
Xanthines (theophylline, administered once weekly intravenously. The usual
aminophylline) adult dosage is 60 mg/kg, and it takes approximately
Oral corticosteroids 30 minutes to infuse the prescribed dose. It is recom-
mended for adult use only because effectiveness in the
pediatric population has not yet been established.
Prolastin is contraindicated in individuals with
patient care and assessing its effectiveness, and they selective IgA deficiency who are known to have an
should explain the distinction to the patients. A sum- antibody against IgA (anti-IgA antibody). Side
mary of the NAEPP categories is provided in Table 7-6. effects and adverse reactions may include flulike
symptoms, allergiclike reactions, chills, dyspnea, rash,
tachycardia and, rarely, hypotension, hypertension,
Drugs Used in the Management and chest pain.10
of COPD
As with asthma, the most important inhaled medications
are the adrenergic bronchodilators, anti cholinergic
Wetting Agents and Mucolytics
bronchodilators (tiotropium bromide in particular), the Bland aerosols and mucolytic agents are used in
selective use of xanthines, and inhaled corticosteroids. respiratory care to humidify the respiratory tract and
Both Advair (a combination of serevent and fluticasone) to loosen, thin, and remove pulmonary secretions.
and Symbicort (foradil and budesonide) have been Bland aerosols (e.g., normal saline, hypotonic or
approved for pharmacologic management of the hypertonic saline, and sterile distilled water) do not
COPD patient. actually disrupt the mucus molecule. Mucolytics
Steroids, both oral and inhaled, are particularly (e.g., n-acetylcysteine, dornase alfa, and sodium
beneficial in the management of COPD because of bicarbonate) actually disrupt (or lyse) the mucus
their anti-inflammatory effect in reducing mucosal molecule (the long mucopolysaccharide chains) to
edema in the bronchi and thereby decreasing airway facilitate secretion removal.
resistance and work of breathing. Steroids may also
potentiate the action of beta-agonist bronchodilators,
increasing airway dilation. However, patients must be BLAND AEROSOLS
aware of potential side effects from long-term steroid Bland aerosols are used primarily to humidify inspired
use, and measures must be taken to avoid or manage air and irritate the airway to promote a cough. Sterile
associated problems such as osteoporosis, hyperten- water, hypotonic saline, and hypertonic saline usually
sion, steroid-induced diabetes, muscular atrophy, and/ cause airway irritation (hypertonic saline may actually
or increased gastric acidity. “draw” additional fluid into the lung to dilute the
In addition, mucolytics such as acetylcysteine solution). They thus increase mucus production, which
(Mucomyst) may be used in COPD patients who have stimulates a cough reflex.11 These solutions are not
considerable mucus production secondary to chronic considered mucolytics, but they may be categorized as
bronchitis and difficulty in expectorating the secretions. expectorants.
S
CASE STUDY 7-1 S Amino acid chain
S
Michael Smith is a 58-year-old white male
who was recently diagnosed with COPD and Sulfur-sulfhydryl
S
asthma. His physician has prescribed bond S
aerosolized albuterol qid via compressor/
nebulizer followed by 2 puffs of Flovent bid S
via MDI. During the first week of therapy, the
patient appeared to respond favorably. S
During the next few weeks, however, Mr.
Smith experienced a disrupted sleeping pattern
S
along with persistent pharyngitis and the pres- FIGURE 7-7 The structure of the mucus molecule.
ence of white patches on his throat. He notified
his physician, who modified his therapy accord-
ingly with improved results.
S
S
Questions S S
1. What change, if any, do you think the
S S
physician made regarding the administration
Disrupts bonds
of aerosolized bronchodilator? S S
2. What was the likely cause of the patient’s S
S
pharyngitis, and what could have been done
to prevent it? S S
S
S
S
S
The AARC has published a CPG on the use of
FIGURE 7-8 Mucolytic action of n-acetylcysteine.
bland aerosols in respiratory care. Specifically, the CPG
suggests that cool bland aerosols (water or saline) used
for upper airway administration have a mass median
aerodynamic diameter (MMAD) ⱖ 5 μm. This size
S
S
ensures that the aerosol is deposited in the upper S S

airway. Hypo- and hypertonic saline solutions used S
for inducing sputum should have a MMAD between
S
S
1 and 5 μm. Finally, heated bland aerosols to correct S
humidity deficits when the upper airway is bypassed,
S S
as in patients with a tracheostomy, requires a MMAD Sodium disrupts amino acid
of 2–10 μm.12 bicarbonate chains
S S
MECHANISM OF ACTION OF MUCOLYTICS S S

The mucus molecule is a mucopolysaccharide chain
S
composed of strands of alternating amino sugars and

amino acids that are connected by disulfide bonds FIGURE 7-9 Mucolytic action of sodium bicarbonate.
(Figure 7-7). The three mucolytics in use disrupt the
mucus molecule in three ways:
• N-acetylcysteine disrupts the disulfide bonds INDICATIONS AND CONTRAINDICATIONS
(Figure 7-8). FOR MUCOLYTICS
• Sodium bicarbonate disrupts the stability of the Mucolytics may be administered by aerosol or by
amino acid chains (Figure 7-9). direct instillation into the airway (e.g., during bronchos-
• Dornase alfa lyses mucus proteins or the protein- copy or lavage). A mucolytic should be considered for
aceous secretions associated with infected patients with thickened secretions who are capable
sputum in cystic fibrosis patients. of protecting their airway and generating a good
spontaneous cough. Mucolytic therapy should be

considered only after adequate systemic hydration CASE STUDY 7-2
(through oral or IV fluids), and the patient still exhibits
persistent coarse rhonchi and difficulty in expectorating Rose Johnson, a 62-year-old black female with
secretions. Both sodium bicarbonate and n-acetylcysteine chronic bronchitis, was prescribed acetylcysteine
may be used for mucolysis; dornase alfa is FDA-approved via nebulizer to help control her bronchial
only for treating patients with cystic fibrosis. secretions and to assist with expectoration of
mucus. Soon after the initiation of therapy, she
experienced dyspnea with audible wheezing.
SIDE EFFECTS OF AND ADVERSE REACTIONS She notified her physician after the first
TO MUCOLYTICS episode and was advised to reduce the dose of
N-acetylcysteine stimulates bronchospasm, especially acetylcysteine. After subsequent treatments,
in patients with bronchial asthma, and should always she still experienced the shortness of breath and
be given with a bronchodilator. When administering a wheezing. Her physician decided to discontinue
mucolytic to any patient whose airway may be compro- the mucolytic therapy.
mised by sudden mucolysis and airway obstruction, the
respiratory therapist should exercise care and always Questions
have suction equipment available. N-acetylcysteine may 1. What caused the patient’s dyspnea and
react with various substances (e.g., rubber, copper, iron, wheezing?
cork) and has a characteristic rotten-egg odor (hydro- 2. Besides discontinuing the acetylcysteine, what
gen sulfide). else could the physician have prescribed?
Dornase alfa has few side effects, and these usually
diminish and resolve in the first several weeks of
therapy. The most common side effects of dornase alfa
are pharyngitis, laryngitis, voice alteration, rash, chest
pain, and conjunctivitis. Dornase alfa must be nebu- Aerosol Antimicrobial Therapy
lized in one of several specifically approved nebulizers Systemic administration of antimicrobial agents is the
[Hudson T Up-draft II disposable nebulizer, Marquest first-line approach in most cases of infection. Certain
Acorn II disposable nebulizer, and PARI LC (reusable) clinical situations and specific antimicrobial agents have
nebulizer with PARI PRONEB compressor]. Other been shown to be appropriate for aerosol administra-
aerosol medications (e.g., beta-agonists, anticholiner- tion. In particular, aerosolized antimicrobial agents in
gics) should never be mixed in the same nebulizer with the prevention and treatment of ventilator-associated
dornase alfa. pneumonia (VAP) are being considered and investigated
because of the emergence of multiple-drug-resistant
gram-negative organisms that are resistant
DOSAGE OF MUCOLYTICS to systemic antimicrobial therapy.13 Currently used
Dosages, concentrations, and trade names of mucolyt- aerosolized antimicrobials include antibiotics, antifun-
ics are provided in Table 7-7. gal drugs, antiprotozoal drugs, and antiviral drugs.
TABLE 7-7 Mucolytic drugs and dosages

Drug (Trade Name) Action Concentration Dosage Comments
Dornase alfa Proteolytic Ampules contain 1 ampule,* once or Approved only for
(Pulmozyme) 1.0 mg in 2.50 mL twice daily CF patients 5 years old
and older
N-acetylcysteine Disrupts disulfide 10% and 20% 3–5 mL, qid Should be used with or
(Mucomyst, Mucosol) bonds solutions after bronchodilator;
10% solution causes
fewer side effects
Sodium bicarbonate Disrupts stability of 4.2% 3–5 mL as needed Few side effects,
amino acid chains mild mucolytic
*Dornase alfa must be nebulized only with approved nebulizers and should never be mixed with other drugs for nebulization; administration by mouthpiece is
recommended to avoid deposition in sinuses.
INDICATIONS FOR AEROSOLIZED this route (e.g., pentamidine, which is used in

ANTIMICROBIAL DRUGS the management of AIDS patients with HIV
There are several generally accepted indications for infections)
administering antimicrobial agents by aerosol: • To eliminate an organism that is colonizing the
respiratory tract (e.g., infected sputum in cystic
• As an adjunct to systemic antimicrobial therapy fibrosis and bronchiectasis patients)
that has been unsuccessful • To help prevent and/or treat ventilator-associated
• For direct topical deposition of an antimicrobial pneumonia (VAP)
that is not appropriate for systemic administra- • To reduce the severity of systemic side effects
tion (e.g., nystatin) (when an antimicrobial is selected that is poorly
• For topical deposition in a pulmonary infectious absorbed through the lungs)
process in which perfusion is limited and
systemic therapy has failed (e.g., aspergillosis) Table 7-8 summarizes drugs, dosages, side effects,
• For topical deposition of an antimicrobial that and clinical indications for currently utilized aerosol
may be more effective, or better tolerated, by antimicrobials.
TABLE 7-8 Selected aerosol antimicrobials

Drug Classification Indication Dosage Side Effects/Comments
Amphotericin B Antifungal Pulmonary 5–10 mg, Fever, headache, anorexia,
aspergillosis, nebulized 2–4 nausea, vomiting, malaise,
coccidiomycosis, times/day muscle and joint pain
candidiasis
Colistin Antibiotic Colonized 100 mg, nebulized Parasthesia, numbness and
pseudomonas in 2–4 times/day tingling of tongue and
CF patients extremities, itching and
urticaria, GI upset, vertigo,
slurring of speech
Nystatin Antifungal Pulmonary 25,000 units, Nausea, vomiting, diarrhea
aspergillosis, nebulized 2–4
Candida albicans times/day or
instilled in ET tube
Pentamidine Antiprotozoal Pneumocystis 600 mg in 6 mL Fatigue is most common side
(Pentam, carinii pneumonia SDW, nebulized* effect; bronchospasm, cough,
Pneumopent) for 20–30 burning sensation in back of
minutes, once/day throat. Bronchodilator should
be given if patient has history
of asthma or smoking.
Ribavirin (Virazole) Antiviral Confirmed respiratory 300 mL of 2% Deterioration of respiratory
syncytial virus (RSV) solution, nebulized function, bacterial
pneumonia for 12–18 hours/ pneumonia, pneumothorax,
day for 3–7 days apnea, ventilator dependence,
rash, conjunctivitis. Drug is
teratogenic and is a risk to
visitors and health care
providers; scavenger systems
should be used. Drug may
also precipitate in exhalation
valve of ventilator circuits,
inline particle filter is
recommended.
*Pentamidine should be nebulized only in an approved micronebulizer.
DISADVANTAGES OF AEROSOL inhalation (nebulization) or by instillation into an

ANTIMICROBIAL THERAPY endotracheal tube. The instillation is followed by
Because the effectiveness of most aerosol therapy is vigorous manual ventilation and positional changes of
patient dependent, the aerosol delivery of antimicrobi- the infant to enhance distribution. Currently available
als is limited and may not achieve its therapeutic goal. exogenous surfactant-replacement drugs fall into three
Limitations and disadvantages of aerosolized antimi- categories based on the source and on the presence or
crobials are as follows: absence of proteins in their chemical composition.
These three categories and their corresponding surfac-
• Bronchospasm is a common adverse reaction. tant preparations are as follows:15
• Systemic side effects may occur.
• The drug may be inactivated by sputum proteins. • Nonprotein surfactants:
• Dosages for the aerosol delivery of antimicrobi- Adsurf (pumactant, which is an artificial
als have not been established. lung-expanding compound [ALEC])
• Optimal delivery and equipment techniques Exosurf (colfosceril palmitate)
have not been determined.
• The drug may not be deposited at the desired • Protein-containing surfactants:
(infected) site. HL-10
• Ambient air may be contaminated by the drug Curosurf (poractant ␣)
(exposing personnel, other patients, and visitors Alveofact (SF-Rl 1)
to the antimicrobial). BLES (bovine lipid extract surfactant)
• The hospital’s population of specific antimicro- Infasurf (Calfactant CLSE)
bial targets may develop a tolerance (see the Newfacten
previous list entry) and hospital-acquired Surfacten (surfactant-TA)
infections may increase. Survanta (beractant)
• Peptide-containing synthetic surfactants:
Surface Active Aerosols Venticute (rSP-C surfactant)
Surface tension is the physical property that creates Surfaxin (lucinactant)
tension at a fluid-air interface. It is the result of the
attraction (cohesion) of like molecules at the surface
of a liquid. Molecules on the surface are attracted Indications for Surfactant-Replacement Drugs.
inward, making the liquid contract to minimize Surfactant-replacement drugs have both prevention and
surface area. Detergents (e.g., surfactant) reduce rescue protocols.
surface tension. The presence of pulmonary surfactant • The prevention protocols recommend the initial
reduces surface tension to ease the inspiratory work of dosage of surfactant drug as soon as possible
breathing; the absence of surfactant (e.g., in infant and after birth (within 15 minutes) for infants born
adult respiratory distress syndromes) increases the with a birth weight of 1250–1350 g or who
surface tension in alveoli, and the increased surface exhibit signs of lung immaturity (e.g., an abnor-
tension, in turn, opposes inflation and contributes to mal lecithin:sphingomyelin ratio).
alveolar collapse. The concept of surface tension is • The rescue protocol is indicated for infants who
applied in two very different clinical situations: infant develop IRDS, as manifested by radiographic
respiratory distress syndrome (IRDS) and fulminating findings and the need for mechanical ventilation.
alveolar pulmonary edema.
Side Effects of and Adverse Reactions to

SURFACTANT REPLACEMENT THERAPY Surfactant-Replacement Drugs. Bradycardia and
Premature or low-birth-weight infants often develop oxygen desaturation occur in 10–20% of infants during
infant respiratory distress syndrome (IRDS). This the dosing procedure. If these occur, the dosing proce-
syndrome is associated with difficulty breathing, poor dure should be interrupted and the infant resuscitated
ventilation and oxygenation, and excessive work of (but not suctioned). Less common adverse effects
breathing, which leads to fatigue, cardiac dysrhythmias, include bronchospasm, vasoconstriction, pulmonary
and deteriorating blood gases. The primary clinical hemorrhage, hypotension, hypocarbia, and apnea.15
feature of the syndrome is a lack of surfactant at birth,
and it may require up to 72 hours for adequate Dosage Guidelines for Surfactant Replacement
endogenous surfactant to be produced.14 Surfactant- Drugs. Trade names and dosages of surfactant-
replacement drugs are generally administered by replacement drugs are summarized in Table 7-9.
TABLE 7-9 Surfactant replacement drugs

Drug (Trade Name) Prevention Protocol Rescue Protocol Supplied/Comments
Beractant (Survanta) Initial dose within 15 Initial dose with 8 hours of Single-dose 8 mL vials
minutes of birth for infants onset of symptoms of IRDS contain 25 mg/mL
weighing less than 1250 g 100 mg/kg birthweight, (200 mg/vial). Usual color
100 mg/kg birth weight, divided into four equal is off-white to light-brown.
divided into four equal quarter-doses and instilled Drug is refrigerated and
quarter-doses and instilled into ET tube* should be warmed by
into ET tube* standing at room
Maximum of four doses
temperature for 20 minutes
Maximum of four doses given no more frequently
or hand-warming for
given no more frequently than every 6 hours
8 minutes before
than every 6 hours
administration; artificial
warming methods should not
be used; unused drug may
be refrigerated only once.
Colfosceril palmitate, Initial dose as soon as Initial does as soon as Sterile lyophilized powder in
cetyl alcohol, tyloxapol possible after birth for possible after onset of 10 mL vials to which 8 mL
(Exosurf Neonatal) infants weighing less than symptoms of IRDS sterile water is added.
1350 g 5.0 mL/kg birthweight, Reconstituted suspension is
5.0 mL/kg birthweight, divided into two equal milky-white and contains
divided into two equal half-doses and instilled into 13.5 mg/mL. If suspension
half-doses and instilled into ET tube* separates, it should be
ET tube* swirled before use; if large
Usually two doses are
flakes or particles persist it
Usually three doses are but adequate but there is no
should not be used.
there is no maximum dosage maximum dosage
*Both manufacturers have specific dosing guidelines, which are provided with illustrations and videotapes.
In 1994, the AARC published a clinical practice quick reduction in the alveolar-capillary diffusion barrier
guideline for surfactant replacement therapy. The created by the frothy, foamy secretions associated with
guideline indicates that repeat doses of surfactant the edema. Ethyl alcohol alters the surface tension of the
should be considered contingent on the continued edema bubbles and causes them to burst. Bursting can
diagnosis of IRDS. The clinical status of the patient be achieved by aerosolizing ethyl alcohol or by passing
dictates the frequency of repeat doses. The recommen- oxygen through a bubble diffuser filled with ethyl
dation is that additional doses of surfactant should be alcohol.17
given at 6- to 24-hour intervals for infants who experi-
ence increased ventilator requirements or who fail to Indications and Contraindications for Ethyl Alcohol.
improve after the initial dose.16 Ethyl alcohol, administered via nebulizer or humidi-
fier, is indicated as an adjunct in the treatment of
acute alveolar pulmonary edema. Treatment of the
DRYING AGENT (ETHYL ALCOHOL) underlying cause of the edema should be ongoing,
Fulminant alveolar pulmonary edema is a rapidly occurring and traditional medical treatments (such as rotating
accumulation of fluid within the alveolar sacs (fulminant tourniquets, diuretics, and digitalis) should continue.
means “coming in lightninglike flashes”). This type of Patients with a history of alcohol abuse or those
edema may be associated with life-threatening acute receiving Antabuse therapy for alcoholism should not
congestive heart failure or with traumatic causes such as receive aerosolized ethyl alcohol.
head injuries (neurogenic), acute mountain (high-
altitude) sickness, heroin overdose, burns, or acute Side Effects of Ethyl Alcohol. Aerosolized quantities
inhalational injuries (e.g., poisonous fumes). of ethyl alcohol rarely cause any adverse reactions, but
The use of ethyl alcohol as a surface active agent in the drying effects may irritate lung mucosa or cause
fulminant alveolar pulmonary edema is based on the bronchospasm. Mild intoxication may occur.
Dosage of Ethyl Alcohol. A short course of therapy pattern, posture, and general appearance. Many
(two to four treatments) is generally sufficient. The institutions require a midtreatment assessment of
recommended dosage is 5–15 mL of 30–50% ethyl respiratory rate and heart rate for all therapy (not
alcohol administered by small-volume nebulizer or just adrenergic drugs).
intermittent positive pressure breathing (IPPB) with After an aerosolized medication treatment, the
oxygen as the source gas. Treatments may be repeated patient should be assessed for a reasonable therapeu-
every 30 minutes. tic response to the drugs and the presence of any
Note: Isopropyl or denatured alcohol must not be adverse reactions. The assessment of the therapeutic
used for this purpose. response must be correlated with the goal of the
therapy (e.g., a patient receiving a fast-acting bron-
chodilator should exhibit some improvement in
Assessing the Effectiveness breath sounds and, if appropriate, peak flow mea-
of Aerosol Medications surement). Patients receiving mucolytic therapy
should be closely monitored for up to 20 minutes
The assessment of a patient before, during, and after after a treatment. The mucolysis will likely continue
receiving aerosol therapy is an integral part of the beyond the treatment period, and the patient may
therapy and care plan. Before administering any require assistance in coughing or clearing the airway.
aerosolized drug, the respiratory therapist should The respiratory therapist can use the immediate
assess basic vital signs, breath sounds, and patient post-treatment period for patient education as well as
status. Except in the case of status asthmaticus, for clinical assessment.
tachycardia in excess of 120 bpm is a general contra-
indication to the administration of beta-agonists. In
status asthmaticus, the patient is in profound respira-
tory distress and is almost certain to be experiencing
Conscious Sedation
anxiety, fatigue, hypoxemia, and acid-base imbalance. Sedation and analgesia imply a physical state in which
In this case, the administration of effective fast-acting a patient is able to tolerate an unpleasant or uncom-
beta 2-selective drugs may actually result in a reduced fortable situation while maintaining adequate
heart rate when respiratory distress and hypoxemia cardiopulmonary function. The patient should also
are relieved. maintain the ability to respond to verbal commands
The clinical decision regarding whether to and tactile stimulation. The patient’s ability to
proceed with a beta-agonist when a patient is respond is important when respiratory therapists
experiencing tachycardia is a medical decision based assist physicians during certain diagnostic and
on all factors in the case. When assessing the therapeutic procedures. Respiratory therapists can
response to an administered bronchodilator, to the minimize associated risks by administering pre-
RT must consider airflow (both inspiratory and scribed medications and closely monitoring patients
forced expiratory maneuvers), along with the pres- during these types of procedures.
ence or absence of an immediate response with Recognizing the fact that respiratory therapists
regard to proper dose, the frequency of administra- assist physicians with the administration of sedative
tion, and overall response to long-term therapy. The and analgesic drugs during certain diagnostic and
clinician must have complete knowledge of the main therapeutic procedures, the AARC published a posi-
effects, mode of action, time course, side effects, and tion statement in December 1997 addressing this
dosage constraints of any medications administered. issue. This statement was revised in March 2000. The
This assessment is critical to documenting the position statement notes that the American Society of
desired patient outcomes and the need for continu- Anesthesiologists (ASA) guidelines call on respiratory
ing prescribed therapy.18 therapists to provide conscious sedation and that
If a patient is unable to perform a reasonable therapists complete formal training and competency
inspiratory maneuver (because of muscle weakness, assessment programs in order to provide this service
confusion, or inability or unwillingness to follow under medical direction. The AARC’s statement fully
directions), then aerosol therapy may not produce the supports this formal training, resulting in competency
desired outcome. Administering the aerosol via IPPB certification, as well as respiratory therapists being
may be appropriate for some patients; alternative permitted to provide the service in accordance with
delivery methods (e.g., oral, intramuscular, or supposi- the ASA guidelines, any institutional policies and
tory) may be required for others (e.g., oral, intramuscu- service operations, the requirements of the Joint
lar, or suppository). Commission [formerly the Joint Commission on
During an aerosol treatment, the therapist Accreditation of Healthcare Organizations (JCAHO)],
should continually monitor the patient’s ventilatory and specific state requirements.19
Anesthesia Drugs Advanced Cardiac Life Support

General anesthesia involves drugs that induce the Pharmacology
absence of all sensation. Probably several types of
Respiratory therapists participate in cardiac resuscitation
mechanisms are at work to produce anesthesia. How-
and may be directed to administer selected cardiovascular
ever, the current theory is that general anesthetics
agents during a cardiac arrest. The American Heart
stabilize the membranes of excitable tissue by influenc-
Association (AHA) publishes standards regarding
ing synaptic transmission and consequently depressing
appropriate drugs, dosages, and sequences of interven-
the central nervous system (CNS). There are four stages
tions during cardiopulmonary resuscitation (CPR).20
of anesthesia:
These standards are routinely reviewed, periodically
• Stage I: State of analgesia (affects midbrain updated, and published through the AHA. Resuscitation
medullary centers and certain spinal drugs primarily include agents that control cardiac
cord areas) rhythm and rate and agents that control cardiac output
• Stage II: State of excitation (affects subcortical and blood pressure. Other advanced cardiac life support
inhibition centers causing excitation, delirium, (ACLS) drugs include narcotic analgesics, volume
and amnesia) expanders, and thrombolytics.
• Stage III: State of surgical anesthesia (affects
midbrain and spinal cord in four distinct planes)
• Stage IV: State of medullary suppression (affects INTRAOSSEOUS (IO) ADMINISTRATION
respiratory and cardiovascular centers, causing OF ACLS DRUGS
apnea, coma, and death) Narcan, atropine, valium, epinephrine, and lidocaine
(NAVEL) may be administered via intraosseous (IO)
There is no one ideal general anesthetic. Anesthesi- access when an IV line cannot be established. This
ologists use a combination of agents to produce safe alternate method is preferred over instillation through
and effective anesthesia, which include: an endotracheal tube because how much drug is
• Gases (nitrous oxide and cyclopropane). actually delivered via the ET route is uncertain.
• Volatile liquids (diethyl ether, halothane, Standard IV doses are used for IO administration. The
methoxyflurane, isoflurane, and enflurane). delivery technique for IO access during CPR20–24 is:
• Intravenous agents (droperidol or diazepam, 1. Insert needle directly through the bone’s hard
fentanyl, ketamine, and propofol). cortex and into the periosteum. Remove stylet
Before surgery, patients are usually given a preanes- and insert catheter.
thetic agent such as morphine, triazolam, a barbiturate, 2. The proximal tibia is often used, but the distal
or atropine to create sedation, reduce apprehension, or femur and iliac spine are alternate administration
decrease salivary and bronchial secretions, depending sites.
on the type of agent used. Finally, some types of 3. Administer drug via IO catheter.
surgery necessitate complete paralysis. In this case, 4. Continue cardiac compressions.
peripheral-acting muscle relaxants are used. These
agents are classified as follows:
DRUGS FOR CONTROL OF CARDIAC RHYTHM
• Nondepolarizing neuromuscular blockers that AND RATE
compete with acetylcholine for the nicotinic-2 Drugs for the control of cardiac rhythm and rate
receptor site at the neuromuscular junction include antiarrhythmics, beta-adrenergic blockers,
(e.g., d-tubocurarine, known as curarin or curare) calcium channel blockers, atropine, isoproterenol,
• Depolarizing neuromuscular blockers that adenosine, and magnesium. Specific clinical indica-
cause a persistent depolarization at the tions, contraindications, mechanisms of action, and
motor end plate so that receptors cannot dosages are provided in Table 7-10.
react with acetylcholine (e.g., succinlycholine
or Anectine)
• Direct-acting neuromuscular blockers that DRUGS TO IMPROVE CARDIAC OUTPUT AND
interfere with the biochemical pathways and BLOOD PRESSURE
prevent the interaction of actin and mysosin in Drugs to improve cardiac output and blood pressure
the muscle (e.g., dantrolene or Dantrium) include beta-adrenergic agents, inotropic agents,
Ventilatory support must always be provided vasopressors, selective vasodilators, and nitrites. Specific
whenever these peripheral-acting muscle relaxants clinical indications, contraindications, mechanisms of
are used. action, and dosages are provided in Table 7-11.
TABLE 7-10 ACLS drugs that affect cardiac rhythm and rate
Mechanism Clinical Contraindications/
Drug of Action Indications Comments Dosage/Route
Adenosine Slows SVT (supraventricular Less effective in 6.0 mg (3mg/mL vial)
conduction tachycardia); narrow- patients taking by rapid IV push over
through AV complex PSVT theophylline 1–2 seconds
node (pulseless SVT)
Atenolol Beta blocker Reduces incidence of Concurrent 5.0 mg (0.50 mg/mL in
ventricular fibrillation (VF) administration with 10 mL vial) by slow IV
in post-MI patients not calcium channel infusion (over 5 minutes)
receiving thrombolytics blockers may cause
hypotension; avoid in
asthmatics
Atropine Inotropic and Symptomatic bradycardia; Use with caution in 0.50–1.0 mg IV repeated
chronotropic second drug (after presence of myocardial every 3–5 minutes up to
epinephrine) for asytole ischemia and hypoxia; maximum of 0.03–0.04 mg/
or bradycardic pulseless increases myocardial kg (usually 3.0 maximum)
electrical activity (PEA) O2 demand
Bretylium Anti-arrhythmic, Persistent ventricular Contraindicated in 5.0 mg/kg IV bolus for
elevates tachycardia (VT), heart block, cardiac arrest from VF or
ventricular VF, multifocal asystole, PEA VT; 5–10 mg/kg over
threshold premature ventricular 8–10 minutes for stable VT
contractions(PVCs)
when lidocaine and
procainamide have failed
Diltiazem Slows Controls ventricular Do not use 15–20 mg IV over
conduction rate in atrial fibrillation concurrently with 2 minutes for acute PSVT;
through SA and atrial flutter beta-blockers or 5–15 mg/hour titrated by
node calcium channel heart rate for maintenance
blockers
Isoproterenol Inotropic and Refractory torsades de Increases myocardial IV infusion 2–10 μg/
chronotropic pointes; temporary O2 demand; do not minute, titrate to heart rate
control of bradycardia in give with epinephrine
heart transplant patients
Lidocaine Anti-arrhythmic, Drug of choice for Contraindicated in IV bolus 1.0–1.5 mg/kg, may
elevates ventricular ectopy, VT, heart block, repeat every 5–10 minutes
ventricular multifocal PVCs, and VF asystole, PEA up to total of 3.0 mg/kg
threshold
Magnesium Magnesium Cardiac arrest associated Renal failure 1.0–2.0 g mixed in
supplement with torsades de pointes 10 mL of D5W IV push in
or hypomagnesemia; cardiac arrest; 1.0–2.0 g
prophylactic after acute in 50–100 mL of
myocardial infarction (MI) D5 IV infusion
Procainamide Anti-arrhythmic, Persistent ventricular Contraindicated in 30 mg/min IV infusion up
elevates tachycardia (VT), VF, heart block, to17 mg/kg for cardiac
ventricular multifocal PVCs not asystole, PEA arrest; 2–8 mg/kg/hour
threshold controlled by lidocaine infusion to control
dysrhythmias
Verapimil Slows Drug of second choice Do not use 2.50–5.0 mg IV bolus over
conduction after adenosine to concurrently with 1–2 minutes; additional
and increases terminate PSVT with beta-blockers or 5.0 mg bolus every
refractoriness narrow QRS and normal calcium channel 15 minutes as needed
in AV node blood pressure blockers (up to 30 mg total dose)
TABLE 7-11 ACLS drugs that affect blood pressure and cardiac output
Amrinone Inotropic; induces Severe congestive heart May exacerbate Initial IV loading dose
reflex peripheral failure (CHF) refractory to myocardial ischemia of 0.75 mg/kg
vasodilation diuretics, vasodilators, or worsen ventricular over 2–3 minutes;
and conventional ectopy; do not mix maintenance infusion of
inotropic agents with dextrose solutions 5.0–15.0 μg/kg/min
or other drugs
Calcium salts Electrolyte Known or suspected Do not routinely use in Initial IV dose,
hyperkalemia or cardiac arrest: do not 10% calcium chloride
hypocalcemia; antidote mix with other drugs solution, 2.0–4.0 mg/kg;
for toxic effects of calcium gluceptate
calcium channel 5.0–7.0 ml; calcium
blocker overdose gluconate 5.0–8.0 mL
Digoxin Slows ventricular Third-line choice for Avoid electrical cardio IV loading dose of
response in PSVT (after adenosine, version if patient is 10–15 μg/kg lean body
fibrillation or diltiazem, verapimil) receiving digoxin (if weight; maintenance
atrial flutter life-threatening, use dose affected by body
lower current settings, size and renal function
i.e., 10–20 J)
Dobutamine Inotropic: may Congestive heart failure Hypotension (systolic 2-20 μg/kg/minute IV
induce reflex or pulmonary congestion pressure <100 mm infusion, titrate so heart
peripheral with systolic pressures Hg) with signs of rate does not increase
vasodilation of 70–100 mm Hg and shock; may cause more than10% of
no clinical signs of tachyarrhythmias, baseline; hemodynamic
shock fluctuations in BP, monitoring
headache, and nausea recommended
Dopamine Dose-related: low Second drug (after Use in patients with Low dose: IV 1–5 μg/kg/
doses cause renal atropine) for hypovolemia only after minute; moderate dose:
and mesenteric symptomatic volume replacement; IV 5–10 μg/kg/min; high
vasodilation, bradycardia; hypotension caution in patients with dose (vasopressor dose):
higher doses cause when systolic BP is cardiogenic shock and IV 10–20 μg/kg/min
peripheral 70–100 mm Hg with CHF; do not mix with
vasoconstriction signs of shock sodium bicarbonate
Epinephrine Increases heart Cardiac standstill; Increased blood 1.0 mg IV push in
rate, force of ventricular fibrillation; pressure and heart cardiac arrest; may
contractions, pulseless ventricular rate may increase repeat every
and coronary tachycardia, pulseless myocardial ischemia 3–5 minutes
perfusing electrical activity (PEA);
pressures: drug of choice in
vasoconstriction anaphylaxis
Nitroglycerin Selective coronary Acute angina pectoris; Do not mix with other Sublingual: 0.3–0.4 mg
vasodilator adjunct in unstable drugs; patient should repeated every 5 minutes
angina and CHF sit or lie down when IV; 10–20 μg/min, titrate
associated with taking this drug; with to effect; hemodynamic
acute MI acute MI, limit systolic monitoring recommended
BP drop to10% in
normotensive and
30% in hypertensive
patients (do not allow
systolic BP to drop
below 90 mm Hg)
(continues)
TABLE 7-11 ACLS drugs that affect blood pressure and cardiac output (continued)
Nitroprusside Potent peripheral Useful in heart failure Hypovolemia Initial IV dose of
vasodilation with hypertension; may 0.1–5.0 μg/kg/minute
be useful in patients
with low cardiac output
and high systemic
vascular resistance
refractory to dopamine
Norepinephrine Potent Severe cardiogenic shock Ischemic heart IV: 0.5–1.0 μg/min
vasoconstrictor; and hemodynamically disease, hypovolemia titrated improve BP
inotropic significant hypotension
OTHER ACLS DRUGS Sodium bicarbonate may be useful in patients with a

Advanced cardiac life support drugs with less direct preexisting metabolic acidosis (i.e., diabetic ketoacido-
myocardial or vasopressor effects may be critical during sis or lactic acidosis), hyperkalemia, or tricyclic or
or after cardiac resuscitation. These drugs include phenobarbitol overdose. In these cases, an initial
analgesics, diuretics, and thrombolytics. Although dosage of 1.0 mEq/kg should be administered once the
sodium bicarbonate has been included in ACLS need has been established by arterial blood gas analy-
protocols, its use has become controversial. Current sis. Specific clinical indications, contraindications,
standards emphasize maintaining oxygenation and mechanisms of action, and dosages for the miscella-
hyperventilation to ameliorate acid-base disturbances. neous ACLS drugs are provided in Table 7-12.
TABLE 7-12 Miscellaneous ACLS drugs

Drug Mechanism Clinical Contraindications/
(Trade Name) of Action Indications Comments Dosage/Route
Flumazenil Reverses Benzodiazepine overdose Do not use suspected 0.20 mg IV over
sedative and or toxicity tricyclic overdose or in 15 seconds; if inadequate
respiratory unknown drug OD; do response administer
depression not use in seizure- 0.30 mg IV over
effects of prone patients 30 seconds; administer
benzodiazepines additional 0.50 mg over
30 seconds once every
minute until adequate
response or total of
3.0 mg is given
Furosemide Loop diuretic Adjuvant therapy of acute Do not use in 0.50–1.0 mg/kg
(Lasix) pulmonary edema in hypovolemic or IV infusion over
patients with systolic dehydrated patients 1–2 minutes
pressure >90 mm
Hg; hypertensive
emergencies; increased
intracranial pressure
Mannitol Osmotic Increased intracranial Monitor fluid status 0.50–1.0 mg/kg IV over
diuretic pressure in management of and osmolarity; 5–10 minutes; additional
neurological emergencies caution in renal failure doses of 0.25–2.0 g/kg
because fluid overload every 4–6 hours as
may result needed; use in conjunction
with mild hyperventilation
TABLE 7-12 (continued)

Drug Mechanism Clinical Contraindications/
(Trade Name) of Action Indications Comments Dosage/Route
Morphine Narcotic Chest pain and anxiety Administer slowly and 1.0–3.0 mg IV (over
analgesic associated with acute titrate to effect, may 1–5 minutes) every
myocardial infarction (MI) compromise 5–30 minutes
or cardiac ischemia respiration; causes
hypotension in volume-
depleted patients
Naloxone Narcotic Respiratory and May cause narcotic 0.4–2.0 mg every
antagonist neurological depression withdrawal 2 minutes (use higher
due to narcotic doses for complete
intoxication or OD narcotic reversal); may
administer up to 10 mg
over short period
(<30 minutes)
Sodium Alkalinizing Preexisting hyperkalemia Not recommended for 1.0 mEq/kg IV bolus,
bicarbonate agent or metabolic acidosis (i.e., routine use in cardiac repeat half dose every
lactic acidosis, arrest patients; 10 minutes; if ABGs
ketoacidosis) adequate ventilation available, manage by
and CPR are major base deficit (BE)
“buffer agents” in according to
cardiac arrest formula-HCO3⫺ dosage ⫽
(–BE) (weight in kg)
(0.3) ⫽ mEq HCO3⫺
Thrombolytic Thrombolytic Acute MI with ST elevation Do not use with active *Alteplase: for AMI, 15 mg
agents (e.g., activity 1 mm or more in at least internal bleeding within bolus, then 0.75 kg/mg
Alteplase two continguous leads, 21 days, history of over 30 minutes, then
TPA tissue given <12 hours from major surgery or trauma 0.50 mg/kg over
plasminogen onset of symptoms; acute within 14 days, aortic 60 minutes not exceeding
activator. ischemic stroke, given dissection, severe 100 mg total; for acute
Streptokinase <3 hours from onset of uncontrolled ischemic stroke: 60 mg
urokinase) symptoms hypertension, known IV first hour, then 20 mg/
bleeding disorders, hour for 2 hours;
lumbar puncture within streptokinase: 1.5 million
7 days, recent IU in a 1-hour infusion
arterial puncture at
noncompressible site,
or history of
cerebrovascular,
intracranial, or
intraspinal event within
3 months
*Dosing guidelines and procedures vary for thrombolytic agents; refer to current information for specific agent being used.
practitioner is administering medicated aerosol

Summary treatments, providing conscious sedation during
A working knowledge of key pharmacological terms certain diagnostic and therapeutic procedures under
and concepts, as well as the dosages, actions, contra- medical supervision, or reviewing medications with
indications, and side effects of the major pharmaceu- a patient, this knowledge makes the respiratory thera-
tical agents, is critical to the practicing respiratory pist more clinically competent. Table 7-13 reviews
therapist in any area of patient care. Whether the and summarizes all of the medications that can be
196
TABLE 7-13 Chart reviewing aerosolized medications used in the delivery of respiratory care (courtesy of Mohawk
Valley Community College, Utica, NY)
Receptors
Generic All Brand % General Chemical Stimulated Administration Adverse Special
Name Names Solution Category Structure or Action & Dosage Effects Considerations
Albuterol Proventil 0.5% Sympathomimetic Saligenin Beta 2 SVN: 2.5 mg MDI: Muscle tremors Used commonly as a rescue
Ventolin Bronchodilator 90 μg/puff inhaler drug (MDI).
Levalbuterol Xopenex Unit dose Sympathomimetic Saligenin Beta 2 SVN: 0.63 mg & Muscle tremors Expensive when compared to
HCL only Bronchodilator R-isomer of 1.25 mg Q6 to cost of Albuterol.
albuterol Q8 MDI:
Salmetrol Serevent DPI only Long-acting Saligenin Beta 2 Diskus DPI: 1 capsule Increases in heart rate Do not use in emergency
xinafoate Sympathomimetic 50 mcg Q12H & cardiac arrhythmias situations!! Slow onset
Bronchodilator if overused. of action
Formoterol Foradil DPI only Long-acting Saligenin Beta 2 Aerolizer DPI: 1 Increased risk of Do not use in emergency
fumarate Sympathomimetic capsule 12 mcg toxicity with overuse situations!! Onset of action
Bronchodilator Q12H of long acting drugs 3 to 4 minutes Peak action
due to accumulation 30–60 minutes
of drug in body.
Ipatropium Atrovent Unit dose Parasympatholytic quaternary Blocks ACH at SVN: 0.5 mg in unit Very few side effects Used for people with problems
bromide only bronchodilator ammonium cholinergic dose MDI: 42 mcg/ associated with taking
compound receptor puff (2p Qid) sympathomimetics. Commonly
given with albuterol.
Tiotropium Spiriva DPI only Long-acting quaternary Blocks ACH HandiHaler DPI: Very few side effects Do not use as a rescue drug in
bromide Parasympatholytic ammonium at cholinergic 1 capsule 18 mcg/day an emergency.
bronchodilator compound receptor
Pirbuterol Maxair MDI only Sympathomimetic Saligenin Beta 2 Autohaler MDI: Muscle tremors Breath-actuated inhaler
Bronchodilator 2 puffs Q4H to Q6H
200 mcg/puff
Racemic Vaponephrine 2.25% Sympathomimetic Catecholamine a, B1, and B2 SVN: 0.25 to 0.5 mls/ Increases in: HR,BP Duration of action is short 25 to
epinephrine Micronephrine Bronchodilator 3 to 5 mis ns 30 minutes for maximum effect.
Terbutaline Bricanyl 0.1% Sympathomimetic Resorcinol B2 > B1 SVN: I to 2 mg. Tremors, increases
Brethaire solution Bronchodilator MDI: 2 puffs in HR
Brethine or MDI
Acetylcysteine Mucomyst 10% 20% Mucolytic NA Breaks the SVN: 3 to 5mls Breaks the disulfide Bronchospasm due to acidity of
solutions disulfide bond TID or QID bond in mucus. solution. Nausea due to the smell.
in mucus Give with a Beta 2 agonist
Dornase alfa Pulmozyme Proteolytic enzyme Breakdown of VN: 2.5 mg in Voice alteration, sore Maintenance therapy drug must
DNA in mucus 2.5 mls ns QD throat, etc. be taken everyday. Uses a
chain special SVN.
Cromolyn Intal Arane SVN Anti-asthmatic NA Blocks SVN: 20 mgs. Coughing and Propholactic type drug, it must
sodium solution ⫹ Mast-cell tid or qid hoarsness be taken everyday. It may take
MDI degranulation up to 2 weeks for maximal
effect.
Flunisolide Aerobid MDI Anti-inflammatory Corticosteroid NA 250 μg/puff Bid Possible immune & Thrush, if mouth is not rinsed
HPA suppression with out after use.
higher doses
Budesonide Pulmicort Liquid Anti-inflammatory Corticosteroid NA SVN: Respules Possible immune & Thrush, if mouth is not rinsed
Respules and DPI UD 0.25 and HPA suppression with out after use.
Pulmicort 0.5 mg QD higher doses
Flexhaler DPI: 90 & 180 mcg/
inhal. BID
Triamcinolone Azmacort MDI Anti-inflammatory Corticosteroid NA MDI: 2 puffs TID.QID Possible immune & Thrush, if mouth is not rinsed
acetonide 100 mcg/puff HPA suppression with out after use.
higher doses
Fluticasone Flovent HFA MDI & DPI Anti-inflammatory Corticosteroid NA MDI: 2 puffs Bid Possible immune & Thrush, if mouth is not rinsed
propionate Flovent DPI: Bid 44 mcg HPA suppression with out after use.
Diskus 50 μg HO mcg higher doses
1OO μg 220 mcg
250 μg
Beclomethasone Qvar HFA MDI Anti-inflammatory Corticosteroid NA MDI: 2 puffs 40 mc/ Possible immune & Thrush, if mouth is not rinsed
dipropionate puff Bid 80 meg/puff HPA suppression with out after use.
Bid higher doses
Pentamidine Pentam via Anti-Protozoal an aeromatic NA SVN: 300 mg of Possible Must take precautions to protect
Nebupent Respigard Anti-Fungal diamidine; it powder in 6 ml sterile bronchospasm and the caregiver and environment.
II neb. Interferes with H2O Q 4 weeks increased risk of Respigard II neb,.neg pressure
cell wall contracting TB from rooms HEPA filters etc.
metabolism HIV patients
Bitolterol Tornalate 0.2% Sympathomimetic PRO-drug/ Beta 2 MDI: No longer available in the USA
mesylate Bronchodilator catecholamine 2 puffs
BID-QID
Salmelrol Advair DPI & MDI Long-acting Saligenin ⫹ Beta 2 DPI MDI Increases in heart Thrush, if mouth is not rinsed
Xinafoate ⫹ HFA Sympathomimetic Corticosteroid 100/50 45/21 rate & cardiac out after use.
Fluticasone Bronchodilator ⫹ 250/50 115/21 arrhythmias if
Propionate Anti-inflammatory 500/50 230/21 overused.
AIbuterol ⫹ Duoneb SVN unit Sympathomimetic Saligenin ⫹ Beta 2 SVN: 3 mg albuterol ⫹ Muscle tremors, same
ipratropium dose Bronchodilator ⫹ Corticosteroid 0.5 mg ipratropium as other
bromide Parasympatholytic bromide sympathomimetics
bronchodilator
albuterol ⫹ Combivent MDI MPI:103 mcg

ipratropium albuteroH-18 mcg
bromide ipratropium bromide
arformoterol Brovana Unit dose Long-acting Saligenin Beta 2 SVN: 15 mcg/2 mls Increases in heart rate Comes in a foil pack. Protect
tartrate only Sympathomimetic Q12H & cardiac arrhythmias from light and excessive heat.
Bronchodilator if overused. Store in a refrigerator.
formoterol Symbicort MDI with Long-acting Saligenin ⫹ Beta 2 2 strengths of MDI: Increases in heart rate Thrush, if mouth is not rinsed
fumarate ⫹ HFA Sympathomimetic Corticosteroid 80/4. 5 mcg or & cardiac arrhythmias out after use.
budesonide Bronchodilator ⫹ 160/4.5 mcg if overused.
Anti-inflammatory
197
administered to the patient in aerosol form, through 4. Epinephrine has which of the following receptor-
either an MDI, a DPI or a nebulizer, in terms of site activities?
brand/generic name, category, chemical structure, a. alpha only
receptor site activity, administration and dosage, b. alpha and beta-1
adverse effects, and special considerations. c. beta-1 and beta 2
d. alpha, beta-1, and beta 2
5. A 1.5% strength solution of a drug contains how
Study Questions many milligrams per milliliter?
REVIEW QUESTIONS a. 0.15
b. 1.5
1. What are the three phases of pharmacology? c. 15
2. What are the mechanisms of action of three types d. 150
of drugs administered by inhalation? 6. How many milliliters of a drug are needed to
3. What are some common indications for, contrain- administer 0.75 mg using a 0.5% strength solution?
dications for, and side effects of, and adverse a. 0.15
reactions to aerosol drugs? b. 1.5
4. Name three aerosol drugs and their appropriate c. 0.3
dosages. d. 3.0
5. How many milliliters are needed to administer 7. A patient is receiving an aerosolized bronchodila-
5 mg of a drug using a 2% strength solution? tor treatment when the respiratory therapist
monitoring the patient notes a heart rate of 140.
6. What drugs are used in the management of
The baseline rate was 84. What action should the
asthma, and why are they used?
therapist take?
7. What are three drugs, including indications and a. Tell the patient to breathe more slowly and
dosages, used in advanced cardiac life support? deeply.
8. What is the appropriate action in a case involving a b. Ask the nurse what should be done.
22-year-old female asthmatic seen in the emer- c. Stop the treatment, notify the patient’s physi-
gency room in respiratory distress? She is presently cian, and document the response in the
taking 16 puffs per day of her albuterol MDI with patient’s medical record.
diminished response. She has been on this medica- d. Add more saline to the nebulizer cup and
tion for 4 years. continue with the treatment.
8. According to the American Heart Association,
which of the following groups of drugs may be
administered by endotracheal instillation as an
1. Delivering a drug via the inhalation route describes adjunct or when an IV line cannot be established?
which phase of pharmacology? a. epinephrine, atropine, and lidocaine
a. pharmaceutical b. norepinephrine, epinephrine, and sodium
b. pharmacokinetic bicarbonate
c. pharmacodynamic c. sodium bicarbonate, adenosine, and lidocaine
d. pharmacologic d. adenosine, atropine, and verapamil
2. Sympathomimetic bronchodilators promote the 9. Which of the following agents produces a muco-
relaxation of bronchial smooth muscle by stimu- lytic effect by disrupting disulfide bonds?
lating the intracellular production of a. nedocromil sodium
a. 5-AMP b. n-acetylcysteine
b. ADP c. sodium bicarbonate
c. ATP d. fluticasone propionate
d. cyclic 39,59 AMP 10. Which of these antimicrobials can be nebulized for
3. Xanthines, such as aminophylline, produce the treatment of Pneumocystis carinii pneumonia
bronchodilation by inhibiting which enzyme? commonly associated with AIDS patients?
a. monoamine oxidase a. amoxicillin
b. catechol-O-methyl transferase b. pentamidine
c. phosphodiestarase c. ribavirin
d. adenyl cyclase d. amphotericin B
CRITICAL-THINKING QUESTIONS 11. Robinson M, et al. Effect of hypertonic saline,

amiloride, and cough on mucociliary clearance in
1. Is it ever possible or permissible for a respiratory
patients with cystic fibrosis. Am J Respir Crit Care
therapist who is administering aerosolized medica-
Med. 1996;153:1503–1509.
tions to patients to alter or change a physician’s
12. American Association for Respiratory Care.
order in the patient’s best interest? Identify a
Bland aerosol administration. Respir Care.
specific instance when a respiratory therapist might
2003;48,5:529–533.
take such an action.
13. Dhand R. The role of aerosolized antimicrobials in
2. A physician orders a medication for a patient who the treatment of ventilator- associated pneumonia.
the respiratory therapist knows is contraindicated Respir Care. 2007;52,7:866–884.
and will result in harm to the patient. What actions 14. Whitaker KC. Neonatal and Pediatric Respiratory
should the therapist take? Explain your answer. Care. Clifton Park, NY: Delmar Cengage Learning;
3. Why is it essential for respiratory therapists to 1996.
be well versed in all areas of pharmacology 15. Sinha S, Moya F, Donn SM. Surfactant for respira-
when it seems as if the only medications they tory distress syndrome: are there important clinical
administer are aerosolized bronchodilators differences among preparations? Curr Opin Pediatr.
and mucolytics? 2007;19:150–154.
16. American Association for Respiratory Care.
Surfactant replacement therapy. Respir Care.
References 1994;39:824–829.
1. Op’t Holt TB. Inhaled beta agonists. Respir Care. 17. Ziment I. Respiratory Pharmacology and Therapeutics.
2007;52,7:820–832. Philadelphia: WB Saunders Co; 1978.
2. Restrepo RD. Use of inhaled anticholinergic 18. American Association for Respiratory Care.
agents in obstructive airway disease. Respir Care. Assessing response to bronchodilator therapy
2007;52,7:833–851. at point of care. Respir Care. 1995;40,12:
3. Bills GW, Soderberg RL. Principles of Pharmacology 1300–1307.
for Respiratory Care. 2nd ed. Clifton Park, NY: 19. American Association for Respiratory Care. Position
Delmar Cengage Learning; 1998. Statement on Administration of Sedative and Analgesic
4. American Association for Respiratory Care. Assess- Medications by Respiratory Care Practitioners. Dallas:
ing response to bronchodilator therapy at point of AARC; March 2000.
care. Respir Care. 1995;40,12:1300–1307. 20. American Heart Association. 2005 American
5. American Association for Respiratory Care. Heart Association (AHA) guidelines for
Selection of device, administration of cardiopulmonary resuscitation (CPR) and
bronchodilator, and evaluation of response to emergency cardiovascular care (ECC) of
therapy in mechanically ventilated patients. Respir pediatric and neonatal patients: pediatric
Care. 1999;44:105–113. advanced life support. Pediatrics. May
6. National Heart, Lung and Blood Institute. Expert 2006;117,5:e1005–e1028.
panel report 3: guidelines for the diagnosis and 21. Banerjee S, Singhi SC, Singh S, Singh M. The
management of asthma: full report 2007. NIH intraosseous route is a suitable alternative to
publication 08-4051. intravenous route for fluid resuscitation in severely
7. Baraniuk JN. Molecular actions of glucocorticoids: dehydrated children. Indian Pediatrics. 1994;
an introduction. J Allergy Clin Immunol. 1996; 31,12:1511–1520.
97:141–142. 22. Brickman KR, Krupp K, Rega P, Alexander J,
8. Phua G-C, MacIntyre NR. Inhaled corticosteroids Guinness M. Typing and screening of blood from
in obstructive airway disease. Respir Care. 2007; intraosseous access. Annals of Emergency Medicine.
52,7:852–858. 1992;21,4:414–417.
9. Holgate ST, Bradding P, Sampson AP. Leukotriene 23. Frascone RJ, Jensen JP, Kaye K, Salzman JG.
antagonists and synthesis inhibitors. J Allergy Clin Consecutive field trials using two different
Immunol. 1996;98:1–13. intraosseous devices. Prehospital Emergency Care.
10. American Thoracic Society/European Respiratory 2007;11,2:164–171.
Society Statement. Standards for the diagnosis and 24. Davidoff J, Fowler R, Gordon D, et al. Clinical
management of individuals with alpha-1 antitryp- evaluation of a novel intraosseous device for
sin deficiency. Am J Respir Crit Care Med. adults: prospective, 250-patient, multi-center trial.
2003;168:818–900. JEMS. Supp. 2005;30,10:20–23.
Suggested Readings Rau JL. Respiratory Care Pharmacology. 4th ed. St. Louis:
Mosby-Yearbook; 1994.
Guntur VP, Dhand R. Inhaled insulin: extending the Rubin BK. Mucolytics, expectorants, and mucokinetic
horizons of inhalation therapy. Respir Care. medications. Respir Care. 2007;52,7:859–865.
2007;52,7:911–922. Siobal, MS. Pulmonary vasodilators. Respir Care.
Noonan M, Rosenwasser LJ, Martin P, O’Brien 2007;52,7:885–899.
CD, O’Dowd L. Efficacy and safety of Szafranski W, Cukier A, Ramirez A, Menga G,
budesonide and formoterol in one pressurized Sansores R, Nahabedian S, Peterson S, Olsson H.
metered-dose inhaler in adults and adolescents Efficacy and safety of budesonide/formoterol in the
with moderate to severe asthma. Drugs. management of chronic obstructive pulmonary
2006;66,17:2235–2254. disease. Eur Respir J. 2003;21:74–81.
CHAPTER 8
Pulmonary Infections
Barbara Ludwig
OBJECTIVES
• Describe the difference between bacterial and viral pneumonias.
• Discuss the effect of immunological disorders on the occurrence, clinical signs and symptoms, and
treatment of pulmonary infections.
• Discuss the diagnosis and medical treatment of pulmonary infections.
• Describe the difference between a tuberculosis exposure and a tuberculosis infection.
• Explain the relationship between tuberculosis and HIV.
• Compare the differences between a tuberculosis infection and MAC infection.
• Discuss the geographic locations of common fungal infections.
• Compare the clinical appearance of a fungal infection in the patient with an intact immune system and the
patient who is immunosuppressed.
CHAPTER OUTLINE
Pulmonary Infections Hospital-Acquired Pneumonia
Community-Acquired Bacterial Patients at Risk for Hospital-Acquired Pneumonia
and Viral Infections Etiologic Mechanism
Viral Infections and Pneumonia Diagnosis
Classifications of Pneumonia Mycobacterium Infections
Community-Acquired Pneumonia Mycobacterium tuberculosis Infection and Disease
Risk Factors of Community-Acquired Pneumonia Etiology and Pathogenesis
Pathogenesis Pathophysiology
Pathologic Changes History and Clinical Manifestations
Bronchopneumonia Diagnosis
Diagnosis of Community-Acquired Pneumonia Respiratory Isolation Requirements
Treatment of Community-Acquired Pneumonia Tuberculosis Resistance
Treatment
(continues)
201
(continued)
Nontuberculous Mycobacterium Infections Histoplasmosis

Clinical Manifestations of NTM Disease North American Blastomycosis
Diagnosis of NTM Disease Diagnosis of Pulmonary
Treatment of NTM Fungal Infections
Fungal Pulmonary Infections Treatment of Fungal Infection and
Fungal Pneumonia
Coccidioidomycosis
KEY TERMS
anergic delayed hypersensitivity mycelium
antibody titer reaction nephrotoxicity
antigenic drift doubling time polymicrobial
antigenic shift empirical primary infection tuberculosis
bullae Ghon complex Ranke complex
caseous necrosis gray hepatization stage reactivation tuberculosis
community-acquired hospital-acquired pneumonia red hepatization stage
pneumonia inflammatory stage resolution stage
coagulopathy miliary tuberculosis
O
n the list of the 10 leading causes of death and the effect on the workplace. The authors concluded
in 2005 in the United States [according to that the cost to the employer for employees with
the National Center on Health Statistics respiratory infections was $112 billion and that
(NCHS)], influenza/pneumonia is the included medical costs and time lost from work.2 A
eighth. In 2005, mortality rate increased significantly comparison of the per-capita expenditures for people
in several diseases; influenza/pneumonia was one of ill with lower respiratory tract infections to those for
them. Of the deaths due to influenza/pneumonia, the average person reveals that the employee costs were
approximately 88% occurred in people 65 years or almost three times more for that employee than for the
older. The age group with the highest death rate was in average employee.3
the oldest sector of the U.S. population, the 85 years
and older group.1 Although the mortality rate is very
high in some vulnerable groups who contract influenza Community-Acquired Bacterial
and pneumonia, complications of pulmonary infection and Viral Infections
can be serious in other age groups, and not all of the
Infections of the respiratory tract are among the most
infections are viral or bacterial. This chapter covers
common afflictions of the human race. In the United
many types of infections, both common and not so
States, respiratory tract infections are responsible for
common. The respiratory therapist needs to know
more visits to physicians than any other disease and
about all of them.
for more time lost from work or school. In 1995, the
National Health Interview Survey (NHIS) estimated
Pulmonary Infections that that there were 174 acute respiratory conditions
Viruses, bacteria, fungi, and parasites are microorgan- per 100 persons per year. The NHIS indicated that,
isms that cause infections of the respiratory system. on average, everyone is afflicted with a respiratory
Some of these infections are contagious and may cause condition or infection at least once a year.2 The
serious respiratory disease with significant mortality in most common bacterial causes of respiratory infection
high-risk groups such as the chronically ill, the elderly, are Streptococcus pneumoniae, Haemophilus influenzae,
and persons with impaired immunity. Besides a Mycoplasma pneumoniae, and C. pneumoniae, and
significant cause of morbidity, a 1997 study reported the most common viral causes are adenovirus,
the costs of medically treating respiratory infections influenza, metapneumovirus, and parainfluenza virus.
CHAPTER 8 ■ Pulmonary Infections 203
Community-acquired respiratory fungal infection is November 2003, nearly 400 cases have appeared
less frequent than bacterial or viral infection, but the in more than a dozen countries. The World Health
common organisms in the United States are Histoplas- Organization is keeping records of human cases, and
mosis capsulatum and Coccidiodes immitis.6 public health officials are closely monitoring outbreaks
because the virus has the potential to change and
become infectious. The potential for an avian flu
VIRAL INFECTIONS AND PNEUMONIA pandemic has resulted in medical communities
Respiratory viral infections cause everything from preparing disaster plans for situations such as a viral
the common cold to severe viral pneumonia. A large pandemic that may be even more severe than the Great
majority of all respiratory infections are viral in origin. Influenza Pandemic of 1918.11
They cause considerable illness but few deaths, except Viruses are transmitted from person to person by
in persons who are immunocompromised. one of two mechanisms.
The most common viral pathogens that cause viral
• The inhalation of virus-contaminated aerosol-
pneumonia in otherwise healthy adults, infants, and
ized secretions expelled into the air during a
children are influenza A and B viruses (50% of cases).
cough or sneeze by the person infected with
The elderly are susceptible to more viruses than healthy
the virus
young adults because of diminishing immunity. Other
• Direct upper airway contact, as would occur by
common viruses that cause viral pneumonia in chil-
getting the virus on your hand and touching
dren are respiratory syncytial virus and parainfluenza
your mouth, eye, or other mucus membrane
virus.6,7
surface9
Influenza viruses A and B frequently cause annual
epidemics and endemics. As the virus passes through With the invasion of the virus through the respira-
the human population, it undergoes frequent antigenic tory tract, the patient may develop a primary viral
mutation owing to viral RNA amino acid recombina- pneumonia or bronchitis. Viral pneumonia is a spread
tions occurring on the viral surface proteins. These of the virus to the bronchi, bronchioles, alveoli, and
changes, called the antigenic drift, are sufficient to alveolar interstitium. The virus damages the bronchi
make the general population’s current immune and bronchioles’ epithelial layer, and the epithelial
defenses inadequate against this new antigen mutation. tissue sloughs to the basement membrane. This loss of
The antigenic drifts are commonly associated with the airway epithelium interferes with normal bronchial
limited epidemics in the community. clearance. The affected areas of the parenchyma
Dramatic changes in viral subtypes can occur become edematous and hemorrhagic. The lungs’
when RNA segments are exchanged between coinfect- intense inflammatory response causes alveolar necrosis
ing viruses. This mutation significantly alters viruses’ and the formation of hyaline membrane.12
genetic makeup by means of new gene formation. This Viral infections affecting the lower respiratory tract
major change is an antigenic shift, and a serious occur in three general situations:
epidemic or pandemic is possible. The population no
• Infections confined to the lung alone, called
longer has immunity against the changed virus.7,9
primary pneumonia, such as respiratory syncytial
Severe influenza outbreaks generally occur every 10
virus, influenza, parainfluenza, and adenovirus
to 30 years. The populations with the highest mortality
• Systemic infections involving the lung, which
in these influenza outbreaks are children, the elderly,
can result from measles, chicken pox, and
and those with comorbid conditions such as chronic
adenovirus
obstructive pulmonary disease, diabetes mellitus,
• Viral infections that occur in the immunosup-
cancer, heart disease, or renal disease. The worst
pressed,12 who are vulnerable to pneumonia
influenza pandemic in history occurred in the closing
from cytomegalovirus, herpes zoster, chicken
years of World War I. An estimated 40 million people
pox, and adenovirus.12
died during the flupandemic of 1918–1919.7,9 The high
death rates occurred in the vulnerable populations: Most viral pneumonias are not fatal. In patients
children under the age of five and adults over who die from their viral illness, the pathologic changes
the age of 70. Surprisingly, a group that is usually less are mainly due to a secondary bacterial infection
affected, adults between the ages of 20 and 40, had called a secondary pneumonia, or superinfection. Injury
devastating death rates that destroyed families and even to the respiratory epithelium with a viral infection
entire communities.10 Avian influenza A has recently allows the bacteria attachment resulting in a bacterial
taken a prominent position among the new viral pneumonia.12 The most common bacteria causing
infections that could develop into a flu pandemic. The postinfluenza pneumonia are Streptococcus pneumoniae,
avian virus usually does not infect humans, but since Staphylococcus aureus, and Haemophilusinfluenzae.7
The patient with an uncomplicated viral infection provides additional protection against other viral
initially presents with classic features of influenza infections and may be helpful in high-risk pediatric
(fever, chills, malaise, headache, and body aches) with patients with an underlying immune deficiency or HIV
recovery after a few days. A worsening of respiratory infection. Neither drug is recommended for use for
symptoms suggests pneumonia. Primary influenzal pediatric patients with congenital heart disease.14
pneumonia is rare, and its presence has a high mortal-
ity rate. The disease can rapid progress, leading to death Treatment
within hours of onset.12 If the viral illness is compli- • Acyclovir is effective against herpes simplex virus,
cated by a secondary bacterial pneumonia, the morbid- herpes zoster, or varicella (chickenpox).
ity and mortality also increase sharply. • Ganciclovir and immune globulin are beneficial
The laboratory findings for a person with viral in the treatment of cytomegalovirus (CMV).4
pneumonia are very different from those for a person Patients with CMV pneumonia either are
with a bacterial infection. In primary viral pneumonia, immunosuppressed by infection with HIV or are
the leukocyte count is normal. If the white count is receiving immunosuppressive drugs (e.g., organ
elevated, the patient may have a superimposed bacte- transplant recipients).
rial infection. Although not often necessary, a specific • Aerosolized ribavirin is no longer a recommended
diagnosis may be made by isolating the virus by treatment for children with respiratory syncytial
demonstrating an elevated antibody titer of the virus. However, ribavirin is effective for treating
person’s serum (the reciprocal of the highest dilution hepatitis C, and it has been administered by
of the serum in which the antibody is detectable). This intravenous in immunocompromised children
test can identify the presence of viral proteins or assay and neonates with adenovirus infection with
the individual’s respiratory secretions or nasopharyn- local and disseminated involvement. The drug is
geal washings for the presence of elevated antibody.6,7 given orally to adults. It is thought to reduce
fever and viral shedding.9
Prevention. Antiviral vaccines (flu shots) play an • Two antiviral drugs—zanamivir and oseltamivir—
important role in preventing influenza infections and are effective against both influenza A and B.
decreasing the severity of the influenza illness. High- Zanamavir is administered by inhaler or nasal
risk groups such as people with comorbid diseases, route and should not be given to patients with
the elderly, or health care workers, are encouraged to reactive airways because of possible broncho-
be vaccinated yearly for influenza prevention.9 The spasm. Oseltamivir is administered orally. The
Centers for Disease Control and Prevention evaluates drugs must be taken early in the onset of influ-
each year the appropriateness of administering the enza symptoms and must be taken for 5 days.7
available antiviral drugs for prophylaxis and treatment Each drug is thought to reduce the viral symp-
of influenza A and B infections. Their recommenda- toms by 1 day.15
tions are based on the circulating influenza A viruses,
including two subtypes (H2N2 and H3N2) and
influenza B viruses. These viruses circulate worldwide, Classifications of Pneumonia
but their prevalence within communities varies. Since In the past, there were only two major classifications of
2006, the neuraminidase inhibitors (oseltamivir and pneumonia: community-acquired pneumonia and
zanamivir) have been the only antiviral drugs recom- hospital-acquired (nosocomial) pneumonia. Today,
mended because of resistance to the admantanes health care changes have caused less clear boundaries
(amantadine, rimantadine). Local health department between the community and the hospital. More
surveillance data and laboratory testing should help hospitalized patients have not totally recovered from
area physicians identify which antiviral drugs to use in their respiratory infections at the time of discharge
preventing or reducing the severity of illness with the from the hospital. Additionally, many patients are
current viral strains.13 receiving medical care from outpatient facilities. In
Other preventive antiviral drugs are the human 2005, the American Thoracic Society and Infectious
monoclonal antibody palivizumab (Synagis) and Diseases Society of America proposed a new category
respiratory syncytial virus immune globulin RSV-IVIG of pneumonia called health-care-associated pneumonia.
(RespiGam). These two medications effectively prevent This classification includes pneumonia cases of patients
the occurrence of respiratory syncytial virus in high-risk who recently had been hospitalized, had received
pediatric patients. Palivizumab is preferred because it hemodialysis or intravenous chemotherapy, or had
does not interfere with vaccinations (measles-mumps- been residents of a nursing home or long-term care
rubella, varicella), is an IM formulation, and has fewer facility. These patients either have serious health care
complications than RSV-IVIG. However, RSV-IVIG issues or are living in institutions designed for senior
citizens. Many are chronically ill. Although these A major mechanism of pneumonia is microaspira-
patients previously were categorized as having tion of upper airway secretions. During sleep, 45% of
community-acquired pneumonia, they are more ill normal subjects aspirate. People with impaired swal-
than the typical case. Their need for hospitalization is lowing reflexes (e.g., stroke, amyotrophic lateral
different, as is their need for different and more potent sclerosis (ALS), muscular dystrophy, postpolio
antibiotics. syndrome) frequently microaspirate when compared
The current classifications of pneumonia are: to normal people. Therefore, their risk for pneumonia
is higher.
• Community-acquired pneumonia.
Chronic excessive alcohol use has many negative
• Health-care-associated pneumonia.
effects that predispose alcoholics to pneumonia.
• Hospital-acquired pneumonia.
Alcoholics routinely are undernourished or malnour-
• Ventilator-associated pneumonia.
ished, and nutritional deficiencies compromise
The last three categories are associated with relatively immune function. The oropharynx of alcoholics can be
serious pneumonias, longer hospital stays, and higher colonized with gram-negative bacteria, and, during
mortality rates.4,5 intoxication, the glottic reflexes are obtunded. This can
lead to microaspiration of upper airway secretions.
Lastly, during sleep, alcohol impairs pulmonary
Community-Acquired Pneumonia clearance mechanisms (e.g., cough reflex, ciliary
According to the National Center for Health, in 1997, clearance). All of these factors combine to make the
86,649 people died of influenza/pneumonia. It was alcoholic more susceptible to pneumonia.6,7
the sixth leading cause of death by any means in the Poor nutritional intake does not give the body
United States, and it was the leading cause of death adequate calories and protein to produce adequate
due to infectious disease.2,11 Most people with numbers of immune cells. Therefore, individuals who
community-acquired pneumonia (CAP) are managed are malnourished have impaired cell-mediated and
by their personal physician and are not admitted to the humoral immunity. Malnourished people frequently
hospital. The most common bacterium found in people have an underlying chronic condition, such as
with CAP is Streptococcus pneumoniae. Other common alcoholism, chronic lung disease, heart disease, or cancer,
organisms causing CAP are Myocoplasma pneumoniae, which may be the basis of their malnutrition.6,7 These
Haemophilus influenzae, viruses, and Legionella species. compounding risk factors put them at a greater risk of
Often, the organism is never identified.7 pneumonia and a fatal outcome.
Smoking also impairs pulmonary defense mecha-
nisms, such as the mucociliary clearance, goblet cell
RISK FACTORS OF COMMUNITY-ACQUIRED function, and secretory IgA function. With lowered
PNEUMONIA lung defenses secondary to smoking, these individuals
Specific risk factors are common among people who are more susceptible to pulmonary infections.7
develop community-acquired pneumonia (CAP): age, People with chronic diseases are susceptible to
alcoholism, poor nutrition, smoking, comorbid bacterial infections. Chronic lung disease patients have
conditions, and institutionalization.7 These risks a greater incidence of CAP than do people with normal
include senior citizens and the chronically ill living lungs. This patient population has a greater incidence
at home, military service personnel who are living in of infections with Streptococcus pneumoniae, Haemophilus
barracks or other communal facilities, and college influenza, and Moraxella catarrhalis.8 People with
students living in dormitories or in fraternity or diabetes mellitus, neurological diseases, heart disease,
sorority houses. or cancer also have a greater incidence of CAP, and
Each year a person lives after the age of 65 they are at a greater risk of developing gram-negative
increases the risk for developing CAP. Research studies infections. Research studies comparing the characteris-
have identified this age group as the one at the highest tics of patients dying of pneumonia with those of
risk of developing pneumonia from Streptococcus patients surviving it have shown that more of the
pneumoniae, the greatest risk of being hospitalized, and deceased patients had comorbid conditions than did
the greatest risk of death from pneumonia. This patient the surviving group.
population also has the greatest incidence of underly-
ing chronic conditions such as cardiovascular disease,
chronic obstructive pulmonary disease (COPD), and PATHOGENESIS
diabetes. An additional problem is that the immune The major mechanisms by which microorganisms invade
function of the elderly is less effective in the presence the lower respiratory tract are by inhalation, by aspira-
of infection than that of younger populations.7 tion, or through the circulation. Community-acquired
pneumonia primarily arises from aspirated bacterial These pneumonic stages are the effects of the bacte-
invasion of the lower respiratory tract, not from inhala- ria on the tissues, the body’s immune response to the
tion or blood-borne bacteria. infection, and the healing process. Not all parts of the
The main reservoir of microaspiration is the lung are in uniform stages of consolidation. Some parts
oropharynx. The oropharynx usually harbors bacteria in of the lung are infected initially, and the infection may
the range of 107–108 organisms per milliliter of saliva, spread. Therefore, one segment of the lung may be in
and it contains many anaerobes and gram-positive the gray hepatization stage while another is in the
bacterial pathogens.16 Streptococcus pneumoniae is a resolution stage.17
common pathogen of the oropharynx. Gram-negative
bacilli are not present as commonly in the oropharynx,
and only a small percentage of the general population BRONCHOPNEUMONIA
harbor gram-negative bacteria in their oropharynx. Bronchopneumonia has the same evolution of consolida-
People normally aspirate oropharyngeal secretions tion, but the infection is not confined to a lobe or
during sleep, when the upper airway glottic reflexes are lobes. The infection usually affects the alveoli contigu-
diminished. Usually, our lower airway defense mecha- ous to the bronchi. The consolidative changes are
nisms cope with this nightly onslaught of bacteria. patchy and follow the pathway of the tracheobronchial
The occurrence of pneumonia is determined by the tree. Streptococcus pneumoniae, Staphylococcus aureus,
interactions among the bacterial growth rate, the Pseudomonas aeruginosa, and Escherichia coli are some
virulence of the organism, and the lower airway organisms that may cause this distribution pattern of
defense mechanisms. The first line of defense is ciliary pneumonia.17
clearance. If the organism reaches the lower airway and
the host defenses are unable to control the prolifera-
tion of the bacteria, colonization swiftly changes to DIAGNOSIS OF COMMUNITY-ACQUIRED
frank infection.6,7 PNEUMONIA
In trying to diagnose CAP, one must look at the
PATHOLOGIC CHANGES individual’s presenting symptoms (see Table 8-1). The
classic constellation of fever, chills, body aches, cough
Bacterial CAP is classically described as a lobar pneumonia.
productive of purulent sputum, chest pain, dyspnea,
It has four distinct pathologic stages:
crackles, and bronchial breath sounds heard on
• In the first 12–24 hours following infection, the auscultation, and dullness to percussion may not be
lung is in the acute inflammatory stage. There present in many patients. Findings vary widely in
is marked inflammatory pulmonary edema with people with CAP. For example, pneumonia in the
engorgement of capillaries and exudation of elderly is frequently atypical in the clinical presenta-
acellular serous fluid into the alveolar spaces. tion. The elderly patient may be afebrile or even
• The next stage of pneumonia progression is the hypothermic. Mental confusion or obtundation is a
red hepatization stage. These changes occur common sign. In many cases, the patient may not
between 24 and 72 hours postinfection. The exhibit abnormal breath sounds on auscultation or
lung has a deep red, liverlike appearance. The show evidence of consolidation on the chest radio-
alveolar spaces are full of coagulated exudate graph.6,7 In recent years, health care practices have
containing fibrin, red blood cells, polymorpho- changed considerably regarding the standard tech-
nuclear leukocytes, and the causative bacteria. niques used to diagnose CAP pneumonia. The routine
• The pneumonic process changes to the gray tests of the past, such as chest X-ray, blood chemistry,
hepatization stage 4–5 days postinfection. The and sputum culture, are not performed unless the
lung is yellow-gray, and the alveoli contain many patient is showing evidence of complications or has
polymorphonuclear leukocytes and very few red risk factors for unusual microorganisms or for a more
blood cells. severe disease.7
• The resolution stage is the final (healing)
phase of the pneumonic process. The enzymes Infections with Specific Microorganisms. Some
released from the leukocytes liquefy the alveolar bacterial organisms cause a clinical picture that can
fibrinous exudate. The phagocytes reabsorb the help physicians identify them.
liquid, and the atelectatic lung starts to reinflate. Mycoplasma pneumonia, an intermediate organism
Necrosis of the lung is uncommon, but a between a bacterium and a virus, causes a pneumonia
transudative pleural effusion (neighborhood process called atypical pneumonia.15 Mycoplasma
reaction) or an exudative pleural effusion or pneumonia accounts for 18% of all community-
empyema may occur.17 acquired pneumonia requiring hospitalization. This is
TABLE 8-1 Pneumonia syndromes

Community-Acquired
Bacterial Viral Immunocompromised Host
Signs Abrupt onset Acute onset of cough, Classic signs may be absent
Productive cough sore throat, nasal New development of worsening
discharge, dry cough, increased respiratory rate
Crackles and rhonchi on
cough, wheezing on
auscultation, dullness to May show new development of
auscultation
percussion over affected purulent secretions, or change
lung areas Mucoid, non-purulent in character or volume of
Purulent sputum, secretions or increased suctioning
⫾ hemoptysis, requirements
Crackles or bronchial
breath sounds
Symptoms Dyspnea, pleuritic chest pain Dyspnea, pleuritic Classic symptoms may be absent,
chest pain ↑ dyspnea
Systemic Toxic chills and high fever, Fever, body aches, Fever, typical systemic
manifestations body aches headache, malaise features absent
Altered mental state ⱖ 70 years/old, altered mental status
Metastatic infection with no recognized cause
may occur
Suggested Attempts to identify a pathogen Diagnostic tests of re- BAL, protected brush or targeted
microbiology not usually indicated. Exceptions spiratory secretions: bronchoscopy recommended
studies for critically ill patients ⫹ Antigen-detection,
⫹ ELISA, Culture
of secretions or
tissue
Chest Localized infiltrates (lobar Diffuse interstitial New or progressive and
radiograph or segmental) infiltrates or patchy persistent infiltrate
Multilobar suggests Streptococcal infiltrates. RSV may OR
pneumoniae or Legionella also show atelectasis
Consolidation
pneumophilia infection and/or hyperinflation.
OR
Interstitial infiltrates suggests
Cavitation
Mycoplasma pneumoniae
infection OR
Pneumatoceles (infants ⬍ 1 year)
Laboratory Leukocytosis, Normal WBC, Drop Leukopenia or leukocytosis
Drop in SaO2, SaO2, Positive blood culture not related
Electrolytes and BUN and to other source
creatinine testing to identify Drop in SaO2,
hydration status Increased oxygen requirements
and/or increased ventilatory
demands
Predisposing Age, smoking history, alcohol, Elderly, children, Organ transplantation, malignancy,
Factors comorbid disease, post-influenza, comorbid disease, immunosuppression, comorbid
immunosuppressive drugs communal living diseases, HIV infection
(dorms, military
barricks)
(continues)
TABLE 8-1 Pneumonia syndromes (continued)

Community-Acquired
Bacterial Viral Immunocompromised Host
Common Streptococcal pneumoniae, Influenza, Parainfluenza, Early onset pneumonia (⬍96 hrs)
microorganisms Mycoplasma pneumoniae Respiratory Syncytial Bacterial: Streptococcal pneumonae,
Chlamydia pneumonia Virus, Adenovirus Staphylococcus aureus, Haemophilus
Haemophilus influenzae, influenza, Moraxella catarrhalis, enteric
Staphylococcus aureus gram-negatives, Serratia marcescens,
(methicillin/oxacillin sensitive), Escherichia coli
K. pneumonae
Viruses:
Influenzae A and B
Respiratory Syncytial Virus
LATE onset pneumonia (⬎96 hrs)
Gram negative bacilli (P. aeruginosa,
Proteus spp. Acinetobacter spp.)
S. aureus (MRSA/ORSA)
VRE,
L. pneumophila,
Viral:
Influenza A and B
Respiratory Syncytial Virus, Adenovirus
Fungal:
Yeasts, fungi, P. jirovecii
a frequency second only to pneumococcal pneumonia. The severity of the infection is determined by the
The outstanding characteristic of this infection is that degree with which the organism is resistant to common
it is a disease of young people. It infects young adults antimicrobials.
or teens in the winter or summer months with a Methicillin-resistant Staphylococcus aureus (MRSA)
higher incidence in small communities such as is a serious staphylococcal infection that is very difficult
schools, colleges, and military barracks. Infected to treat with common antimicrobials. Resistance to
individuals usually present with influenzalike signs methicillin implies resistance to all beta-lactam
and symptoms, which worsen over several days. antimicrobials such as penicillins, cephalosporins,
Sufferers may also complain of headache and may carbapenems, and beta-lactamase inhibitor–beta-
have severe sore throat, earache, laryngitis, and lactam combinations. Hospitalized patients with MRSA
conjunctivitis. The chest X-ray usually shows hilar infection are placed in barrier isolation to prevent the
infiltrates that may be bilateral. The mortality rate is spread of infection to others. The patient can be
low, and the chest X-ray changes usually resolve during isolated in a private room or cohorted (roomed with
convalescence.6,7,12 other patients with the same infection). Personnel
Staphylococcus aureus is a gram-positive coccus that should wear gloves and gowns for direct contact and
usually appears on microscopic examination in should wash their hands after removing their gloves. A
clusters. This microorganism is seen as a cause of mask should be worn if aerosolization or secretion
pneumonia in three major settings:13 splashing possible.
MRSA is transmitted commonly through the
• Secondary complication of a preceding viral transiently contaminated hands of health care
respiratory tract infection workers who have direct contact with an infected
• Hospitalized patients who have host defense patient or with a contaminated surface and do not
impairment and whose oropharynx is colonized wash their hands properly. Airborne transmission can
with Staphylococcus aureus also occur. MRSA may also be transmitted by persons
• Complication of staphylococcus bacteremia or who carry MRSA in their nasopharynx. People who
sepsis are nasal carriers of MRSA (patients or health care
workers) can transmit the infection to other C. pneumoniae and severe chronic adult asthma.
hospitalized patients; this mode of transmission, It has been reported that 8.9% of patients presenting
however, is uncommon. with acute asthma had serological evidence of
The topical antibiotic Mupirocin has excellent C. pneumoniae infection.21 In elderly people with a
antibacterial activity against staphylococcal infections comorbid disease, it may have a lethal clinical course.
and MRSA. Intranasal administration has been suc- This organism has been known to cause hospital-
cessfully used in patients and health care workers acquired pneumonia.20
during MRSA outbreaks to reduce nasal carriage of the Haemophilus influenzae is a small coccobacillary
organism. Mupirocin use has reduced the number of gram-negative organism that is found in two forms: the
MRSA outbreaks in a variety of clinical areas (e.g., unencapsulated strain and the capsulated strain. It is
neonatal nurseries, hemodialysis units, cardiothoracic often found in the nasopharynx of normal healthy
surgery). At home, nasal carriers have not been identi- individuals and in the lower airways of people with
fied as a source of infection to other healthy family chronic obstructive lung disease.19 The infected are
members.18 often elderly or predisposed to pneumonia by alcohol-
In severe cases, staphylococcal pneumonia is ism or chronic bronchitis. The person with chronic
known to cause formation of bullae (enlarged alveoli) obstructive lung disease frequently develops an exacer-
and pneumothorax, as well as microabscesses, pleural bation of the lung disease secondary to infection with
effusion, and empyema. After recovery from pneumo- the unencapsulated strain, which may cause pneumo-
nia, the patient may have residual pulmonary lung nia or acute bronchitis.13
damage such as fibrosis bronchiectasis and pulmonary The pneumonia may take the form of either lobar
cavities.7,17 pneumonia or bronchopneumonia. Factors that
Legionella pneumophila is an aerobic, gram-negative predispose the individual to oropharyngeal coloniza-
intracellular bacillus. This bacillus differs from others tion by gram-negative bacteria and subsequent pneu-
in that it fails to grow on standard media and requires monia are current or recent hospitalization, underlying
a different culture technique. The organism thrives in disease or compromised host defenses, and recent
warm, moist conditions such as soil or stagnant water antimicrobial therapy. Gram-negative pneumonia is
reservoirs (e.g., faulty air-conditioning cooling towers, frequently associated with abscess and empyema, and,
hospital showerheads, and faucets). Bacteria usually after recovery, the person may be left with pulmonary
spread by air, and outbreaks commonly occur in the fibrosis.3,4
summer or autumn. Legionella pneumonia is most
common in the elderly and cigarette smokers, as well as
in people with chronic lung, heart, or kidney disease, TREATMENT OF COMMUNITY-ACQUIRED
diabetes, or suppressed immunosystems.19 It is sug- PNEUMONIA
gested that Legionella be tested for only if the patient is The definitive treatment for CAP is antimicrobial
not responding to beta-lactam antibiotics or is immu- therapy (Table 8-2). The treatment varies according to
nosuppressed or if the suspicion of Legionella infection the microorganism and the sensitivity of the organism
is high. Legionella organisms are known to affect to specific drugs. The initial antimicrobial chosen for
multiple body organ systems in addition to the lung; the person with CAP is empirically chosen (based on
they may cause liver dysfunction, kidney failure, or experience). Frequently, the organism is never iso-
muscle necrosis.6,7 lated. Despite this lack of ability to isolate the
Chlamydia psittaci is the cause of psittacosis, causative organism, knowledge of a patient’s health
which can be spread to humans by infected birds history and risk factors, a physical examination, and
(e.g., parakeets, canaries, parrots). The more common simple testing (SpO2, chest X-ray) enable the physi-
clinical cause of chlamydia infection is the Chlamydia cian to diagnose CAP and to identify a possible
pneumoniae, or TWAR, organism. It was named TWAR causative organism. An infiltrate on a chest X-ray has
because of its similarity to a conjunctival isolate from predictive values for specific clinical signs that, when
Taiwan (TW-183) and a pharyngeal isolate from the present, increase the likelihood that the infiltrate is
United States (AR-39).15 TWAR is a very common due to pneumonia. Increasing the probability that
organism that is known to cause pneumonia in the the patient has pneumonia are the presence of fever
elderly and young adults, but its exact incidence is greater than 37.8ºC, heart rate greater than 100
not known. Young adults have a clinical presentation beats/minute, crackles on auscultation, and decreased
similar to Mycoplasma pneumonia. By age 20, breath sounds in a nonasthmatic.6 For the person
approximately 50% of the population has had the hospitalized for CAP, additional diagnostic
infection and reinfection appears to be common.20 procedures (see Table 8-1) may be necessary so
Research studies have shown a connection between that the appropriate antimicrobial therapy can be
TABLE 8-2 Antibiotic therapy in bacterial pneumonia

Treatment for Resistant
Microorganism 1st Line Antibiotic Alternative Antibiotics Strains
Streptococcal Semi-Synthetic Newer Fluoroquinolones Intermediately resistant
pneumoniae Penicillins e.g. Penicillin e.g. Sparfloxacin, Gatifloxacin; 3rd generation Cephalosporin
G or V 1st generation Cephalosporins Cefotaxime; Ceftriaxone
e.g. Cephalexin, Cefazolin;
Highly resistant
Macrolides e.g. Erythromycin;
Clindamycin Vancomycin + 3rd
generation Cephalosporin
Ceftriaxone,
Cefotaxime; OR Fluoroqui-
nolone e.g. Levofloxacin
Staphylococcal Strains sensitive to 1st or 2nd generation Cephalosporin Methicillin/Oxacillin
aureus penicillinase–resistant e.g. Cefazolin, Cefuroxime; Clindamycin resistant staphylococcus
penicillins (Oxacillin, Carbapenenems e.g. Imipenem, aureus
Cloxacillin, Nafcillin) Merepenem; Macrolides e.g. (MRSA/ORSA)
Erythromycin; Clindamycin; Gentamycin Vancomycin
Vancomycin
Chlamydia Tetracycline e.g. Sulfonamide e.g. Trimethaprim- Treatment based on
pneumoniae Doxocycline Sulfamethoxazole; Macrolides susceptability testing.
(TWAR strain) e.g. Erythromycin; Fluoroquinolone
e.g. Ciprofloxacin
Mycoplasma Tetracycline e.g. Macrolides e.g. Clarithromycin, Treatment based on
pneumoniae Tetracycline; Macrolides Azithromycin; Fluoroquinolone susceptability testing.
e.g. Erythromycin e.g. Levofloxacin
Hemophilus Bronchitis: Sulfonamides Bronchitis: 2nd or 3rd generation Treatment based on
influenzae e.g. Trimethaprim- Cephalosporin e.g. cefuroxime, susceptability testing.
Sulfamethoxazole; cefotaxime; Fluoroquinolones
Serious infections: e.g. Ciprofloxacin; Macrolides
3rd generation e.g. Azithromycin;
Cephalosporin e.g. Serious infections: 2nd generation
Cefotaxime Cephalosporin e.g. Cefuroxime;
Chloramphenicol; Carbapenems
e.g. Meropenem
Legionella Macrolides e.g. Tetracycline e.g. Doxycycline ⫾ Treatment based on
pneumophilia Azithromycin, Rifampin; Sulfonamide e.g. susceptability testing.
Erythromycin ⫾ Rifampin Trimethaprim-Sulfamethoxazole
Fluoroquinolone e.g.
Levofloxacin ⫾ Rifampin;
Klebsiella 3rd or 4th generation Carbapenems e.g. Imipenim; Treatment based on
pneumoniae Cephalosporin e.g. Aminoglycoside e.g. Gentamicin; susceptability testing.
Cefotaxime, Cefepime Extended spectrum penicillin
e.g Pipercillin/Tazobactam (Zosyn)
Sulfonamide e.g. Trimethaprim-
Sulfamethoxazole
Stenotrophomonas Sulfonamide e.g. Tetracycline e.g. Minocycline; 3rd gen- Treatment based on
Maltophilia Trimethaprime- eration Cephalosporin e.g. Ceftaxidime; susceptability testing.
Sulfamethoxazole Fluoroquinolone e.g. Ciprofloxacin
(continues)
TABLE 8-2 Antibiotic therapy in bacterial pneumonia (continued)

Treatment for Resistant
Microorganism 1st Line Antibiotic Alternative Antibiotics Strains
Pseudomonas Aminoglycoside e.g. Carbapenems e.g. Imipenem, Treatment based on
aeruginosa Tobramycin, Gentamicin Meropenem PLUS Aminoglycoside susceptability testing.
PLUS Extended Spectrum e.g. Gentamicin
Penicillin e.g. Ticarcillin,
Pipercillin
Escherichia coli 3rd or 4th generation Penicillin e.g. Ampicillin ⫾ Treatment based on
Cephalosporin Aminoglycoside e.g. Gentamicin; susceptability testing.
e.g. Cefotaxime, Extended Spectrum Penicillin
Cefepime; e.g. Pipercillin, Aminoglycoside alone
In severe illness: Add e.g. Tobramycin
Aminoglycoside
e.g. Gentamicin,
administered. The decision regarding the need to The microorganisms causing HAP reflect the
hospitalize the patient is based on several indicators: number of days after admission that the patients
develop pneumonia.
• Severe leukocytosis or leukopenia
• Significant hypoxemia (PaO2 less than 60 mm • Patients with early-onset HAP develop symptoms
Hg and SaO2 less than 90%) or hypercarbia in fewer than 5 days after admission to the
(PAO2 less than 50 mm Hg), acidosis (pH less hospital, and the organisms are closer to the
than 7.30) causative agents of CAP. The common
• Signs of multiple organ dysfunction microorganisms causing early-onset HAP are
• Severe clinical manifestations (tachypnea, S. pneumonia, S. aureus, H. influenzae,
tachycardia, chest pain, high fever, cyanosis, Enterobacteriaceae, S. marcescens, and E. coli.12
hypotension)6,7 • In late-onset HAP, the infection occurs after
day 5 of admission. The causative agents are
If the patient is hospitalized, in addition to
different from early-onset HAP and reflect the
intravenous (IV) antimicrobials, the following support-
patients’ susceptibility to infection. Common
ive therapies are frequently necessary: hydration with
organisms causing late-onset HAP are gram-
IV fluids, oxygen therapy, and bronchodilator therapy.
negative bacilli (H. influenza, P. aeruginosa),
If the patient’s oxygenation or ventilatory defect is not
S. aureus (MRSA), Acinetobacter spp.,
reversed or controlled with intensive bronchial hygiene,
K. pneumoniae, and viruses.
invasive or noninvasive mechanical ventilation may be
necessary until lung mechanics and oxygenation
improve. PATIENTS AT RISK FOR HOSPITAL-ACQUIRED
PNEUMONIA
Hospital-Acquired Pneumonia The following is a list of the findings from numerous
research studies examining which hospitalized patient
Hospital-acquired pneumonia (HAP) is defined as a
groups are at the greatest risk for developing hospital-
pulmonary infection not present or incubating at the
acquired bacterial pneumonia.21
time of the patient’s admission to the hospital.20
HAP accounts for only about 15% of hospital- • Older than 60 years of age
acquired infections, but it significantly affects patient • Chronic lung disease or systemic disease
morbidity, mortality, and hospitalization costs. The • Intubation (including surgery)
excess duration of length of stay attributed to hospi- • Recent antibiotic history
tal-acquired pneumonia has been estimated to be • Large volume aspiration
6.8–30 days.3 • Depressed level of consciousness
Other clinical situations not listed put the patient its pattern is not pathogen specific, and organism
at risk but to a lesser degree. Also increasing the specific recovery and culture are needed. In addition, the
patient’s risk for hospital-acquired pneumonia is a host presence of sputum or a change in its quantity or
of factors (extremes of age, immune status, comorbid quality is also deceiving. Purulent sputum may be
conditions, ICU admission) and clinical conditions. present with or without pneumonia. The upper airway
Patients for whom the ventilator circuit is changed sinusitis may be the source of the secretions. Other
every 24 hours have an increased risk of airway con- criteria, such as fever, leukocytosis, and immunoglobu-
tamination. Patients receiving stress ulcer bleeding lin elevation, may also not be present in the patient
prophylaxis with H2 blockers are at risk because H2 with HAP. Many patients who are at risk for hospital-
blockers suppress gastric acidity and permit bacterial acquired pneumonia are immunosuppressed, and the
survival in the stomach. Patients who are in the supine immune system may not respond appropriately to the
position have a greater risk of aspiration.21,22 presence of infection.12,21
Bronchoalveolar lavage is the recommended way
to obtain respiratory specimens and identify potential
ETIOLOGIC MECHANISM pathogens and to provide a guide to therapy. Fiberoptic
The mechanisms for development of HAP have similari- bronchoscopy is a common diagnostic device that
ties to those for CAP, but there are important differ- provides access to distal airways. Using a protected
ences. A highly significant shared etiology between CAP brush-sampling catheter or performing a bronchoal-
and hospital-acquired pneumonia is that of microaspi- veolar lavage (BAL) or mini-BAL to obtain lung wash-
ration of upper airway secretions, which is still by far ings can recover uncontaminated specimens for culture.
the most frequent cause of pneumonia. CAP and Uncontaminated specimens are necessary for proof of
hospital-acquired pneumonia are frequently caused by pneumonia and for determining which antimicrobial
self-infection.21 Other shared mechanisms are: will be the most effective for treatment.
These distal airway–sampling techniques have
• Inhalation of contaminated aerosols (common).
limitations when used in the patient with a suspected
• Blood-borne spread from a distant site
hospital-acquired infection. The protected specimen brush
(uncommon).
(PBS) catheter has eliminated the problem of upper
• Translocation of organisms from the gastrointes-
airway contamination of the sample, but the patient’s
tinal tract into the systemic circulation (increases
current antimicrobial therapy reduces the diagnostic
the risk for bacterial overgrowth).
yield of organisms. False negatives are a big problem
• Mucosal disruption of the bowel and impaired
using this technique. Bronchoalveolar lavage is a diagnos-
lymphatic clearance of organisms from the
tic bronchoscopic procedure involving infusion of
bowel.
diluent or washing a lung segment and then aspirating
• Cross-contamination from the hands of
and recovering the fluid for culture. A protected BAL
health care workers or contaminated gloves or
catheter device is available. Normally, this technique
devices (an important shared mechanism).
involves lavaging the lung with approximately 20 mL
• Contaminated water supplies (showers, hospital
of diluent, but a smaller lavage sample may be used
cooling towers).21
with as little as 10 mL of diluent. The smaller lavage
Significant differences between the etiological technique is termed a mini-BAL. When comparing the
mechanisms of CAP and hospital-acquired pneumonia BAL and PSB in diagnosing pneumonia, researchers
are the additional sources of infection that the hospi- found that BAL was more accurate in diagnosing
talized patient is exposed to in the hospital environ- hospital-acquired pneumonia but that PSB was the
ment and the organism pool of that specific hospital. more specific in diagnosing pneumonia.5,22 “A positive
With good handwashing among the hospital staff, BAL culture has a relatively low sensitivity (66%) but
bacterial monitoring, and infection control, these high specificity (90%) for a diagnosis of pneumonia.
sources of infection can be reduced. This means that a negative PSB culture does not
exclude the presence of pneumonia, but a positive PSB
culture confirms its presence with 90% accuracy.”23
DIAGNOSIS
The clinical criteria for the diagnosis of hospital- Treatment. When treating a newly admitted patient
acquired pneumonia are very general and may not be with community-acquired pneumonia, the physician
very helpful.12,21 There are problems with using should start an empirically determined antimicrobial
common criteria in diagnosing HAP pneumonia, immediately, with or without the organism identified.
especially in the ventilator patient. The chest X-ray is The antibiotic regimen should include agents that are
an insensitive tool, and it may show no changes even in a different antibiotic class than what the patient had
in the presence of infection. If an infiltrate is present, received previously.5 Starting antimicrobial therapy
very early reduces the likelihood that the infection will Many patients with hospital-acquired pneumonia,
be fatal, providing the therapy is adequate. The treat- ventilator-associated pneumonia, or health-care-
ment associated with the greatest patient survival is associated pneumonia are infected with multi-drug-
starting very early with the correct empiric antimicro- resistant microorganisms.5 The American Thoracic
bial therapy—possibly with a simple Gram stain Society has identified four principles of antibiotic
coupled with patient signs and symptoms and knowl- management:
edge of patient history and clinical course.24
• Avoid untreated or inadequately treated HAP,
• If the Gram stain indicates a great number of VAP, or HCAP, because the failure to initiate
gram-negative bacilli with a likely Pseudomonas prompt appropriate and adequate therapy has
pneumonia, the patient is treated with combina- been a consistent factor associated with
tion therapy to cover the pseudomonas. increased mortality.
• If the infection is thought to be gram-positive • Recognize the variability of bacteriology from
cocci, the assumption is an infection with one hospital to another, specific sites within the
Streptococcus pneumoniae or Staphylococcus hospital, and from one time period to another,
aureus.23 Since there is a greater risk for MRSA and use this information to alter the selection of
infection or penicillin-resistant streptococci, an appropriate antibiotic treatment regimen for
vancomycin is preferred. any specific clinical setting.
• The presence of mixed flora with no predominance • Avoid the overuse of antibiotics by focusing on
on the Gram stain may indicate an anaerobic accurate diagnosis, tailoring therapy to the results
infection or a polymicrobial aerobic infection (by of lower respiratory tract cultures, and shortening
more than one species). This must be treated by a duration of therapy to the minimal effective period.
carbapenem such as imipenim, with a possible • Apply preventative strategies aimed at modifi-
addition of an antipseudomonal antibiotic.16 able risk factors.5
CASE STUDY 8-1

Hans Shultz is a 68-year-old male who lives in chest, especially in the middle lobe. He has slight
an assisted living facility and who has multiple end-expiratory wheeze in both bases.
hospital admissions for exacerbation of COPD. Prior Extremities: 2⫹ pitting edema
to admission, he experienced two days of increasing
HEENT: Jugular venous distention
dyspnea and cough. He complained of chills, fever,
and body aches, and he was coughing grayish Laboratory Results:
mucus. Mr. Shultz was admitted to the hospital and CXR: Hyperlucent lung fields with infiltrates present
was taken to the pulmonary ICU. in right middle and upper lobes, flat diaphragm with
The following laboratory studies and admitting blunting of the costophrenic angle on the right,
clinical findings were obtained in the hospital’s increased bronchial markings. Chest film from
emergency department during initial evaluation and 3 months previously also had a lateral chest film
treatment. available for review. The lateral chest film showed
increased AP diameter and a large retrosternal
Physical Exam:
airspace. Prominent pulmonary arteries were present.
Mr. Shultz is a cachetic (physical wasting with loss
of weight and muscle mass due to disease), white ABG pH 7.28, PaCO2 66 mm Hg, PaO2 58 on
male in obvious respiratory distress. He is using his 4 L/min. nasal cannula
accessory muscles to breathe and cannot lie flat. Hb. 13 g., Hct. 42%, WBC 13,000 mm3
Vital Signs: HR 116 beats/min, RR 23, BP—
130/86 mm Hg, Temperature 38.3°C, SpO2 85% Questions
on 2 liters nasal cannula. The oxygen liter flow rate 1. What information in this case is consistent with
was increased to 4 L/min. health-care-associated bacterial pneumonia?
Sensorium: Lethargic but arousable 2. What risk factor does this patient have for
Respiratory System: He states that he needs bacterial pneumonia?
two pillows to sleep (he cannot lie flat). He has
3. What complications of COPD and bacterial
distant breath sounds with inspiratory and expira-
pneumonia is this patient manifesting?
tory wheezing and crackles present in the right
CASE STUDY 8-2

Mary Beth Allen is a 35-year-old Caucasian female Na⫹ 132 mmol/dL, K⫹ 2.7 mmol/dL Cl⫺ 106 mmol/dL
with a history of multiple sclerosis and immune BUN 6 mg/dL Creatinine 0.9 mg/dL, Lactic acid 2.4
deficiency who presents to the hospital emergency mmol/L
department with worsening cough and increasing 3/11/11: Patient was admitted through the
shortness of breath. The patient was hospitalized emergency department and transferred to the
4 weeks ago with H. influenza pneumonia, and she general medicine floors. The next morning she
has been hospitalized 3 times in the last 12 months developed respiratory distress. The rapid response
for health-care-associated pneumonia (HCAP) team was activated, they stablilized her, and a
(MRSA ⫻ 1). Patient states she has experienced blood gas was drawn. It revealed a pH 7.35,
increased dyspnea over last 24 hours with cough PaCO2 39 mm Hg, PaO2 36 mm Hg BE 4.1, HCO3
production of brown “nasty” nonbloody sputum. 21.1 mmol/dL on a nonrebreathing mask. She was
She is still working as a nurse and “everyone has then transferred to the Medicine ICU where they
been sick” at home. performed a bronchoscopy and a bronchial alveolar
lavage (BAL). The BAL was negative for malignant
Social History:
cells. The Grocott stain was negative for pneumo-
Patient smokes a half a pack/day of cigarettes.
cystis and other fungal organisms. Bronchial wash
She works as a nurse at a local hospital, and she
fluid revealed the majority of cells were T cells with
has been taking care of patients with worsening
low CD4:CD8 ratio, which can be seen in a variety
pneumonia.
of lung diseases. The CXR showed bilateral subhilar
Vital Signs: infiltrates extending toward the lung bases consis-
RR 16/min, HR 63, BP 147/80 tent with pneumonia.
Height 172 cm, Weight 83.1 kg
Medications:
Chest X-ray results: Bilateral lower lobe
Respiratory medications: Fluticasone/Salmeterol
pneumonia
inhaler (500/50) and an Albuterol MDI
Auscultation: Right upper, middle, and lower lobe
Nonrespiratory medications: Levofloxacin,
have diminished breath sounds
Pipercillin/Tazobactam, Vancomycin, Enoxaparin
Left upper lobe and left lower lobe show
injection, Fluoxetine, Interferon B-1A, Oxycodone/
crackles
Acetaminophen, Modafinil
ABG
pH 7.55, PaCO2 20 mm Hg, PaO2 68 mm Hg Critical Thinking Questions
BE 3.5, HCO3 17.2 mmol/dL on 2 L/min nasal
1. What risk factors does this patient have for
cannula
health-care-associated pneumonia?
Lab Chemistry:ds 2. Why were ER staffers checking for malignancy
Hb 11.2 gm/dL, Hct. 33.4%, RBC 4.0 m/uL, and fungal infections?
WBC 10.4 k/uL, Platelets 283 k/uL
3. What bacterial organisms are possible causes
for her pneumonia?
Mycobacterium Infections MYCOBACTERIUM TUBERCULOSIS

INFECTION AND DISEASE
Several diseases are caused by organisms in the
In the year 2000, the World Health Organization
Mycobacterium genus, but the most common is
estimated that nearly 2 billion people, or about a third
tuberculosis (TB). Tuberculosis is a significant health
of the world’s population, had latent TB infection.
problem throughout the world. Nontuberculous
This huge number of people could develop an active
mycobacterial infections are more prevalent in
disease in their lifetime. Tuberculosis kills more
immunocompromised patients, such as people who
adolescents and adults than any other infectious
have HIV infections, although they may appear in
disease. The greatest proportions of people infected
patients with normal immune function. “HIV infection
with tuberculosis are in developing countries, and the
is the greatest single medical risk factor because
spread of tuberculosis is increasing. Many key determi-
cell-mediated immunity, which is impaired by HIV, is
nants of health are outside the control of health
essential for defense against TB.”25
killing ability of the macrophage. If it survives inside

Spotlight the macrophage, the organism may multiply slowly
On and eventually kill the macrophage. Inflammatory cells
are attracted to the area and cause a tubercle and
Tuberculosis and HIV Infection sometimes pneumonitis.
The role that HIV infection has in tuberculosis is The organisms, now in greater numbers, spread in
considerable. In 2006, there were an estimated the lung and to distant body organs by way of the
710,000 HIV-positive TB patients globally. lymph system and the bloodstream. When the organ-
Approximately 85% of them live in sub-Saharan isms reach areas of high oxygen partial pressures (the
Africa. The World Health Organization estimated apices of lungs, kidneys, brain, long bones, vertebral
that about 10.9 million people were coinfected bodies), further multiplication occurs. It takes 8 to 12
with HIV and M. tuberculosis and have up to weeks for the immune system to process the organism
15% risk of developing TB every year. The largest and “recognize” it as foreign and nonself before the
population infected with both organisms lives in body’s cell-mediated immune (CMI) system focuses on
sub-Saharan Africa, but South-east Asia also has the organism.25,27
a high incidence of this double infection. Myco- The activation of the CMI system activates macro-
bacterium tuberculosis is the leading killer in the phages to ingest and kill the organisms and directs
HIV-positive population and is responsible for T lymphocytes (killer T cells) to the bacillis, where they
more than 50% of AIDS-related deaths. release lymphokines and other chemical killers. The
From World Health Organization, “Tuberculosis,” Fact Sheet 104
CMI system contains the organisms and controls the
(November 2010). http://www.who.int/mediacentre/factsheets/ spread of infection by walling off the organisms with
fs104/en/index.html a granuloma. A granuloma is the result of directed
immunological cellular activity characterized by the
presence of organized white blood cells (e.g., lympho-
officials and physicians (e.g., sanitation and water cytes, macrophages) and capillaries that surround the
supply, education, trade, and environmental and organisms. In some of the granulomas, tissue necrosis
climate change). The governments of many developing occurs, producing a cheese-like material, in a process
countries lack the resources to significantly change called caseous necrosis. The necrotic core of the
these risk factors.26 granuloma contains latent live tuberculous bacteria.
The initial pulmonary lesion of tuberculosis consists of
a caseating granuloma and the adjacent enlarged hilar
ETIOLOGY AND PATHOGENESIS lymph node. The granuloma will calcify in time.
Mycobacterium tuberculosis is a nonmotile, non-spore- Fibrosis and calcification of the layers of the granuloma
forming, aerobic, acid-fast bacillus. Unlike infections frequently occur, seen as an isolated calcified density,
by the other mycobacterial organisms, M. tuberculosis called a Ghon complex, on the chest radiograph in the
infection is transmissible from person to person by way middle or lower lung zones. The term Ranke complex
of inhalation of organisms suspended in aerosolized describes the lesion that includes the Ghon complex
drops of saliva, respiratory secretions, or other body and the patient’s calcified hilar lymph nodes.25,27
fluids. The infected person’s coughing, sneezing, or The other change secondary to activation of the
talking suspends the organism in the air. There are CMI system is that the infected individual’s TB skin test
other means of transmission: will convert from negative to positive.25,27 The skin test
conversion indicates that the immune system has an
• Ingestion of nonpasteurized milk from infected
immunological memory of a previous infection with
cattle
the M. tuberculosis organism. When re-exposed to the
• Lab accidents causing direct inoculation through
tuberculin protein in a TB skin test, the immune system
the skin
shows a tissue reaction on the skin. The entire process
• Inhalation through contaminated fluids or
of initial infection with the organism and the body’s
materials (urine, feces, and sinus drainage).
response is called primary infection tuberculosis.
However, touching inanimate objects such as eating Many people with primary infection tuberculosis are
utensils or clothing cannot transmit tuberculosis.27 asymptomatic and are unaware of the infection. If the
Once the organism is inhaled, it is preferentially initial primary infection occurs in someone who is
transmitted to the bases of the lungs, usually in only immunosuppressed, the CMI system does not respond
one site. When the infectious particle reaches the appropriately, and the infection progresses. Granuloma
alveoli, it may be ingested by a macrophage. Its survival do not form, and M. tuberculosis spreads throughout
depends on the virulence of the organism and the the lungs and to other areas of the body.25,27
Three to five percent of people with a history of • Country or region of birth and residence.
M. tuberculosis infection develop the disease tuberculosis • Exposure history.
within 1 year of initial infection. The occurrence • Recent travel.
represents poor immunological control of the infection. • Socioeconomic status.
Other at-risk populations for progression from primary
The risk factors for postprimary TB are:
infection to tuberculosis disease are diabetics, cancer
patients, and people who are HIV positive or poorly • HIV-positive status.
nourished or who have other causes of immunosup- • Silicosis.
pression. Any decrease in immune function allows • Immunosuppression secondary to disease.
granulomata to break down, and M. tuberculosis organ- • Drugs.
isms escape, causing disease activation. This condition • Medical therapy.
is called postprimary tuberculosis, or reactivation • Lifestyle.
tuberculosis. The lung areas frequently affected in
The clinical signs and symptoms that suggest
postprimary tuberculosis are the apical and posterior
pulmonary tuberculosis are:
segments of the upper lobe. Fifteen percent of the
patients also have extrapulmonary disease. In this form • Respiratory symptoms (cough for longer than
of tuberculosis, active granulomata form, but, because 3 weeks, hemoptysis, chest pain, and dyspnea).
immune function is reduced, it breaks down and • Constitutional symptoms (fever of unknown
continues to allow organisms to escape.25,27 origin, fatigue, night sweats, and weight
Tuberculosis disease, if not controlled with drug loss).25,27
therapy, causes lung necrosis, cavity formation, lung
distortion, and fibrosis. Another form of tuberculosis DIAGNOSIS
is disseminated tuberculosis, known as miliary
Various tests can be performed to help in the diagnosis
tuberculosis. It occurs when a tuberculous lesion
of tuberculosis. The chest X-ray and the tuberculin skin
erodes into a blood vessel and a large innoculum of
test are the initial screening tests and are good prelimi-
organisms is disseminated throughout the body. It
nary indicators of individuals who actually have the
creates millions of metastatic tuberculous lesions
disease. If the results from these tests create a high
2–3 mm in diameter. The condition was named miliary
index of suspicion that the patient has tuberculosis,
because the lesions resemble millet seeds on an X-ray.
then the procedures for organism recovery and sputum
The classic chest radiograph of miliary tuberculosis
smear cultures are performed. With the help of these
shows seeding of the lung with soft nodules approxi-
radiological and laboratory tests, a diagnosis of tuber-
mately 2 mm in diameter. Other body organs are also
culosis infection and disease can be made.25,27
seeded with infection and develop small abscess
pockets. This fulminant spread of infection throughout
the body can be rapidly fatal. The most vulnerable
Chest Radiograph. The chest radiograph is one of the
most common diagnostic procedures used in the initial
population groups to this type of infection are the
medical screening of a patient with suspected tubercu-
elderly, newborns, children, and people with AIDS.27
losis infection. If the patient has chest X-ray changes
consistent with tuberculosis, then additional confirma-
PATHOPHYSIOLOGY tory testing is indicated. Computed tomography (CT)
The changes in pulmonary function in people offers better imaging of possible cavities and is more
with active tuberculosis show a restrictive pattern accurate in locating lung involvement than is a regular
(i.e., decreased lung volume) late in the disease. chest X-ray.
Because tuberculosis is equally unsparing of both the In primary TB, the chest X-ray shows the mid- and
alveoli and the pulmonary blood vessels, the person’s lower lung zone, with or without nodular infiltrates, in
ventilation/perfusion relationship remains balanced, the hilar adenopathy. The chest X-ray of an immuno-
and hypoxemia and hypercarbia are infrequent.27 competent patient with postprimary tuberculosis
shows upper lobe infiltrates (apical and posterior
HISTORY AND CLINICAL MANIFESTATIONS segments) with or without cavity formation. That of an
HIV-positive or immunosuppressed patient shows hilar
Health history is important in providing diagnostic
adenopathy, pleural effusion, and infiltrates in either
clues, possibly giving the physician vital information
the upper or lower lung zone.
necessary to make an accurate diagnosis.28 The risk
factors for infection are:
Skin Testing. Skin testing (Mantoux test) is an important
• Age. diagnostic tool to identify people with prior primary
• Prior TB or a positive TB skin test. tuberculosis or asymptomatic active infection. A person
infected with M. tuberculosis shows a characteristic recently introduced automated culture system using
reddened induration when tuberculin protein (PPD) carbon-14 as a liquid culture medium has reduced this
is intradermally injected. This skin reaction is a time to 1–3 weeks.26
delayed hypersensitivity reaction that is the result
of the individual’s T cells having been sensitized to Direct Recognition of Mycobacterium Species. Rapid
the tuberculosis organism in a previous exposure. direct tests that detect M. tuberculosis nucleic acid are
Five tuberculin units (TU), or 0.1, mL is injected more desirable than the slow, expensive, and some-
intradermally. The diameter of the induration is read times insensitive sputum cultures. For the patient who
at 48–72 hours.28 has a positive sputum smear, the DNA probe and the
polymerase chain reaction (PCR) are direct tests of the
• ⱖ20-mm induration indicates infection.
sputum that give a faster confirmation than the tradi-
• 15-mm induration is positive if the patient is
tional sputum culture and are very sensitive and
from a geographic area where nontuberculous
specific.29
mycobacterial infections are common.
Under evaluation and not clinically available
• ⱖ10-mm induration is a positive test in U.S.
for rapid detection of TB are monoclonal antibodies,
regions where nontuberculous mycobacterial
ELISA, radioimmunoassay, and dot-blot
infections are uncommon.
immunoassays.28,30
• ⱖ5-mm induration is suspicious in HIV-positive
or immunosuppressed individuals or in those in
close contact with a person who has active TB. RESPIRATORY ISOLATION REQUIREMENTS
False negative rates may be as high as 25%, and In the patient with unconfirmed suspected TB, all the
false positives are also common. risk factors for infection and disease progression are
identified. The patient’s clinical presentation, the chest
Sputum Testing. The actual percentage of people in the radiograph findings, and the risk factors are carefully
United States with active tuberculosis is small. How- examined. If the patient information is suggestive of
ever, patients with an unknown history of tuberculosis active tuberculosis, then respiratory isolation should be
exposure who have a positive skin test must have their initiated pending the sputum smear results. The
sputum tested for the presence of infection. Conse- respiratory isolation recommendation can be commu-
quently, the steps involved in testing the sputum for nicated to the Public Health Services’ TB control office,
mycobacterium are important for physicians, nurses, and the patient can be managed on an outpatient basis.
and respiratory therapists to know.25,27 Hospitalization is recommended only if the patient is
acutely ill, if noncompliance is likely (due to alcohol-
Mycobacterial Culture. Does a sputum specimen that ism or past history of noncompliance), or if the home
stains positive for the presence of acid-fast bacilli (AFB) environment or social situation is unstable.25,28
represent active tuberculosis or colonization by nontu-
berculous mycobacterium? To diagnose the patient TUBERCULOSIS RESISTANCE
correctly, the clinician must culture the sputum smear.
An egg- or agar-based medium could be used. Cultur- Multi-drug-resistant tuberculosis (MDR TB) is defined as
ing is a slow process, taking from 3 to 8 weeks. A resistance to more than one antituberculosis drug. This
label mainly refers to the two most common TB
drugs—isoniazid and rifampin. Extensively drug-resistant
tuberculosis (XDR TB) is defined as “resistance to at least
Best Practice isoniazid and rifampin among first line anti-tubercular
drugs, resistance to any fluoroquinolone, and resistance
Sputum Testing to at least one second-line injectable drug (amikacin,
• Morning sputum samples are taken or capreomycin, or kanamycin).”31 In 2006, the U.S.
sputum is induced with warm saline for National TB Surveillance System (NTSS) published that
3 consecutive days. 49 TB cases reported between 1993 and 2004 were
• If sputum samples are negative or sputum XDR-TB. The NTSS found that the cases from the years
could not be obtained, fiberoptic bron- 2000–2006 were likely to be foreign born and less
choscopy (protected brush, BAL, or trans- likely to be persons with HIV infection. Drug resistance
bronchial biopsy specimens) is employed. in the United States varies demographically and
• For children who cannot cooperate with geographically. Mycobacterium tuberculosis resistance is
sputum induction, an early morning gastric common in dense population centers with large
aspirate can be successful. concentrations of people with HIV-positive disease or
foreign-born Hispanic, Asian-Pacific Islanders, or
CASE STUDY 8-3

Ronald Carlyle recently discovered that he was HIV Laboratory findings: Normal fluid and electro-
positive. His physician was performing a complete lytes, Helper T cells (CD4) 660 mm3, other skin
battery of tests, including chest radiograph, blood tests normal.
chemistry, urinalysis, and skin tests. One of the
tests included a TB skin test. Ronald came back Questions
to the physician’s office to have the skin test site 1. Does this patient have tuberculosis infection or
examined. His tuberculin skin reaction was consis- tuberculosis disease? Explain your answer.
tent with a positive skin test. 2. What is the definition of positive PPD test for
Clinical Manifestations: Fatigue, cough, weight an HIV-positive patient?
loss of 10 pounds in the last 3 months, and night
3. Describe two possible mechanisms that would
sweats.
cause TB disease in Mr. Carlyle.
Laboratory Workup: 4. Is a positive sputum test for acid-fast organisms
Chest radiograph: Infiltrates in the upper posterior necessary for an initiation of drug therapy for
and apical segments of both upper lobes. The hilar active tuberculosis?
lymph nodes are enlarged.
African Americans. There is overlap among the indi- • Have known exposure to someone who has
viduals in ethnic groups with the HIV disease group.25 isoniazid-resistant tuberculosis.
• Have known exposure to MDR-TB.28
TREATMENT There are specific indications for antitubercular

drug treatment in the patient who is HIV-positive.
Chemoprophylaxis is a term used to describe the drug
Individuals in this category are persons who:
treatment for an individual who is asymptomatic, is
not shedding organisms in the sputum, and has a • Currently have a positive skin test or a docu-
positive skin test. This person has a primary tuberculo- mented history of a positive skin test without
sis infection but not tuberculosis disease. If the person known exposure to drug-resistant organisms.
never received antituberculosis drug treatment, then he • Are anergic (have diminished hypersensitivity)
or she still has live organisms in lung granulomata, but and a known exposure to drug-sensitive TB.
the organisms are in the resting state. The small focus • Have a positive skin test and a known exposure
of infection that could potentially reactivate is treated to someone with isoniazid-resistant tuberculosis.
by administration of a single drug to kill the still • Have a known exposure to MDR-TB and a high
present occult infection. The drug needs to be taken likelihood of infection (recent skin test converter
over several months because of the slow doubling or anergic to skin tests).28
time (the time it takes to double in number) of the
The drug treatment for tuberculosis disease has
organisms in the resting state.25
varying schedules based on the individual’s drug
Drug treatment (see Table 8-3) should be initiated
sensitivity, immune state, social and economic circum-
as soon as an adequate sputum specimen is obtained
stances, and treatment compliance history. Antituber-
and saved for culture.25 With a negative smear and a
culosis drugs can be toxic, and some patients may not
high likelihood of infection, empiric therapy should be
be able to tolerate certain medications. These patients
considered pending culture results. However, the
will require drug substitutions and possibly longer
presence of a negative smear may indicate that the
treatment schedules.28
patient is not highly infectious.
There are specific indications for antitubercular
drug treatment in the patient with intact immune Nontuberculous Mycobacterium
function who has a positive skin test. Individuals in Infections
this category include persons who:
These organisms can be referred to in several ways:
• Recently developed a positive skin test. nontuberculous mycobacteria (NTM), atypical myco-
• Have an unknown exposure history. bacteria, and mycobacteria other than tuberculosis
• Have known exposure to someone who has (MOTT).25,31 This chapter will refer to infections with
isoniazid-sensitive tuberculosis. these organisms as NTM.
TABLE 8-3 Treatment for acid-fast bacilli infection

Acid-Fast Never Treated Give First
Microorganism Line Drugs Multi-Drug Resistant Specialized Treatment
Mycobacterium First 2 months Treat 18–24 mos Extensively Drug Resistant
tuberculosis Isoniazid (INH) Rifampin Use remaining first 3 drugs in order of preference:
(RMP) Pyrazinamide (PZA) line drugs Capreomycin, PZA, Ethionamide,
Ethambutol (EMB) (PZA, Streptomycin) Cycloserine, Clofazimine,
Stop EMB and PZA after PLUS Fluoroquinolone e.g. Ofloxacin/
2 mos. Levafloxacin; Aminoglycoside
Fluoroquinolone
e.g. Kanamycin, Amikacin
Additional 4 mos of antibiotics
INH ⴙ RMP AND INH resistant
Neg. sputum, cultures Other Aminoglycoside RMP ⫹ EMB ⫹ PZA
and CXR antibiotics if resistant to HIVⴙ – same as conventional drug
OR streptomycin treatment but administer 3 mos.
Pos. sputum, cultures and Alternative Drugs longer
neg. CXR Levofloxacin/Ofloxacin/ Pregnant women – same as conven-
Additional 7 mos of Ciprofloxacin; Cycloserine; tional drug treatment but exclude
INH ⴙ RMP Capreomycin or PZA and Streptomycin
Pos. sputum, cultures and Ethionamide; Clofazamine;
pulmonary cavities on CXR Aminosalicylic Acid
Mycobacterium Pos sputum and cultures Not common Drug resistant
kansasii and CXR Not specified. Treatment based
INH ⫹ RMP ⫾ EMB or on susceptability testing.
Aminoglycoside antibiotic
Streptomycin
Mycobacterium Treat 12–18 mos. or Common Prophylaxis Therapy (1 or more)
avium complex cultures neg for 12 mos. Add RMP; Macrolide antibiotics:
Macrolide antibiotics Aminoglycoside antibiotic Azithromycin, Clarithromycin;
Clarithromycin/Azithromycin Amikacin Rifabutin
PLUS ⱖ 1 of the following: Disseminated disease in
EMB, Fluoroquinolone advanced AIDS
antibiotic Ciprofloxacin, and/
Combinations of 4 to 6 drugs that
or Rifabutin
include: Rifabutin, Fluoroquinolone
antibiotic Ciprofloxacin,
Clofazimine, Aminoglycoside
antibiotic Amikacin
These organisms are commonly occurring and have • M. marinum: Swimming pool granuloma,
been recovered in many parts of the world and in crustacean bites
varied environmental areas (soil, water, dairy products, • M. scrofulaceum: Granulomatous lymph nodes;
house dust, animals).32 The following is a noninclusive found more in children than in adults
list of nontuberculous mycobacterial infections, with • M. fortuitum: Penetrating skin wounds and
some general information about the infection, where foreign body infections (porcine heart valves,
exposure to the organisms could occur, and the popu- breast implants)
lation usually affected. • M. xenopi: Causes pulmonary disease in humans;
water contaminant
• M. avium complex: Common in AIDS patients,
frequently disseminated throughout the body In past years some geographic areas had a high
• M. kansasii: Common in midwestern states; incidence of NTM but little reported NTM disease,
second most common NTM in AIDS patients suggesting an environmental reservoir of infection.
In the United States, scientists report that the appear- MAC be given to all AIDS patients with a CD4 count of
ance of NTM disease appears to be increasing. In recent ⬍75/mm3 and who have had prior opportunistic
years, the number of isolates and the diagnosis of infections (see Table 8-3).31
clinical disease are increasing. These results are mir- Mycobacterium kansasii is the second most com-
rored elsewhere in the world. For example, in France, mon NTM infection in AIDS patients. As is seen in
the incidence of NTM in HIV-negative persons was at people with MAC disease, it appears in people who
one time estimated to be about 0.73 cases per 100,000 are HIV positive late in the clinical course of the
population with MAC (Mycobacterium avium-complex), disease when the CD4 count is ⬍100/mm3. The
M. xenopi, M. kansasii, and rapidly growing mycobacte- disease remains confined to the lung in most cases but
ria commonly seen in the isolates (M. abscessus, can disseminate to the bone marrow, lymph nodes,
M. chelonae, M. fortuitum). Other than better laboratory and skin.33
diagnostic techniques, additional reasons for this Other diseases—such as COPD, cystic fibrosis,
increase in the number of NTM infections are a greater: gastroesophageal reflux disease, and chest wall
disorders—are all associated with NTM. The exact
• Understanding of the disease.
relationship of these problems with NTM is unknown.
• Availability of chest CT scanning.
However, the conditions could facilitate the develop-
• Number of people who are at risk for NTM
ment of NTM infection, and the organism’s presence
(people with compromised immune systems
could certainly worsen these existing diseases. NTM
and older adults).
infection is also a complicating condition in people
Despite the fact that the organism is common, the with bronchiectasis and aspergillus lung disease.
medical community does not know the mode of Apparently, NTM infection in people with bronchiecta-
transmission of NTM to humans. However, it is known sis increases the risk for developing pulmonary asper-
that the transmission of disease, either from person to gillosis. including the invasive form and aspergilloma
person or from animals to people, is not significant. (fungus balls).32
Therefore, people with active NTM do not require
respiratory isolation unless the patient also has a
transmissible coinfection, such as M. tuberculosis. CLINICAL MANIFESTATIONS OF NTM DISEASE
There are three common presentations of NTM has nonspecific signs and symptoms. It can be a
pulmonary NTM in people with normal immunity. pulmonary infection or a disseminated infection, and
the clinical manifestations reflect its origin. In pulmo-
• The first presentation is a tuberculosislike
nary NTM, chronic cough with sputum production and
pattern with upper lobe involvement that
fatigue are common but fever and night sweats appear
appears in older men with a history of smoking
in only 50% or fewer of cases.32 The chest radiograph
and COPD.
may be variable: with or without cavities, bronchiecta-
• The second common presentation is in thin,
sis, patchy infiltrates and nodules in the upper lobes, or
nonsmoking women with skeletal abnormalities
isolated nodules without infiltrates.25
who complain of cough and have nodular
In AIDS patients with MAC infection, since the
bronchiectasis.
initial site of infection is thought to be the gastrointes-
• The last occurs in people who develop a
tinal (GI) tract, this patient population has GI symp-
hypersensitivity pneumonitis after using a hot
toms (nausea, vomiting, diarrhea, enlarged liver or
tub or a spa.
spleen, weight loss, and anorexia).32 The infection
M. kansasii, M. xenopi, M. malmoense, and rapidly disseminates to the bone marrow, liver, spleen, and
growing mycobacteria are commonly associated with lymph nodes. Since the lung is not directly infected,
the first two presentations, and MAC is associated with the lung may have colonies of organisms but not MAC
all of them.32 lung disease. If the AIDS patient also has MAC lung
People with AIDS have an increased incidence for disease, the chest radiograph is often normal but may
all of the NTM mycobacterial infections, but MAC is show nodular or non-nodular infiltrates but no
particularly worthy of mention. MAC is one of the cavities.31–33
AIDS-defining diseases.27,31,33 It is the third most
common opportunistic disease of AIDS patients in the
United States, causing lung infection or bacterial DIAGNOSIS OF NTM DISEASE
colonization and frequently disseminating throughout Unlike that of tuberculosis, the diagnosis of NTM is not
the body. Up to 50% of HIV-positive individuals will made from simply culturing the organism from the
develop disseminated MAC before their death.33 It is lung. Using the high-resolution CT results with the
now suggested that prophylaxis drug treatment for microbiologic studies is essential for diagnosis.
The presence of organisms could represent coloni- reveal the diagnosis with information on recent travels,
zation but not infection. Diagnosing NTM infection is geographic residence, and immunological function.
made according to the following criteria: Several fungal infections cause lung disease that
predominate in certain areas of the United States:
• Clinical criteria: Clinical manifestations consis-
coccidioidomycosis, histoplasmosis, blastomyocosis.34
tent with NTM, with the exclusion of other
The fungal organism is a normal inhabitant of soil in
possible conditions, such as tuberculosis or
the specific location, existing in the mycelium form (as
cancer
a mat of long, branching filamentous tubes). The spore
• Imaging: Chest X-ray with infiltrates, nodules, or
breaks off from the fungus and becomes airborne. It is
cavities OR HRCT showing multiple small
inhaled and deposits in the airways and alveoli. In the
noncalcified nodules and multiple locations of
warm moist environment of the lung, it undergoes
bronchiectasis with variable presence of cavities
complex biochemical reactions and changes into the
• Bacteriology (any met within 1 year): ⬎2 positive
yeast form. The pulmonary scavenger macrophages
cultures from expectorated sputum; ⬎1 positive
ingest the yeast. The yeast survives and multiplies
culture from BAL or wash; transbronchial or
inside the macrophages. It then spreads throughout the
other biopsy showing acid-fast bacillus or
lung and possibly throughout the body by way of the
granulomatous inflammation32
lymphatic and the bloodstream.
The immune response to the infection is in the
TREATMENT OF NTM form of a delayed hypersensitivity reaction mediated by
the lymphocytes. This reaction promotes granuloma
The treatment of NTM in the immunocompetent
formation that is similar to the body’s response to the
population is very challenging. Unlike people with
mycobacterial organisms.34 In the immunocompetent
tuberculosis, most people with NTM are often resistant
host, the organisms disseminate infrequently. If
to many antimycobacterial drugs (e.g., isoniazid,
dissemination occurs, the skin and organs, such as the
pyrazinamide). They must be given a regimen of three
liver, spleen, kidney, bones, brain, and meanings of the
or four antituberculous drugs (see Table 8-3).32 For
brain, could become involved. When the infection is
progressive disease, even other drugs might have to be
confined to the lung, the disease is usually self-limiting,
added to this regimen. Consequently, there may be
and the host may be unaware of the infection. If the
drug interactions or drug toxicity with complications.
organism disseminates, the disease becomes chronic
Treating MAC pulmonary disease or disseminated
and slowly progressive. The person’s symptoms are
MAC in people with AIDS poses even more challenges
similar to those of tuberculosis (night sweats, fever,
to the physician than the immunocompetent group.
anorexia, weight loss) and, once diagnosed, can be
These patients are also receiving medications for their
treated with antifungal agents.34
HIV disease, as well as possible prophylactic or defini-
In the immunosuppressed, the infection is usually
tive treatment for other opportunistic diseases (e.g.,
subacute or chronic. The person has complaints that
Pneumocystis carinii). Adding three more drugs to the
are subtle and vague, such as fatigue, weakness, and
treatment regimen may be difficult for the patient to
malaise. In the person with HIV disease, the symptoms
tolerate.19 Drug interactions, toxicity, and patient
manifest as an unexplained worsening. With progres-
compliance are issues that must be carefully watched.
sion and dissemination, the person could develop
Unlike MAC, M. kansasii responds well to the usual
acute pneumonia, respiratory failure, and other signs of
antimycobacterial antibiotics.31
systemic involvement, such as hypotension and
coagulopathy (a disorder in the blood’s clotting
Fungal Pulmonary Infections system).33,34
Fungal pulmonary infections are uncommon in the
immunocompetent host. Many fungal infections are COCCIDIOIDOMYCOSIS
classified as opportunistic infections that cause disease Coccidioidomycosis is a fungal disease caused by the
in people with depressed immune function (e.g., AIDS, organism Coccidioides immitis. The organism is found in
chronic diseases, steroid therapy, cancer drugs). These the soil in the southwestern United States, including
diseases are in fact so pervasive in the immunosup- the Central Valley of California, Arizona, and parts of
pressed that the presence of specific fungal infections New Mexico and western Texas. The area extends into
places the HIV-positive patient in the AIDS category of northern Mexico, with some disease cases appearing in
disease severity.33 Central America and South America.34,35 Because of its
In immunocompetent people who develop fungal geographic predominance, this disease is also known as
infections, the disease occurs as an acute, benign, San Joaquin Valley Fever or Valley Fever.35 If the
self-limiting respiratory infection. Patient history helps infection disseminates, it affects many body organs and
may penetrate into the cerebrospinal fluid and cause DIAGNOSIS OF PULMONARY FUNGAL
meningitis. Untreated disseminated coccidioidomyco- INFECTIONS
sis with meningitis is always fatal. Even when treated, Serological tests of the patient’s immune response
fungal meningitis in HIV-positive patients has a very may be helpful in diagnosing the fungal infection.
high mortality rate.34,35 Some of the organisms (e.g., Histoplasma capsulatum
and Cryptococcus neoformans) have specific antigenic
products that can be detected on blood sera studies.
HISTOPLASMOSIS Diagnosis is usually confirmed by isolating the
Histoplasmosis is a fungal disease caused by the organ- causative organism. Helpful in diagnosing the specific
ism Histoplasma capsulatum. This infection occurs fungal organism are biopsy of skin lesions, cultures
throughout the world, but in the United States the of sputum, urine, and blood, and bone marrow
organism is endemic to the Ohio and Mississippi river samples. Sputum culture alone is insufficient to
valleys, extending into Maryland, southern Pennsylva- diagnose actual fungal disease; the patient may have
nia, New York, and Texas. The organism is present in fungal colonization of the lung without infection.
soil contaminated by avian droppings (e.g., chickens) The invasiveness of the infection is the true
and bat droppings. Inhalation of the airborne spores diagnostic determination. To confirm the diagnosis of
causes acute infection. systemic fungal infection, cultures or biopsy findings
The infected individual may be asymptomatic or from sites other than the lung, clinical evidence of
complain of a flulike illness. If the person inhaled a infection, and the other clinical and laboratory
heavy concentration of spores, the infection could be findings are necessary.34
severe and lead to severe hypoxemia and respiratory
failure.34,36 Chronic lung disease is a complication of
chronic histoplasmosis. HIV-positive individuals with TREATMENT OF FUNGAL INFECTION AND
disseminated histoplasmosis have a 10% mortality FUNGAL PNEUMONIA
rate.33 Drugs used to treat systemic fungal infections include
flucytocine, amphotericin B, and others in the azole
chemical family (see Table 8-4).34 Amphotericin B is
NORTH AMERICAN BLASTOMYCOSIS very nephrotoxic; patients receiving this drug must be
The organism Blastomyces dermatitidis causes North monitored for nephrotoxicity (a kidney disorder
American blastomycosis. Its geographic distribution is resulting from ingestion of a toxic substance). If
similar to that of H. capsulatum but extends farther patients with normal kidney function at the beginning
north into the north-central Midwest, mid-Atlantic of therapy have a significant elevation in serum creati-
states, upstate New York, southern Canada, and the nine (3–4.5 mg/dL) or if the blood urea nitrogen
southeastern United States. The organism is con- (BUN) increases to ⬎50 mg/dL, the dose of amphoteri-
tained in soil contaminated with animal excrement cin B should be reduced. Permanent damage to the
and decaying organic material. Blastomyces dermatiti- kidneys could occur. Aerosolized amphotericin B has
dis exists in the mycelium form until inhaled into been used to treat patients with colonization of fungal
the airway and alveoli, where it converts into organisms in the lung. In addition to antifungal drugs,
yeast.34,37 surgery to remove sites of localized infection may be
The immunological response is a delayed hyper- effective in a limited number of cases.34
sensitivity reaction that is monocyte derived. Macro-
phages phagocytize the yeast, and monocytes and
giant cells infiltrate the infection site. They cause an
Summary
inflammatory tissue reaction with granuloma forma- Infections of the respiratory tract are among the most
tion and tissue necrosis with subsequent pulmonary common infections of the human race. In the United
fibrosis. Like other fungi, the organism can dissemi- States, respiratory tract infections are responsible for
nate and cause bodywide infection and granuloma more visits to physicians than any other diseases and
formation.34,37 This fungal disease is known for for more time lost from work or school.
causing skin lesions that abscess and scar. Other Viruses, bacteria, fungi, and parasites are organisms
frequently affected areas are the bone, thyroid, that cause infections of the respiratory system. Some of
prostate, epididymis, testes, and kidneys. The disease these infections are contagious and may cause serious
course is usually slowly progressive, but in some respiratory disease. Pneumonia, an infection of one or
cases it can have a fulminant course. Untreated both lungs, is extremely contagious and is the result of
blastomycosis is fatal. Antifungal drugs are usually breathing in small droplets that get into the air when
effective.37 an infected person coughs or sneezes. Pneumonia can
TABLE 8-4 Fungal lung disease treatment

Alternative Drug
Microorganisms Drug of First Choice Treatment Specialized Treatment
Aspergillus spp. Invasive infections: Oral Itraconazole Unresponsive Infection: Lipid-
IV Amphotericin B ⫾ associated formulations of
Flucytosine Amphotericin B
Blastomyces Itraconazole Mild disease in Life-threatening infections
dermatitidis Itraconazole-intolerant Amphotericin B
Fluconazole or
Amphotericin B
Candida albicans Esophageal candidiasis Itraconazole Invasive infection
Fluconazole Amphotericin B
Unresponsive Disseminated Disease
esophageal candidiasis Caspofungin
Voniconzole
Voriconazole
Coccidiodes immitis Mild/moderate Itraconazole AIDS-associated severe disseminated
non-meningeal infection: Amphotericin B initially;
extrapumonary infection maintenance with Itraconazole OR
Fluconazole Fluconazole
Severe illness Unresponsive Infection: Lipid-associated
Amphotericin B formulations of Amphotericin B
Cryptococcus Systemic disease Fluconazole, AIDS patients
neoformans without meningitis Itraconazole; alternative Fluconazole and Flucytosine
Fluconazole maintenance (HIV⫹)
AIDS–associated meningits:
More severe cases Amphotericin B
Amphotericin B and Flucytosine
IV Amphotericin B by HIV⫹ maintenance Fluconazole or
Fluconazole mainte- Itraconazole
nance in HIV+ patients
Histoplasma Itraconazole Amphotericin B AIDS-associated severe disseminated
capsulatum infection: Amphotericin B initially;
maintenance with Itraconazole
also result when bacteria or viruses from the mouth, are able to multiply in the lung, they can spread there
throat, or nose inadvertently enter the lungs. and into other organs. Any patient with an evaluation
Antibiotics are used to treat pneumonia caused by suggestive of active tuberculosis should be placed in
bacteria, the most common cause of the condition. respiratory isolation.
Pneumonia can also be caused by viruses, such as those
that cause influenza (flu) and chickenpox (varicella).
Varicella pneumonia, which is rare, can be treated with
antiviral medicine.
Study Questions
In most cases pneumonia is a short-term, treatable REVIEW QUESTIONS
illness. But frequent bouts of pneumonia can be a
serious complication of a long-term (chronic) illness, 1. Name the common microorganisms that cause
such as chronic obstructive pulmonary disease community-acquired bacterial pneumonia.
(COPD). 2. Patients in the hospital are at risk for developing
M. tuberculosis infection is transmissible from hospital-acquired pneumonia due to the fact that
person to person by way of inhalation of organisms most suffer from immunological disorders. Which
suspended in aerosolized drops of saliva, respiratory group of patients is at the most risk for developing
tract secretions, or other body fluids. If the organisms hospital-acquired pneumonia?
3. Tuberculosis is a pulmonary disease that is 8. What community-acquired pneumonia is associ-

becoming more problematic because of the ated with a high incidence in small communities
drug-resistant nature of some of the mycobacterium. such as schools, colleges, and military barracks?
What are the procedures for a diagnosis of a. Klebsiella pneumonia
tuberculosis? b. Staphylococcus pneumonia
4. Name common fungal diseases of the lung and c. Chlamydia pneumonia
the procedures for the diagnosis of this type of d. Mycoplasma pneumonia
disease. 9. What are clinical manifestations of community-
acquired pneumonia?
a. afebrile but acutely ill
MULTIPLE-CHOICE QUESTIONS b. change in sputum color
1. Which of the following organisms is a virus? c. chills, high fever, body aches
a. Influenza d. diffuse infiltrates on chest X-ray with normal
b. Haemophilus influenzae breath sounds
c. Klebsiella pneumoniae 10. What patient is not at risk for health-care-associated
d. Legionella pneumophila pneumonia?
2. How long after the Mantoux test must you wait a. a 68-year-old woman living with her daughter
before checking for a tissue reaction? b. a 10-year-old receiving outpatient chemotherapy
a. 8–16 hours for a brain tumor
b. 24–36 hours c. a 75-year-old man residing in an assisted living
c. 48–72 hours facility
d. 96–120 hours d. a 50-year-old woman going to an outpatient
dialysis center 3 times a week
3. What is the drug of choice for mycobacterium
tuberculosis chemoprophylaxis?
a. isoniazid CRITICAL-THINKING QUESTIONS
b. rifampin
c. pyrazinamide 1. During the acute inflammatory or consolidative
d. gentamycin stage of pneumonia, appropriate therapy selection
would include antibiotics, bed rest, fluids and
4. Which of the following nontuberculous mycobac-
supplemental oxygen. Why might the use of other
terial organisms causes a common opportunistic
modalities be needed during the resolution stage?
infection in AIDS patients?
What other modalities might you include? What
a. Mycobacterium chelonae
would be the rationale for each of the modalities
b. Mycobacterium kansasii
you would add?
c. Mycobacterium fortuitum
d. Mycobacterium avium-intracellulare 2. Why are the Occupational Safety and Health
Administration guidelines for care of patients with
5. What fungal infection is endemic to the Ohio and
active tuberculosis more complex than for patients
Mississippi river valleys?
with most other pulmonary infections?
a. coccidioidomycosis
b. histoplasmosis 3. Why might the various fungal diseases that
c. cryptococcus impact the pulmonary system have geographical
d. North American blastomycosis associations?
6. What is the recommended antibiotic for MRSA 4. With all of the drug-resistant strains of bacteria
infections? being discovered, what could the health care
a. oxacillin community do to decrease the incidence of this
b. erythromycin problem?
c. amikacin
d. vancomycin
7. What changes in the virus is responsible for References
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CHAPTER 9
Airflow Limitation Diseases

Barbara Ludwig
OBJECTIVES
• Describe the difference between chronic bronchitis and emphysema.
• Describe the pharmacologic treatment of airflow limitation and compare the recommended drug therapy
treatment of asthma to that of COPD.
• Describe the differences between COPD and asthma.
• Describe the clinical categories of asthma.
• Compare the clinical presentation of a patient with emphysema to that of a patient with asthma.
• Describe the different causes of bronchiectasis.
• Identify the bacteria commonly found in patients with chronic bronchitis and bronchiectasis.
CHAPTER OUTLINE
Asthma Pathogenesis and Pathophysiology
Demographics and Statistics Diagnosis of COPD
Atopic and Nonatopic Asthma Clinical Manifestations
Asthma Triggers Stages of COPD
Airway Inflammation and Airflow Limitation Complications
Diagnosis of Asthma Treatment
Asthma Classifications Bronchiectasis
Asthma Management Diagnosis
The Acute Asthma Attack Etiologies
Chronic Bronchitis (COPD) and Emphysema Treatment
Definitions
Risk Factors
227
KEY TERMS
asthma direct costs paraseptal emphysema
atopy indirect costs vagal tone
centriacinar emphysema panacinar emphysema
T
he primary airflow limitation diseases days, workdays, productivity, and productive years
discussed in this chapter are asthma, bronchi- secondary to premature death. In 1998, the indirect
ectasis, chronic bronchitis, and emphysema.1 cost of asthma was projected at $5.33 billion per year.4
Asthma is in a separate category of airflow This includes family loss of income and productivity
limitation because it is a reversible disease that when parents stay home to take care of their asthmatic
responds to bronchodilator therapy. Bronchiectasis, child. In 1999, over 5000 deaths were attributed to
chronic bronchitis, and emphysema are known by the asthma, with most of the deaths in the 65-year-and-
acronym COPD (chronic obstructive pulmonary disease). over age bracket.3,4
The airway obstruction in these diseases is not reversed
by bronchodilators, and the diseases result in perma-
nent and progressive changes. See Table 9-1 for the ATOPIC AND NONATOPIC ASTHMA
differences among these four disease states.
Asthma is classified as a chronic inflammatory disease.
The inflammation is a consequence of the effects of
Asthma activated inflammatory cells. This immune system
response is classified as a type 1 hypersensitivity reaction,
Asthma is a chronic inflammatory disorder of the
which is characterized by an IgE antibody–mediated
airways in which many immunological cells play a role.
inflammatory response. The immune reaction is
The predominant cellular elements are mast cells,
initiated by exposure to an antigen protein to which
T lymphocytes, eosinophils, macrophages, and neutro-
that individual is sensitive; this sensitivity is called
phils. In people who are susceptible to this disease, the
atopy. After birth, the mature immune system develops
inflammation causes recurrent episodes of wheezing,
immunological tolerance. Atopic people’s immune
dyspnea, chest tightness, and coughing. The airflow
systems are intolerant of certain antigens, and they
obstruction may reverse spontaneously, or it may
respond excessively to exposure to those antigens.2,5
require treatment for reversal.
It is thought that atopy is a familial tendency, and it is
Asthma has several key characteristics. When these
considered the strongest predisposing factor for
characteristics are committed to memory, the asthmatic
developing asthma.6,7
patient’s signs, symptoms, and treatment are easier to
An individual with atopy has elevated IgE in the
understand:2
serum that has formed against specific antigens (aller-
• Chronic inflammatory disorder gens). The patient also has a positive skin test against
• Recurrent episodes of breathing difficulties the offending allergens. Many environmental sub-
• Characterized by airflow limitation stances are potential allergens or triggers (e.g., house
• Reversible dust mites, cats, pollen, and fungi), and each atopic
person has a distinct allergic profile. The individual’s
immune system determines the strength of the inflam-
DEMOGRAPHICS AND STATISTICS matory response to the allergen stimulus. Atopic
Asthma is the most common chronic childhood asthmatics have an exaggerated or hypersensitive
disease. It affects 22 million people, including approxi- response to a trigger that would not elicit a response
mately 6.5 million children.2,3 The most recent statis- in a nonallergic individual.5
tics (2007) from the Centers for Disease Control and A type IV hypersensitivity reaction may also cause
Prevention estimated that people with asthma account asthma in susceptible individuals. It is an IgG-
for approximately 444,000 hospitalizations annually mediated immune response. This immunological
with an average length of stay of 3.2 days. The inpatient reaction may be secondary to exposure to environ-
hospital services are the largest single direct cost of mental allergens, but it can also be secondary to
asthma, at an estimated $1 billion per year. The triggers such as viral infections or aspirin. Some
indirect costs of asthma are related to a loss of school antigens are unknown.8
CHAPTER 9 ■ Airflow Limitation Diseases 229
TABLE 9-1 Airflow limitation diseases

Chronic Bronchitis Emphysema Bronchiectasis Asthma
Etiology Cigarette smoking, Cigarette smoking, Infants and children Non-specific bronchial
environmental homozygotic 1- Congenital cause from hyperreactivity to a variety
pollution antitrypsin deficiency, a developmental arrest of stimulants: airborn aller-
some connective of the bronchial tree gens, infection, pollution,
tissue disorders, drugs, emotion, exercise,
Adults
IV drug abuse, gastroesophageal reflux
Infectious insult
Airway drainage
impairment
Airway obstruction
Defect in host
defense
Pathologic Bronchial mucus gland Air space enlarge- Abnormal bronchial Smooth muscle hypertro-
changes hyperplasia, basement ment of respiratory dilation with bronchial phy, hyperplasia of mucus
membrane thickening, bronchioles and/or wall destruction glands and goblet cells,
hyperplasia of mucus alveolar ducts, alveoli and transmural mucosal and submucosal
gland and goblet cells, (Centriacinar and/or inflammation edema, ↑ number of
narrowing of small Panacinar) Airway dilation is inflammatory cells,
airways cylindrical, cystic, or subepithelial fibrosis with
varicose collagen deposition
Clinical Chronic productive Dyspnea, barrel General Findings: During asthma attack
Features cough (copious, chest, cachetic, Digital clubbing, weight Tachypnea, dyspnea,
purulent in acute pursed lip breathing, loss, nasal polyps, and accessory muscles use,
exacerbations), accessory muscles chronic sinusitis pursed lip breathing,
hemoptysis, use, diminished wheezing on auscultation
Respiratory Findings:
wheezing and rhonchi breath sounds
on auscultation, Cough, daily
systemic evidence of mucopurulent
cor pulmonale sputum production,
hemoptysis, pleuritic
chest pain related to
coughing
Aucultation: crackles,
rhonchi, wheezing,
/ dyspnea,
Multiple episodes of
infection with increased
sputum production over
baseline, increased
sputum viscosity, and
foul odor of sputum
Precipitating Infection, atmospheric Infection, atmo- Infection, other Increased exposure to
Factors pollutants, temperature spheric pollutants, conditions related asthma triggers, infection
temperature to the causes of
bronchiectasis
(continues)
TABLE 9-1 Airflow limitation diseases (continued)

Chronic Bronchitis Emphysema Bronchiectasis Asthma
Chest ↑ bronchial markings, Hyperradiolucency, General Findings: During asthma attack
radiograph prominent pulmonary wide intercostal Increased pulmonary Hyperradiolucency, wide
arteries spaces, flattened markings, honeycomb- intercostal spaces,
diaphragm, long, ing, atelectasis, pleural flattened diaphragm, long,
narrow heart, changes narrow heart, ↑ retrosternal
↑ retrosternal airspace (lateral)
Specific Findings:
airspace (lateral)
Cylindrical form: Linear
lucencies, and parallel
markings radiating from
the hila
Varicose form: dilated
bronchi
Cystic: clustered cysts
Pulmonary ↓ Expiratory flows ↓ Expiratory flows / Normal ↓ Expiratory flows,
Function mild ↑ FRC, normal or ↑ RV, FRC If abnormal, ↑ RV, FRC (in severe
Changes ↑ RV, normal DLCO ↓ Expiratory flows, asthmatics) normal DLCO
↓ DLCO
↑ RV, FRC
Arterial Blood ↓ PaO2, ↑ PaCO2 ↓ PaO2 (worsening in ↓ PaO2 during acute During asthma attack
Gas (worsening in acute acute exacerbations) exacerbations ↓ PaO2, variable PaCO2
exacerbations) Hypercapnia in acute
exacerbations
Complications Frequent pulmonary Frequent pulmonary Recurrent pneumonia Bronchopulmonary
infections, respiratory infections, respiratory requiring hospitaliza- Aspergillosis,
failure, cor pulmonale failure, cor pulmonale tion, empyema, lung
Respiratory failure
abscess, hemoptysis,
progressive respiratory
failure, cor pulmonale
ASTHMA TRIGGERS • Cockroach proteins are a known allergic trigger.

Exposure to environmental triggers elicits an Roach-infested areas are a source of allergens for
immunoglobulin-mediated hypersensitivity reaction in asthmatics.
the bronchial epithelium of allergic patients. Patients • Animal dander from pets is in the house envi-
who have inadequate control of their asthma or who ronment, permeates the house, and can even be
have been exposed to a high concentration of allergens carried on clothing.5
experience a rapid worsening in respiratory function
secondary to asthma exacerbation (an asthma attack). Infections. Infection by respiratory tract virus is a
common cause of disease exacerbation in both chil-
Allergic Triggers. Re-exposure to allergens in an atopic dren and adults. Viral infections elicit an immune
individual who is sensitized (who has elevated IgE in response with similarities to the allergic mechanism.
the serum) to that allergen has a worsening of asth- Infections also modulate the immune system and may
matic symptoms. Common allergic triggers are house enhance the allergic response. Viral infections increase
dust and dust mites, pets, especially cats, pollens (tree, the airways’ responsiveness to triggers; this abnormality
grass), roaches, and feathers. increases the response to activated inflammatory
mediators and results in a severe worsening of
• House dust contains organisms that may initiate symptoms.6
an allergic reaction. Molds are a common cause.
• Dust mites are microscopic arachnids that eat Exercise. Exercise in an individual with hyper-
the scales of human skin. They are present in responsive airways triggers a worsening of asthmatic
cushioned furniture, carpet, and bedding. symptoms. The reaction is more severe in cold
environments than in warm, moist environments membrane. The airway is swollen. The mast cells are
(e.g., exercising outdoors versus exercising indoors). activated and release their intracellular mediators,
It is thought that the reaction is secondary to airway and there is inflammatory cellular infiltration of
cooling resulting from water evaporation from airway the airway with eosinophils, neutrophils, and
mucosa. In addition, the evaporation of water results in lymphocytes.9
hyperosmolarity of the sol layer on the mucosal surface Airway inflammation contributes to airway hyper-
and induces chemical mediator release. These effects responsiveness, airflow limitation, symptoms, and
are exaggerated in exercise because of increased minute chronicity. Three phases of airway inflammation are
ventilation. The cooling and increased mediator secondary to the activation of the inflammatory cells
concentration in the hyper-reactive airway triggers produced when the individual is exposed to an allergen
asthma symptoms: wheezing, cough, chest tightness, (an acute asthma attack or exacerbation):
and dyspnea.7
• The initial tissue changes in the acute inflamma-
tory reaction are called the acute phase response.
Medications and Preservatives. Certain drugs are This is the initial cellular airway response to
known to trigger asthma symptoms. Sensitivity to chemical mediator release from the mast cells of
aspirin and other nonsteroidal anti-inflammatory drugs the airways and the basophils. The primary
(NSAIDs) is a known problem in some people with mediator in this response (histamine), along
asthma. Other drugs that may worsen asthma symp- with many other mediators, creates inflamma-
toms are beta-blockers, both in oral tablets and topical tory changes. This response is classically seen in
forms.5 Sulfite is a common preservative used in food the initial hours after an asthma exacerbation.
and beverages such as processed potatoes, shrimp, The patient has bronchospasm, an outpouring of
dried fruit, beer, and wine. If people develop asthma secretions, and mucosal edema with significant
symptoms after eating these items, asthma experts airflow limitation.
advise them to avoid those foods. Following exposure, • In the subacute phase, the asthmatic patient’s
they are at a greater risk for developing a severe asthma initial symptoms are being treated and con-
exacerbation or perhaps even status asthmaticus.2 trolled with appropriate medication, but a
continuous inflammatory pattern is present. The
Environmental Pollution. Asthmatics are extremely patient’s airflow limitation is still significant, and
sensitive to environmental irritants, including cigarette the patient’s pulmonary function shows reduced
smoke. If the concentration is significant, indoor and expiratory flows. This phase continues for days to
outdoor irritants trigger an asthmatic response. weeks after an asthma exacerbation.
• Indoor pollutants, such as chemical fumes given • The chronic inflammation phase is present in
off by synthetic materials like rugs, furniture, asthmatics between asthma exacerbations. This
aerosol sprays, particle board, wall coverings, is the inflammation that maintenance therapy is
and recent painting, may all cause symptoms in attempting to control.2,10 Drug therapy with
the asthmatic. corticosteroids or drugs that control specific
• Outdoor pollutants from motorized vehicles, chemical inflammatory mediators, such as mast
manufacturing plants, and ozone can act as a cell or leukotriene modifiers, are the primary
trigger for asthma or add to the individual’s means for control.
existing breathing difficulties.
• Local meteorologists frequently broadcast air
AIRWAY INFLAMMATION AND
quality alerts, especially in the summer months,
AIRFLOW LIMITATION
and the asthmatic should try to limit the time
spent outdoors and, when outside, should wear Airway inflammation causes airway hyper-responsiveness,
a protective mask. that is, an exaggerated bronchospasm response to a
stimulus (allergen, exercise, cold air, or infection). The
Exposure to pollutants may increase airway inflamma- individual has postexposure wheezing and breathless-
tion and increase the risk of allergic sensitization with ness. The degree of airway hyper-responsiveness is
exposure to multiple environmental allergens.2,5 correlated with asthma severity. Pulmonary function
testing using methacholine/histamine inhalation
Pathophysiology of Asthma. The cellular pathologic challenge or nondrug stimuli inhalation such as cold,
changes that occur in chronic inflammation are dry air can measure airway hyper-responsiveness. The
significant. The airway epithelium is damaged testing includes the measurement of pre-exposure and
through its layers to the basement membrane. postexposure expiratory flow rates. The patient who has
Collagen is deposited in the airway basement a significant reduction in postexposure expiratory flows
is diagnosed with hyper-responsive/hyper-reactive The signs and symptoms of someone presenting

airways.2,5 with undiagnosed asthma are very helpful in arriving
Airway inflammation also causes bronchospasm. at a diagnosis of asthma. In the asthmatic individual
Bronchospasm is caused by many factors: IgE mediator who is not having an asthma exacerbation, the
release, aspirin or NSAIDs ingestion, non-IgE response, clinical signs are less severe than those during an
stress, or airway edema. Bronchospasm causes airflow acute asthma attack. The asthmatic complains of
limitation with wheezing and dyspnea.2,10 wheezing and postexercise shortness of breath. Chest
Chronic inflammation increases the rigidity of the tightness and cough are frequent problems. The
airways, resulting from the chronic leakage of fluid patient’s symptoms are worsened with exposure to
from the blood vessels in the airway caused by chronic allergens or irritants. The typical signs and symptoms
mediator release, mucosal thickening, and airway swell- of an adult asthmatic in an asthma exacerbation are
ing. Acute airway rigidity is a type of airflow limitation listed in Table 9-1.
in acute asthma that does not respond to bronchodila- Usually asthma attacks begin acutely. The patient
tors. Rigidity can be reduced and controlled with has wheezing and chest tightness with intermittent
anti-inflammatory medications. coughing episodes. The cough is usually tight, non-
However, if the chronic inflammation is not productive, and common at night. The wheezing
controlled with maintenance therapy, this aspect of worsens, is heard during inspiration, and is audible
airflow limitation becomes permanent because of without a stethoscope. As airflow limitation increases,
airway structural changes. This end point of chronic the ventilation/perfusion relationship becomes abnor-
inflammation is called airway wall remodeling. When the mal, and hypoxemia results. Dyspnea increases in
patient’s airflow limitation is predominately secondary severity, and the use of accessory muscles to breathe is
to airway wall remodeling, bronchodilators have no obvious. Tachycardia and increased blood pressure are
effect and the airflow limitation is fixed.2,9 Mucus responses to stress and anxiety, as well as to hypox-
plugging also causes airflow limitation. The outpouring emia. In severe asthma, which does not respond to
of secretions in the acute inflammatory phase can beta-adrenergic drugs and other treatment modalities
form plugs that obstruct the airway. Plugging usually (status asthmaticus), hypoventilation occurs second-
occurs in the smaller airways and can seriously reduce ary to fatigue and severe ventilation/perfusion mis-
airflow.2,10 matching. In this scenario, the patient needs to be
hospitalized and admitted to the intensive care unit.
A critical element of an asthma attack is that a silent
DIAGNOSIS OF ASTHMA chest is a serious finding. If the airflow limitation is
The key elements of characterizing asthma mentioned so severe that a wheeze cannot be heard, then this
earlier are very consistent with the cardinal diagnostic patient is critical and needs maximal therapy to avoid
findings.2,5 These clinical findings support the diagno- ventilatory failure and possible cardiopulmonary
sis of asthma: arrest.2,5,10
• The presence of episodic symptoms of airflow
limitation
• Airflow obstruction that is partially reversible
• The ruling out of alternative diagnoses Age-Specific Competency
The techniques used to establish the diagnosis of
asthma are:
Asthmatic Children
Asthmatic children who are not in an asthmatic
• Patient history. attack may show clinical manifestations that are
• Physical exam (respiratory tract, skin, and chest). not typically seen in the adult:
• Pulmonary function spirometry (demonstrate
reversibility). • Frequent headaches
• Other studies. • Irritability and depression
• Dark circles under the eyes (allergic
Additional studies: “shiners”)
• Evaluate alternative diagnoses. • Rhinorrhea with yellow or green mucus or
• Identify precipitating factors. congestion with cough
• Assess asthma severity. • Sleeping difficulty, awakening with
• Identify potential complications (pneumotho- nightmares
rax, atelectasis, and cor pulmonale).10
TABLE 9-2 Asthma classifications published by Asthma Expert Panel Report 2007
Symptoms Lung Function
Asthma Severity Daily Night Activity Limitation Expiratory Flows PF Variability
Intermittent Asthma 2 days/wk 2 nights/ No limitations except 80% of predicted 20%
mos during infrequent
exacerbations
Mild Persistent 2/wk but 2/mos Exacerbations may 80% of predicted 20%–30%
1/day affect activity
Moderate Persistent Daily 1/wk 2/wk; may last days; 60% – <80% 30%
exacerbations affect of predicted
predicted activity
Severe Persistent Continual Frequent Frequent exacerbations 60% of predicted 30%
ASTHMA CLASSIFICATIONS ASTHMA MANAGEMENT

Asthma has four severity classifications, and the Asthma management takes two main directions. First,
intensiveness of the treatment varies directly with the reduce the individual’s exposure to environmental
asthma severity. With increasing asthma severity, the allergens. If allergen exposures can be significantly
symptoms are more frequent, the airflow limitation is reduced, then the individual’s asthma classification can
more severe, and the disease has a greater impact on be reassessed and the need for drug therapy reduced.
the quality of life. The four asthma classifications The second main element of asthma management is
(Table 9-2) are: drug therapy. The principles of asthma control are
based on how the prescribed medications and reduc-
• Intermittent asthma
tion of environmental exposure improves the quality of
• Mild persistent asthma
life, reduces disease impairment, and lowers the risk of
• Moderate persistent asthma
asthma exacerbations.3 Table 9-3 summarizes the goals
• Severe persistent asthma
of asthma therapy.
The patient’s asthma severity is determined by assessing:
Reduction of Exposure. Exposure reduction is an
• Symptom frequency per week and at night, as
important part of asthma management. Controlling
well as activity restriction.
the environment of the asthmatic patient is one
• Expiratory flow measures (e.g., peak expiratory
method of reducing exposure to the allergen. In fact,
flow (PEF) or forced expiratory flow in the first
minimizing the contact with allergens cannot be
second of exhalation (FEV1) and the flow rate
stressed enough. If successful, exposure control reduces
variability during the day).2,5,10
TABLE 9-3 Goals of asthma therapy published by the Asthma Expert Panel Report 2007
Reducing Impairment Reducing Risk
Prevent chronic and troublesome symptoms Prevent recurrent exacerbations of asthma and minimize
need for ED visits and hospitalizations
Require infrequent use (2/wk) of Short Acting Beta 2 Prevent progressive loss of lung function; for youths
Agonist (SABA) for quick relief 12 years of age prevent reduced lung growth
Maintain (near) normal pulmonary function
Maintain normal activity levels Provide optimal pharmacotherapy with minimal or no
adverse effects
Meet patients’ and families’ goals of asthma care
asthma severity and improves the patient’s quality of relief of acute symptoms or to prevent exercise-induced
life.2 bronchospasm. This drug group is the most effective
treatment available for acute bronchospasm. The beta 2
• Control animal dander.
agonists are taken by the inhaled route and give faster
• Remove the pet from home or keep it out of
peak action with minimal side effects. These drugs
the bedroom.
should be taken only on an as-needed basis. If more
• Close off the bedroom from free air circulation
than one canister of drug a month is used, then
and place filters over air outlets.
maintenance drug therapy should be changed. The
• Control dust mites.
regular use of short-acting beta 2 bronchodilators
• Essential: Encase mattress and pillows with
indicates a lack of pharmacological control of asthma
allergen-impermeable covering; wash bedding
and may result in frequent exacerbations requiring
weekly in hot water.
hospital treatment. Beta 2 medications have no effect
• Desirable: Remove the carpet from the bed-
on acute or chronic inflammation and are used
room; minimize stuffed toys and wash them
to relieve patient symptoms arising from airway
weekly; keep the home humidity less than
hyper-reactivity secondary to an acute worsening of
50%; avoid sleeping on upholstered furniture;
inflammation.2
remove carpets laid on concrete.
Anticholinergic bronchodilators make up the second
• Control cockroach allergen by the chemical
medication group used for the quick-relief treatment of
control of cockroach infestation.
asthma. Ipratropium bromide may provide additional
• Control indoor fungi by controlling dampness
bronchodilation when used in conjunction with beta 2
(dehumidifier); control fungi growth.
agonists. Ipratropium helps patients with broncho-
• Control exposure to outdoor allergens by staying
spasm secondary to increased vagal tone (hyperexcit-
in air conditioning with doors and windows
ability of the parasympathetic nervous system). The
closed (not so realistic a measure for children). If
drug may also serve as a primary bronchodilator for
going out, try to schedule activities in the early
people who do not respond to beta 2 agonists. The lack
morning.
of response indicates that either beta 2 bronchodilator
has met with resistance secondary to overuse or that a
Pharmacological Treatment. The drugs used to treat
larger element of increased parasympathetic tone is the
asthma are divided into two main categories: quick-
cause of bronchospasm. The lack of response to the
relief and long-term control medications (Figure 9-1).
short-acting beta 2 drugs is more likely to occur in
Two drug groups are used as quick-relief medications:
severe asthma exacerbations. One study reported that
• Short-acting beta 2 bronchodilators (SABA) and when pediatric asthma patients in an emergency
anticholinergic bronchodilators. department were given a maximum of three doses of
• Long-term control medications, such as the ipratropium, they had 13% shorter duration of treat-
following drugs or drug groups: corticosteroids ment and they received fewer beta 2 drug doses before
(inhaled, oral, or IV), long-acting beta 2 ago- discharge. However, the hospital admission rates did
nists, leukotriene receptor antagonists, cromolyn not change.11 Another research study reported a
sodium and nedocromil sodium, and methylx- significant reduction in hospitalization rates for
anthines (see Table 9-4). children in a severe asthma exacerbation who were
given ipratropium in the emergency department.12 In
Quick-Relief Medications The short-acting beta 2 another study, adult asthmatics admitted to the
bronchodilators are used to provide the asthmatic quick emergency department in an acute exacerbation of
Persistent Severe Systemic and inhaled steroids and/or mast-cell

stabilizers and long-acting bronchodilator, (drug
Step 3 doses may increase) plus step 1
Persistent Moderate Inhaled steroids and/or mast-cell stabilizers and
long-acting bronchodilator, with or without leukotriene modifiers
Step 2 (drug doses may increase) plus step 1
Persistent Mild Inhaled steroids/mast-cell stabilizers or slow-release theophylline

and leukotriene modifiers plus step 1
Step 1
Intermittent PRN beta-2 bronchodilator
FIGURE 9-1 Steps in the pharmacological control of asthma.

TABLE 9-4 Long-term asthma control published by Asthma Expert Panel Report 2007
Alternative Not
Step Phase Preferred Treatment Preferred Treatment
Intermittent Asthma
Step 1 No Daily Medications None
PRN SABA
Asthma Exacerbations
• SABA Q4–6 hrs
• Short course of oral steroids
Persistent Asthma
Step 2 Low-dose Inhaled Steroids Cromolyn
AND OR
SABA (PRN) Leukotriene Receptor
Antagonists (Nedocromil)
OR
Sustained-Release Theophylline
Step 3 Low-dose Inhaled Steroids Medium-dose Inhaled Steroids
AND OR
SABA (PRN) Low-dose Inhaled Steroids
AND AND
Inhaled Long-acting Beta2 agonists Leukotriene Receptor
Antagonists (Nedocromil) OR
Sustained-Release Theophylline OR Zileuton
Step 4 Medium-dose Inhaled Steroids Medium-dose Inhaled Steroids
AND AND
SABA (PRN) Leukotriene Antagonists OR Sustained
AND Release Theophylline
Inhaled Long-acting Beta2 agonists OR
Zileuton
Step 5 High-dose Inhaled Steroids No alternatives identified
AND
SABA (PRN)
AND
Inhaled Long-acting Beta2 agonists
Consider adding Omalizumab
Consult with asthma specialist
Step 6 High-dose Inhaled Steroids No alternatives identified
AND
SABA (PRN)
AND
Inhaled Long-acting Beta2 agonists
AND
Oral Steroids
Consult with asthma specialist
asthma were given ipratropium in addition to beta 2 these two drugs are different from each other, but they
bronchodilators, and there was a distinct improvement both affect airway inflammation. Both drugs block
in the patients’ FEV1 or PEF. In this study, the addition of chloride channels, which are thought to be the mecha-
ipratropium resulted in fewer hospital admissions.13 nism by which mast cell inflammatory mediator release
Therefore, it is suggested that combination ipratropium– is controlled. As a second-generation anti-asthmatic
beta agonist therapy can be given to both children and drug, nedocromil has a modulating effect not just on
adults in an acute asthma exacerbation. the mast cell but also on the airway epithelial cells,
eosinophils, and sensory neurons. Both drugs are used
Long-Term Control Medications. The asthmatic takes in the treatment of asthma and may be used in place of
the long-term medications daily to control the disease. or in addition to steroids. Their anti-inflammatory
Minimizing asthma symptoms, decreasing the number activity may be sufficient to control asthma in some
of exacerbations, and increasing the person’s quality of people and may be preferred in the treatment of
life are the goals of long-term asthma control. Because childhood asthma because they do not inhibit growth
asthma is classified as a chronic inflammatory airway and development. Cromolyn and nedocromil are used
disease, the primary direction of asthma management to prevent asthma exacerbations and exercise-induced
is to reduce airway inflammation. Corticosteroids, asthma. These drugs are not effective in the treatment
leukotriene receptor antagonists, and cromolyn sodium of an asthma exacerbation.2
or nedocromil reduce inflammation through different The duration of action of the long-acting beta 2
mechanisms. The patient takes one or more of these adrenergic agent salbutamol is approximately 12 hours.
drugs.2,10 In providing long-term bronchodilation, salbutamol
Corticosteroids (steroids) globally suppress the prevents nocturnal symptoms and helps provide
inflammatory response by suppressing the migration of attenuated control of exercise-induced bronchospasm.
polymorphonuclear leukocytes and fibroblasts. Inhaled This drug has a prolonged duration of action because it
steroids are the preferred therapy and are started when is lipid soluble and has a delayed peak effect. There-
persistent asthma is diagnosed. Initiating inhaled fore, salbutamol should not be used for quick relief of
steroids early in the disease course results in a height- symptoms or to treat an acute exacerbation of asthma.
ened objective improvement in lung function. Steroids The short-acting beta 2 drugs are indicated for those
do not cure asthma, but research studies suggest that emergency situations.
their early use, in conjunction with beta agonists, can Methylxanthines have long been used in the
reduce airway wall remodeling.2,14 Steroids control treatment of asthma. Their role in asthma treatment
airway inflammation in a dose-dependent fashion. has been open to question, but it is now accepted that
Using the lowest possible dose of inhaled steroids is theophylline is an alternative therapy for suppressing
recommended. The inhaled form is employed the most nocturnal asthma symptoms. Sustained-release prepa-
frequently in long-term asthma control because of rations of the methylxanthine theophylline are an
lower systemic effects. Since systemic or even inhaled acceptable substitute for the long-acting beta 2 bron-
steroids can inhibit growth and development in chodilator salbutamol. Issues such as cost may require
children, children’s growth should be monitored for the use of the less expensive methylxanthine. The drug
any abnormal slowing while they are taking steroids.2 is still not well understood and has been reported to
Oral steroids also have a role in asthma therapy have effects that may contribute to the overall reason
and are used in addition to inhaled steroids the for its effectiveness in asthma. Theophylline is a
asthmatic is taking. Oral steroids are indicated for modest bronchodilator that is reported to have a slight
asthmatics experiencing an acute exacerbation of anti-inflammatory effect and to strengthen diaphrag-
symptoms but either not responding to or resistant to matic contraction. Since the difference between the
short-acting beta 2 bronchodilators.2 Steroid adminis- therapeutic blood level and theophylline toxicity is
tration can reverse or partially reverse the beta recep-
tors’ desensitization to sustained beta-adrenergic
stimulation. A short course of systemic corticosteroids Best Practice
is recommended after an acute exacerbation of asthma.
The temporary use of steroids reduces the number of
asthma relapses and decreases use of the quick-relief Salbutamol
beta 2 bronchodilator that the asthmatic usually needs Asthmatics using salbutamol should be carefully
in the postexacerbation period.15 instructed that this drug should not be used in
Cromolyn sodium and nedocromil are not preacute breathing problems and that to rely on this
ferred anti-inflammatory drugs but can be used as an drug for relief is dangerous.
alternative medication. The individual properties of
small, the drug blood levels must be regularly moni- THE ACUTE ASTHMA ATTACK
tored for drug toxicity. People with theophylline The classification system of asthma severity is helpful
toxicity complain of nausea, vomiting, and cardiac in determining the maintenance treatment of the
arrhythmias.4 asthmatic. However, any asthmatic with intermittent or
Other types of anti-inflammatory drugs used in persistent asthma who has an acute worsening of
long-term control of asthma are the leukotriene asthma symptoms—an asthma attack—can develop
modifiers. Leukotrienes are eicosanoids derived from severe symptoms and need emergency department care
arachidonic acid, a cell membrane phospholipid. The and even hospitalization before the asthma can be
leukotriene molecules—LTC4, LTD4, LTE4—were controlled. There are three stages of an acute attack.4
formerly known as the slow-reacting substance of Treatment failure results in a seriously ill asthmatic at
anaphylaxis (SRSA). These chemicals are important risk of respiratory arrest (see Table 9-5).
mediators in asthmatic bronchoconstriction and airway Stage 1 is considered a mild attack. In this severity
inflammation. Bronchoconstriction persists in acute of asthma exacerbation, the asthmatic’s respiratory rate
asthma exacerbations well beyond the acute phase is increased, and end expiratory wheezing is heard on
because of the presence of these and other chemical auscultation. But the attack does not limit the ability to
mediators. Researchers have found that leukotrienes are lie flat, and the patient can talk in complete sentences
acutely increased in the urine of atopic asthmatics without having to stop to breathe. If blood gases were
exposed to an allergen to which they are sensitive. Also measured, they’d be normal. The PAO2 and SAO2 are
the urine of asthmatics with aspirin sensitivity contains maintained within normal range because of the
chronically elevated levels when compared with the patient’s hyperventilation. The heart rate and the blood
urine levels in non-aspirin-sensitive asthmatics.6–9 pressure are still in the normal range.
Treatment with leukotriene modifiers inhibits the Stage 2 is a moderately severe asthma attack. The
production of leukotrienes, which control bronchocon- asthmatic’s respiratory rate is more elevated than in the
striction in people with atopic asthma, exercise- previous stage, with obvious use of accessory muscles
induced asthma, and aspirin-sensitivity-induced and audible inspiratory and expiratory wheezing. The
asthma. In addition, inhibiting leukotrienes reduces asthmatic does not like to lie flat, and, because of
the airway hyper-responsiveness associated with airway dyspnea, talking is restricted to simple phrases. The
inflammation. arterial blood gases reveal two abnormalities: respira-
The FDA approved the medications zafirlukast and tory alkalosis and mild hypoxemia with an oxygen
zileuton for use in mild to moderate persistent asthma. saturation greater than 90%. A moderately severe
They should not be used in patients with severe asthma attack is stressful, creating anxiety, ventilatory
persistent asthma. The leukotriene receptor antagonists work, and mild to moderate hypoxemia, which causes
are approved for use in the pediatric patient. Zileuton an elevated blood pressure and tachycardia (100 and
is listed as an alternative leukotriene modifier in the 120 bpm).
adult and youths over the age of 12, but it is not a Stage 3 is a severe asthmatic attack. The asthmatic
preferred drug because liver function monitoring is has a very rapid respiratory rate and must sit upright to
required. breathe. He or she refuses to lie supine and is too short
TABLE 9-5 Asthma attack severity stages

Signs and Symptoms Mild Attack Moderate Attack Severe Attack
RR Increased over baseline Tachypnea Tachypnea
Dyspnea Walking, Can lie flat Talking, Prefers sitting At rest, tripod position
to lying down to breathe
Speaking Full sentences Partial sentences Words
Wheezes (auscultation) End expiratory Inspiratory and expiratory Decreased or Inaudible
Alertness Normal Agitated Agitated or Drowsy
Pulsus Paradoxus Normal 10 mm Hg 10 mm Hg 10 mm Hg
SpO2 95% 90–95% 90%
PaO2 (mm H) Normal (ABG not necessary) 60 60 (possible cyanosis)
PCO2 (mm Hg) 35 35–45 45
PEFR % personal best 70–90% 50–70% 50%
of breath to talk except in single words. Accessory patient who is responding may receive treatment in the
muscle use is prominent during breathing, and wheez- emergency department for up to 5 hours before being
ing may still be audible or it may decrease or even discharged from the hospital. The patient who shows a
disappear. The heart rate is over 120 bpm, with accom- partial response to emergency department treatment
panying hypertension. The extremely hyperinflated may be admitted to the hospital or may be discharged.
patient shows a paradoxical pulse (decreased pulse or The decision is based on the patient’s individual
blood pressure during inspiration). The arterial blood situation. The patient who shows poor response to
gas shows an elevated PACO2 with hypoxemia, and treatment is admitted to the hospital. A good standard
oxygen saturation is less than 90%. Findings that for discharge is pulmonary function performance. It is
herald respiratory arrest are: suggested that the PEFR should be greater than 70% of
predicted or personal best unless otherwise directed by
• Paradoxical chest or abdominal movement
the attending physician.2,5 Additionally, before dis-
during breathing.
charge, the respiratory therapist should check the
• Minimal wheezing in a patient in severe respira-
patient’s inhaler technique and reinstruct the patient
tory distress.
on its use.
• Exhaustion in presence of respiratory acidosis.
Discharge medications commonly include systemic
• Decreased level of consciousness.
and inhaled steroids and quick-relief and long-acting
• Bradycardia.
beta 2 bronchodilators. The systemic steroids are
• Cyanosis.
gradually tapered off under the guidance of the physi-
In general, many asthmatics experiencing an acute cian and with careful monitoring of asthma symptoms.
exacerbation of asthma have a preliminary period of The patient’s long-term pharmacological control
increased asthma symptoms that results in a visit or regimen should be reassessed. An exacerbation of
phone call to the physician’s office. Drug treatment at asthma is considered treatment failure and indicates
home is intensified without alleviation of symptoms. reexamination and adjustment of home medications to
The most critical element of asthma care for the prevent future exacerbations.2,5
asthmatic or the family is recognition of when to go to
the emergency department. Asthma deaths occur with
failure to come to the hospital or with delay in coming Chronic Bronchitis (COPD)
to the hospital until after deterioration into a treat-
ment-refractory state.5 and Emphysema
In 2006 in the United States, 8.9 million noninstitu-
When to Come to the Emergency Department. If, tionalized adults were diagnosed with chronic bronchi-
after the patient has consulted the family physician or tis, and 3.8 million were diagnosed with emphysema.
asthma specialist, the intensive home therapy is Chronic lower respiratory tract disease was the fourth
unsuccessful in controlling asthma symptoms (peak greatest cause of death with 121,987. Most of the
expiratory flow rate (PEFR) less than 60% of predicted respiratory deaths were secondary to chronic obstruc-
or personal best), the patient should go to the hospital tive pulmonary disease (COPD), and the majority of
emergency department. Before starting for the hospital, them were over the age of 55. This disease is one of
the primary instructions for the patient are to: senior citizens.16
The economic burden of a disease is reported as
• Continue taking the short-acting beta 2
direct costs and indirect costs.
bronchodilator.
• Take steroid tablets before leaving. • Direct costs are the value of health care
• Use oxygen if available. resources devoted to the diagnosis and manage-
• Call 911 if unable to drive.15,17 ment of a disease, including hospitalization,
drug therapy, rehabilitation. These costs are
The management of the patient in the emergency
generally reimbursed by health insurance.
department is very intense and complete. Emergency
• Indirect costs are the monetary consequences
department treatment of the asthmatic includes
of disability, missed work, premature death, and
oxygen, high-dose bronchodilators by nebulization,
the caregiver or family costs resulting from the
and steroids. The treatment regimen is determined by
illness. These costs reflect the shortened contri-
assessing asthma exacerbation severity and the
bution of the afflicted individual to society and
response to that therapy; it follows the National Heart,
the burden on the family.
Lung, and Blood Institute’s Expert Panel guidelines on
asthma management.2 In developed countries, COPD exacerbations
The goals of treatment are to relieve acute symp- account for the greatest burden on the health care
toms and to prevent hospitalization. The asthmatic system. For example, the total direct costs of respiratory
CASE STUDY 9-1

This is one of numerous emergency department Cardiovascular: Regular rhythm with sinus
visits for Latonya Brewster, a 20-year-old female, tachycardia
for acute asthma exacerbation. She had been Medications taken for asthma: MDIs fluticasone,
attending a family picnic when she started to feel albuterol, salbutamol; montelukast. Her parents
chest tightness that was not relieved by using her stated that her personal best PEFR is 70% of
albuterol inhaler. She became progressively more predicted, and it varies ~30%–35% throughout
short of breath (SOB) despite taking her albuterol the day.
every 20 minutes. Her parents called the family
Oxygen therapy was started at 2 Lpm by nasal
physician. He told them to take her to the emer-
cannula. The respiratory therapist gave Latonya
gency department, and he would meet them at the
albuterol and Atrovent (ipratropium) administered
hospital. The following were noted at the emergency
by small-volume nebulizer every 20 minutes. An IV
department.
was started, and she was given the IV corticosteroid
Physical examination: This 20-year-old female is in methylprednisolone.
obvious respiratory distress. She is using her
accessory muscles to breathe and can talk only Questions
in short phrases. 1. In which stage of asthma exacerbation severity
Vital signs: Heart rate 110, blood pressure 130/90, would you categorize Latonya Brewster’s asthma
respiratory rate 25 breaths per minute, tem- attack?
perature 36.8°C, SpO2 92%, peak expiratory 2. On the basis of information supplied by her
flow rate ~60 Lpm. parents, in which asthma classification would
Chest examination: Breath sounds revealed inspira- you place Latonya? Explain your reasoning.
tory and expiratory wheezing throughout the 3. Would replacing Latonya’s albuterol with a
chest. Expiratory wheezing audible without a long-acting bronchodilator be a better treatment
stethoscope. while she is in the emergency department?
HEENT (head, eyes, ears, nose, throat): Atraumatic 4. Methylprednisolone was added to Latonya’s
normocephalic; she was using neck muscles emergency care. What is the benefit of methyl-
during breathing. prednisolone in the asthmatic?
disease in the European Union is about 6% of the total cause of their disease, and they respond differently to
health care budget, with COPD responsible for approx- bronchodilator therapy and steroids.17
imately 56% of respiratory disease costs. In 2002, the Emphysema is defined in pathological terms.
direct and indirect costs of COPD to the United States’ Emphysema is present when there is abnormal perma-
health care system were $18 billion and $14.1 billion, nent dilation and destruction of lung units distal to the
respectively.1 Despite the higher direct costs, indirect terminal bronchioles, which include the respiratory
costs have the largest impact on countries, reflecting the bronchioles, alveolar ducts, and alveoli. Distribution in
loss of human capital, which is the most important the lung is variable, but the involved areas exhibit
asset of any country. abnormal lung architecture and abnormal exchange of
oxygen and carbon dioxide. There are three main types
of emphysema: panacinar, centriacinar, and paraseptal
DEFINITIONS emphysema.
COPD is characterized by the presence of chronic • Panacinar emphysema, also known as panlobar
bronchitis, emphysema, or both. The COPD patient emphysema, has the same definition as emphy-
has progressive airflow limitation that may be partially sema. The entire lung unit—including the
reversible in those with hyper-reactive airways. respiratory bronchioles, alveolar ducts, and
Although asthma is sometimes included in the label of alveolar sacs—is involved, hence the prefix
COPD, asthma is a very different disease from bronchi- “pan-,” indicating “all.” Panacinar emphysema
tis or emphysema. For many people with chronic usually occurs in the lower lobes of the lung. It
bronchitis or emphysema, smoking is the underlying can be caused by smoking and occurs in people
with a genetic disease, alpha-1 antitrypsin Cookbook drug treatment does not work in treating
deficiency. patients with this disease. The figure helps to explain
• Centriacinar emphysema is the enlargement of why medications are used in short-term trials. If the
the central part of the acinus and spares the drug is beneficial, the medication is added to that
distal lung units. It commonly occurs in the patient’s maintenance or emergency treatment
upper lobes of the lung and is strongly associ- regimen. If the drug does not improve the patient’s
ated with smoking. clinical condition, the drug is stopped. Physicians
• Paraseptal emphysema preferentially involves attempt to discover the best treatment regimen for
the distal airway structures, such as the alveolar each person.
ducts and sacs. while sparing the respiratory Asthma overlapping with chronic bronchitis is a
bronchioles. This type of emphysema occurs in patient group that needs special mention. This group is
subpleural areas or along interlobular septa. It also described as having chronic asthmatic bronchitis.
commonly occurs in the apices of the lung and Some asthmatics have less than expected reversibility of
is associated with bullae formation and subse- their airflow limitation in response to beta 2 broncho-
quently is a cause of secondary pneumothorax in dilators. In addition, they have chronic bronchitis. But
people with lung disease. this mix of asthma and bronchitis can also be exam-
ined when studying the chronic bronchitis patient
In most patients with COPD secondary to emphysema,
population. Some patients with chronic bronchitis
these different forms of emphysema coexist.18
have significant partial reversibility of their airflow
Chronic bronchitis is the predominant cause of
limitation that is not a characteristic of chronic bron-
COPD and accounts for approximately 90% of the
chitis. These bronchitics have airway hyper-reactivity
COPD population. Chronic bronchitis is defined not
that is significantly responsive to beta 2 bronchodila-
pathologically but functionally. An individual with a
tors. Therefore, a diagnosis of chronic asthmatic
chronically productive cough lasting 3 or more con-
bronchitis can describe these patients.17,19
secutive months for 2 successive years is diagnosed
with chronic bronchitis. Before this diagnosis can be
made, other diseases that cause similar symptoms— RISK FACTORS
such as tuberculosis, lung cancer, and congestive heart Specific risk factors are common among people who
failure—must be excluded from consideration.17,19 develop chronic bronchitis and emphysema: cigarette
The classic relationship of asthma, emphysema, smoking, environmental pollution, and genetics.
and chronic bronchitis is illustrated in Figure 9-2, Knowledge gained from the Human Genome Project
which shows the variability of the COPD population. may show that genetic predisposition to lung disease is
more important as a risk factor than was previously
thought.
No Airflow
Limitation
E w/o AL CB w/o AL
Cigarette Smoking. Cigarette smoking is the primary
risk factor for COPD. Cigarette smokers have both a
greater prevalence of COPD and a greater severity of
E, CB
E alone CB alone clinical symptoms. The smoking variables that have
the greatest effect on COPD morbidity and mortality
A, E
CB are the age at which the COPD patient started
A, E A, CB Airflow smoking, the total pack-years, and the current smoking
Limitation status.17,19
Chronic
AL w/o
Despite the greater risk for COPD, only 20% of
A, E, CB A alone smokers actually develop COPD. Intensive research has

been devoted to identifying why this population of
A w/o AL cigarette smokers is predisposed to lung disease.1,20
No Airflow
Limitation Environmental Tobacco Smoke and Air Pollution.
FIGURE 9-2 The combinations of disease overlap in Environmental tobacco smoke, which has also been
populations diagnosed as having COPD. The rectangle called secondhand smoke, is known to produce
represents airflow limitation as identified by a clinically respiratory irritation such as cough, eye irritation, and
significant decrease in FEV1 or PEF. All patients with increased respiratory infections. It is a known risk
one or more of the three diseases in the rectangle can factor for lung cancer, and it may be an allergen trigger
be classified as having COPD. CB
chronic bronchitis; in asthmatics. Its role in COPD pathogenesis, however,
E
emphysema; A
asthma; AL
airflow limitation. is unknown.21,22
Air pollution is a respiratory irritant. Its role in protection. This question is being closely studied in
precipitating sickness in people with cardiopulmonary COPD research.21
disease is well documented. Officials who monitor air Pulmonary emphysema results from the proteo-
quality in urban and suburban areas announce alerts lytic destruction of elastin, which is a large component
during the summer because of dangerously high levels of the structural matrix of the lung acinus. People with
of pollutants. High pollutant levels are a risk factor for normal levels of alpha-1 antitrypsin can develop
exacerbation of COPD, but their role as a cause of emphysema when the normal antiprotease-protease
COPD is small in comparison with cigarette smoking. balance is disturbed by the addition of proteases such
High levels of pollution, dust, or chemical fumes as neutrophil elastase, which is a product of cigarette
irritate the respiratory tract and increase the patient’s smoke–induced inflammation. Smoking over an
underlying airflow limitation.19 extended period of time produces a state of chronic
inflammation. The pulmonary cells involved in the
Alpha-1 Antitrypsin Deficiency. Alpha-1 antitrypsin inflammatory reaction release chemical mediators that
deficiency is a genetic disease in which there is a attract neutrophils to the lung. Neutrophil-derived
decreased ability to produce the glycoprotein antitryp- elastase lyses lung tissue elastin. The injury is cumula-
sin. Antitrypsin is necessary to block the activity of tive and becomes clinically evident when the patient
inflammatory proteases (proteolytic enzymes). Alpha-1 has extensive destruction to the lung.
antitrypsin is a protein circulating in body fluids such In some cases, chronic bronchitis occurs in non-
as respiratory secretions, GI secretions, and saliva. A smokers. Research studies of the smoking and non-
deficiency in this enzyme causes unopposed proteolysis smoking populations with chronic bronchitis support
of elastin in the lung and liver. The chronically the hypothesis that the molecular and cellular charac-
increased breakdown of elastin, which is an important teristics of chronic inflammation that occur in the two
protein in the lung parenchyma structures, causes different groups are different. Thus, the pathogenesis of
widespread lung destruction and panacinar emphy- chronic bronchitis in the smoker is different from that
sema. Liver disease or liver cirrhosis may also develop in the nonsmoker, although the end state is the
secondary to protease destruction of hepatocytes. Liver same.20,23 Table 9-6 lists the different presentations of
failure occurs in all ages, but this condition is especially smokers and nonsmokers with chronic bronchitis.
severe in newborns. People who are born with this This distinction indicates that the inflammatory
disorder and who smoke cigarettes develop early-onset process is different and that the initiating stimulus or
panacinar emphysema in their twenties and thirties. trigger is different.23 During acute exacerbations, the
Approximately 100,000 people in the United States inflammatory cells are present in the airway wall
have the severe form of the deficiency, and lung and epithelial tissue and mucus, and, during these episodes,
liver transplantation are the only cure after the damage bronchial injury is more severe. Chronic injury is
has occurred.17,19 thought to take place because of a disruption in the
antiprotease-protease balance secondary to smoking
irritants. The major proteases are neutrophil derived.
PATHOGENESIS AND PATHOPHYSIOLOGY Chronic bronchitis causes tissue changes that are
Cigarette smoking is a cause of both pulmonary apparent both on gross examination and by micro-
emphysema and chronic bronchitis. Why only 20% of scope. The epithelial layer is red and edematous, with
smokers develop COPD is not understood. Research increased secretions pouring from the enlarged mucus
scientists have discussed the possibility of individual, glands. The affected bronchial epithelial layer has
genetic, familial, or environmental factors that provide undergone permanent structural changes from the
TABLE 9-6 Differences between smokers and non-smokers with chronic bronchitis
Smokers Non-Smokers
Increased macrophages Increased mast cells
Increased neutrophils* Increased non-activated eosinophils
Increased nonactivated eosinophils Increased activated CD4 T-lymphocytes
Increased activated CD8 T-lymphocytes Increased Interleukin-5
Increased tumor necrosis factor alpha Increased granulocyte-macrophage colony-stimulating factor genes
Increased interleukin-2 genes Increased proteins
Increased proteins
normal pseudostratified ciliated columnar epithelium A diffusion study is a pulmonary function test that
to squamous, with a loss of the normal cilia. The differentiates between emphysema and the other
smooth muscle may also hypertrophy. All of these COPD diseases. Pulmonary emphysema is the only
changes decrease the bronchial lumen, especially in the disease under the COPD triad (pulmonary emphy-
smaller airways (the terminal bronchioles and respira- sema, chronic bronchitis, and bronchiectasis) and
tory bronchioles). As the disease progresses, the larger asthma that shows a reduced single-breath carbon
bronchi become more involved and the disease monoxide–diffusing capacity. Emphysema causes a loss
becomes apparent clinically.19 of a large percentage of the alveolar capillary bed, and
the reduced alveolar surface area decreases the diffu-
sion capacity of the lung.17
DIAGNOSIS OF COPD Arterial blood gas measurement is used as supporting
The history and physical examination are helpful in documentation in diagnosing COPD. Hypoxemia is
establishing a diagnosis. Looking closely at risk factors present in both chronic bronchitis and late-stage
for COPD, asking questions regarding the incidence of emphysema. Hypercarbia is characteristic of a subpop-
emphysema in the family (alpha-1 antitrypsin defi- ulation of patients with chronic bronchitis and is seen
ciency), asking about morning cough, sputum produc- in people with end-stage emphysema (FEV1 1 L).17
tion, and shortness of breath provide the clinician
valuable clues about the likelihood of COPD.17 After
identifying that a diagnosis of COPD is possible, the
CLINICAL MANIFESTATIONS
patient undergoes additional testing. Normally, patients do not have pure emphysema or
pure chronic bronchitis. The signs and symptoms of
Chest Radiograph. The chest radiograph can identify COPD are a composite of the signs and symptoms of
X-ray changes consistent with chronic bronchitis or patients with varying combinations of asthma, emphy-
emphysema. People with emphysema show all the sema, and chronic bronchitis. Patients with elements of
X-ray hallmarks of hyperinflation: low flat hemidia- more than one disease show combined symptoms:
phragm (on lateral), wide intercostal spaces, hypovas- • Dyspnea on exertion or at rest (emphysema)
cular lung showing excessive air, retrosternal air space • Productive cough of mucoid sputum (chronic
(lateral), and long narrow heart. The chest X-ray bronchitis)
changes classically seen in people with chronic • Wheezing (chronic bronchitis)
bronchitis are less dramatic. Increases in lung mark- • Distant breath sounds and use of accessory
ings indicate thickened airways containing mucus. muscles (emphysema)
These markings show as radiopaque linear densities • Barrel chest (emphysema)
on chest X-ray, and the pulmonary arteries are promi- • Hypoxemia (chronic bronchitis, end-stage
nent in the hilar area. COPD patients with both emphysema)
disorders show a varying combination of these • Hypercarbia in end-stage disease (chronic
changes.17,19 bronchitis, end-stage emphysema)
• Slightly reversible airflow limitation in response
Pulmonary Function Changes. Basic spirometry testing to bronchodilators (chronic bronchitis)
is the gold standard in diagnosing airflow limitation. • Systemic signs of cor pulmonale (early in
Forced expiratory maneuvers identify airflow limitation chronic bronchitis, late in emphysema)17,19
and its severity. Testing the improvement of the FEV1
after administering a short-acting beta 2 bronchodila- The COPD patient with hyper-reactive airways
tor identifies the degree of reversibility of the airflow (asthmatic component) demonstrates partial reversibility
obstruction. of airflow limitation in response to beta 2 bronchodila-
tors. Emphysema patients may show no or little improve-
• The presence of a postbronchodilator FEV1/ ment in expiratory flows after bronchodilator therapy,
FVC 70% and an FEV1 80% of predicted is and chronic bronchitics may be somewhere between the
diagnostic for airflow limitation that is not fully two extremes.17,19
reversible.1
• An increase of 12% or more in the FEV1 or FVC
is the minimal improvement required for STAGES OF COPD
maintenance bronchodilator therapy. The Global Initiative for Chronic Obstructive Lung
• If the expiratory volumes improve more than Disease (GOLD) identified four stages of COPD: mild,
20%, the patient is diagnosed with an additional moderate, severe, and very severe. These classifications
asthmatic condition; this degree of increase are defined by postbronchodilator spirometry results
indicates partial reversibility.24 (Table 9-7). The most general criterion for COPD is the
TABLE 9-7 GOLD classifications of COPD

Stages of COPD Pulmonary Function Criteria Clinical Manifestations
Stage I Mild COPD FEV1/FVC 70% Unaware of limitations
FEV1 80% of predicted Cough, sputum production
Stage II Moderate COPD FEV1/FVC 70% Seeks medical attention because of symptoms
FEV1 50% to 80% of predicted or exacerbation episode
Dyspnea on exertion
Cough, sputum production
Stage III Severe COPD FEV1/FVC 70% ↑ Dyspnea, reduced exercise tolerance, fatigue
FEV1 30 – 50% of predicted Cough, sputum production
↑ number of exacerbations
Stage IV Very Severe COPD FEV1/FVC 70% Evidence of cor pulmonale (pitting ankle
FEV1 30% of predicted edema, jugular venous distention)
OR Dyspnea at rest, fatigue
FEV1 50% plus chronic respiratory ± Cough, sputum production
failure (PaO2 60 mm Hg, PaCO2 Life-threatening exacerbations
60 mm Hg)
presence of airflow obstruction as indicated by FEV1/ results from the effects of chronic hypoxemia on the
FVC 0.70. Severity is determined by the FEV1 in pulmonary vasculature. Hypoxemia causes pulmonary
relation to its predicted value based on age, height, sex, vasoconstriction that increases the right ventricle’s
and race. afterload. Pumping against the chronically high
pulmonary vascular pressures increases right heart
muscle work, which eventually causes right-sided heart
COMPLICATIONS failure. The treatment of cor pulmonale is to treat the
The major complications of COPD are frequent underlying cause: lung disease. Maximizing the COPD
infections, cor pulmonale, respiratory failure, sleeping patient’s lung function and gas exchange is the best way
disorders, and pneumothorax. These complications can to definitively treat cor pulmonale. Continuous oxygen
cause deterioration in the patient’s quality and length therapy may be necessary to raise the PAO2 and to
of life.17,19 eliminate the stimulus for vasoconstriction. If pulmo-
nary hypertension persists, long-term alpha-adrenergic
Infections. An acute exacerbation is the cause of antagonist therapy may be helpful in treating pulmo-
considerable morbidity and mortality in patients with nary hypertension and thus in improving heart
COPD. Most of the exacerbations are secondary to function.17,19
lower respiratory tract infections. The most common
microorganism strains cultured from the sputum are Sleep Quality. Sleep quality is significantly affected in
Haemophilus influenzae, Streptococcus pneumoniae, and patients with COPD.25 Insomnia, sleep-disordered
Moraxella catarrhalis.17,19 COPD patients in an acute breathing, and obstructive sleep apnea affect COPD
exacerbation show a worsening of respiratory symp- patients, many of which have multiple health prob-
toms. They may have fever; the sputum changes from lems. Insomnia is common among people with COPD.
mucoid to purulent; the dyspnea worsens; and pulmo- Factors that could contribute to the inability to remain
nary function measurements deteriorate, with a drop in asleep at night are cough, dyspnea, and arousals
the PAO2, possible hypercarbia, and a decrease in FEV1 associated with increasing PACO2, oxygen desaturation,
or PEFR. They may also have a worsening of cor and medications that help breathing function but
pulmonale in conjunction with the acute exacerbation. promote wakefulness.26 During sleep, alveolar ventila-
As the disease worsens, the acute exacerbation episodes tion and PAO2 decrease and CO2 increases in normal
occur more frequently and may cause acute respiratory subjects. However, in the COPD population, their
failure.17,19 oxygen baseline values are lower than normal and their
hypoventilation during sleep results in more severe
Cor Pulmonale. Cor pulmonale is defined as right drops in oxygen saturation, especially in REM (rapid
heart failure secondary to lung disease. Cor pulmonale eye movement) sleep. The acute episodes of hypoxemia
during sleep lead to pulmonary vasoconstriction and symptoms may be appreciable. The goals of drug
put the person with COPD at a greater risk for develop- therapy in the treatment of COPD are to:
ing persistent pulmonary hypertension and cor pulmo-
• Increase the positive effects of smoking cessation
nale. Obstructive sleep apnea (OSA) can occur in the
or reduction.
COPD population. If they complain of disrupted sleep,
• Relieve dyspnea using bronchodilator therapy.
daytime sleepiness, it may not be just insomnia.
• Treat the episodic exacerbations of COPD.
OSA should be considered by the physician as a
• Preserve lung function and reduce its rate of
possible problem in a patient who is complaining
decline.17,19
of insomnia.26
Acute respiratory failure is defined by a deterioration Bronchodilator medications are central to the manage-
in the patient’s arterial blood gas secondary to a ment of people with COPD. They are given as rescue
worsening in lung function brought about by an acute drugs for relief of persistent or worsening COPD and as
infection, pneumothorax, or exacerbation of cor maintenance drugs. The principle bronchodilators are
pulmonale. Respiratory failure is described as a state of beta 2 agonists, anticholinergics, and methlyxanthines.
alveolar hypoventilation in which the pH is less than These medicines can be used alone or in combination.1
7.25, the PACO2 is more than 60 mm Hg, and the PAO2 Beta 2 bronchodilators, used for many people with
is less than 50 mm Hg. Intensive bronchial hygiene COPD, reduce airway obstruction secondary to bron-
may help to avert intubation and mechanical ventilation. choconstriction. People with COPD have an irrevers-
For the patient who is chronically hypercarbic, the ible or slightly reversible airflow limitation. If a patient
arterial pH and PAO2 are used as the primary guidelines does not initially respond to short-acting beta 2
to determine respiratory failure.19 agonists, a lengthy maintenance trial of this drug
frequently results in symptomatic or pulmonary
Pneumothorax. Pneumothorax is a possible complica- function improvement sometime after the bronchodi-
tion of COPD. People with bullae are very vulnerable lator trial. The relief of dyspnea without an accompany-
to rupture and subsequent pneumothorax. Other ing increase in FEV1 is sufficient cause for continuing to
causes of pneumothorax are mechanical ventilation or prescribe bronchodilator therapy to the patient with
other medical procedures that may lacerate the lung chronic lung disease. Improving quality of life is an
(e.g., a central IV line placement, thoracentesis).19 important determinant of treatment efficacy.
Beta 2 agonists are available for inhalation as dry
powder for self-actuation, in an MDI (metered-dose
TREATMENT inhaler), and as liquids for nebulizing. The choice of
Maintenance therapy in patients with COPD is very the inhaler device depends on the physician, availabil-
important in decreasing life-crippling symptoms, in ity, costs, and individual coordination skills. People
decreasing the number of exacerbations, in improving who have difficulty with the system can have an MDI
quality of life, and possibly in extending life. The space chamber added or use a breath-activated device.1
treatment regimen depends on disease severity (based The anticholinergic drugs (ipratropium, oxitro-
on FEV1) and on whether the patient has asthma as a pium, and tiotropium bromide) have a greater role for
component of the airflow limitation. relief of bronchospasm in COPD than in asthma. This
The first step in the treatment for COPD is to drug group causes bronchodilation by blocking
encourage the patient to stop smoking. This step is acetylcholine’s effect on the M3 (muscarinic 3) recep-
critical in mild to moderate COPD because smoking tors. They may also inhibit airway hyper-reactivity to
cessation slows disease progression. In severe COPD, nonspecific agents such as smoke or strong scents in
smoking cessation reduces symptoms and exacerbation cosmetics. This drug group has a longer duration of
frequency. Many smoking cessation programs, quitting action than the short-acting beta 2 bronchodilators.
strategies, and behavior modification techniques may Tiotropium, the longest acting of all the anticholinergic
help the long-term smoker quit. When attempting to drugs, has a duration of action of 24 hours. It is
quit, the smoker is prone to relapses and may attempt suggested that ipratropium be used in mild to severe
to quit many times before being successful.17,19 COPD. Combination therapy with a beta 2 drug
should be added in moderate COPD. Anticholinergic
Drug Therapy. The drugs used to treat COPD have drugs are available in an MDI or as a liquid for
many similarities to those used for asthma. An impor- nebulization.1,19
tant difference is that the airflow limitation in COPD Theophylline-based medications have been used in
without an asthmatic component does not respond chronic lung disease for decades. The mechanism of
well to bronchodilator therapy. In COPD, the improve- bronchodilation is not well understood. Theophylline
ment is mild (about 12–15%), but the alleviation of is known to have many beneficial effects for some
people with COPD. Improvement in diaphragmatic life for patients with a terminal illness, as in pulmonary
contraction has been reported as well as an anti- rehabilitation.
inflammatory effect. One study of the therapeutic effects Most COPD patients on the waiting list for lung
of theophylline reported the anti-inflammatory effect transplantation have emphysema. The types of lung
that theophylline demonstrated in a study on transplants are single-lung, double-lung, and living-
asthmatics.27 The report indicated that, in the treatment related lung. Not all emphysema patients qualify for
of COPD, theophylline, when used in conjunction with lung transplantation. They must meet stringent criteria
other bronchodilator drugs, adds to the other drugs’ before they are put on the transplant waiting list.28 The
bronchodilator effects. However, because of the potential criteria for lung transplantation are:
for drug toxicity, inhaled bronchodilators are preferred.1
• Limited life expectancy.
The routine use of antimicrobials in COPD is not
• No alternative effective medical or surgical
indicated. Antimicrobial therapy is suggested as
therapy.
treatment for patients in an acute exacerbation second-
• Being currently ambulatory.
ary to a lower respiratory tract bacterial infection. The
• Having adequate nutritional status and accept-
choice of antimicrobial therapy is based on the suscep-
able left ventricular function without significant
tibility of the likely pathogens. Drug-resistant strains
coronary artery disease.
are becoming a problem in treating pneumonia.1,17,19
• Age (single lung, younger than 65; double lung,
Unlike their effect in asthma cases, oral and
younger than 60; heart-lung, younger than 55).
inhaled corticosteroids do not modify the progressive
deterioration in lung function. However, the regular The exclusionary criteria are followed closely
use of inhaled steroids in symptomatic Stage III and because of the desire to give the organ to people with
Stage IV COPD patients reduces the frequency of the greatest chance of a successful outcome. The
exacerbations and improves quality of life. Currently, situations that disqualify a person for a lung
maintenance treatment with inhaled steroids, espe- transplant are:
cially the inhaled steroid combined with the long- • Recurring or active drug-resistant infections.
acting beta 2 agonist, is recommended for a patient • Noncompliance with medical regimens.
with more advanced COPD who is demonstrating • Being HIV-positive, hepatitis B–positive, or
repeated exacerbations.1 hepatitis C–positive status.
In the recent past, a trial of oral steroids was • Ventilator dependency.
suggested for patients who are receiving optimal • Receiving prednisone therapy of more than
therapy and are still symptomatic. Discouraging steroid 20 mg/day.
trials is the lack of clinical evidence that a short course • Mental instability.
of steroids can be used to predict the long-term • Current substance abuse.
response to inhaled steroids in COPD. Steroids cause • Malignancy within past 2 years.
too many serious side effects—such as diabetes, • Dysfunction of other major organs.28
hypertension, and increased infections—in exchange
for simply a greater sense of well-being.1,17 The most common type of lung transplant in the
The use of oral steroids in COPD has changed in COPD patient is the single-lung transplant. This
recent years. Short-term therapeutic trials of oral procedure is simpler than the others, does not require
steroids are not recommended. Evidence suggests that a cardiopulmonary bypass, and has lower surgical and
short-term trial of steroids does not predict the success postoperative morbidity and mortality rates. Patients
of inhaled steroids in patients not responding to will need to be on immunosuppressive therapy for the
bronchodilator therapy. Additionally, evidence-based rest of their lives.
research does not support long-term treatment with Successful lung volume reduction surgery (LVRS)
systemic steroids. The systemic side effects are too helps to reduce the number of COPD patients on the
severe to use these drugs without solid proof of their waiting list for lung transplantation. The surgery has
effectiveness.1 reemerged as a treatment for end-stage COPD. Non-
functioning areas of the emphysematous lung are
Other Treatment. Other directions for treating the removed to reduce hyperinflation and to improve lung
patient with COPD are lung transplantation, lung mechanics and gas exchange. The National Emphysema
volume reduction therapy, the replacement of alpha-1 Treatment Trial identified four subgroups of patients
antitrypsin, and pulmonary rehabilitation. These who had different surgical risks and different benefits
treatments are widely different in their impact on the from the surgery:
patient’s life. Their effects range from curative, as in the • Group 1 patients have mostly upper lobe
case of a lung transplant, to improving the quality of emphysema and low exercise capacity.
• Group 2 patients have mostly upper lobe “Bronchiectasis is an anatomic distortion of the
emphysema and high exercise capacity. conducting airways that results in chronic cough,
• Group 3 patients have diffuse emphysema and sputum production and recurrent cough.”30 It was first
low exercise capacity. described by Laennec in 1819 as abnormally dilated
• Group 4 patients have diffuse emphysema and bronchi and bronchioles due to recurring episodes of
high exercise capacity. infection and inflammation.30,31 The airway dilation
is chronic and irreversible and usually affects the
Groups 1 and 2 consist of the types of the patients who
medium-sized bronchi (4th–9th generations). The
would benefit the most from lung volume reduction.
chronic airway inflammation and pooling of infected
They have localized disease, and removing the diseased
secretions sets up a cycle of repeated serious pulmonary
lung decreases the areas of hyperinflation and improves
infections with damage that is progressive and causes
lung mechanics, exercise tolerance, and quality of life.
deteriorating lung function.
Groups 1 and 2 would benefit the most from lung
volume reduction. Groups III and IV have disease that
affect the entire lung so that, despite removing hyperin- DIAGNOSIS
flated lung areas, the remaining lung would be still very
Someone with suspected bronchiectasis presents to the
diseased. These patients do not demonstrate significant
physician with a chronic cough productive of mucopu-
improvement after surgery and are not candidates for
rulent secretions. Although the physical findings are
LVRS. Their only possible avenue is lung transplant
generic for many types of lung problems, the clinical
surgery.28,29
findings are less common: hemoptysis, digital clubbing,
Small numbers of patients with COPD have
and excessive sputum production with position change.
premature emphysema secondary to alpha-1 antitryp-
Pulmonary function findings are unrevealing, with
sin deficiency (AAT). To qualify for alpha-1 proteinase
airway limitation ranging from mild to severe. The
inhibitor replacement therapy, patient must:
imaging study that definitively diagnoses bronchiecta-
• Be a nonsmoker. sis is the high-resolution CT (HRCT) scan. It has
• Be over the age of 18. replaced the bronchogram as the gold standard for
• Have low serum concentration of A1-A 50 mg/dL radiologic diagnosis of bronchiectasis.30 HRCT findings
or 11μM/L or 0.8g/L (35% of normal). reveal bronchial dilation with the appearance of the
• Have progressive emphysema with a documented classic signet ring sign (the internal bronchial diameter
rate of decline in FEV1. is greater than the diameter of the accompanying
• Be vaccinated with the hepatitis B vaccine series bronchial artery) and the lack of bronchial tapering of
before administration. the affected bronchial segmental generations. The three
classic patterns of airway distortion in bronchiectasis
The API drug is given by IV once per week or every
are cylindrical, varicose, and saccular/cystic. Many
2–4 weeks, and the usual dose is 60 gm/kg/week.
people with bronchiectasis have all three abnormal
Patients must remain on this drug for the rest of their
changes to their bronchi. Those with a predominance
lives. There is a national registry for people who qualify
of the saccular/cystic bronchiectasis have a higher
for replacement therapy.17
incidence of Pseudomonas aeruginosa cultures and a
poorer prognosis.30,31
Bronchiectasis ETIOLOGIES
It is estimated that approximately 100,000 people in
The causes of bronchiectasis are organized as idio-
the United States have non–cystic fibrosis bronchiecta-
pathic, postinfection, or underlying disease. These
sis. Most of the people with this type of bronchiectasis
categories overlap.
are over the age of 75. In recent years, the disease
In the idiopathic category is a long list of diseases or
appeared to be more of historical interest. However,
conditions that frequently are unknown at the time the
with the advent of more advanced imaging such as the
person is identified as having bronchiectasis but that
high-resolution CT, the disease has been found to be
are diagnosed at a later time. The idiopathic cause has
more prevalent than previously thought.30 Certain
subtypes such as:
demographic groups have an increased risk for devel-
oping bronchiectasis, such as people with decreased • Secondary genetic immunologic dysfunction or
access to health care, those with high rates of child- autoimmune abnormalities.
hood pulmonary infections (cystic fibrosis is a promi- • Genetic causes, such as cystic fibrosis, primary
nent risk), and those with chronic airway disease such immotile cilia syndrome, and alpha-1 antitryp-
as chronic bronchitis. sin deficiency.
• IgG immune deficiency and immune-related dys- causes adverse side effects in patients with
function, such as allergic bronchopulmonary non-CF bronchiectasis.
aspergillosis collagen vascular diseases and • Nebulized hypertonic saline (7%), a new form
inflammatory bowel diseases. of therapy in CF-bronchiectasis, may be benefi-
• Chronic gastric aspiration, foreign body aspira- cial in non-CF bronchiectasis, but more evi-
tion, and endobronchial tumors. dence-based research should be performed
before it is routinely used.
Nontuberculous mycobacteria (NTM) infections
• Mechanical aids to augment sputum mobiliza-
are associated with bronchiectasis, but it is not clear
tion are effective in CF-bronchiectasis, but little
whether NTM actually causes or bronchiectasis or if
research in the non-CF type of bronchiectasis is
bronchiectasis increases the patient’s susceptibility to
available. These treatments may still be used in
NTM.
both types of bronchiectasis, but their effective-
Another group with a significant incidence of
ness is unproven.
coexisting bronchiectasis is the COPD population.
A study using HRCT revealed that 50% of a cohort
of patients with stable COPD who had a mean FEV1
<0.96 L had bronchiectasis. Additionally, COPD
Summary
patients with bronchiectasis had more severe exacerba- The airflow limitation diseases discussed in this chapter
tions, more colonization of their lower airway with are asthma, chronic bronchitis bronchiectasis, and
bacteria, and more inflammatory markers in their emphysema. Asthma is in a separate category of airflow
sputum. Although asthmatics have a much lower limitation because it is a reversible disease that
reported incidence of bronchiectasis, a research study responds to bronchodilator therapy. Chronic bronchi-
revealed a 3% incidence of bronchiectasis in a group tis, bronchiectasis, and emphysema are known by the
of patients with severe persistent asthma.30,32 acronym COPD. The airway obstruction in these
diseases is not reversed by bronchodilators, and the
disease results in permanent and progressive changes.
TREATMENT In people who are asthmatic, the inflammation causes
recurrent episodes of wheezing, dyspnea, chest tight-
Treatment of bronchiectasis is directed toward reducing
ness, and coughing. The airflow obstruction may
the frequency of exacerbations and improving quality
reverse spontaneously, or it may require treatment for
of life. The organisms commonly cultured from the
reversal. Exposure to environmental triggers elicits a
diseased bronchi are nonenteric gram-negative bacteria,
hypersensitivity reaction in the bronchial epithelium of
Staphylococcus aureus, and NTM. Cystic fibrosis (CF)
allergic patients, which may result in a rapid worsening
should be ruled out in those with chronic cultures of
in respiratory function. Other causes of exacerbation
Staphylococcus aureus. Approximately one-third of
are viral infection, exercise, and inhalation of irritants.
bronchiectasis patients are colonized with Pseudomonas
COPD is characterized by the presence of chronic
aeruginosa; these patients have a greater number of
bronchitis, emphysema, or both. The COPD patient
exacerbations and greater deterioration in lung
has progressive airflow limitation that may be partially
function.30
reversible in those patients with hyper-reactive airways.
Oral or IV antibiotics are used only in acute
Emphysema is present when there are permanent
exacerbations. However, studies on the benefit of
dilation and destruction of lung units distal to the
inhaled maintenance antibiotics indicate that it may
terminal bronchioles.
be beneficial to use a regimen of inhaled tobramycin
Chronic bronchitis is the predominant cause of
or colistin in patients with frequent exacerbations.
COPD. Chronic bronchitis is defined functionally as
However, the concern is that the patient may develop
an individual having a chronically productive cough
antibiotic resistance.
lasting 3 or more consecutive months for 2 successive
Using the same respiratory medications and
years. Bronchiectasis is an anatomic distortion of the
mechanical mobilization of secretions for CF-
conducting airways that results in chronic cough,
bronchiectasis and non-CF bronchiectasis is not
sputum production, and recurrent cough. The airway
recommended.
dilation is chronic and irreversible, usually affecting
• Short-acting or long-acting beta adrenergic medium-sized airways. It is the result of recurring
bronchodilators and anticholinergic bronchodi- episodes of infection and inflammation.
lators are commonly used as maintenance A deficiency of alph-1 antitrypsin is a genetic
therapy, but their effectiveness is not clear. disease involving a decreased ability to block the
• The mucolytic agent, recombinant human dornase activity of proteolytic enzymes. A deficiency in the
alfa, a standard of care in CF-bronchiectasis, enzyme results in the unopposed proteolysis of elastin
in the lung and the liver. The increased breakdown 4. What is a common bacterial organism cultured
of elastin leads to the development of panacinar from the sputum of patients with chronic
emphysema. bronchitis?
Basic spirometry is the gold standard for diagnos- a. Pseudomonas aeruginosa
ing airflow limitation. Forced expiratory maneuvers b. Haemophilus influenzae
identify airflow limitation and its severity. The c. Staphylococcus aureus
differentiation between emphysema and other d. Mycoplasma pneumonia
diseases that limit airflow is based on the measure- 5. What medication is preferred in patients receiving
ment of carbon monoxide diffusing capacity. Because step 5 asthma maintenance therapy?
emphysema results in the loss of alveolar surface a. low-dose inhaled steroids and a long-acting
area, the carbon monoxide diffusing capacity of the beta 2 bronchodilator
lung is decreased. b. medium-dose inhaled steroids and sustained-
The major complications of COPD are frequent release theophylline
infections, cor pulmonale, respiratory failure, sleeping c. high-dose inhaled steroids and inhaled
disorders, and pneumothorax. These complications long-acting beta 2 bronchodilator
can cause deterioration of the patient’s quality and d. high-dose leukotriene antagonist and low-dose
length of life. inhaled steroids
6. This asthma patient has an FEV1 of 72% and
Study Questions complains of awakening at night about 1–2 times a
week because of difficulty breathing, and his peak
REVIEW QUESTIONS flow rates varies about 35% during the day. What is
1. What are the differences between asthma, chronic this patient’s severity of asthma?
bronchitis, and emphysema? a. mild intermittent asthma
b. mild persistent asthma
2. List and define the clinical categories of asthma.
c. moderate persistent asthma
3. Compare the clinical presentation of a patient with d. severe persistent asthma
emphysema to that of a patient with asthma.
7. What is the recommended rescue medication for
4. Differentiate between atopic and nonatopic the patient with asthma?
asthma. a. high-dose inhaled steroid
5. What are the three main types of emphysema? b. inhaled cromolyn sodium
What are the differences among them? c. leukotriene receptor antagonist
d. short-acting beta 2 bronchodilator
8. This COPD patient has an FEV1/FVC of 65%, FEV1
of 62%. Using the GOLD classification, what is the
1. What postbronchodilator change in FEV1 or FVC is severity of his COPD?
considered a minimally acceptable improvement a. Stage I
for prescribing bronchodilator therapy? b. Stage II
a. 6% c. Stage III
b. 12% d. Stage IV
c. 18% 9. What radiographic changes are consistent with
d. 20% pulmonary emphysema?
2. Which of the following diseases is not classified as a. air bronchogram extending to the peripheral
an airflow limitation disease? lung fields
a. pneumothorax b. increased radiodensity of the lung in the lower
b. asthma lobes
c. bronchiectasis c. increased bronchial markings
d. chronic bronchitis d. low flat diaphragm
3. Which of following is not an etiology of 10. What clinical manifestation is commonly observed
bronchiectasis? in patients with pulmonary emphysema?
a. cystic fibrosis a. pronounced expiratory wheezing
b. immunologic dysfunction b. dyspnea on exertion
c. inflammatory bowel disease c. digital clubbing
d. allergy to tree pollen d. cyanosis
CRITICAL-THINKING QUESTIONS in the pediatric emergency department. Pediatrics.

1999;103,4:748–752.
1. How are COPD with emphysema and emphysema
12. Qureshi F, Pestian J, Davis P, Zaritsky A. Effect of
caused by alpha-1 antitrypsin deficiency different?
nebulized ipratropium on the hospitalization rates
Briefly describe the typical course of therapy for
of children with asthma. N Engl J Med.
each.
1998;339,15:1030–1035.
2. Define the two main elements of an asthma 13. Rodrigo GJ, Rodrigo C, Burschtin O. A meta
management program. analysis of the effects of ipratropium bromide in
3. What are the three stages of an asthma attack? adults with acute asthma. Am J Med. 1999;
What are the differences between them? How 107,363–370.
would the treatment plan differ between stages? 14. Pedersen S. Why does airway inflammation persist?
Is it failure to treat early? Am J Resp Crit Care Med.
2000;161,S182–S185.
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CHAPTER 10
Diffuse Parenchymal Lung Diseases

Barbara Ludwig
OBJECTIVES
• Describe the difference categories of diffuse parenchymal lung diseases (DPLDs).
• Identify the four types of idiopathic interstitial pneumonias.
• Discuss the diagnosis and medical treatment of DPLDs.
• Describe an organization of different types of DPLDs.
• Identify the proposed mechanism of inflammation and fibrosis in diffuse lung disease.
• Describe the general X-ray changes in patients with DPLD.
CHAPTER OUTLINE
Diffuse Parenchymal Lung Diseases Phase 2: Chronic Inflammation
Incidence and Prevalence in the Population General Clinical Appearance
Mortality Rates Diagnosis
Etiology Complications
Pathogenesis Treatment
Phase 1: Antigen Trigger
KEY TERMS
basement membrane idiopathic
etiology pathogenesis
extracellular matrix video-assisted thoracoscopic surgery (VATS)
honeycomb lung
251
T
he terminology used to talk about diffuse thickening of the alveolar capillary membrane with
parenchymal lung diseases is inconsistent. In an associated decrease in lung compliance and gas
various sources, these diseases may be exchange. The wide variety of diseases that cause
referred to as restrictive lung diseases, intersti- diffuse parenchymal and interstitial damage range,
tial lung diseases (ILDs), or pulmonary fibrosis. The among many others, from idiopathic lung diseases,
American Thoracic Society/European Respiratory environmental lung diseases, drug toxicity, and
Society International Multidisciplinary Consensus collagen vascular diseases to hemorrhagic diseases of
Group refers to this disease group as diffuse parenchymal the lung.1,2
lung diseases (DPLDs). That organization also changed Approximately 190 disorders can cause diffuse
the classification of idiopathic (of uncertain or parenchymal lung disease. The individual diseases
unknown origin) interstitial pneumonias. (See or disorders are complex and are not specifically
Table 10-1 for the new terminology.)1 discussed in this chapter. Rather, employing a
Diffuse parenchymal lung diseases encompass all general perspective, the aim is to impart a broad
of the pulmonary and systemic diseases that cause understanding of the pathology, pathophysiology,
infiltration into the alveolar airspace and the intersti- clinical features, diagnosis, and treatment of diffuse
tium of the lung. The infiltration results in the parenchymal lung disease.
TABLE 10-1 Classification of diffuse parenchymal lung diseases

Categories Specific Diseases
DPLD of Collagen vascular diseases
Known Cause Rheumatoid arthritis, Scleroderma, Systemic Lupus Erythematosus, Ankylosing spondylitis,
Sjogren Syndrome, Mixed Connective Tissue Disease
Drug-induced interstitial disease
Cytotoxic agents, Certain antibiotics, Certain antiarrhythmics, Illicit drugs, Anti-inflammatory drugs
Radiation Exposure
Pulmonary Alveolar Proteinosis
Environmental Lung Diseases
Hypersensitivity Pneumonitis: Farmers Lung, Baggassosis, Bird Breeder’s Lung
Pneumoconiosis: Asbestosis, Berylliosis, Silicosis, Anthracosilicosis, Coal worker’s lung
Inherited DPLD
Familial IPF or Sarcoidosis, Tuberous sclerosis,
Neurofibromatosis, Niemann-Pick disease, Gaucher disease, Hermansky-Pudlak syndrome
Idiopathic Idiopathic interstitial fibrosis Other interstitial pneumonias:
Interstitial Formerly known as Usual interstitial Desquamative interstitial pneumonia (DIP),
Pneumonias pneumonia (UIP) or end-stage lung Acute interstitial pneumonia (AIP) or
Hamman-Rich syndrome,
Non-specific interstitial pneumonia (NSIP),
Respiratory bronchiolitis ILD, Cryptogenic
organizing pneumonia (COP) formerly
idiopathic BOOP
Lymphocytic interstitial pneumonia (LIP)
Granulomatous Sarcoidosis
DPLD
Other DPLD Lymphangioleiomyomatosis (LAM)
Langerhans’ cell Histiocytosis/Histiocystosis X
Pulmonary/Renal vasculitis: Wegener’s Granulomatosis, Goodpasture’s Syndrome
Pulmonary Eosinophilic Syndromes
Loeffler’s Syndrome (eosinophilic pneumonia), Churg-Strauss Syndrome
CHAPTER 10 ■ Diffuse Parenchymal Lung Diseases 253
Diffuse Parenchymal ETIOLOGY

Many of the DPLDs have an unknown etiology (the
Lung Diseases cause of a disease). However, of the diseases having
The DPLDs are a heterogeneous group of disorders that known etiologies, a large group of diseases consists of
damage the pulmonary parenchyma secondary to the environmental (occupational) lung diseases.
various disease-causing processes. The type of inflam- Environmental lung diseases are the most common
matory cells activated and the inflammatory pathway disease classification of all the DPLDs. These diseases
leading to lung injury depends on the etiologic trigger are distributed geographically according to the industry
or antigen stimulus. Despite these differences, the end and occupational concentrations in specific areas of
results are the same: widespread inflammation and the country.8
fibrosis.3 However, even though their effects are the Environmental lung disease (Tables 10-2 and 10-3)
same, their treatments, their responses to treatment, is secondary to the inhalation of allergens, chemical
and their prognoses all vary. gases, and environmental pollutants that elicit an
immunological reaction in the lung, causing deposi-
tion of fibroblasts in the airways or alveolar tissue.9–12
INCIDENCE AND PREVALENCE IN THE POPULATION Whether disease occurs in any one individual depends
Studies of people with intrinsic lung diseases revealed on several variables:
an overall prevalence (i.e., people already diagnosed)
• Pollutant particle density.
of 3 to 6 cases per 100,000 persons and a prevalence of
• Duration of exposure.
idiopathic pulmonary fibrosis of 27 to 29 cases per
• Chemical properties of the pollutant.
100,000 persons. When examining people over the age
• The individual’s susceptibility to that environ-
of 75, the prevalence exceeded 175 cases per 100,000
mental material.8
persons.4–6 The prevalence of sarcoidosis in the United
States is 10 to 40 cases per 100,000 persons. The
incidence (i.e., people just diagnosed) of DPLD in Duration of Exposure. The particle size for optimal
people with collagen vascular disease is increasing for deposition in the respiratory bronchioles and alveoli is
most of the diseases in this category.4 in the range of 0.5–5 ␮m. The density of environmen-
tal pollutants of this size determines the dose (quantity
of an agent administered). If fewer than 10 particles per
MORTALITY RATES milliliter of air are inhaled, then all the pollutant
The morbidity and mortality rates of people with DPLD particles are eliminated from the lung by its defense
vary with the disease. Factors that directly increase the mechanisms. If 1000 particles per milliliter are inhaled,
mortality rate of the patient with DPLD are: then 90% of the particles are eliminated. However, if
the particle density is 1 million particles per milliliter,
• Increased age.
then a high percentage of these pollutants will be
• Male sex.
retained in the lung. This type of pollutant density
• Smoking history.
overwhelms the lung’s normal defenses, and the
• Severe dyspnea.
particles cannot be removed by the normal mecha-
• Severe loss of pulmonary function.
nisms (e.g., cough, mucociliary escalator). For example,
• Severe X-ray changes.
if dust exposure occurs over months to years, then the
• Poor response to therapy.
dust may cause a low-level inflammatory response that
• Prominent fibroblasts on pathology report
causes progressive lung injury.
are all.
The following mean mortality rates of people diag- Chemical Nature of the Pollutant. The chemistry of a
nosed with idiopathic interstitial pneumonias have pollutant’s impact on the individual should be
widely disparate time measures because they are from answered by the following questions:
different research reports:7
• Does the pollutant easily elicit an immunologi-
• Idiopathic pulmonary fibrosis mean mortality cal reaction from the individual?
rate: 68% (5–6 years) • Is the pollutant a known agent that causes
• Acute interstitial pneumonia mean mortality: fibrosis formation (e.g., silicosis, asbestosis)? If
62% (1–2 months) the pollutant is fibrinogenic, then the damage is
• Desquamative interstitial pneumonia mean progressive and continues even if the individual
mortality rate: 27% (12 years) is removed from possible exposure. In this
• Nonspecific interstitial pneumonia mean situation, disease may appear years after the
mortality: 11% (17 months) exposure has ceased.
TABLE 10-2 Environmental lung diseases

Extrinsic Allergic Alveolitis or Hypersensitivity
Pneumoconiosis (inorganic dusts) Pneumonitis (organic dusts)
Silicosis Silicone Dioxide Malt workers Lung Moldy Malt
Occupations: rock mining, Antigen: Aspergillus
rock quarrying, tunneling, clavatus or Aspergillus
foundry work, fumigatus
manufacturing (pottery,
porcelain, abrasives), Farmers Lung Moldy hay, bedding,
sandblasting, stonecutting compost
Antigen: Micropolyspora
Asbestosis Fibrous silicate faeni
Occupations: insulation,
shipyard and construction Toxic chemicals Acid fumes, aldehydes,
workers, auto repair (see Table 10-3) ammonia, anhydrides,
workers exposed to cadmium fumes
brake linings
Bird Breeders Lung Parrots, parakeets,
Coal Workers Silica pigeons, chickens, etc.
Occupation: coal mining Antigen: Bird serum
proteins in droppings
Berylliosis Beryllium
Bagassosis Moldy sugar cane
Occupations: workers in
aerospace, nuclear Antigen:
weapons and electronic Thermoactinomyces
industries saccharii, candidus,
or viridus
Susceptibility of the Individual. The third factor that subsequent parenchymal injury. How the initial stimu-
determines disease occurrence with environmental lus or antigen begins the fibrotic process varies with
exposure is the susceptibility of the individual to the the disease. The antigen trigger could be a virus or toxin,
pollutant. The individual’s atopy or immune function an inhaled organic or inorganic agent, an antibody
affects the person’s susceptibility or tolerance to any released from the immune system, or an unknown
exposure to environmental pollution.2,8 trigger. Fibrosis is the result of chronic inflammation
due to persistent or recurrent exposure to a stimulant,
irritant, or antigen causing parenchymal injury.1,13
PATHOGENESIS
With the existence of approximately 190 disorders
causing DPLD, the pathogenesis (origination and PHASE 2: CHRONIC INFLAMMATION
development of a disease), or evolution, of disease will The release of inflammatory cell activation and media-
not be uniform. The pathogenesis of DPLD is described tor from the injured lung’s epithelial cells and vascular
only in general terms so that the details of specific endothelial cells is the second phase of pulmonary
diseases do not cause confusion. Numerous pathways fibrosis development. The types of immune cells
can lead to pulmonary fibrosis, and this description released and chemical mediators produced vary with
may not include all the ways in which inflammation, the antigen trigger and determine the pathway of
lung and interstitial injury, and fibrosis develop. inflammation and subsequent fibrosis. Specifically
activated inflammatory cells could include eosinophils,
mast cells, macrophages, neutrophils, lymphocytes,
PHASE 1: ANTIGEN TRIGGER and multiple types of cytokines. Activated inflamma-
The first phase in the pathogenesis of diffuse lung tory cells are attracted to the area of injury, where they
disease is the antigen trigger. It is the initial underlying release chemicals that damage and fibrose the alveolar
cause of lung and/or vascular inflammation and capillary membrane (ACM).
TABLE 10-3 Toxic gas inhalation injury

Inhalant Information General Injury
High Water Solubility
Ammonia Industries: Fertilizer production and use; refrigeration; manufacturing of dyes Primarily upper
and plastics respiratory
Household cleaners tract: drooling,
mucosal
Besides inhalation it can be ingested and injure the GI tract or injure by direct
edema, cough,
contact with skin, or eyes
stridor, eye
On airway tissue forms ammonium hydroxide in an exothermic reaction causing irritation, skin
significant thermal injury irritation
Alkaline burn causes liquefaction necrosis and deeply penetrates tissue Serious cases
Mild exposures: Conjunctival and UA inflammation, pain pulmonary
Moderate exposures: exaggerated mild symptoms edema and
ARDS
Severe exposures: respiratory distress, productive cough, pulmonary edema, dysphagia
Chloramine Industries: Disinfectant in munciple water systems,
Risk for hemodialysis patients and fish (denature Hb. and causes hemolytic anemia)
Methyl Industries: Carbamate pesticides, adhesives, and rubber production
isocyanate Involved in Bhopal disaster ~3800 deaths immediately and thousands
experienced morbidity and premature death
Respiratory tract, skin, and mucus membrane irritation
Eye exposure causes: burning, photophobia, blepharospams, tearing, lid edema,
corneal ulceration with reversible blindness
Prolonged exposure: vomiting, diarrhea, dyspnea, cough progressing to pulmonary
edema and possible ARDS
Sulfur dioxide Industries: winemaking, winery sanitation, refrigerant, reagent or solvent in
laboratories, combustion of fossil fuels, smelting of sulfide ores, volcanic emissions
On airway tissues forms sulfuric acid and sulfurous acids
Contributes to formation of acid rain
Causes Bronchoconstriction in asthmatics
Besides inhalation it can injure by direct contact with skin, or eyes
Exposure: intensely irritating to the eye and respiratory tract
• UA irritation, nosebleeds, dysphagia, coughing
• In 5–15 minutes – bronchospasm
• Continued exposure – high pitched crackles, chest pain, tracheitis,
laryngeal edema, chemical bronchopneumonia, pulmonary edema,
cyanosis, asphyxia, death
Most common form of death is asphyxiation from glottic spasms
Intermediate Water Solubility
Chlorine Industries: Chemical, paper, textiles; sewage treatment; Household and swimming Affects all
pool accidents; airways,
Largest single cause of major toxic On airway tissue forms hypochlorous and potential for
hydrochloric acids delayed
symptoms.
Hallmark: Non-cardiogenic pulmonary edema
Combination of
Residual effects: non-specific airway hyper responsiveness, some people develop
high and low
fibrosis or bronchiolitis obliterans release incidents
water soluble
symptoms
(continues)
TABLE 10-3 Toxic Gas Inhalation Injury (continued)

Inhalant Information General Injury
Hydrogen Industries: petroleum, viscose rayon, rubber, and mining
Sulfide Other: volcanic eruptions, exposure to sewers, liquid manure pits, ships’ holds,
sulfur springs
Also called “acid rain”
Forms sulfuric acid and sulfurous acids
Inhalation, direct contact, possible histotoxic hypoxia resulting in asphyxiation
• Low levels – irritation to mucus membranes and respiratory system
• High levels – neurologic and pulmonary symptoms
• Very high levels – cardiopulmonary arrest due to brainstem toxicity
Nitrogen oxides Industries: arc welders, firefighters, military and aerospace personnel, Terminal airway
explosives, farmers epithelial injury
NO2 converted to NO, HNO3 (nitric acid) and HNO2 in distal airways
• Toxic to alveolar Type I cells and ciliated airways
• Alters macrophage and immune function, causing impaired resistance
to infection
• Methhemoglobinemia
• ARDS
2–6 weeks post exposure patients can develop Bronchiolitis obliterans or diffuse
alveolar damage
Low Water Solubility
Phosgene Industries: Production of aniline dyes, polycarbonate resins, coal tar, pesticides, Lower airway
isocyanates, polyurethane, pharmaceuticals injury with
Found in: household solvents, dry cleaning fluid inflammation
and necrosis
Produced in the combustion of methylene chloride in paint remover or
trichloroethylene in degreasing agents Causes
non-cardiogenic
A chemical warfare agent
pulmonary
Known as: carbonic dichoride, carbon oxychloride, carbonyl dichloride, edema (ARDS)
chloroformyl chloride, d-stoff, and green cross
Mechanisms of injury:
• Hydrolysis: Forms CO2 and hydrochloric acid in distal airways
• Acylation: Denatures protein, disrupts enzymes activates inflammatory cascade
Acute ACM injury results in the destruction of The interstitial matrix is present between cells in
Type I alveolar epithelial cells and the complementary the interstitial space and acts as a protective
pulmonary capillary endothelial cells. Chronic buffer against stresses placed on the ECM. In
inflammation causes permanent loss of the ACM diffuse parenchymal lung diseases, the damaged
extracellular matrix, including the basement membrane, extracellular matrix does not allow the reestab-
obliteration and fibrosis of the alveoli with fusion of lishment of normal lung structure.
adjacent basement membrane tissue remnants. • The basement membrane is the anchor for
organ cells. It is a thin membrane made up of
• The extracellular matrix consists of all the
proteins held together by type-IV collagen that is
connective tissues and fibers that are not part of
a vital component of the extracellular matrix. It
a cell but that provide support. It includes the
forms an integrated structure that controls cell
interstitial matrix and the basement membrane.
position, cell motility, the permeability barrier, the patient about occupational and domestic
extracellular signal transmission to cells, and environments—especially about asbestos, silica, and
regulation of growth factors important to farm and animal dust exposures. The patient is also
survival of alveolar epithelial and vascular questioned about travel history and drug history,
endothelial cells. The epithelial cells of each especially medications implicated in the genesis of
body organ are anchored to this membrane and DPLD, such as cytotoxic agents, amiodarone, gold,
resemble a layer of tiles. and some antimicrobials. Additionally, the physician’s
pursues the family history related to connective tissue
The focal areas of fibrosis are fused by connective
diseases, sarcoidosis, and other genetically caused
tissue. It is thought that the focal organizing fibrotic
diffuse lung disease.2,14
areas represent permanent loss of alveolar structure
to a respiratory lobule of the lung (terminal bronchi-
Pulmonary Function Testing. All forms of DPLD
oles to the alveoli). If the fibrotic process goes on
decrease lung volumes but preserve expiratory flow
unchecked, it ultimately destroys the entire lung
rates unless the patient has airway involvement, is a
lobule. This describes the idiopathic pulmonary
smoker, or has an airflow limitation lung disease. The
fibrosis (usual interstitial pneumonia) found in
patients have a reduced total lung capacity, vital
end-stage lung in people with asbestosis (persistent
capacity, functional residual capacity, and FEV1, along
exposure to the irritant), hypersensitivity pneumoni-
with a normal or increased FEV1/FVC ratio. Studies of
tis (recurrent exposure to the antigen), collagen
gas transfer typically show a reduction of carbon
vascular disease (scleroderma, rheumatoid arthritis),
monoxide–diffusing capacity. The primary reason for
or idiopathic (e.g., idiopathic pulmonary fibrosis
the reduced diffusion is the destruction of alveoli and
[IPF]).13
their capillaries, decreasing available surface area for
gas exchange. This loss of surface area is the basis of the
Phase 3: Granuloma Formation. Depending on the
patient’s hypoxemia. The patient’s PaO2 may be
type of DPLD, the third phase in pathogenesis may
adequate at rest and drop with mild exertion, such as
include the intermediate step of granuloma forma-
walking. Carbon dioxide is elevated only in end-stage
tion in addition to fibrosis development. Granuloma-
pulmonary fibrosis.2,14
tous pulmonary fibrosis is present in the lungs of
people with hypersensitivity pneumonitis, eosino-
Chest Radiograph and Other Radiographic
philic pneumonia, and sarcoidosis. The inflammatory
Studies. DPLD characteristically affects both lungs,
pathways that promote the granuloma formation in
and in some diseases it tends to dominate a particu-
sarcoidosis are postulated to be mediated by acti-
lar lung zone. Sarcoidosis, silicosis, and hypersensi-
vated T lymphocytes (CD4 cells) and activated
tivity pneumonitis have upper lobe predominance;
macrophages. Idiopathic interstitial pneumonias have
idiopathic interstitial pneumonias and asbestosis
a different pathway for fibrosis development than
have lower lung zone predominance. Enlargement of
does sarcoidosis.14
the mediastinal lymph nodes is often associated with
sarcoidosis or silicosis.
GENERAL CLINICAL APPEARANCE A common term used to describe severe pulmo-
The major clinical manifestation of people with nary fibrosis on the chest radiograph is honeycomb
interstitial lung disease is dyspnea. It is usually gradual lung, as seen in Langerhans histiocytosis X or late
in onset, with the patient believing that he or she is just phase pulmonary fibrosis. The fibrotic lung zones of
“out of shape” until the dyspnea progresses ultimately honeycomb lung are composed of cystic fibrotic air
to dyspnea at rest. In the very early stage of DPLD, spaces, and the normal alveolar architecture is replaced
dyspnea may be absent. The classic patient with DPLD with dense acellular collagen.2,14
is a 50- to 55-year-old male. His dyspnea worsens with High-resolution computed tomography (HRCT)
exertion; he has bibasilar inspiratory crackles, a cough brings much more definition to the usual CT scan. It
that is perhaps paroxysmal but nonproductive, and samples 1- to 2-mm samples of lung tissue at 1-cm
clubbing of his fingers and toes.2,14 intervals and uses a high-resolution computer software
algorithm. HRCT can bring into focus more detail than
was possible with conventional CT scans (e.g., ground-
DIAGNOSIS glass opacification, diffuse or local involvement, airway
For a diagnosis of DPLD (Table 10-4), the physician structures). HRCT is valuable in detecting fine fibrotic,
takes an extensive history of the patient’s external risk inflammatory changes, making it very helpful in identify-
factors and blood chemistry changes. During the ing disease activity. Therefore, HRCT not only helps
evaluation of risk factors, the physician questions physician diagnose early fibrotic disease, but it also allows
258
TABLE 10-4 Diagnosis of interstitial lung disease

Diagnostic Clues
Clinical signs and Chest X-ray Laboratory Pulmonary Function Other Diagnostic
Diseases History symptoms Findings Findings Test Findings Test Findings
Idiopathic Progressive Dyspnea at rest or Diffuse basilar Hypoxemia at Restrictive VTLB findings – areas of nml.
Interstitial DOE R/O exertion, digital predominance rest or during pattern with lung, interstitial fibrosis &
Pneumonias occupational or clubbing, bibasilar (⫾ nml. in early activity ↓ DLCO honeycombing ⬎ periphery
drug related crackles, disease) HRCT – intralobular intersitital
thickening, bronchiolar
distortion with traction
bronchiectasis peripheral
honeycomb changes
Hypersensitivity Environmental Acute exposure: Nml or ↑ lung Acute exposure: Acute or Subacute BAL – ↑ T-lymphocytes
Pneumonitis exposure Flu-like illness, markings Hypoxemia & Restrictive pattern (ⱖ60% of total lymphocytes)
Diagnosis from respiratory distress, between attacks hypocarbia ↓ DLCO for all forms in acute exposure
history fever, cough, Acute exposure: IgG serum of HP ↑ neutrophils, ↑ mast cells.
headache, diffuse diffuse alveolitis, precipitins to Many are hypoxemic TTB of lung, lymph nodes
Variable illness
fine bibasilar ground glass inducing organic at rest and desaturate diagnosing patients with
depending on
crackles appearance agent (↓’s in with exercise inadequate history.
dose, exposure
frequency, Chronic disease: Chronic exposure: disease Chronic disease Chronic HP disease May
individual Progressive DOE, Diffuse progression) Severe restrictive OR mimic idiopathic pulmonary
susceptibility bibasilar inspiratory fibrosis with mixed obstructive & fibrosis or nonspecific
crackles, fatigue, honeycombing restrictive pattern interstitial pneumonia.
weight loss, ⫾
clubbing
Cor Pulmonale in
end-stage lung
Langerhans Cell Smoking may Mild disease: Reticular-nodular ⫾ hypoxemia at May have obstructive HRCT – Thin-walled irregular-
Histiocytosis play a role Asymptomatic or infiltrates rest. and restrictive shaped cysts, nodules ⫾
(LCH) ⬎ common in mild symptoms predominance in ⫾ desaturation disorder. cavitation, reticular densities
3 syndromes: infants and Systemic disease: UL, ML, clear with exercise Obstruction may be 2° & ground glass appearance.
young children; Dyspnea, wheezing, costophrenic to LCH &/or smoking BAL or TTB – presence of
Eosinophlic
also affects hemoptysis, chest angles Langerhans’ positive cells in
granuloma ↓ DLCO
adults pain, fatigue, weight Advanced disease: lung fluid or presence of
Hand-Schuller- Abnml. exercise test
Affects loss, fever bullae, cystic Langerhans’ cells in tissue
Christian disease
ⱖ1 organs Bone lesions, changes, sample
Letterer-Siwe pneumothorax
diabetes insipidus, VTLB or bone lesion biopsy
disease
⫾digital clubbing
Sarcoidosis 2:1 male to 5% asymptomatic Bilateral hilar Hypoxemia or Restrictive pattern HRCT may be helpful for
female DOE, cough, chest lymphadenopathy, during exertion some show staging and help locating site
US – southeast pain, crackles on diffuse infiltrates in moderate- to- obstruction for biopsy
auscultation fever, ML, UL, severe Common- An isolated TBB of lymph nodes &
⬎ incidence in
anorexia, muscle End-stage: sarcoidosis, ↓ DLCO discrete, non-caseating
African-
Americans aches, honeycomb lung Abnml lab tests Exercise testing granulomas. Epithieliod cell
specific to organ indicates lung, heart is dominant
involvement involvement
(skin, eyes,
heart, lungs,
neurological)
Asbestosis Environmental Progressive DOE, Lower lobe Earliest change Early: HRCT
exposure dry cough predominance is exertional ↓ FEF25–75% Pleural or pleural-based
Appropriate (⫾ paroxsymal), with an irregular hypoxemia abnormalities and cancer
↓ FEV1 with normal
latent period bibasilar end- reticular pattern in changes.
ratio
expiratory crackles, periphery.
High cancer risk Late: Better definition of infiltrates.
digital clubbing
with smoking Early asbestos changes
~40% Restrictive pattern
with ↓ DLCO Peripheral septal thickening,
Advanced:
honeycombing, areas of
Cor Pulmonale in pleural thickening (placque),
end-stage lung and bronchiolar thickening.
Cryptogenic Flu-like onset, Expiratory wheezing, Bilateral, patchy, Restrictive pattern HRCT – patchy consolidation
Organizing predromal URI no clubbing migratory alveolar with ↓ DLCO and/or ground glass
Pneumonia Not described infiltrates Airflow limitation may appearance
(COP) in children be present Transbronchial biopsy or VTLB
lung biopsy – intraluminal
plugs of fibrobastic tissue in
the conducting airways and
alveolar ducts
Goodpastures Predromal viral Severe dyspnea, Progressive, Presence of Not necessary for Open lung biopsy –
Syndrome upper hemoptysis, migratory, anti-basement diagnosis. If intraalveolar hemorrhage,
respiratory progressive renal asymmetric membrane performed, the macrophages containing
infection failure infiltrates found antibody in the patient shows a hemosiderin
bilaterally blood ⫹ blood restrictive pattern Immunofluorescent staining
and protein in of lung and kidney tissue
urine showing deposition of
anti-basement membrane
antibody in the alveolar and
glomerular basement
membranes
259
close monitoring of the effects of drug treatment on active oxygen use, and lower total lung capacity (TLC) helps
disease. In addition, information from this radiological to identify poor candidates for surgical biopsy.15
technique can be used to identify potential locations to The advantage of surgical lung biopsy is that it
biopsy lung tissue for histopathologic diagnosis.2,14 In provides a histopathological diagnosis. The biopsy
some cases, HRCT is used to diagnose a patient with sample allows the pathologist to identify the type of
DPLD using information gained from patient history, inflammatory cells present in the lung sample, catego-
bronchoalveolar lavage results, and pulmonary function rize the pulmonary changes and the extensiveness of the
testing. If more specific information is necessary (e.g., fibrosis, and arrive at a diagnosis. The pathologist can
pathology results), then surgical lung biopsy is necessary. also help the physician ascertain whether the disease is
Common changes seen on HRCT performed on patients at the end stage or whether the physician can give the
with DPLC are diffuse, patchy, reticular opacities with patient some hope that the disease might respond to
irregularly thickened interlobular fissures and honeycomb treatment. Recognition of ongoing inflammatory
changes, especially in the bases.14 changes indicates that treatment with anti-inflammatory
drugs may delay the progression to end-stage lung.2,14
Clinical Laboratory Studies. Laboratory testing Another technique of obtaining a lung sample for
information is suggestive of some DPLD, but it is biopsy is through the fiberoptic bronchoscope. A trans-
nondiagnostic. However, specific abnormalities can bronchial needle biopsy (TBB) permits sampling in the
support a diagnosis of DPLD. For example: central, peribronchial areas. This technique is acceptable
in testing for the presence of a DPLD associated with
• Abnormal erythrocyte sedimentation rate
central lung involvement. Hilar lymph node sampling
indicates autoimmune disease.
may provide sufficient tissue to permit a histopathological
• The presence of serum precipitins is supportive
diagnosis for sarcoidosis or hypersensitivity pneumonitis.
of hypersensitivity pneumonitis.
If the suspected DPLD involves primarily the peripheral
• Antinuclear antibody and rheumatoid factors are
lung, as would idiopathic pulmonary fibrosis, then OLB
supportive of collagen connective tissue diseases.
or VATS is necessary to obtain a large enough sample.2,14
• Available blood tests, provide good supportive
evidence of diffuse parenchymal lung disease.
• When used with clinical manifestations, pulmo-
Bronchoalveolar Lavage. Bronchoalveolar lavage (BAL)
is a diagnostic procedure promoted as a possible
nary function test results, chest radiographs, and
technique to diagnose DPLD and eliminate the
HRCT may be sufficiently specific to allow for a
need for surgical lung biopsy. However, BAL has
diagnosis without the need for a surgical lung
not proven to be an adequate substitute for surgical
biopsy or a transthoracic lung biopsy.2,14
biopsy. Performing a pulmonary lavage and collecting
the washing sample theoretically produce a represen-
Surgical Lung Biopsy. In most patients, surgical lung
tative sampling of the inflammatory cells responsible
biopsy is not necessary to diagnose DPLD. A thorough
for the lung injury. However, BAL does not provide
history and physical exam, including appropriate blood
enough information for a diagnosis or determina-
chemistry studies, chest X-ray, and a HRCT imaging test,
tions about the current state of the patient’s lung
are performed before a surgical lung biopsy is consid-
disease.2,14
ered. If the HRCT is not conclusive or more information
is necessary, then the tissue biopsy may be needed.
Open lung biopsy (OLB) used to be the gold
standard for the diagnosis of DPLD. Now many COMPLICATIONS
physicians use the less invasive video-assisted The major complications of DPLD are cor pulmonale,
thoracoscopic surgery (VATS) in the place of OLB. exacerbation of idiopathic pulmonary fibrosis, and
Risks are associated with doing any surgical biopsy progressive oxygenation failure. These complications
procedure. Patients with relatively severe cardiovascular- can cause a significant decrease in quality and length
pulmonary impairment appear to be at the greatest of life.
risk for possibly fatal complications, such as acute
exacerbation of idiopathic pulmonary fibrosis or Cor Pulmonale. Cor pulmonale is defined as an altera-
unexplained acute lung injury. It is unclear whether tion in the structure and function of the right ventricle
the cause of the accelerated decline in lung function is secondary to lung disease. The chronic effects of
the rapid disease progression in this population or a hypoxemia on the pulmonary vasculature cause cor
response to the anesthetic, to the surgical procedure, pulmonale in patients with DPLD disease.
or to positive pressure ventilation. Before this proce- Doppler echocardiography is the most reliable
dure is performed, careful screening of patients for the noninvasive technique to estimate pulmonary artery
presence of pulmonary hypertension, preoperative pressure. Two-dimensional echocardiography identifies
CASE STUDY 10-1

Diffuse Parenchymal Lung Disease Mr. O’Connor denied exposure to any dusts or
Sean O’Connor, a 55-year-old male, went to his contaminants and denied any drug use. The doctor
personal physician complaining of increased made arrangements for him to receive a full workup
shortness of breath during exertion that had become at the Pulmonary Function Lab that would include a
worse over the last several months. He also com- diffusion study.
plained of a dry nonproductive cough that interfered A week later, Mr. O’Connor came back to the
with sleep. His doctor performed a physical exam doctor for discussion of his test results. The PFT
and general blood chemistry workup. revealed a restrictive ventilatory defect with a
reduced total gas volume, normal expiratory flows,
Physical Examination:
and a moderately reduced CO transfer. His walk test
Vital Signs: HR 90, BP 145/85, RR 18,
showed desaturation while walking to a nadir of
Temperature 36.8°C, SpO2 94%
89%. His doctor told him that he had some type
Respiratory: Inspiratory crackles heard bilaterally
of diffuse interstitial pulmonary problem and that
in the bases.
he would need to perform more diagnostic testing
PFT: Simple spironmetry in the doctor’s office:
to see what type of diffuse disorder he had.
↓ FEV1 and ↓ VC, FEV1/FVC 85%
Mr. O’Connor was given the facts that this may be a
Chest-radiograph showed ground-glass haziness
progressive disease and that the available treatment
in the bases, some streaky opaque shadows
options may help.
at the diaphragms, elevation of both
diaphragms. Critical-Thinking Questions
Cardiovascular: RRR without murmurs
1. What additional tests may be helpful in diag-
ECG: 12 lead – no obvious problems visible
nosing Mr. O’Connor’s lung disease?
Extremities: No pitting edema in the legs,
digital-clubbing present 2. What type of DPLD is Mr. O’Connor likely to
Blood chemistry sent to Laboratory Services for have? Discuss the reasons for your choice.
analysis. 3. Discuss why interstitial lung disease causes this
The patient was then intensively questioned pattern of pulmonary function abnormalities.
regarding occupational exposure history.
the signs of chronic right ventricular overload and its all possible treatments that may reduce pulmonary
effect on cardiac function. If more precise measure- pressure and improve right heart function.16
ments are necessary, right heart catheterization is the
most accurate invasive test to confirm the diagnosis of Exacerbation of Idiopathic Pulmonary Fibrosis. The
cor pulmonale and to quantify the degree of pulmonary causes of acute exacerbations of IPF are in many cases
hypertension.16 It can also give information about the unknown. The effect may be the result of an acute
patient’s underlying lung disease that may aid in direct stress on the lung, accelerating the speed of the
therapy. fibrotic process or secondary to an occult viral infec-
The treatment of cor pulmonale is directed toward tion or aspiration. Patients have no obvious infection,
treating the underlying cause: lung disease. Maximizing pulmonary embolism, or decompensated heart
the DPLD patient’s lung function and gas exchange failure, but they demonstrate an acute pulmonary
is the best way to definitively treat the condition. deterioration with worsening symptoms, gas
Continuous oxygen therapy may be necessary to raise exchange, and lung function. It is common for
the PaO2 and relieve hypoxic vasoconstriction. If patients to present with severe hypoxemia, requiring
pulmonary hypertension persists or is disproportion- mechanical ventilation.17
ately high, a trial use of one or more drugs in primary Although the definition of acute exacerbation of
pulmonary hypertension may improve exercise capacity IPF is not standardized, an international group of
and hemodynamics, as well as slow the rate of clinical pulmonary experts recommend the following diagnos-
deterioration in patients with secondary pulmonary tic criteria to identify the patient in such a state:
artery hypertension. Sustained-release calcium channel
blockers (nifedipine or diltiazem), intravenous or • A diagnosis of IPF previously or on this admission
inhaled prostacyclin analog therapy, endothelin- • Unexplained appearance or worsening of
receptor antagonists (bosentan), and sildenafil are dyspnea within 30 days
• HRCT showing new bilateral ground glass abnor- Continuous oxygen therapy is another treatment
mality and/or reticular or honeycomb pattern with option that is predominately supportive. Continuous
superimposed consolidation consistent with UIP oxygen therapy may support the patient’s oxygenation
• No bronchoscopic or tracheal aspirate evidence temporarily, but disease progression causes hypoxemia
of infection that is increasingly unresponsive to oxygen. Without a
• Exclusion of new acute lung injury lung transplant, the patient will die when the disease
• Left heart failure or pulmonary embolism.17 process is so extensive that oxygenation cannot be
maintained with supplemental oxygen.4
Cough, fever, and flulike symptoms can also be
Lung transplantation is a definitive treatment for
present, and many patients are admitted to the hospital
the patient with DPLD. Ideally, there should be early
with severe respiratory failure. The causes of acute
referral for lung transplantation. Waiting until the
respiratory failure in patients with DPLD are deteriora-
patient has end-stage pulmonary fibrosis may be too
tion in the patient’s PaO2 secondary to a worsening in
late. Many patients won’t survive long enough to
lung function brought about by an acute infection,
receive a new lung.18
disease progression, or exacerbation of cor pulmonale.
Research is ongoing on identifying new agents that
Intensive bronchial hygiene and increased FIO2 may
may be more effective in treating people with DPLD.
help improve the patient’s clinical status. Patients with
The current treatment is minimally effective. Other
end-stage pulmonary fibrosis have refractory hypoxemia
forms of therapy must be developed to attack the
and do not benefit from higher oxygen concentrations
disease process at the cellular level. Some treatment
or continuous mechanical ventilation. These patients
options under investigation are:18
should be considered for organ transplantation.4
• Antifibrotic therapy.
• Anti-inflammatory agents that directly control
TREATMENT specific inflammatory cells (e.g., macrophage or
Treatment of DPLD varies with the underlying disease, T cell).
but the general treatment has not changed in some years. • Agents affecting the interaction of the fibroblast
The initial direction in treatment is to control exposure with lung parenchyma cells in the alveolar
to the precipitating antigens. Since many diseases causing epithelium and capillary endothelium.
DPLD do not have a known etiology, this measure is • Molecular therapy to promote lung repair
effective only in cases of environmental exposure. (e.g., growth factors).
The drug treatment used for people with DPLD is The number of diffuse parenchymal lung diseases makes
to prevent disease progression by suppressing the the task of developing new effective therapies for this
inflammatory process in the lung. This goal is accom- group of diseases all but insurmountable. Currently,
plished by administering high-dose corticosteroids scientists are spending considerable research dollars and
and monitoring disease activity by chest radiograph, time in investigating new treatments for the diseases
HRCT, or other techniques. If steroids effectively with the poorest prognosis and for the greatest number
reduce inflammation, the patient’s dose is tapered to a of people. Idiopathic pulmonary fibrosis has no known
level where inflammation suppression is sustained; cause and no effective treatment. If scientists are
this daily dose is maintained for long-term adminis- successful in developing therapies for this devastating
tration. Other drugs that may be used are cytotoxic disease, the diagnosis does not have to mean a terminal
drugs such as cyclophosphamide or azathioprine. illness.
Patients’ responses to steroids or cytotoxic drugs are
variable, and the positive effects may not be sustained.
For example, patients with idiopathic pulmonary fibrosis
may initially respond to treatment early in the inflamma- Summary
tory phase of the disease with some stabilization of lung Diffuse parenchymal diseases encompass all of the
function, but, with disease progression, therapy becomes pulmonary and systemic diseases that cause infiltra-
ineffective. In general, patients in end-stage pulmonary tion into the alveolar airspace and interstitium of the
fibrosis do not respond to steroid therapy because the lung. The infiltration results in the thickening of the
fibrotic process is well established at the time of diagno- alveolar capillary membrane with an associated
sis with little inflammation.4,14 The median survival time decrease in lung compliance and gas exchange. The
for patients with interstitial pulmonary fibrosis is fewer wide variety of diseases that cause diffuse parenchy-
than 3 years. Factors that affect survival are smoking mal and interstitial damage range, among many
history, pulmonary function deterioration, X-ray changes, others, from idiopathic lung diseases, environmental
response to therapy, and lung biopsy findings indicating lung diseases, drug toxicity, and collagen vascular
loss of functional lung units.4 diseases to hemorrhagic diseases of the lung.
Many of the DPLDs have an unknown etiology. maintained with supplemental oxygen.4 Lung trans-
However, of the diseases having known etiologies, a plantation is a definitive treatment for the patient with
large group of diseases consists of the environmental DPLD. Ideally, there should be early referral for lung
(occupational) lung diseases. Environmental lung transplantation.
diseases are the most common disease classification of
all the DPLDs. These diseases are distributed geo-
graphically according to the industry and occupational Study Questions
concentrations in specific areas of the country.
REVIEW QUESTIONS
Fibrosis is the result of chronic inflammation due
to persistent or recurrent exposure to a stimulant, 1. Briefly define the three phases of the pathogenesis
irritant, or antigen causing parenchymal injury. of DPLD.
The major clinical manifestation of people with 2. Describe the typical pattern of changes that might
interstitial lung disease is dyspnea. It is usually gradual be seen on the pulmonary function tests performed
in onset, with the patient believing that he or she is just on a patient with DPLD.
“out of shape” until the dyspnea progresses ultimately
3. What is cor pulmonale?
to dyspnea at rest.
All forms of DPLD decrease lung volumes but 4. Define hypersensitivity pneumonia.
preserve expiratory flow rates unless the patient has 5. Describe the general appearance of an individual
airway involvement, is a smoker, or has an airflow with interstitial lung disease.
limitation lung disease. The patients have a reduced
total lung capacity, vital capacity, functional residual
capacity, and FEV1, along with a normal or increased
FEV1/FVC ratio. Studies of gas transfer typically show a 1. Which of the following would cause
reduction of carbon monoxide–diffusing capacity. The hypersensitivity pneumonitis?
primary reason for the reduced diffusion is the destruc- a. bird breeder’s lung
tion of alveoli and their capillaries, decreasing available b. rheumatoid arthritis
surface area for gas exchange. c. asbestosis
The major complications of DPLD are cor pulmo- d. silicosis
nale, exacerbation of idiopathic pulmonary fibrosis, and 2. Which of the following diffuse parenchymal
progressive oxygenation failure. These complications can lung diseases is caused by exposure to inorganic
cause a significant decrease in quality and length of life. dusts?
Treatment of DPLD varies with the underlying a. systemic scleroderma
disease, but the general treatment has not changed in b. farmer’s lung
years. The initial direction in treatment is to control c. anthracosilicosis
exposure to the precipitating antigens. Because many d. Niemann-Pick disease
diseases causing DPLD do not have a known etiology, 3. Which of the following diseases do/does not have
this measure is effective only in cases of environmental a known cause?
exposure. a. environmental lung diseases
The drug treatment used for people with DPLD is b. pulmonary eosinophilic syndromes
to prevent disease progression by suppressing the c. idiopathic interstitial pneumonias
inflammatory process in the lung. This goal is accom- d. Wegener’s granulomatosis
plished by administering high-dose corticosteroids and
monitoring disease activity by chest radiograph, HRCT, 4. What occupations are associated with causing
or other techniques. If steroids effectively reduce asbestosis?
inflammation, the patient’s dose is tapered to a level a. coal mining
where inflammation suppression is sustained; this b. aerospace industry
daily dose is maintained for long-term administration. c. harvesting sugar cane
Other drugs that may be used are cytotoxic drugs such d. shipyard and construction
as cyclophosphamide or azathioprine. 5. What pulmonary function changes are seen
Continuous oxygen therapy is another treatment in patients with idiopathic interstitial
option that is predominately supportive. Continuous pneumonias?
oxygen therapy may support the patient’s oxygenation a. restrictive pattern with reduced DLCO
temporarily, but disease progression causes hypoxemia b. obstructive pattern that is refractory to
that is increasingly unresponsive to oxygen. Without a bronchodilator therapy
lung transplant, the patient will die when the disease c. mixed obstructive and restrictive pattern
process is so extensive that oxygenation cannot be d. cardiac limitation on exercise stress test
6. What clinical signs and symptoms are present CRITICAL-THINKING QUESTIONS

in patients with chronic hypersensitivity
1. Why are high-dose corticosteroids used in the
pneumonitis?
treatment of DPLDs? What are the limitations of
a. asymptomatic except during acute
high-dose corticosteroids in treating DPLDs?
exacerbations
b. hemoptysis, chest pain, fatigue, and 2. Describe the role of lung transplantation in the
weight loss treatment of DPLDs.
c. progressive DOE, bibasilar inspiratory 3. What is the difference between hypersensitivity and
crackles, fatigue allergic reaction?
d. rhonchi, wheezing, and pleural friction rub on
auscultation
7. Which of the following is not definitive but very References
important in helping to diagnose hypersensitivity 1. American Thoracic Society/European Respiratory
pneumonitis? Society International Multidisciplinary Consen-
a. history of environmental exposure sus Classification of the Idiopathic Interstitial
b. pulmonary function tests and Pneumonias. This Joint Statement of the Ameri-
reduced DLCO can Thoracic Society (ATS) and the European
c. chronic respiratory acidosis with Respiratory Society (ERS) was adopted by the ATS
hypoxemia Board of Directors, June 2001 and by The ERS
d. transbronchial needle biopsy Executive Committee, June 2001. Am. J. Respir.
8. What is a common cardiovascular complication of Crit. Care Med. 2002;165,2:277–304.
patients with severe DPLD? 2. Britton J, Evans A. Diffuse lung diseases: approach
a. left ventricular failure and chronic pulmonary to diagnosis. In: Albert R, Spiro S, Jett J, eds.
edema Comprehensive Respiratory Medicine. St. Louis:
b. cor pulmonale and secondary pulmonary Mosby: 1999:44.1–44.8.
hypertension 3. Mason RJ, Schwarz MI, Hunninghake GW, Musson
c. hypertensive heart disease secondary to RA. Pharmacological therapy for idiopathic
systemic hypertension pulmonary fibrosis. Past, present, and future. Am. J.
d. noncardiogenic pulmonary edema Respir. Crit. Care Med. 1999;160,5:1771–1777.
9. What medication(s) is/are commonly used in the 4. Sharma S. (June 5, 2006) Restrictive lung disease.
treatment of patients with DPLD? eMedicine Specialties: Pulmonology; Interstitial
a. bronchodilators and inhaled steroids Lung Diseases.
b. vasodilators and anticoagulants 5. Coultas D, Zumwalt R, Black W, Sobonya R. The
c. systemic anti-inflammatory drugs epidemiology of interstitial lung diseases. Am. J.
d. inotropic medications and vasodilators Respir. Crit. Care Med. 1994;150,4:967–972.
6. Raghu G, Weycker D, Edelsberg J, Bradford WZ,
10. What granulomatous DPLD is commonly associ-
Oster G. Incidence and prevalence of idiopathic
ated with multiple organ involvement?
pulmonary fibrosis. Am. J. Respir. Crit. Care Med.
a. systemic lupus erythematosis
2006;174,7:810–816.
b. systemic scleroderma
7. Katzenstein AA, Myers JL. Idiopathic Pulmonary
c. Goodpasture’s syndrome
Fibrosis: clinical relevance of pathologic
d. sarcoidosis
classification. Am. J. Respir. Crit. Care Med.
11. What is a common problem with patients with 1998:157,4:1301–1315.
DPLD during exertion? 8. Newman LS. Environmental pulmonary
a. oxygen desaturation with exercise diseases. In: Beers M, et al, eds. The Merck
b. bradycardia with exercise Manual of Diagnosis and Therapy. Whitehouse
c. leg pain and peripheral cyanosis Station, NJ: Merck Research Laboratories;
d. syncope and hypotension during exercise 2006:469–480.
12. What DPLD is known to cause lung and kidney 9. Peterson JS, Miller SM, Cairns CB. (June 10, 2008)
disease? Toxicity, Nitrous Dioxide. eMedicine Specialties:
a. sarcoidosis Emergency Medicine: Toxicology.
b. Langerhans cell histiocytosis 10. Mandavia S. (March 24, 2009) Toxicity, Hydrogen
c. Goodpasture’s syndrome Sulfide. eMedicine Specialties: Emergency
d. Wegener’s granulomatosis Medicine: Toxicology.
11. Noltkamper D, Burgher SW. (July 10, 2008) et al. Complications of video-assisted
Toxicity, Phosgene. eMedicine Specialties: thoracoscopic lung biopsy in patients with
Emergency Medicine: Toxicology. interstitial lung disease. Ann Thorac Surg.
12. Issley S, Lang E. (March 14, 2007) Toxicity, 2007;83,3:1140–1144.
Ammonia. eMedicine Specialties: Emergency 16. Sovari AA, Dave RH. (September 3, 2008) Cor
Medicine: Toxicology. Pulmonale. eMedicine Specialties: Cardiology;
13. Strieter RM. What differentiates normal lung Myocardial Disease and Cardiomyopathies.
repair and fibrosis? Inflammation, resolution 17. Collard HR, Moore BB, Flaherty KR, Brown KK,
of repair, and fibrosis. Proc Am Thorac Soc. Kaner RJ, King Jr TE, et al. Acute exacerbations of
2008;5,3:305–310. idiopathic pulmonary fibrosis. Am. J. Respir. Crit.
14. King Jr TE, Kline J. Interstitial lung diseases. In: Care Med. 2007;176,7:636–643.
Beers M, et al, eds. The Merck Manual of Diagnosis 18. Wells AU, Hogaboam CM. Update in diffuse
and Therapy. Whitehouse Station, NJ: Merck parenchymal lung disease 2006. Am. J. Respir. Crit.
Research Laboratories; 2006:443–461. Care Med. 2007;175,7:655–660.
15. Kreider ME, Hansen-Flaschen J, Ahmad NN,
Rossman MD, Kaiser LR, Kucharczuk JC,
CHAPTER 11
Atelectasis, Pleural Disorders, and Lung Cancer

Barbara Ludwig
OBJECTIVES
• Identify the four main cell types of malignant lung cancer.
• Discuss the diagnosis and the clinical manifestations of lung cancer.
• Describe the treatment for small-cell and non-small-cell lung cancer.
• Explain the different types of pneumothorax and their causes.
• Describe the clinical signs and symptoms a person shows with a tension and a nontension pneumothorax.
• Discuss the four mechanisms of pleural fluid formation in people with a pleural effusion.
• Identify the radiologic appearance of the various pleural disorders (effusion, empyema, pneumothorax).
• Explain the treatment for pleural disorders.
• Compare and contrast the types of atelectasis.
• Identify the radiologic changes seen in patients with atelectasis.
CHAPTER OUTLINE
Atelectasis Lung Cancer
Obstructive Actelectasis Risk Factors
Nonobstructive Actelectasis Histological Cell Types of Lung Cancer
Special Types of Atelectasis Clinical Manifestations
Diagnosis Paraneoplastic Syndromes
Treatment Diagnosis and Staging
Pleural Disorders Treatment
Pneumothorax
Pleural Effusion and Empyema
266
CHAPTER 11 ■ Atelectasis, Pleural Disorders, and Lung Cancer 267
KEY TERMS
adjuvant therapy decortication pleural effusion
atelectasis empyema pneumothorax
benign tumor exudates radiation therapy
brachytherapy malignant tumor secondary spontaneous
carcinogen metastasis pneumothorax
carcinoma in situ open pneumothorax thoracentesis
chemotherapy palliative transudate
cytology paraneoplastic syndrome
Atelectasis do not occur across lung fissures; so the complete

obstruction of the lobar bronchus results in the
Atelectasis means the incomplete expansion of the collapse of the entire lobe because collateral air drift
lung. It may be secondary to incomplete expansion at cannot occur between lobes.4
birth, called primary atelectasis, or secondary to a
condition or disease that causes diminished volume for Bronchial Neoplasms. Primary bronchogenic carci-
all or part of a lung. The different types of atelectasis noma is the most frequently encountered cause of
can be categorized in several ways, but the simplest is localized bronchial obstruction. Squamous cell carci-
dividing it into obstructive, nonobstructive, and special noma and small cell carcinoma occur more in the
types of lung collapse. central airways, and patients may initially come to their
doctor because of respiratory problems.1,5,6
OBSTRUCTIVE ATELECTASIS Foreign Bodies. Especially in children, inhaling

Obstructive atelectasis, the most common type, results foreign bodies is a common problem. Adults can also
from the reabsorption of gas from the lung distal to the aspirate foreign bodies when they lose control of their
obstruction. The obstruction can occur at the level of airway protective mechanisms, such as in automobile
the mainstem bronchi, or at lower-division bronchus. crashes, during seizures, or after an overdose of depres-
The most important of the many causes of a localized sant drugs. If a foreign body is aspirated because of
obstruction are tumors, aspirated foreign bodies, vomiting, the presence of highly acidic gastric contents
mucus plugs, or compression of the airway due to the in the vomitus can produce acute lung injury and
enlargement of an adjacent structure. possible acute respiratory distress syndrome (ARDS).
The speed of lung collapse depends on two factors. The diagnosis of an endobronchial foreign body
First, if the person is breathing room air, atelectasis may not be identified immediately or seen on X-ray. If
takes longer. The gas in the lung distal to the obstruc- delayed, the signs and symptoms are consistent with a
tion contains approximately 80% nitrogen, which localized respiratory infection such as lobar pneumo-
absorbs into tissue spaces very slowly and slows the nia, or a lung abscess.5
rate of lung deflation. The higher the FIO2 is, the faster
Mucus Plugging. A mucus plug may become impacted
gas resorption occurs.
in a bronchus and remain indefinitely. If infection
Second, collateral air drifts through:
develops, it can produce a classical clinical presentation
• Small holes between adjacent alveoli (pores of identical to lung cancer. Diseases that can cause this
Kohn). type of problem are cystic fibrosis, asthma, and bron-
• Small channels between terminal and respiratory chopulmonary aspergillosis.5
bronchioles and adjacent alveoli (canals of
Lambert). External Compression of a Bronchus. Possible causes
• Intersegmental respiratory bronchiole-to- of external compression of the airway are:
bronchiole connections (Martin’s channels).
• Enlarged lymph nodes infiltrated with cancer
The collateral air drift affects the pattern of atelectasis cells from bronchogenic carcinoma of the lung
despite the presence of an obstruction interfering with or lymphoma, which can compress, invade, and
normal airflow distribution.1–3 Segmental and subseg- obstruct the bronchial lumen.
mental lung collapse is less common because of collateral • Malignant or benign tumors of the mediasti-
air drift through the alveolar and bronchiole communica- num, which can compress the airway to the
tion channels. However, these communication channels point of occlusion.
• Tuberculosis, which compress the airway by Plate or Discoid Atelectasis. Classic chest X-ray signs
means of an infected lymph node putting diagnose this type of atelectasis. Segmental and
pressure on the bronchus.5 subsegmental atelectasis in the lung bases manifests on
X-ray as narrow, straight bands or lines that run parallel
NONOBSTRUCTIVE ATELECTASIS to the diaphragm. Since the atelectasis does not follow
known anatomical subdivisions of the lung, it is not
Nonobstructive types of atelectasis are caused by an
obstructive. Because of its location in the peripheral
abnormal relationship between the visceral and
bases of the lungs, it is likely the result of small areas of
parietal pleura, a loss of surfactant, or the replacement
atelectasis secondary to hypoventilation, pulmonary
of normal lung parenchyma with scar tissue or cellular
embolism, pain associated with breathing (pleuritis or
infiltrates.1,5
surgical pain), or poor diaphragmatic movement
Pleural effusion, hemothorax, and pneumothorax
observed in obesity.1,5
are common causes of localized atelectasis secondary
to a disruption of the normal lung-pleura relationship.
The presence of fluid or air in the pleural space creates DIAGNOSIS
a positive intrapleural pressure, which is transmitted to Physical examination and laboratory studies assist in
the adjacent alveoli. The positive pressure in that part the diagnosis of atelectasis. However, chest X-rays and
of the lung causes an appreciable decrease in ventila- CT scans confirm the diagnosis. Other problems that
tion to it. Consequently, underventilation and atelecta- show a similar clinical picture to atelectasis, such as
sis occur in the lung areas directly adjacent to the pneumonia, pneumothorax, lung cancer, and other
affected pleura. Large accumulations of fluid or air can pulmonary diseases, need to be eliminated as the
cause significant lung collapse and a decrease in lung possible cause.1,5
compliance.
Adhesive atelectasis occurs because of increased Clinical Findings. The seriousness of the patient’s
surface tension secondary to surfactant loss. This clinical manifestations is related to the size of the
problem can occur as the result of blunt chest trauma affected lung area and to any other complicating
with significant lung contusion, radiation injury, and problems, such as pneumonia. Patients will have
the many causes of acute lung injury and ARDS. The dyspnea, tachypnea, fever, low SPO2 secondary to
loss of surfactant makes the alveoli unstable, resulting ventilation/perfusion mismatching, and possible
in alveolar collapse. The atelectasis can be diffuse or cyanosis if the hypoxemia is severe. On physical
localized. exam, the patient will show dullness to percussion
Diseases that cause scarring (fibrosis) of the lung, and diminished or absent breath sounds in the
along with the replacement of the normal alveolar affected area, and the trachea will deviate to the
epithelium with collagen, also cause diffuse atelectasis. atelectatic side.1
The scar tissue distorts the normal architectural struc-
ture of the lung, causing the scarred areas to collapse Radiographic Findings. The chest X-ray and CT scans
and other areas to overdistend. Diseases associated show direct and compensatory changes that occur
with this type of atelectasis are interstitial pulmonary following alveolar collapse. The direct X-ray changes
fibrosis, chronic tuberculosis, or severe fungal infec- are:
tions. This type of atelectasis is known as cicatrization
• Increased radio-opacity of the affected lung.
atelectasis.1
• With nonobstructive atelectasis, the presence of
an air bronchogram beyond the hilum appearing
SPECIAL TYPES OF ATELECTASIS over the collapsed lung tissue.
This third category of atelectasis consists of several • A fissure line with lobar lung collapse.
types of special cases.
The compensatory changes reflect the loss of lung
volume:
Postoperative Atelectasis. Acute atelectasis after
surgery, especially procedures involving the thorax or • The chest structures move to fill the vacated
upper abdomen, has long been associated with the loss space left when the lung collapsed.
of lung volume, causing complete or partial alveolar • The mediastinal structures (heart and trachea)
collapse. Pain, medications, increased secretions, and move to the affected side.
the inability to cough and to take deep breaths are • The hemidiaphragm is elevated on the
common causes of postoperative atelectasis.5 Postop- affected side.
erative atelectasis commonly affects areas of the lung in • The unaffected lung shows increased radiolucency
a segmental or subsegmental distribution.1 because of overinflation.
The direct and compensatory changes are more pro-

nounced with large areas of atelectasis.1,5 Spotlight
On
TREATMENT Spontaneous Pneumothorax
The treatment of atelectasis depends on the underlying Primary spontaneous pneumothorax is most
cause. The goal of treatment is lung reinflation by predominant among male smokers between the
removing the cause of the lung collapse. If the problem ages of 20 and 40. They are classically described
is obstructive, the treatment is to remove the obstruc- as ectomorphs, having a tall, lean body frame.
tion by flexible fiberoptic bronchoscopy or treat the Cigarette smoking is the predominant risk factor.
cause of the obstruction, such as lung cancer or tuber- Smoking increases the risk for pneumothorax in
culosis. If the patient has fluid in the pleural space, females by a factor of 9 and in males by a factor
drainage (thoracentesis or chest tube) is the only way of 22, with a direct relationship between the
to improve ventilation and reinflate the atelectatic areas occurrence of spontaneous pneumothorax and
of the lung. the number of cigarettes smoked each day.
In patients with postoperative atelectasis, preven-
tion is really the optimal approach.
• Limiting pain and sedative medications when
practical. pneumothoraces occur at rest or during quiet activities.
• Early ambulation. However, sometimes they occur during activities in
• Hyperinflation maneuvers (see Chapter 22). which there may be an unequal transmission of
• Antibiotic therapy if indicated. pressure in the lung, such as skiing, sky- or underwater
• Oxygen therapy (if needed). diving, or just flying in an airplane.8
• Suctioning if the patient’s cough is ineffective.1,5 The classical clinical appearance of people with a
primary pneumothorax is pleuritic chest pain and
dyspnea. Frequently, the pneumothorax is small, and
Pleural Disorders symptoms may subside within 24 hours even if the
Pleural disorders are pleural abnormalities that develop condition goes untreated. If the pneumothorax is large,
because of another primary disease or disorder. The the person will come to the emergency department for
pleural surface may become inflamed or irritated, or treatment.7 In a person with recurrent pneumothorax,
the pleural space may be filled with air, gas, or fluid. chemical pleurodesis or surgical intervention is
For the pleura to regain its normal function, the indicated.5
underlying cause of the pleural abnormality must be
corrected or controlled. The pleural disorders discussed Secondary Spontaneous Pneumothorax. A second-
here are pneumothorax, hemothorax, and pleural ary spontaneous pneumothorax occurs in people
effusion. with chronic or acute lung disease. Commonly, it
occurs because of rupture of a bleb or bullae in people
with severe COPD or other lung diseases that cause
PNEUMOTHORAX injury to the lung parenchyma, such as interstitial lung
Pneumothorax is the presence of free air in the diseases, infectious diseases, malignancies, connective
pleural space that causes partial or complete collapse tissue diseases, and many more. The clinical sequelae
of the affected lung. The classification of pneumotho- are more severe because these patients have a poor
rax are primary spontaneous pneumothorax, cardiopulmonary reserve as a result of their pulmonary
secondary spontaneous pneumothorax, traumatic disease. They have severe dyspnea, worsening hypox-
pneumothorax, catamenial pneumothorax, and emia, and possible hypotension. In people with
iatrogenic pneumothorax.7,8 chronic lung disease, the pneumothorax is more
difficult to diagnose because its signs and symptoms
Primary Spontaneous Pneumothorax. This type of are similar to those of an acute exacerbation of these
pneumothorax occurs in people without underlying patients’ lung disease.7
lung disease. Typically, the person is an apparently A subtype of secondary spontaneous pneumotho-
healthy, young adult male in his teens or early twenties. rax is AIDS-associated pneumothorax. This subtype is
The pneumothorax is thought to occur because of the associated with infection with pneumocystis carinii
rupture of subpleural apical blebs or bullae that may pneumonia (PCP), caused by the organism Pneumocys-
be present at birth or that may develop in those that tis jiroveci. PCP causes cystic changes in the lung, and
smoke.8 Ninety percent of primary spontaneous these cysts can rupture and cause a pneumothorax.7
Because of the underlying lung disease, ventilatory affects the right lung (90–95%) and is a recurring
and oxygenation defects are present. The sudden onset problem in many women.
of pneumothorax places an added burden on the
patient’s breathing, with sometimes life-threatening Iatrogenic Pneumothorax. This type of pneumothorax
consequences. The individual’s acute or chronic is secondary to medical procedures that could damage
symptoms suddenly worsen significantly, with marked the pleura or lung tissue. Thoracentesis, transthoracic
dyspnea, cyanosis, tachycardia, subcutaneous emphy- or transbronchial needle aspiration, central venous line
sema, and possible circulatory shock. These patients placement, cardiopulmonary resuscitation, and
require emergency decompression of the pneumotho- mechanical ventilation are well documented proce-
rax with needle aspiration and chest tube placement dural causes of pneumothorax.7,8. CPR is considered an
for continuous air drainage. With recurrent pneumo- iatrogenic, or hospital-induced, type of blunt chest
thorax, chemical pleurodesis is a treatment option. trauma. After any medical procedure that has a risk of
Because of the underlying severe lung dysfunction, pneumothorax, the patient should have a chest radio-
surgery may be contraindicated, but chemical graph as a precautionary measure.9
pleurodesis may prevent further episodes.9
Tension Pneumothorax. Tension pneumothorax can
Traumatic Pneumothorax. Traumatic pneumothorax is develop in any category of pneumothorax. This condi-
the result of direct or indirect trauma to the chest. It tion occurs when the pleural pressure exceeds atmo-
may be a complication of a medical diagnostic or spheric pressure during the entire expiratory phase.
therapeutic procedure, or it may be caused by penetrat- This condition arises when a “one-way valve” condition
ing or blunt chest trauma.8,10,11 is present in the patient’s injured lung. Simply
Penetrating injury to the chest directly damages the explained, the air can enter the pleural space through
chest wall, pleura, and lung. The injury to the lung and the ruptured alveoli, but it cannot exit. The air accumu-
chest wall creates an open pneumothorax. The lates until the pressure of the trapped gas in the pleural
opening in the chest wall allows open communication space exceeds atmospheric pressure. This type of
between the atmosphere and the pleural space, and pneumothorax is frequently seen in patients receiving
consequently air moves freely between the two areas positive pressure ventilation.9
during breathing. The pressure changes in the pleural Tension pneumothorax is a life-threatening situa-
space during breathing cause air to move from the tion and a medical emergency. The high pleural pres-
atmosphere into the pleural space during inspiration. sure compresses the affected lung and may completely
As a result, free lung movement is inhibited, causing air collapse it. The pressure also compresses the mediasti-
to retreat out of the pleural space during expiration. num and causes it to shift into the space occupied by
The results are large changes in pleural pressure and the opposite lung. The shift distorts the structures inside
significantly reduced ventilation. The large changes in the mediastinum (trachea, aorta, vena cava, and heart)
intrathoracic pressure may also affect venous return to and causes cardiovascular instability. The patient with
the heart and cardiac output. The situation can be tension pneumothorax shows all the signs of acute
controlled quickly by placing a bandage over the open respiratory failure and circulatory shock:8,9,11
chest wound. The accumulating pleural air must also
be removed with a chest tube.8 • Sudden deterioration in the clinical condition
Blunt trauma to the chest can also cause pneumo- • Rapid labored breathing, cyanosis
thorax. Rib fractures that lacerate the lung tissue or • Tachycardia, hypotension
alveolar rupture from sudden chest compression (by a • Physical exam of the chest: marked hyperexpan-
steering wheel or explosive energy). The person sion of the affected lung and tracheal deviation
frequently has subcutaneous air from the air leak and to unaffected side
experiences respiratory distress.2 • Arterial blood gas: severe hypoxemia, with or
without hypercarbia and respiratory acidosis
Catamenial Pneumothorax. This type of pneumotho- Immediate decompression of the tension is

rax represents 3–6% of all people with pneumothorax. necessary using a 50-mL syringe. The needle should be
It typically occurs within 48 hours of the onset of inserted into the second anterior intercostal space at
menstruation in premenopausal women or in post- the midclavicular line. Large volumes of gas can be
menopausal women receiving estrogen. The cause is aspirated quickly. Then a chest tube is inserted once the
intrathoracic endometriosis. It is thought that endome- patient is stabilized.8,9,11
trial tissue migrates through diaphragmatic openings,
or it is released into the pelvic veins, travels to the Clinical Manifestations. The severity of symptoms
lungs, and forms a pulmonary embolism. It usually varies widely from person to person. The scale ranges
from the person who is asymptomatic to the person to prevent a tension pneumothorax. To treat the
who is near death with respiratory failure and shock.8 symptomatic patient, possible interventions that may
The identified manifestations include common signs be used include:
and symptoms in addition to those the patient mani-
• Rest.
fests with severe respiratory compromise.9–11
• Observation.
• Respiratory distress: dyspnea; chest pain, • Supplemental oxygen.
usually localized to side of pneumothorax; • Needle aspiration.
decreased SPO2 • Chest tube insertion and drainage of air.
• Subcutaneous emphysema (may be expanding) • Chemical pleurodesis.
• Chest exam: reduced or absent breath sounds • Video-assisted surgery (VATS) with chemical
on affected side; ipsilateral expansion of the pleurodesis (a procedure that causes the
chest, with or without tracheal deviation to membranes around the lung to adhere and
unaffected side; hyper-resonance to percussion prevents the build-up of fluid in the pleural
on affected side space), surgical clamping of bullae, or laser
• Circulatory signs: tachycardia, with or without eradication of bullae.11
hypotension and shock
Chemical pleurodesis is a treatment for people with
recurrent pneumothorax. Instilling talc slurry or 3 g of
Diagnosis. The chest radiograph or the computerized
tetracycline into the pleural space through a chest
tomography (CT) confirms the diagnosis of pneumo-
intercostal tube scleroses the pleural space. This
thorax. To be detectable on a routine chest radiograph,
procedure is painful, so lidocaine can be added to the
the free pleural air must occupy approximately 20% of
sclerosing mixture and a sedative drug be given before
the thoracic volume. If a small pneumothorax is
the procedure.5
suspected, an expiratory chest film or a lateral decubi-
tus chest radiograph may make the pleural air more
Classification. Certain groups of patients are vulner-
visible.
able to specific types of pneumothorax. If a patient is
The chest radiograph findings in the patient with
particularly susceptible to pneumothorax, the therapist
pneumothorax identify the presence of pleural air with
must incorporate a routine assessment for this compli-
its attendant changes and indicate whether the air is
cation into the patient’s care so that rapid treatment
under tension and is affecting the cardiovascular
can be initiated to ensure a good outcome.
system.9–11
• Displacement of the mediastinum toward the
normal or unaffected side PLEURAL EFFUSION AND EMPYEMA
• Visible visceral pleural line on the side of the Pleural effusions are an accumulation of fluid in the
pneumothorax pleural space. The estimated incidence of pleural
• Absence of lung markings distal to the visceral effusion is 1 million cases per year.12 They are a
pleural line complication of a primary illness, with most effusions
• Depressed hemidiaphragm on the side of the caused by infections, congestive heart failure, cancer,
pneumothorax collagen diseases, pulmonary emboli, or cirrhosis of
the liver. The most common cause of pleural effusion is
Visible subcutaneous air in the soft tissue spaces
congestive heart failure (30–40% of cases). The remain-
or mediastinal air surrounding the heart. In addition,
ing 60–70% of the cases of pleural effusion are divided
the diagnosis of pneumothorax should be considered
among nine primary diseases, with pneumonia as the
if a patient who is being mechanically ventilated
second most common cause and malignancy as the
suddenly becomes agitated or begins “fighting the
third.13 Of all the diseases that produce pleural effu-
ventilator.”9
sion, four underlying physiological mechanisms can
Chest CT is increasingly used to predict the risk of
explain the reason for the effusion:
pneumothorax recurrence. It is able to detect people
with large or numerous blebs who are at high risk for • Increased hydrostatic pressure (congestive heart
recurring pneumothorax.7 failure)
• Increased capillary permeability (inflammatory
General Treatment. The type of pneumothorax, the and malignant effusions)
size of the pneumothorax, and the severity of the • Decreased plasma oncotic pressure (cirrhosis
individual’s symptoms determine the intervention. Any secondary to low serum protein)
patient with a pneumothorax who is receiving positive • Impaired lymphatic drainage (malignancy,
pressure ventilation should have a chest tube inserted parasitic infections)
TABLE 11-1 Clinical signs of pleural effusion

Volume of Pleural Mediastinal
Effusion Lung Expansion Tactile Fremitus Percussion Breath Sounds Shift
⬍300 mL Normal High Normal Vesicular None
300–1000 mL Decreased Medium Dull Decreased vesicular None
1000–2000 mL Decreased Low Dull Decreased broncho- Present
vesicular
⬎2000 mL Decreased None Dull Decreased Present
bronchovesicular
There are two types of pleural fluid: transudate and the low frequencies are filtered out. The bleating “A”
exudate. sound is called egophony.
When removing pleural fluid during a thoracente-
• A transudate is an ultrafiltrate of plasma, with a
sis, inspecting the aspirated effusion fluid for odor and
low concentration of protein. Transudate fluids
appearance provides important diagnostic information
form as the result of elevated hydrostatic pres-
and may even confirm the cause. For example, the color
sure and decreased plasma oncotic pressure in
reveals considerable clues:
the pulmonary circulation.
• An exudate is similar to plasma in that it has a • Blood-tinged fluid may be due to the thoracentesis.
high protein concentration. Increased capillary • Red fluid is blood secondary to trauma or
permeability and disturbed lymphatic drainage bleeding.
cause exudative fluid to form. • Black fluid indicates an aspergillus infection.
• Yellow-green fluid may be a rheumatoid pleuritis
In some diseases, the pleural fluid can be a transudate
or pancreatic effusion.
or an exudate.13
If more specific information is necessary, the pleural
Diagnosis. Pleural effusion is diagnosed with the help fluid is analyzed. The minimum tests performed in the
of physical signs and symptoms (see Table 11-1), laboratory analysis of the pleural fluid are total protein
imaging techniques, and thoracentesis (the extraction and cytology. Total protein of the fluid identifies the
of fluid by inserting a needle into the pleural space). fluid as a transudate or an exudate. Cytology examines
Common complaints that accompany a pleural the white count for the presence of infection and
effusion are dyspnea (particularly if the patient has checks for the presence of bacteria and malignant cells.
chronic lung disease or if the effusion is large) and Additional clinical laboratory analysis may check
chest discomfort or pain. More than 300 mL of glucose content, lactate dehydrogenase (LDH), choles-
effusion fluid is necessary for abnormal chest percus- terol, amylase, hematocrit, and tumor markers. The
sion, but only 200–300 mL must be present to be information from these tests is the basis for a diagnosis
visible on the chest radiograph. For smaller effusions, and also indicates whether further diagnostic tests are
a lateral decubitus chest radiograph or ultrasound needed.8,13
may be necessary to identify its presence. The actual Empyema exists when pus is present in the pleural
presence of effusion fluid can be confirmed only by space. A complication of pneumonia, empyema is most
thoracentesis.8,11 likely to appear in the person with an underlying
An additional vocal sound heard in pleural chronic condition such as COPD, diabetes, or renal
effusion is egophony. “Egophony is a change in timbre failure. It should be suspected in the person who is still
(E to A) but not pitch or volume. It is due to a decrease febrile despite receiving appropriate antimicrobial
in amplitude and increase in the intensity of the therapy or in the person who may be afebrile but still
second formant, produced by solid (including com- sick. A chest radiograph or CT scan identifies the
pressed lung) interposed between the resonator and presence of effusion. A thoracentesis confirms the
the stethoscope head.”14 When auscultating a patient presence of pus.13
with an effusion, the clinician asks the patient to say
the letter “E” and listens to the chest in the area of the Treatment. The treatment of pleural effusion is to treat
effusion. The sound of the patient saying “E” is heard the underlying cause and to relieve the patient’s
as an “A” through the stethoscope. The high-frequency symptoms (i.e., give palliative care). Removing the
sounds are heard in compressed areas of the lung, and fluid by either thoracentesis or chest tube drainage
allows the lung to reexpand and may relieve dyspnea. If National Cancer Institute on the stage of lung and
hypoxemia is present, oxygen therapy is indicated. bronchus cancer at the time of diagnosis:19
In a patient with an empyema, immediate and
• 16%—diagnosed while the cancer is still
complete drainage by chest tube system is necessary. If
confined to the primary site (localized stage)
tube drainage is unsuccessful, rib resection and surgical
• 25%—diagnosed after the cancer has spread to
drainage of loculated pus pockets by blunt dissection
regional lymph nodes or directly beyond the
or decortication (the removal of part or all of the
primary site (regional stage)
outer surface of an organ) of the pleura may be neces-
• 51%—diagnosed after cancer has metastasized
sary. Because an empyema usually indicates the
(distant stage)
presence of an anaerobic infection, antimicrobial
• 8%—staging information unknown
therapy should be modified; additional antimicrobial
changes may be necessary when culture results are Diagnosis of advanced lung cancer in more than 75%
known. The sequellae of inadequately treated empy- of the cases explains why the 5-year survival rate for
ema include fibrothorax, or “trapped lung.”8,13 lung cancer is low and why the associated productivity
costs are the highest.
The highest recorded 5-year survival rates are in the
Lung Cancer United States with 12.5% for men and 15.6% for
women.15,19 These values reflect the survival for all cell
The American Cancer Society (ACS) identified cancer as types of primary lung cancer. The developing world’s
the number two cause of death in the United States. 5-year survival is approximately 8%.
Cancer accounted for nearly one-quarter of yearly
deaths (559,312), exceeded only by heart disease
(652,091). Lung cancer is the most common fatal RISK FACTORS
cancer in both men (31%) and women (26%). Since Risk factors are the extrinsic or intrinsic elements in the
1990, the age-adjusted lung cancer death rate of men environment that predispose an individual to a disease.
has decreased by 40%. In contrast, the lung cancer Examples of factors are genetic predisposition to a
death rate for women more than doubled in the past disease, an antigen the individual is allergic to, social
27 years, and in 1987, lung cancer mortality exceeded habits, and the state of the individual’s immune
breast cancer, becoming the primary cause of cancer function.
deaths in women.15
These statistical changes are reflected in cigarette Cigarette Smoking. Lung cancer results from a combi-
smoking statistics. More women are smoking than are nation of continued exposure of the bronchial mucosa
men, and fewer women are quitting.16,17 The death to carcinogens and genetic susceptibilities.20 Cigarette
rates are higher in men than in women in every racial smoking is by far the most important risk factor for
and ethnic group. African American men and women lung cancer and thought to be the primary risk factor
have the highest cancer mortality, followed by whites, for approximately 80% of all lung cancers.21 About
then American Indian/Alaskan natives, Hispanics, and 15% of all people who smoke develop lung cancer,
finally Asian/Pacific Islander. Asian American and with the risk varying depending on the age at which
Pacific Islander men and women have the lowest cancer smoking started and the number of cigarettes
death rates, about half of the rate of African American smoked.22 Lung cancer risk increases by approximately
men and women, respectively.17 the fourth power of smoking duration and by the
The productivity costs to the U.S. economy second- square of the number of cigarettes smoked every day.23
ary to cancer deaths—loss of paid employment, Tobacco smoke contains many carcinogens that are
caregiving, and housekeeping activities—are signifi- known to cause molecular abnormalities in bronchial
cant. The estimated productivity losses in 2000 were epithelia. Respiratory epithelial chromosome damage
approximately $116 billion. If the current survival rate is found in all chronic smokers.
does not improve, the costs will increase to $147.6 People exposed to environmental tobacco smoke,
billion in 2020. The economic impact of death from including spouses and children of smokers, have an
lung cancer has been the most costly. Lung cancer increased risk of about 17% for lung cancer.24 In one
alone was responsible for more than one-quarter of the study, people who had been exposed to tobacco smoke
total costs ($39 billion in 2010). Death from colon and as children but not as adults did not appear to have any
rectum cancer was the second most costly ($12.8 increased risk. Exposure to the smoking of family
billion in 2010), and death from female breast cancer members and friends seems to be associated with the
was the third ($10.9 billion in 2010).”18 initiation of adolescent smoking.23
The following Surveillance and Epidemiology and There are conflicting data regarding the relative
End Results (SEER) statistics were released from the risks of developing lung cancer from smoking for men
and women. Two examples of conflicting reports are Asbestos workers’ statistics are even more abysmal. An
from the American Cancer Society and the Nurses asbestos worker who does not smoke has a five-fold
Health Study of Women and Health Professional increased risk of lung cancer compared to other
Follow-up Study of Men. The ACS performed two nonsmokers. But the asbestos worker who smokes has
cancer prevention studies and identified that men who a 92-fold increased risk of lung cancer compared to
smoke had an increased risk of lung cancer compared nonsmokers. This risk is much greater than that of
to women who smoke.15 Another large study studying someone who smokes over two packs of cigarettes a
cancer data from former and current smokers in both day (64-fold risk increase).16,30
sexes found that women do not appear to have greater
susceptibility to lung cancer than men.25 Radon Gas. Radon gas is a breakdown product of
These conflicting results indicate the complexity of uranium and an environmental risk factor for lung
the subject and the need for further study. Reported cancer. Approximately 2–3% of lung cancer is thought
differences in the histological subtypes are also not to be caused by radon.29 Because it is ubiquitous in the
well understood. environment, it can seep into any dwelling. Many
people are unaware that they are exposed to this
• Women smokers appear to be at a higher risk of
pollutant in their own homes. A fact that is not appre-
small-cell lung cancer than men smokers are.
ciated is that radon and cigarette smoking may have a
• Men smokers seem to have an equal risk for
synergistic effect on lung cancer rates. Smokers, and
squamous-cell and small-cell cancers.
possibly nonsmoking residents of smokers’ house-
• Women smokers have a greater incidence of
holds, may be at increased risk of lung cancer even
adenocarcinoma than men smokers do, with a
when radon levels are relatively low. Kits are available
possible influence by estrogen.26,27
to test the home for radon, and methods exist to
• Up to 15% of lung cancers in never-smokers are
remove it.
thought to be caused by second-hand smoke.
(Cigarette smoke contains many carcinogens,
such as aromatic polycyclic hydrocarbons and Family History. Genetics is under intense scrutiny as a
N-nitrosamines.) Urinary levels of tobacco- possible lung cancer risk factor. One area of research is
specific carcinogens were elevated in nonsmoking investigating the possibility of genetic susceptibility to
women exposed to environmental tobacco environmental tobacco smoke. One study reported that
smoke. A nonsmoking woman has a 24% greater individuals with a family history of lung cancer had a
risk of developing lung cancer, if living with a two-fold greater risk of developing lung cancer and that
smoker.28 this risk was more pronounced in women.15 The study
found that women tend to carry more gene mutations
Quitting smoking is the primary way to prevent that can increase their susceptibility to developing lung
lung cancer. However, it might be 15–20 years before cancer.
the risk assumes a rate almost as low as nonsmokers’ Another direction of cancer research is in the area
risk of lung cancer. Research has shown that the of familial tendencies to develop certain cell types of
difference in risk between people who continue cancer, cancer at certain organ sites, and so on.31 For
smoking and those who quit is explained by the example, current research suggests that a family history
differences between the two groups in the duration of cervical, ovarian, or uterine cancer may increase the
of smoking—the length of the exposure, not its risk of lung cancer in postmenopausal women. One
intensity.16,29 study reported that a family history of ovarian cancer
increases the risk by two-fold for adenocarcinoma of
Air Pollution. The pollutants emitted from motor the lung, and a history of uterine and cervical cancer in
vehicles, manufacturing, and the burning of coal a first-degree relative increases the risk slightly for
contain carcinogens. The risk of lung cancer attributed squamous-cell and small-cell lung cancers. The higher
to environmental pollution is thought to be small, but risk occurred in both smokers and nonsmokers.32
its real effect on cancer rates is not yet established.16 Studies also have indicated that women may have a
greater genetic susceptibility to specific types of lung
Occupations Linked to Lung Cancer. Uranium and cancer due to female, X-linked inheritance (the inheri-
asbestos workers have a much greater risk of lung tance of genes located on the X chromosome).15
cancer than any other occupational groups. A uranium
worker who does not smoke has a seven-fold increase Hormonal Influences. Hormones could present an
in cancer risk when compared with other nonsmokers. increased risk for lung cancer. Researchers are looking
A uranium worker who smokes increases the risk of at hormone replacement therapy, the age onset of a
lung cancer to 38-fold compared to other nonsmokers. woman’s first period, and the length of her menstrual
cycle as possible risk factors for lung cancer. Estrogen is significant airway obstruction secondary to the tumor
known to have a role at many levels in tumor produc- and may be diagnosed with lung cancer after coming to
tion, and researchers are studying how estrogen affects the doctor for treatment of pneumonia.16,29,30
abnormal cell growth as well as its role in cellular Large-cell cancer accounts for 10–15% of all lung
damage. Research in this area is one of the new direc- cancers, and it is strongly associated with smoking. It is
tions in lung cancer studies.15 described as an undifferentiated cell type because it
lacks glandular (adeno characteristics) and squamous
characteristics. These tumors are often diagnosed by
HISTOLOGICAL CELL TYPES OF LUNG CANCER default when all other cell types have been excluded.
They appear in the middle to peripheral lung areas and
The two major classifications of lung cancer are non-
may extend to involve segmental and subsegmental
small-cell lung cancer (NSCLC) and small-cell lung
bronchi. The large cell tumors are big, bulky, well-
cancer (SCLC). NSCLC accounts for approximately
defined masses with extensive hemorrhage and necro-
75% of all lung cancers, and it is a heterogeneous
sis. They grow rapidly and metastasize early through
collection of three histological cell types: adenocarci-
the lymphatics and bloodstream.
noma, squamous-cell carcinoma, and large-cell carci-
Giant-cell, a variant of large cell, is extremely
noma. These histologies are classified together because
aggressive and carries a very poor prognosis. The
the approaches to diagnosis, staging/prognosis, and
people with these tumors usually present with a large
treatment are similar. Small-cell lung cancer is very
peripheral mass. The tumors do not involve the large
different from the other cancer classification with a
airways unless they are spreading directly.16,29,30
different staging process, treatment approach, and
prognosis (Table 11-2). Small-Cell Cancer. Small-cell lung cancer (SCLC) is a
major classification as well as a cell type. SCLC has the
Non-Small-Cell Cancers. Adenocarcinoma accounts highest association with cigarette smoking. Approxi-
for about 35–40% of all lung cancers, and it is the most mately 98% of patients with SCLC have a smoking
common type of NSCLC lung cancer in the United history.33 The disease originates in lung tissue next to
States. It occurs in smokers, but it is also the most central airways and major blood vessels. Because it
common lung cancer found in nonsmokers. It is the grows so rapidly, SCLC is characterized by early metas-
usual cell type of 60–80% of cancers in nonsmokers.6 tasis to distant sites such as the mediastinal lymph
Adenocarcinoma may arise from a previous scar, nodes, liver, bones, adrenal glands, and brain; therefore,
and it usually does not cavitate. The tumor usually most patients already have detectable metastasis by the
arises in the lung periphery and metastasizes early to time it is first diagnosed. This cell type is also known
other body organs through the circulatory and lym- for causing paraneoplastic syndromes, of which the
phatic systems. It usually metastasizes to the lymph most common are syndrome of inappropriate antidi-
nodes, pleura, adrenal glands, central nervous system, uretic hormone (SIADH) and syndrome of ectopic
and bone. Adenocarcinoma tends to have a worse adrenocorticotrophic hormone (ACTH) production.
prognosis than squamous-cell cancer in all stages.6 Neurologic syndromes may also occur such as Eaton-
Bronchoalveolar cell carcinoma is a subtype of Lambert syndrome and sensory disturbances.16,30,33
adenocarcinoma that usually accounts for about 5% of
all bronchogenic carcinomas. This type of cancer occurs
in people with underlying interstitial lung disease and CLINICAL MANIFESTATIONS
parenchymal scarring. It appears to arise from type II Fifteen percent of the people with lung cancer do not
pneumocytes and may appear as a solitary periph- have symptoms at the time of diagnosis. Seventy
eral nodule, multifocal disease, or a pneumonic form. percent of lung cancer patients have signs and symp-
The cancer may spread to other parts of the lung or to toms of intrathoracic or distant metastasis at the time
the other lung by transbronchial spread or by growing of diagnosis. Clinical manifestations in individuals
along the pulmonary interstitium. Spreading by these with lung cancer include:
mechanisms is associated with a poor prognosis.6
• Dyspnea (possible airway obstruction).
Squamous-cell accounts for 20–25% of all lung
• Stridor and fever (possible atelectasis and
cancers. It is strongly associated with cigarette smoking.
infection).
The tumor commonly arises from large bronchi and
• Hoarseness (involvement of the recurrent
spreads by direct invasion of neighboring tissues or
laryngeal nerve).
lymph node metastasis. Squamous-cell cancers are
• Chest pain (pleural involvement).
frequently slow growing and can take several years to
progress from a localized tumor to an invasive cancer.6 Other clinical manifestations are listed in
On initial presentation, the patient frequently has Table 11-2.16,30
TABLE 11-2 Lung cancer

Non-Small Cell Lung Cancer Other
Small Cell Adenocarcinoma Large Cell Squamous Cell Many Cell Types
Distribution of 13 35–40 10–15 25–30 5
cell types (%)
Specific Highest Most frequent cause Smokers Smokers Carcinoid: slow
Information correlation with of lung cancer in Undifferentiated Central lesion growing malignant
smoking non-smokers in a proximal tumor ~2% of all
Large peripheral
Central airways Peripheral lung bronchus primary lung tumors
mass with
and blood vessels Bronchoalveolar necrosis Cells shed and Lymphoma: primarily
non-Hodgkin’s <1%
Highest occur- carcinoma is Metastasizes early can be detected
rence of distant subtype from cytology Mucoepidermoid:
Cavitary lesion
metastasis Cavitary lesion studies Derived from salivary
↑ occurrence of May be present gland tissue
paraneoplastic for years before Hamartoma:
syndromes diagnosis Commonest benign
No Cavitation tumor
Metastatic: All cell
types; result of
spread from
primary tumors
(breast, head, neck)
Local Asymptomatic: ~25% of patients
Manifestations Symptomatic: Cough, new cough onset in smoker, hemoptysis, chest heaviness, dyspnea, digital
clubbing, obstructive atelectasis or pneumonia
Local metastasis: pleural involvement (pain, effusion), regional lymph node enlargement, superior
vena cava syndrome (dilated neck veins, prominent veins on chest, facial edema, red coloring),
superior sulcus tumor (Horner’s syndrome, bony destruction, hand muscle atrophy)
Metastasis 65–70% have The more differentiated the cells, the slower the tumor growth and spread. Every
disseminated or body tissue could be the site of distant metastasis.
extensive disease Clinical manifestations give clues of metastasis
at diagnosis
Common: bone,
liver, adrenal
glands, pleura,
CNS
Symptoms
give clues of
metastasis
Paraneoplastic Associated systems: muscloskeletal, cutaneous, neurologic, endocrine, hematologic/vascular
Syndromes Musculoskeletal: hypertrophic osteoarthopathy, myopathy
Cutaneous: clubbing, pruritis, scleroderma
Endocrine: Cushing’s syndrome, syndrome of inappropriate antidiuretic hormone secretion (SIADH),
hypercalcemia, carcinoid syndrome, thyroid-stimulating hormone, ACTH syndrome
Neurologic: Lambert Eaton syndrome, neuropathy, psychosis, dementia
Vascular/hematologic: anemia, polycythemia, arterial thrombosis, eosinophilia, hypercoagulability
Other: wasting syndrome
TABLE 11-2 Lung cancer (continued)

Non-Small Cell Lung Cancer Other
Small Cell Adenocarcinoma Large Cell Squamous Cell Many Cell Types
Laboratory Hypercalcemia: bony metastasis or secondary to parathyroid-like hormone from tumor cells
Anemia: nutrition-related, bone marrow involvement, chemotherapy
Decreased clotting time: not understood
Hyponatremia and low serum osmolality: SIADH
Diagnosis Initial screen: patient symptoms, chest x-ray (incidental or first step in diagnosis)
Cell type diagnosis: Bronchoscopy, needle aspiration, bronchial brushings, and washings,
transbronchial biopsy, sputum cytology, or CT guided biopsy
Staging: bronchoscopy with bronchial biopsy and lymph node biopsy, HRCT, pleural fluid cytology,
mediastinoscopy and biopsy of mediastinal nodes, PET scan
Treatment Solitary pulmonary Varies with stage:
nodule Surgery: Lobectomy; pneumonectomy; or segmental, wedge, or sleeve resection
Limited disease: as appropriate if pulmonary function is adequate
surgical resection,
Systemic chemotherapy in combination with thoracic radiotherapy
chemotherapy,
radiotherapy OR combined chemoradiotherapy
Other cases: Palliative tumor reduction
Chemotherapy, Experimental – Biologic testing (various stages of testing)
radiotherapy,
palliative tumor
reduction, stent
placement
Prognosis Untreated: All stages: 16.8% All lung cancers
(2005 data) Limited disease - Localized – 51.2% (at diagnosis confined to Localized – 49.5%
median survival primary site) Regional – 20.6%
12 wks
Regional – 21.8% (spread to regional lymph nodes Distant – 2.8%
Extensive disease - or directly beyond the primary site)
median survival Unstaged – 8.3%
Distant – 2.9% (diagnosed after metastasis to
6 wks
distant sites)
Treated:
Unstaged – 8.5% (unknown stage)
All stages: 5.9%
Compared with people with squamous cell cancer,
Localized (at
more patients with adenocarcinoma had cerebral
diagnosis confined
metastasis within 5 years
to primary site) –
19.5% IIB disease – surgery and weight loss are significant
independent predictors of 5-year survival
Regional (limited
disease) – 12.5%
Distant (extensive
disease) – 2.2%
Unstaged (stage not
known) – 6.4%
PARANEOPLASTIC SYNDROMES clubbing, a common manifestation of lung cancer,

Paraneoplastic syndromes are nonpulmonary involves the fingers and toes, with selective enlarge-
disorders that are caused by lung cancer. Many types ment of the connective tissue to the distal phalanges. It
are secondary to hormonelike chemicals or other is diagnosed by the loss of the angle between the
substances released from the tumor that have meta- cuticle and the base of the nailbed. The most common
bolic or neurological effects. For example, digital paraneoplastic problems (5–10%) are syndrome of
inappropriate antidiuretic hormone (SIADH) and This technique can be used to determine cell type and
syndrome of ectopic adrenocorticotrophic hormone cancer stage. Other organs, such as the liver and
(ACTH) production. Neurologic syndromes may also adrenal glands, can be directly biopsied with needle
occur, such as Eaton-Lambert syndrome and sensory aspiration to aid in cancer staging.
disturbances.16,30 Video-assisted surgery has proved useful in cancer
diagnosis of indeterminate isolated pulmonary nod-
ules. This visual technique has also been used in
DIAGNOSIS AND STAGING surgical removal of the lung in high-risk or elderly
patients. Its current use in the management of patients
Diagnosing the cancer and staging the invasiveness of with malignancy is being studied.34,35
the involvement are intricately intertwined. The chest
radiograph is a screening tool. Abnormalities on the Lung Cancer Staging. Cancer staging criteria help the
chest radiograph, coupled with the patient’s clinical clinician identify the extent and prognosis of tumors.
manifestations, indicate whether further diagnostic Lung cancer staging criteria are different for the two
tests are necessary. Cytology or histology aids in the main cell types. The cell type of the lung tumor and the
diagnosis of lung cancer. The following tests are used in degree of invasiveness determine treatment options
the initial diagnosis and staging of disease severity:16,30 and patient prognosis.
• History and physical exam Cancer clinical staging, which describes the extent
• Laboratory studies: complete blood count, blood of disease, is determined following completion of the
chemistry, including liver function tests diagnostic work-up. The work-up includes the:
• High-resolution computer tomography (HRCT) • Pathology report from tissue obtained during
of chest as well as CT of the liver, brain, and bronchoscopy, needle (or other technique)
adrenal glands to identify distant metastasis. biopsy.
• Bone scintigraphy if bone metastasis is suspected • Blood tests.
• Positron emission tomography (PET scan) • Imaging tests (e.g., abdominal ultrasound of the
The PET scan is more sensitive and accurate in staging liver, radionuclide bone scans, HRCT, MRI scan
mediastinal spread of the cancer. It can detect abnor- of brain, chest and abdomen) that were indi-
malities not visible on CT scans. cated by a high index of suspicion based on
patient clinical manifestations.6,30,33
Techniques Used in Cancer Diagnosis. The fiberoptic The purpose of staging is to determine resectability
bronchoscope is frequently used in both cancer diagnoses and operability because surgical resection is the only
and staging, especially if the suspicious lesion is cure for lung cancer. Pulmonary function tests should
centrally located: be performed in people with resectable cancer to
• Obtaining tissue samples by transbronchial decide operability. If the estimated postoperative lung
biopsy enables the clinician to determine cell function (⬍40% FEV1 and ⬍40% DLCO) indicates that
type. the patient is inoperable, then exercise testing is
• It permits biopsy of regional lymph nodes for performed to confirm this estimation. If surgery is not
tumor staging. indicated, the patient receives other definitive care.4
• If the tumor is endobronchial, the bronchoscope
also allows direct visualization of the tumor as Staging of Non-Small-Cell Lung Cancer. The TNM
help in later surgical resection. staging system was implemented in 1997 after revisions
of the stage groupings: T is the primary tumor, N is for
Sputum samples for cytology testing can also be
the regional lymph nodes, and M is for distant metasta-
obtained when the tumor is too peripheral to be
sis. The system is used for all lung carcinomas except
directly biopsied using the bronchoscope.
small cell.
Mediastinoscopy is usually performed to visualize
directly the mediastinal lymph nodes. It allows medias- • T describes tumor size and its location in relation
tinal node biopsy, which aids in cancer staging. The to bronchi, carina, major blood vessels, pleura,
CT-guided biopsy is helpful when the lesion is located and chest wall (TX, T0, Tis, T1, T2, T3, T4).
in the periphery of the lung. The CT identifies where the • N describes lymph node involvement and
physicians should insert the biopsy needle to obtain a whether the involvement is on the ipsilateral
good tissue sample for determining malignancy. side or contralateral side of the primary tumor
If the patient has a pleural effusion, the fluid can (NX, N0, N1, N2, N3).
be aspirated by thoracentesis and tested for cancer cells. • M is either present or absent (MX, M0, M1).
The X designation in each category indicates that the circumscribed anatomical area is based on the
subset was unable to be assessed, and the Tis indicates fact that it falls within 1 radiation field, using
carcinoma in situ. radiation therapy settings as the limitation.29
Carcinoma in situ is a premalignant neoplasm in [Radiation therapy is treatment with high-
which the tumor cells are confined to the epithelium of energy rays (such as X-rays) to kill or shrink
origin and have not invaded the basement membrane. cancer cells. The radiation may come from
A diagnosis of carcinoma in situ is associated with a outside the body (external radiation) or from
high incidence of progression to invasive cancer. radioactive materials placed directly in the tumor
Neoplastic changes in squamous or glandular epithe- (brachytherapy or internal radiation). This
lium can occur in the body wherever these cells are therapy may be used to shrink the cancer before
common, such as in the cervix, anus, bronchi, esopha- surgery, to destroy any remaining cancer cells
gus, uterine endometrium, or vagina. after surgery, or as the main treatment. It may
There are four stages for NSCLC, with further also be used as palliative treatment for advanced
subdivisions of stages I–III into A and B designations. cancer.]
The severity of the disease worsens with the increased • Extensive disease is disease that has spread
numerical designation. The A and B designations in beyond the limited-stage anatomical area and
stages I, II, and III are expansions of the classification cannot be encompassed in 1 radiation field.
system to indicate gradations of severity within the Any tumor cells found in contralateral lymph
stage. There are many possible combinations of tumor nodes, tumor-laden lymph nodes above the
size, tumor invasiveness, and lymph node metastasis in clavicle, malignant pleural effusion, or distant
stages IIB, IIIA, and IIIB.6,16,30 organ metastasis is classified as extensive
disease.29
• Stage 0 (carcinoma in situ)
• Stage IA (T1N0M0), Stage IB (T2N0M0)
• Stage IIA (T1N1M0), Stage IIB (T2N1M0 or
T3N1M0) TREATMENT
• Stage IIIA (T3N1M0, T1N2M0 or T2N2M0 or The treatment of lung cancer depends on the cell
N3N2M0) type: non-small-cell lung cancer or small-cell lung
• Stage IIIB (T4N0M0, T4N1M0 or T4N2M0 or cancer. The sensitivity of the tumors to radiation,
T1N3M0, T2N3M0 or T3N2M0, T4N3M0) chemotherapy, and the ability to surgically remove
• Stage IV (any T, any N, M1) the tumor all vary in these two cancer classifications.
Staging is the primary method used to determine
Non-Small-Cell Lung Cancer. The 5-year survival
whether surgery will benefit the patient. In stages I, II,
rate of lung cancer is reported to be approximately
and IIIA, the tumors are operable if the patient has no
16%. Approximately 50% of all patients with NSCLC
complicating medical problems.16 Additionally, the
have distant metastasis at the time of diagnosis
oncology team needs to know the individual’s cancer
(stage IV). There is no cure for these people, but
severity stage to design the treatment plan.6
oncologists are developing treatment regimens that
may in the future prolong life. Currently, treatment
Staging of Small-Cell Lung Cancer. The TNM system
focuses on the palliation of symptoms and disease
is primarily used to stage NSCLC. In very few patients
control.16,29,30
with small-cell lung cancer (⬍5%), a very detailed
The primary treatments for non-small-cell lung
staging is helpful. However, in most cases, the TNM
cancer are surgery and radiation therapy. Stages I, II,
staging system is of limited use in determining a
and in some cases IIIA are considered operable. Stage
prognosis for patients with SCLC because most of the
IIIA may be surgically curable, but the risk is high
patients are in stage III/IV at the time of diagnosis. An
and the benefit is marginal. Surgery provides the best
older system, developed by the Veterans Administration
5-year survival rates in the treatment of NSCLC:
group, is still used today to stage patients with SCLC.
stage 1A, about 70%; stage IB, 50–60%; stage
This system consists of two stages: limited disease and
IIA, 40–55%; stage IIB, 40%; and stage IIIA
extensive disease.
about 25%.16
• Limited disease is disease that is confined to one Radiation therapy is sometimes indicated before
hemithorax and its ipsilateral mediastinal and surgery to shrink the tumor, after surgery to kill
supraclavicular lymph nodes. Malignant pleural remaining cancer cells, or at both times. But, even with
effusion is excluded. Thirty-five to forty percent the surgical removal of the lung, the recurrence rates
of patients are in this stage when diagnosed. This are high.
Chemotherapy (or chemo) is an adjuvant

therapy (an auxiliary treatment) to kill any cancer Spotlight
cells present in the body. In cases of recurrence, On
radiation and chemotherapy are used to relieve
patient symptoms such as coughing and shortness of Racial Disparities
breath. Tumor reduction is one of the goals of adju- in Lung Cancer
vant therapy. It relieves airway obstruction secondary
Lung cancer death and survival rates differ
to the endobronchial tumor, enabling the patient to
between African Americans and non-African
breathe more comfortably. Other adjuvant therapies
Americans. According to statistics released from
are:16,30,36
the American Cancer Society, African Americans
• Stent implantation (maintains airway patency have the highest death rate and the shortest
in the presence of external compression of the survival rate of any racial and ethnic group in the
trachea from tumor). United States. The reasons are complex and
• Laser therapy (palliative reduction of endobron- include social and economic differences. “These
chial tumor mass). include inequalities in work, wealth, income,
• Photodynamic therapy (causes tumor light education, housing and overall standard of living,
sensitivity and induces tumor cell death when barriers to high-quality health care, and racial
the tumor is exposed to a concentrated laser discrimination.” Although, this disparity is
beam). decreasing, as of 2010, the overall cancer death
• Brachytherapy (intraluminal application of rate was still 33% higher in African American men
radiation to patients with tumor-caused airway and 16% higher in African American women.
obstruction). Source: Statistics for 2009: Cancer Facts and Figures for
African Americans 2009–2010, American Cancer Society
Inc. http://www.cancer.org/docroot/STT/STT_0.asp.
Small-Cell Lung Cancer. Surgery has a very limited
place in the treatment of SCLC. It is suggested that
patients with a solitary pulmonary nodule have lung
resection followed by chemotherapy and thoracic
radiotherapy. Other presentations of SCLC do not Summary
show improved survival with surgical resection. Atelectasis is the incomplete expansion of the lung. It
Limited-stage SCLC is treated with multiple-drug can be categorized in several ways, but the simplest is
chemotherapy usually containing a platinum-containing dividing it into obstructive, nonobstructive, and special
regimen and concurrent thoracic radiotherapy (see types of lung collapse. Obstructive atelectasis, the most
Table 12-1). The patient who goes into complete common type, results from the reabsorption of gas
remission should be offered prophylactic cranial from the lung distal to the obstruction. Nonobstructive
radiation therapy. Approximately 50% of patients types of atelectasis are caused by an abnormal relation-
achieve complete remission, but they relapse within ship between the visceral and parietal pleura, a loss of
2 years. surfactant, or the replacement of normal lung paren-
Approximately two-thirds of SCLC patients have chyma with scar tissue or cellular infiltrates. One of the
extensive-stage disease when initially diagnosed. common special types of atelectasis is acute atelectasis
Patients with extensive-stage SCLC respond to after surgery, especially procedures involving the thorax
combination chemotherapy using a platinum- or upper abdomen, has long been associated with the
containing regimen, but the relapse rate is very rapid. loss of lung volume, causing complete or partial
Prophylactic cranial irradiation should be offered to alveolar collapse. Pain, medications, increased secre-
all patients with extensive-stage disease who are tions, and the inability to cough and to take deep
responding to chemotherapy. It reduces brain metas- breaths are common causes of postoperative atelectasis.
tasis, improves disease-free time, and prolongs life.33 The treatment of atelectasis depends on the underlying
The adjuvant therapy available to patients with SCLC cause. The goal of treatment is lung reinflation by
is the same as in NSCLC. New chemotherapy agents removing the cause of the lung collapse.
for SCLC have not appeared, but some experimental Pleural disorders are pleural abnormalities that
treatment strategies in the area of angiogenesis develop because of another primary disease or disor-
blocking agents have been are tested. Researchers der. The pleural surface may become inflamed or
hope that these drugs can stop blood flow to the irritated, or the pleural space may be filled with air, gas,
tumors and starve them of the nutrients necessary or fluid. Pneumothorax is the presence of free air in the
for growth.16,30,33 pleural space that causes partial or complete collapse of
the affected lung. Pleural effusions are an accumulation 3. What is a cause of obstructive atelectasis?
of fluid in the pleural space. The most common cause of a. pleural effusion
pleural effusion is congestive heart failure (30–40% of b. bronchogenic carcinoma
cases). The remaining 60–70% of the cases of pleural c. decreased lung surfactant
effusion are divided among nine primary diseases, with d. lung fibrosis
pneumonia as the second most common cause and 4. What findings are present in a patient with a
malignancy as the third. pleural effusion of 700 mL?
The two major classifications of lung cancer are a. increased bronchovesicular breath sounds
non-small-cell lung cancer (NSCLC) and small-cell b. hyper-resonance to percussion over the affected
lung cancer (SCLC). NSCLC accounts for approxi- area
mately 75% of all lung cancers, and it is a heteroge- c. mediastinal shift on chest X-ray
neous collection of three histological cell types: d. decreased lung expansion in the effusion area
adenocarcinoma, squamous-cell carcinoma, and
5. What cell type of lung cancer is associated with
large-cell carcinoma. These histologies are classified
causing paraneoplastic syndromes?
together because the approaches to diagnosis, staging/
a. adenocarcinoma
prognosis, and treatment are similar. Small-cell lung
b. squamous cell
cancer is very different from the other cancer classifica-
c. large cell
tion with a different staging process, treatment
d. small cell
approach, and prognosis.
The treatment of lung cancer depends on the cell 6. In which type of lung cancer is extensive
type: non-small-cell lung cancer or small-cell lung disease present in 65–70% of patients at
cancer. The sensitivity of the tumors to radiation, diagnosis?
chemotherapy, and the ability to surgically remove the a. adenocarcinoma
tumor all vary in these two cancer classifications. b. squamous cell
c. large cell
d. small cell
Study Questions 7. What is the curative treatment for the patient
REVIEW QUESTIONS with non-small-cell cancer?
a. surgery
1. Identify the four main cell types of malignant lung b. chemotherapy
cancer. c. radiation therapy
2. Discuss the four mechanisms of pleural fluid d. b and c
formation leading to the development of a pleural 8. What are the radiographic findings in a patient
effusion. with a tension pneumothorax?
3. Compare and contrast the types of atelectasis. a. mediastinal shift to the affected side
4. Describe the clinical signs and symptoms of b. absence of pulmonary vascular markings on the
tension pneumothorax. affected side
c. increased radio-opacity of the lung on the
5. Describe the treatment for small-cell and non-
affected side
small-cell lung cancer.
d. blunting of the costophrenic angle on the
affected side
9. What type of atelectasis is associated with lobar
1. Which lung cancer is most frequently found in collapse?
nonsmokers? a. compression atelectasis
a. small cell b. nonobstructive atelectasis
b. adenocarcinoma c. obstructive atelectasis
c. large cell d. adhesion atelectasis
d. squamous cell 10. What are the characteristics of a transudate?
2. What is/are the cause(s) of collateral air drift in a. The fluid is an ultrafiltrate of plasma and
the lung? contains less protein than plasma.
a. pores of Kohn b. The fluid is similar to plasma and has a higher
b. canals of Lambert level of protein.
c. Martin’s channels c. Transudates are usually present in pneumonia.
d. all of the above d. b and c
CRITICAL-THINKING QUESTIONS 12. Rubins J. Pleural effusion. eMedicine Specialties:

Pulmonology. June 5, 2008. http://emedicine.
1. How might external compression of a bronchus
medscape.com/article/299959-overview.
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13. Loddenkemper R. Pleural diseases: pleural effusion.
the atelectasis caused by external compression of a
In: Albert R, Spiro S, Jett J, eds. Comprehensive
bronchus.
Respiratory Medicine. St. Louis: Mosby: 1999:
2. How would decreased lung expansion after surgery 66.1–66.10.
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you recommend to prevent the development of 865–867.
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3. In a patient with significant atelectasis, compensa- Future Oncol. 2008;4,5:705–716.
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Describe the compensatory changes and provide a Spiro S, Jett J, eds. Comprehensive Respiratory
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17. Cancer Facts & Figures. American Cancer Society.
2008. http://www.cancer.org/docroot/STT/STT_0.asp.
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CHAPTER 12
Diseases That Affect the Pulmonary

Vasculature
William Atkinson and Barbara A. Ludwig
OBJECTIVES
• Describe the pathophysiology of the various forms of pulmonary edema.
• List the differences between hemodynamic pulmonary edema and edema associated with acute lung injury.
• Explain the various ventilation/perfusion imbalances associated with acute pulmonary embolism and the
mechanism of restoring balance as the clot dissipates and blood flow is restored.
• Name major causes of venous stasis in the lower extremities that are risk factors in the development of deep
venous thrombosis.
• Explain cor pulmonale and discuss the various lung pathologies that are precursors to the condition.
• Name several mechanisms by which patients develop pulmonary hypertension.
• Discuss the hypoxemia that occurs by means of many different mechanisms in heart and lung disease.
CHAPTER OUTLINE
Hemodynamic Pulmonary Edema Idiopathic (Primary) Pulmonary Hypertension
Physiologic Considerations (IPH)
Pathophysiology Pulmonary Vasculitis
Diagnostic Features Pulmonary Embolism
Bedside Monitoring Noncardiogenic Pulmonary Edema:
Acute Lung Injury
Oxygenation and Mechanical Ventilation
Risk Factors
Drug Therapy
Diagnosis of ALI/ARDS
Pulmonary Heart Disease
Clinical Presentation of ALI/ARDS
Obstructive Lung Diseases
Other Causes
284
CHAPTER 12 ■ Diseases That Affect the Pulmonary Vasculature 285
KEY TERMS
ACE inhibitors diaphoresis loop diuretics
acute respiratory distress diastolic dysfunction lupus erythematosus
syndrome (ARDS) diastolic gallop mitral regurgitation
amyloidosis fibrinolysis mitral stenosis
angiotensin receptor granulomatous oncotic pressure
blockers (ARBs) hepatojugular reflux palpitations
aortic insufficiency (AI) Homan’s sign paroxysmal nocturnal dyspnea
aortic stenosis (AS) hydrostatic pressure perfusion pressure
barotrauma intrapulmonary shunting pulmonary edema
cardiac markers J-type juxtapulmonary pulsus alternans
cardiogenic shock receptors sarcoidosis
constrictive pericarditis Kerley’s lines systolic dysfunction
CT angiogram (CTA) kyphoscoliosis Westermark’s sign
T
his chapter explains various syndromes so under these circumstances, it can increase its clearance
that the respiratory therapist is able to capacity to up to 200 mL per hour.1
understand their pathophysiology and As a consequence of increased lung water, the lung
mechanisms. Diagnosing is discussed, and, in stiffens, with decreased compliance requiring increased
some cases, treatment strategies are outlined. Special work of breathing and dyspnea, even though there may
emphasis is placed on respiratory therapy modalities as not be deterioration of oxygen transfer early in the
they apply to this group of illnesses. process. As pulmonary venous pressures increase,
interstitial water continues to accumulate. The accumu-
lation of fluid in the interstitium can compromise the
Hemodynamic Pulmonary Edema small airways and lead to mild hypoxemia. J-type
Hemodynamic pulmonary edema is the accumulation of juxtapulmonary receptors J-receptors, which
hypotonic fluid in the interstitial space of the lung modulate respiration, are stimulated and lead to
caused by an imbalance of the capillary perfusion tachypnea. With accumulations of more than 500 mL
pressure and the pulmonary venous pressure. of interstitial fluid, the alveolar epithelium is violated,
and alveolar flooding and frank pulmonary edema
follow, with severe hypoxemia and respiratory failure.
PHYSIOLOGIC CONSIDERATIONS Physiologic note: Even given high pulmonary venous
Fluid accumulates in the interstitial space of the pressures, the structure of the alveolar capillary rela-
lung if either the capillary perfusion pressure or the tionship prevents leakage into and the flooding of the
pulmonary venous pressure is too high. In the first alveolar space until late in the process. On one side of
instance, the capillary bed is stretched, and the spaces the vascular space is wide interstitial space that is away
between the vascular endothelial cells allow for from the alveolar membrane; this space allows fluid to
leakage of fluid into the interstitial space under the accumulate in the interstitium without violating
increased pressure. In the second instance, leakage is airspace. On the opposite side of the capillary wall, the
caused by increased hydrostatic pressure in the alveolar membrane abuts the capillary endothelial
pulmonary venous system resulting from a number membrane and protects the alveolar airspace with tight
of cardiac causes. intercellular junctions between the alveolar lining cells.
If the changes in pressure are small, the increase Only after these tight junctions break down can
in interstitial water can be cleared by the lymphatic alveolar flooding occur.2
system. This system can remove 18–20 mL of fluid per
hour and direct it to the pleural space, ultimately
clearing it through the thoracic duct. An acute rise in PATHOPHYSIOLOGY
the capillary perfusion pressure can far exceed the The outflow of blood from the left atrium is the
oncotic pressure in the interstitium and flood the common denominator for most causes of cardiogenic
space. In that case, the lymphatic system cannot keep pulmonary edema. The edema (fluid from inside
up with this rapid water accumulation even though, blood vessels seeps outside the blood vessel into the
surrounding tissues) may take the form of obstruction DIAGNOSTIC FEATURES

at the level of the mitral valve, as seen in the mitral Pulmonary edema is often caused by heart failure. As
stenosis or acute mitral regurgitation associated with the heart fails, pressure in the pulmonary venous
papillary muscle dysfunction during acute myocardial system starts to rise. As the pressure in these blood
infarction. vessels increases, fluid is forced into the interstitial
So-called systolic dysfunction occurs with spaces and ultimately into the alveoli. This fluid
syndromes that interfere with the cardiac output (CO) reduces oxygen diffusion into the blood, resulting in
and stroke volume of the cardiac pump: acute infarc- hypoxemia.
tion, left ventricular outflow obstruction and overload Pulmonary edema may be caused by damage
(the case with aortic valve disease), and septal hyper- directly to the lung or severe infection. Lung damage
trophy and obstruction. with a build-up of body fluid is also seen in kidney
Diastolic dysfunction as a cause of cardiogenic failure. Pulmonary edema may also be a complication
pulmonary edema occurs when the left ventricle is of a mechanical inefficiency due to heart attack, leaking
incompletely filled during diastole, as seen in severe or narrowed mitral or aortic valves, or weakening or
hypertensive disease associated with left ventricular stiffening of the heart muscle.
hypertrophy. Infiltrative cardiac disease, such as seen in The health care provider will perform a history,
amyloidosis, produces the same picture. Pericardial physical exam, laboratory evaluation, measurement of
effusion and constrictive pericarditis prohibit blood oxygen levels, chest X-ray, electrocardiogram
diastolic relaxation and filling of the left ventricle, (ECG), and other tests.
leading to increases of left atrial pressure and cardiac
failure. History. The patient often has a history of previous
The classification of systolic and diastolic heart heart disease or a heart murmur. At times, a family
failure may be a bit artificial because many of these member has had premature heart disease or a congeni-
conditions are associated with the features of both. tal lesion that had to be corrected. Some types of
• Fluid overload and increased left ventricular end arrhythmias and metabolic defects that run in families
diastolic pressures are common to many of these may be important, and one should ask about previous
conditions, especially when the left ventricle kidney and lung disease.
starts to dilate. Typically, these are the effects of The usual symptoms are as follows:
aortic insufficiency (AI) and end-stage aortic • Air hunger and dyspnea are symptoms,
stenosis (AS). but unassociated with cough and sputum
• They are also a consequence of mitral regurgita- production.
tion because the L ventricle is not protected as it • When sputum is present, it is usually not thick
is in mitral stenosis. Noncardiac conditions or purulent, but thin, colorless, and foamy. It
associated with fluid overload occur in renal may be pink or blood tinged, but not bloody.
failure, the hypoproteinemic state associated with • Patients tend to want to sit and not lie down
nephritic syndrome and iatrogenic overinfusion because the dyspnea increases as a consequence
of fluids and blood products. of gravity and redistribution of fluid from the
• Often unrecognized causes of pulmonary edema lower extremities. Often, a patient is much more
occur in the elderly and chronically ill patients comfortable sleeping with several pillows
who have a number of comorbidities, including (orthopnea). There may or may not be a history
low serum albumin from poor nutrition, of ankle and leg edema.
anemia, and modest levels of hypoxemia • Because of the redistribution of fluid with
associated with unappreciated pulmonary gravity, some patients will waken from sleep
disease. These patients develop interstitial fluid with acute dyspnea and sit on the side of the bed
and edema at much lower L atrial pressures than or go to the window to catch their breath
normal because of low intravascular oncotic (paroxysmal nocturnal dyspnea).
pressures. In addition, oxygen-carrying capacity • A patient with ischemic heart disease may
and delivery in the presence of anemia, coupled complain of precordial pressure, jaw pain, or
with hypoxemia associated with primary pulmo- pain radiating to the L shoulder and medial
nary disease, further impair cardiac function. portion of the L arm.
Even with only minimal impairment of cardiac • Diaphoresis and palpitations are common,
function such as in a small myocardial infarction and the patient may be peripherally vasocon-
that would otherwise not cause edema, these stricted and cyanotic, complaining of being cold.
comorbidities can lead to life-threatening • Patients are almost never febrile and do not
pulmonary edema.3 complain of chills or rigor.
TABLE 12-1 Comparison of pulmonary edema with pneumonia

Characteristics Pulmonary Edema Pneumonia
Profound Dyspnea Variable
Non-productive and unusual Cough Productive
Thin and foamy occas. Sputum Copious, thick, and colored gray,
pink tinged yellow, or green
Never unless associated pneumonia Fever Usual often with chills and rigor
or sepsis
Diffuse Distribution Localized
Rare Leukocytosis and left shift Usual unless viral
Common Cardiomegaly Never unless associated cardiac
disease
Common Peripheral edema Never
Usual Tachycardia Common
Usual S3 Rare unless concomitant CHF
Table 12-1 distinguishes the presentation of pulmonary BUN with normal creatinine if renal perfusion is
edema from pneumonia. decreased or the patient is dehydrated. The blood
chemistries should also reveal abnormalities of potas-
Physical Examination. The patient presents with sium and magnesium, which could be the result of
varying degrees of respiratory distress. Unless the left excess diuresis. A low serum albumin suggests malnu-
heart failure has led to subsequent right-sided overload trition and makes the treatment of the edema and
and right heart failure, or both sides are involved (as diuresis all the more difficult.
can be seen in pericardial tamponade, cardiomyopathy, Cardiac markers should be done to be sure that
and infiltrative myocardial disease), peripheral signs of myocardial ischemia or myocardial cell death has not
right heart failure are absent. These include ankle and occurred. These include serial measurements of CPK-MB
leg edema, liver engorgement and enlargement, and Treponon levels. B-naturetic peptide levels add
hepatojugular reflux, and distended pulsatile neck very little to the diagnosis, but they are useful as guides
veins at 45 degrees of head elevation. to the effectiveness of treatment and to follow the
The main physical findings of cardiogenic pulmo- treatment over the long-term course of the disease.
nary edema are fine inspiratory rales at the posterior
lung bases. As the edema becomes more severe and the Electrocardiography. The electrocardiogram has no
alveolar space is flooded, coarse, bubbly rales can be specific findings caused by pulmonary edema and
heard throughout, in addition to harsh breath sounds congestive heart failure. However, the presence of left
and severe respiratory distress. Tachycardia is always ventricular hypertrophy or left bundle branch block
present in the absence of heart block, and the primary may suggest aortic valve disease or a hypertensive heart.
auscultatory findings are a ventricular diastolic gallop An electrocardiogram can also be very helpful when it
(S3) and pulsus alternans. Patients are usually shows evidence of ischemia or of current injury,
cyanotic. The hectic cardiac rhythm often precludes suggesting acute myocardial damage as the cause of
identifying other abnormalities or valvular lesions by the pulmonary edema. Various arrhythmias may also
auscultation. provide clues to the reason the heart suddenly failed
to pump efficiently. These patients should be put on
Laboratory Evaluation. A blood count should deter- continuous electrocardiographic monitoring as soon as
mine whether the patient is anemic. Normally, the they come to the hospital to detect any arrhythmias or
white blood cell count is minimally elevated, but there heart block.
rarely is a left shift with immature neutrophils present,
which should make infectious disease (pneumonia) Arterial Blood Gasses and Pulse Oximetry. Initial
less likely. arterial samples should be taken as part of the assess-
A metabolic panel assesses the degree of renal ment. The arterial blood gasses (ABG) gives not only the
insufficiency. One may see modest elevations of the level of oxygenation, but also the effectiveness of
ventilation from the pCO2 and the acid-base state to be Urinary output must be maintained even in hypoten-
sure there is no underlying acidosis as overventilation. sive states. In addition to diuretics, a low-dose dopa-
Alkylosis should be present in uncomplicated cases. mine drip might be used to increase renal blood flow.
Pulse oximetry should be used only to follow the The pulmonary capillary wedge pressure and the
patient’s ability to oxygenate. It is not a measure of pulmonary artery diastolic pressure reflect L atrial
ventilation and often misleads caregivers toward wrong pressure. As cardiac output improves with inotropic
conclusions about the effectiveness of their therapy. therapy, afterload reduction, diuresis, and oxygenation,
the wedge pressure, and the pulmonary artery diastolic
Imaging. Standard posteroanterior (PA) and lateral chest pressure should all increase, as well as the mixed
X-rays may not be possible if the patient is in respiratory venous O2 content. Instances of cardiogenic shock with
distress. So some of the subtleties and classical features low cardiac output and low blood pressure call for
of cardiac failure and congestive heart failure cannot be adrenergic blood pressure support with dopamine and
appreciated. Portable PA chest films are then done to dobutamine. If that fails, intra-aortic balloon place-
help establish the diagnosis. Classical findings include: ment through the femoral artery and counterpulsation
therapy may be warranted until cardiac function and
• Cephalization of the pulmonary vessels with
blood pressure are restored.4
fuzzy indistinct definition of their outlines.
• Cardiac enlargement.
• Blunting of the costophrenic angles and/or
OXYGENATION AND MECHANICAL VENTILATION
obvious pleural effusion.
• Kerley’s lines leading to the pleura, indicating Oxygen, one of the hallmarks of therapy, must be given
engorged lymphatics and a hazy ground glass to all patients in cardiac failure. If patients can main-
appearance of the lung fields themselves tain ventilation on their own, assisted ventilation may
(see Chapter 14). not be needed. In most instances with pulmonary
edema and alveolar flooding, neither oxygenation nor
Two-dimentional echocardiography can often be ventilation can be sustained, and mechanical ventila-
done at the bedside with portable machines. Valvular tion is required. In recent years, BiPAP (bidirectional
disease, as well as presence of pleural effusion, can be airway pressure) therapy without intubation has
easily detected. Adynamic segments of L ventricular become popular. BiPAP gives a ventilatory assist and
myocardium are ominous signs of ischemia or maintains intratracheal expiratory pressure in an
infracted segments of the ventricular wall. Diastolic attempt to recruit alveoli and increase functional
volume of the left ventricle and ejection are good residual capacity.
indications of cardiac output and efficiency. If the Hypoxic patients are often confused and combative
pulmonary edema is the consequence of an acute because of air hunger and are therefore intolerant of
ischemic cardiac event, the patient should be stabilized the BiPAP mask. In such instances, sedation and
and taken to the cardiac catheterization lab where the intubation are necessary before the patient deteriorates.
coronary arteries can be imaged and a revascularization With the newer, more sophisticated mechanical
procedure performed. ventilators available today, many techniques can be
employed. Often one starts with plain assisted ventila-
tion, but often the patient overrides the ventilator
BEDSIDE MONITORING
because of air hunger and tachypnea. Ineffective
The goals of treatment can be reached with monitoring ventilation and oxygenation are the result. A better
as a guide to therapy. In addition to continuously tactic is to use volume-controlled ventilation with
monitoring vital signs, urinary output and oxygenation pressure limitation and autoflow. Another effective
should be tracked. maneuver is to use positive end-expiratory pressure
By means of the following tools, pulmonary (PEEP). Both techniques tend to recruit new alveoli,
arterial pressure monitoring and periodic measure- increase lung compliance, and, within limits, enhance
ments of pulmonary capillary wedge pressure are used oxygenation and cardiac output. If PEEP is used in
to track cardiac output. excess, the mean intrathoracic pressure is increased,
• In mechanically ventilated patients, frequent and venous return impaired, thus decreasing cardiac
arterial blood gas analysis is warranted. output.5
• In patients with pump failure, overwhelming
pulmonary edema, or cardiogenic shock,
intra-arterial continuous blood pressure (BP) DRUG THERAPY
monitoring and right heart catheterization with In addition to oxygen and ventilation therapy, several
a Swan-Ganz line are frequently employed. drugs are useful in treating pulmonary edema.
Diuretics. Loop diuretics, especially furosamide, are inotropic activity and increases cardiac output. It
central to the treatment of pulmonary edema. The produces significant vasodilatation; if the patient
patients have water excess and are often hypervolemic becomes hypotensive, the dose has to be reduced.
with decreased renal blood flow. Loop diuretics are the
most effective agents to clear fluid from the intravascu- Norepinephrine. Norepinephrine is an alpha adrener-
lar space and ultimately improve cardiac function. The gic agonist reserved for patients in profound shock
medication is usually given intravenously to patients in whose BP cannot be supported by other means. It
the acute state, either by direct injection or continuous increases afterload and decreases cardiac output.
infusion. The drug acts quite quickly, and diuresis
is substantial as long as renal blood flow can be Newer Agents. Nesiritide is a recombinant BNP
maintained and the patient is not hypovolemic. (B-Naturetic peptide) that decreases right-sided pres-
sures, wedge pressure, and systemic vascular resistance,
Nitroglycerine and Nitroprusside. Nitroglycerine in increasing cardiac output.
its varying forms reduces preload rapidly and reduces Phosphodiesterase inhibitors have a positive
afterload to some degree. Given intravenously in a inotropic effect, decrease afterload, and decrease
drip, the dose can be titrated gradually up to as high pulmonary vascular resistance. They work by increasing
as 100 μg/min. intracellular cyclic AMP by preventing its breakdown.
Nitroprusside is a potent preload and afterload
reducer that causes smooth muscle relaxation. Given in
an intravenous drip, it rapidly increases cardiac output Pulmonary Heart Disease
but can cause significant reduction in BP, which must be Diseases of the lungs can cause right heart disease and
monitored. Prolonged use can cause thiocyanate toxicity. subsequent right heart failure—a condition referred to
as cor pulmonale. In 84% of cases, the hypertrophy of
ACE Inhibitors and Angiotensin Receptor Blocker. the right ventricle associated with this condition is
ACE inhibitors and angiotensin receptor blockers caused by chronic obstructive lung disease (COLD).
(ARBs) reduce afterload, increase cardiac output, and Other causes are:
lower BP. They are given orally and are usually reserved
for the outpatient setting and the general hospital • Interstitial lung disease.
setting. Better drugs can be used in the acute setting. • Thoracic cage deformity.
However, after an acute episode, these drugs need to be • Obstructive sleep apnea.
given when the patient is discharged to the nonacute • Neuromuscular diseases.
setting, either in the hospital or home. • Obesity hypoventilation syndrome.
• Pulmonary fibrosis associated with a number of
Morphine Sulfate. Morphine sulfate has been used systemic diseases, the most common of which
for many years in the treatment of acute pulmonary are the collagen vascular diseases.
edema. It reduces preload to some degree, but its Separate consideration should be reserved for the
main effect is to reduce the anxiety and rapid shallow syndromes of idiopathic (primary) pulmonary hyper-
breathing associated with the syndrome. Its main tension and recurrent pulmonary embolism. Acute
problems are oversedation, decreased cardiac output, massive pulmonary embolism is often a lethal cause
and respiratory depression, often leading to intubation of acute cor pulmonale.
and ICU admission.
Dopamine and Dobutamine. Dopamine and dobuta- OBSTRUCTIVE LUNG DISEASES

mine are both useful adrenergic agents in the treatment The common denominator in the development of
of acute pulmonary edema and cardiac failure. pulmonary hypertension in the obstructive lung
The effects of dopamine are dose dependant, and it diseases (emphysema, chronic bronchitis, and
is given by continuous intravenous infusion. In low chronic asthma) is chronic hypoxemia. This leads to
doses, the drug increases renal blood flow and hence endothelial proliferation and vasoconstriction in the
urinary output. Higher doses increase cardiac contrac- pulmonary arterial bed. The toxic effects of cigarette
tility and cardiac output. Very high doses have an alpha smoke (vasoconstriction and oxidation) are the
adrenergic effect, cause vasoconstriction, and increase primary, but not the only, causes of the pathological
blood pressure. Higher doses are arrhythmogenic and evolution of these changes.6 Over time, the changes
should be used with caution. become permanent, leading to so-called fixed pulmo-
Dobutamine is a beta-1-receptor agonist and to nary hypertension. Ultimately, right heart failure
some degree has beta 2 activity. It has significant follows.7
CASE STUDY 12-1

A 75-year-old man presented to the emergency White blood cell count was normal without a left
room with the chief complaint of shortness of shift, and he was not anemic. Cardiac markers were
breath, which had become progressive over the past normal.
4 days. He had additional complaints of cough and Initial treatment consisted of oxygen, third-
fever up to 102ºF and was producing gray-green generation cephalosporins, and doxycycline.
sputum. On the day of admission, he produced After arriving to the floor, the nurse noted that
sputum mixed with blood. Upon questioning, he he desaturated to 88% on 4 L nasal oxygen and
admitted to being short of breath for a considerable improved to only 94% with 5 L nasal O2 and deep
amount of time prior to this present illness. He had breathing. He had persistent, blood-tinged sputum.
been able to walk to the light pole on the street A standard two-view PA and lateral chest showed
without dyspnea. He also complained of sharp right only right-sided atelectasis and a small pleural
supraclavicular pain, which was worse with respira- effusion. Subsequent CT angiogram (CTA) of the
tion and associated with precordial chest heaviness. chest showed multiple filling defects bilaterally in
The patient had a known elevated right hemidia- the pulmonary arterial system. He was subsequently
phragm, which was presumed to be from a para- anticoagulated with intravenous heparin, which was
lyzed phrenic nerve. later switched to low-molecular-weight heparin
His past history included treatment for hyper- subcutaneously. A 2-D echocardiogram showed
tension, left knee arthroplasty, and colonoscopy elevated right-sided pressures (estimated) but no
with removal of benign polyps. A prostatectomy was other abnormalities of significance.
done 6 years prior to admission for adenocarci- On the second hospital day, the patient devel-
noma. When he developed recurrence the year prior oped acute respiratory distress while moving from
to admission, he underwent a course of radiation his bed to the chair. Oxygen saturation at that time
therapy. Following his knee surgery, he developed was 93% on 4 L nasal O2. Breath sounds were
chest pain. Evaluation for ischemic cardiac disease reduced in the lower lobes, and the episode
proved negative, but he was later shown to have resolved with bronchodilator inhalation. Electrocar-
esophageal candidiasis and, when he was given diogram revealed a right bundle branch block.
antifungal agents, the chest pain resolved. X-ray was unchanged.
He never smoked. Over the next few days, the patient showed
System review was negative except for chronic progressive improvement, was switched to warfarin,
constipation and anxiety. and was discharged using oxygen at night to be
followed as an outpatient.
Physical Examination:
He was in moderate respiratory distress on oxygen Outpatient Follow-up Visit:
with a temperature of 102ºF. His BP 137/76, pulse The patient was seen in the outpatient department
102 and regular, respiratory rate of 20 and an O2 12 days after discharge and was found to be
saturation of 86% on room air, which increased adequately anticoagulated. He continued to be
to 92% on 2 LO2 by nasal cannula. There were desaturated at night and thus remained on noctur-
decreased breath sounds at both lung bases, greater nal oxygen. His vital signs were normal, but he
on the right, with a right-sided pleural friction rub continued to be in mild respiratory distress, espe-
over the lateral chest. There were no cardiac cially in the supine position. He had some airway
abnormalities except the tachycardia, and the sounds, but the rest of the physical exam was
remainder of the physical examination was normal. normal. He had no evidence of deep venous throm-
X-ray of the chest showed atelectasis of both bosis. Repeat pulmonary CT angiogram showed
lower lobes and bilateral apical pleural parenchymal persistent filling defects, which had only partially
scarring. He had no pleural effusion or pneumotho- resolved and which appeared to be adherent to
rax. The sputum culture showed no pathogens and the vessel walls.
only normal oropharyngeal flora.
Laboratory data was normal except for mild Assessment:
elevation of the transaminases and bilirubin, an Since his dyspnea can be traced back to the
arterial PO2 of 61 torr and a slightly low PCO2. prostate surgery and radiation, it is likely that at
(continues)
(continued)
least some of the emboli are old, especially since 2. What are the causes of hypoxemia in acute
they failed to resolve after a considerable period of pulmonary embolism?
anticoagulation. The acute illness appeared clini- 3. In this specific case, describe the possible
cally to be an infectious process that precipitated sources of the emboli.
respiratory failure. Some of the clots could have
4. In this case, describe the features that favor
been new, but there was no obvious source. This
embolism and those that favor pneumonia.
patient will likely need prolonged and even lifetime
anticoagulation. 5. In pulmonary embolism, describe the changes
that occur in ventilation and perfusion that
Discussion Questions compensate for the imbalance and restore
1. Describe the changes in ventilation and perfu- effective oxygenation in the days after the
sion that occur acutely in pulmonary embolism. acute event.
Cor pulmonale can often be suspected clinically in some immunogenic. The disease usually has a pro-
patients with chronic lung disease who are shown to tracted course with fibrosis and ultimately the destruc-
be chronically hypoxemic. They often have a history tion of the architecture of the lung and so-called
of repeated episodes of respiratory failure and show honeycombing, a characteristic radiographic finding. At
clinical evidence of diminished air entry, hyperaera- end stage, severe irreversible pulmonary hypertension
tion, cardiac enlargement (by chest X-ray), and results in cor pulmonale and right heart failure. Sudden
peripheral edema. These patients often have very loud death often results from fatal cardiac arrhythmias or
pulmonic second heart tones with a widely split second sudden cardiac collapse with low cardiac output state.
sound, a right ventricular heave, and a tricuspid An acute form of the disease has been described and
regurgitant murmur. Two-dimensional echocardiogra- referred to the as Hamman-Riche syndrome, which is
phy is usually sufficient to establish right ventricular rapidly progressive and fatal; its histopathology is
hypertrophy, but right heart catheterization and indistinguishable from the more protracted form of
measurement of pulmonary artery pressures with the disease.
and without oxygen prove the diagnosis. The wedge The chronic granulomatous diseases of the lung
pressure must be normal to rule out left heart disease, deserve special mention, primarily because the fibrosis
and there must not be evidence of left to right is often patchy and the infiltrates nodular, not linear
shunting, overloading the right heart.8 and diffuse. For example, sarcoidosis is a granuloma-
tous inflammatory process in the lung; the immuno-
logic reaction has gone wild, leading to fibrosis and the
OTHER CAUSES destruction of the lung architecture. The etiology is not
Kyphoscoliosis and other severe deformities of the known, but some cases respond to anti-inflammatory
chest wall lead to underventilation of large portions and immunosupressive therapy.
of one or both lungs with overdistention of other Berylliosis, a granulomatous disease with a known
portions, leading to a large imbalance between ventila- etiology (inhalation of beryllium dust from machined
tion and pulmonary perfusion. Over time, as the metal alloy) causes an immunologic reaction in the
abnormality progresses, chronic hypoxemia ensues, lung with progressive granuloma formation and
resulting in pulmonary hypertension, which ultimately fibrosis, leading to pulmonary hypertension.
becomes fixed and leads to cor pulmonale and right
heart failure. Obstructive Sleep Apnea (OSA) and Obesity
There is a long list of lung diseases (see Chapter 10), Hypoventilation Syndrome (OHS). Obstructive sleep
many of whose etiologies are not known, that cause apnea (OSA) and obesity hypoventilation syndrome
diffuse infiltration of the lung parenchyma. In their (OHS) are considered together because they often
chronic states, these processes, whatever their cause, occur together and because they both result from
result in lung fibrosis and interference with oxygen chronic hypoxemia. The entities are often accompanied
diffusion at the level of the alveolar-capillary mem- by COLD, but not always. Although obesity is universal
brane. An example is idiopathic interstitial fibrosis in OHS, it is not always in OSA. In obesity hypoventila-
(IPF), often called usual interstitial pneumonia (UIP). tion, chronic hypoventilation results in both hypox-
This disease has a number of etiologies; some are emia and hypercarbia and eventual in pulmonary
inhalational, some infectious and inflammatory, and hypertension. In sleep apnea, the patients obstruct
their upper airway during sleep and become apneic. accompanied by inflammatory cells seen in the pulmo-
They oxygen-desaturate during these episodes, develop nary vessel walls as opposed to the pathologic changes
pulmonary as well as systemic hypertension, and in scleroderma. These forms of pulmonary hyperten-
experience chronic sleep deprivation. Over a prolonged sion are usually responsive and largely reversible with
period of time, without intervention, the pulmonary corticosteroid or immunosupressive therapy.
hypertension in both diseases becomes fixed. In the
case of OSA, treatment includes nocturnal continuous
positive airway pressure breathing (CPAP); in OHS, it PULMONARY EMBOLISM
consists of weight reduction, assisted ventilation, and Embolization of the pulmonary vascular bed usually
low-flow oxygen. comes from clots formed in the deep veins of the
femoralpopliteal system in the lower extremities. Stasis
Neuromuscular Diseases. A number of neuromuscular in these veins is the precursor to clot formation. The
diseases, such as muscular dystrophy of the Duchenne’s stasis may be associated with diseased veins, long
variety and amyotrophic lateral sclerosis (Lou Gehrig’s periods of immobility such as occurs in prolonged bed
disease), cause progressive loss of skeletal muscle rest or hospitalization, long bus or plane rides, under-
function including the muscles of respiration. Progres- lying right-sided cardiac failure, or the immobility
sive ventilatory failure occurs, terminally leading to associated with restricting plaster casts applied for
pulmonary hypertension. Additionally, the heart fractures of the lower extremity. In rare instances,
muscle itself may be affected further, adding to the circulating clotting factors, either hereditary or acquired
cardiopulmonary insult. Progression of the pulmonary as a result of a systemic disease, can predispose one to
complications can be delayed by oxygen supplementa- clot as part of a hypercoaguable state. Such is the case
tion, but eventually assisted ventilation is needed to with lupus erythematosus, where proteins C and S are
maintain life. Other diseases, including poliomyelitis, identified with clotting; in these cases, the clotting need
Guillain–Barré syndrome, and myasthenia gravis, have not be restricted to the leg veins. These clots at times
similar consequences in their terminal state. dislodge and travel to the pulmonary arterial bed.
This event leads to wide discrepancies between
ventilation and perfusion with dead space ventilation,
IDIOPATHIC (PRIMARY) PULMONARY intrapulmonary shunting, and overperfusion of the
HYPERTENSION (IPH) remaining lung, producing hypoxemia. Local hypoxemia
This term is reserved for a syndrome that occurs in the lung may lead to bronchospasm and redistribu-
primarily in young women and that is rapidly fatal. The tion of the inspired air.11 If the embolism is not large
disease is thought to be immunologically mediated and occludes less than 50% of the pulmonary vascular
with a primary change in the pulmonary arterioles bed, cardiac output can usually be maintained. If the
themselves. An endothelial proliferation of the vessels obstruction is greater than 50%, circulatory collapse,
is the primary lesion with progressive onion skinning low cardiac output, and a hypotensive state can lead to
of the arteriole and ultimate obliteration of the vessels catastrophic consequences, including arrhythmia and
and progressive pulmonary hypertension.9 IPH is often sudden death. Normally, the percentage of intrapulmo-
accompanied by a number of markers of collagen nary shunt is less than 10%. When the intrapulmonary
vascular diseases, such as antinuclear antibodies, shunt is greater than 30%, resultant hypoxemia does
without findings of the disease itself. Occasionally not improve with supplemental oxygenation because
scleroderma or another collagen vascular disease the shunted blood does not come in contact with the
becomes obvious after pulmonary hypertension is well high oxygen content in the alveoli. PAO2 continues to
established.10 Because of this relationship and similar fall proportionately as the shunt increases.
pathology, the collagen diseases and IPH are often In the diagnosis of pulmonary embolism:
lumped together. • The patient usually complains of a sharp pleu-
ritic pain in the chest with the sudden onset of
dyspnea.
PULMONARY VASCULITIS • Hemoptysis (the coughing up of bloody
Rapidly developing pulmonary hypertension occurs in sputum) may or may not occur.
vasculitis of the pulmonary vessels. This inflammatory • Patients often have a sense of impending doom
process can be part of a connective tissue disease such and are very air hungry.
as lupus erythematosus or rheumatoid arthritis. It can • A pleural rub is often not present.
also be the primary lesion as in Churg-Strauss disease, • Wheezing is occasionally heard.
which is associated with eosinophilia and usually • Tachycardia is almost always present, along with
presents as asthma. Pathologically, these diseases are varying degrees of hypoxemia.
Signs of right-sided cardiac overload and hypertension washed out in one sitting. The radio-labeled albumin
are common if a significant clot load has migrated to was trapped in the pulmonary capillary bed, and the
the pulmonary vascular bed. These signs include: chest was subsequently scanned to determine the
evenness of perfusion. One looked for wedge-shaped,
• Distended neck veins.
pleural-based areas of nonperfusion. A second scan was
• Loud pulmonary component of the second
done for xenon distribution, and the evenness of
sound.
ventilation was determined. The two scans were
• Increased split of S2 and an occasional right-
matched, looking for areas of ventilation that are not
sided third heart sound (gallop).
perfused. It is largely accepted that a normal perfusion
One must search diligently for signs of deep vein excludes a significant pulmonary embolism. However,
thrombosis of the lower extremities, including: the patient with underlying pulmonary disease already
has an existing mismatch of ventilation and perfusion,
• Unilateral calf tenderness and edema. such that the significance of perfusion defects is less
• Varicosities and signs of stasis. certain.
• A positive Homan’s sign (pain in the ipsilateral Until recently, the pulmonary angiogram has been
calf when the calf is flexed passively).12 regarded as the gold standard test to confirm the
Laboratory tests are helpful but not diagnostic. presence of pulmonary embolism. The test required a
pulmonary artery catheterization, rapid injection of
• Low arterial PO2s are the rule. It has been said iodinated dye, and a sophisticated vascular radiology
that, if the arterial PO2 is above 90 torr, a suite. In the presence of pulmonary hypertension,
pulmonary embolism is not present. This cutoff arrhythmias often occur, leading to an occasional
does not exclude many patients because most cardiac arrest. The dye loads were substantial, and
of them have depressed blood oxygen values transient renal insufficiency frequently occurred,
anyway due to underlying cardiac or especially if the patient had preexisting renal disease.
pulmonary disease. Now, with the advent of advanced CT scanners and
• Elevated blood transaminases in the past have digital radiography, dye can be rapidly dripped in a
been used to help confirm pulmonary emboli, peripheral vein, and the patient can be scanned shortly
but they are rarely helpful. after the diagnosis is suspected. The images can be
• Elevated blood fibrin split products and other rapidly transmitted digitally by phone lines or by
markers of clot formation and dissolution are satellite to off-site reading stations, either to distant
not helpful. radiographic reading rooms or to the covering radiolo-
• An electrocardiogram can be helpful if it shows a gist’s home. CT angiography is now accepted as the
mean QRS axis that has shifted to the right and standard of care.13
back to the left again. One may also see EKG In both procedures, iodine hypersensitivity
evidence of right ventricular overload and strain, requires the pretreatment of the patient with corticoste-
right bundle branch block, and various atrial roids, which does not absolutely eliminate the possibil-
tachyarrhythmias, none of which are diagnostic. ity of an allergic reaction.
• Ventilatory function studies, including diffusion The goals of treatment are to maintain oxygenation
capacity, are not useful and should not be done and to prevent further extension of the clot until
in an acute situation. fibrinolysis can occur.
The standard PA and lateral chest X-ray is usually • Oxygen is always given to maintain an O2
normal. If abnormalities exist, they are often subtle. saturation above 90%. In a few cases, ventilatory
Occasionally one sees a small pleural effusion or an support is required.
elevated diaphragm on the side of the pain. A unilat- • Heparin is the anticoagulant of choice to prevent
eral segment of lung with no lung markings and a further clotting while fibrinolysis occurs. The
prominent proximal pulmonary artery on that side most common practice is to give an 8- to
(Westermark’s sign) or a wedge-shaped density with 10-thousand-unit bolus of heparin intravenously
bowing of the fissures and pleural effusion (Hampton’s and follow that with a heparin drip of 1000 units
hump) indicate not only pulmonary embolism, but an hour. The partial thromboplastin time (PTT)
frank infarction of a portion of lung. However, these is usually checked every 4 hours until a stable
are rarely seen. and therapeutic value is achieved.
In the past, ventilation/perfusion lung scans were • Thrombolysis can be enhanced with thrombo-
used to confirm the diagnosis. Albumin tagged with plastin activation (TPA), urokinase, or streptoki-
iodine 131 was infused in the venous system, and nase intravenous thrombolytics. The preferred
radioactive xenon was inhaled, held in the lungs, and drug is TPA because it can be directly injected
into the pulmonary artery and has fewer idiosyn- TABLE 12-2 Clinical risk factors for the
cratic allergic reactions. If thrombolytics are to development of ARDS
be used, the heparin needs to be stopped and
the PTT normalized. Sepsis syndrome
Aspiration of gastric contents
Initially, patients are kept in bed until they are
hemodynamically stable and there is no residual Drug overdose
evidence of deep venous thrombosis. They can then be Near drowning
ambulated and the anticoagulation changed to an oral Pulmonary contusion
agent (warfarin). Minimum treatment is 6 weeks, but
Multiple transfusions
persistent venous thrombosis or severe stasis may
require longer anticoagulation. Multiple major fractures
Surgical intervention with thrombectomy is a Head trauma
last-resort measure reserved for patients with massive Hudson LD, Millierg JA, Anardi D, et al. 1995. Clinical risks for the
clotting and cardiovascular collapse in a low cardiac development of the acute respiratory distress syndrome. Am. J. Respir. Crit.
Care Med. 151:298–301.
output state. In these instances, BP and adequate
oxygenation cannot be maintained. This operation
requires putting the patient on cardiac and pulmonary
bypass therapy and manually extracting the clot RISK FACTORS
from the pulmonary artery. Rarely successful, the Many risk factors are commonly associated with ALI/
procedure is statistically not as good as early use ARDS. Hudson and coworkers, who studied 695 ICU
of thrombolytic. patients with a predisposing risk for ARDS (acute
respiratory distress syndrome), reported that one
out of four patients developed the syndrome.14 Patients
Noncardiogenic Pulmonary with sepsis syndrome and patients who had received
multiple blood transfusions were the most common
Edema: Acute Lung Injury groups that developed ALI/ARDS. Garber and cowork-
Acute lung injury (ALI) was first described in the 1960s ers found in a retrospective study of multiple research
during the war in Vietnam, and it was then called publications that the risks for ALI/ARDS with the
DaNang Lung. Exsanguinated battlefield casualties strongest supporting evidence for a cause-and-effect
facing delayed transfusion were often supported in the relationship were sepsis, aspiration, trauma, and
field with plasma to maintain blood pressure and multiple transfusions. The weakest connection of cause
transported rapidly by helicopter to hospitals where and effect for developing ALI/ARDS was disseminated
they were resuscitated and stabilized. After reperfusion, intravascular coagulation.15
a progressive hypoxemia developed, requiring increas-
ing inspired concentrations of oxygen. Ultimately
many of these patients required mechanical ventilation DIAGNOSIS OF ALI/ARDS
to maintain oxygenation, and even then the oxygen In 1994 an American-European Consensus Conference
requirements increased relentlessly. The clinical picture established clinical criteria for the diagnosis of ARDS.
was one of hemorrhagic atelectasis with stiff, low- The criteria include five basic categories:
volume lungs that were difficult to ventilate. It was later
• Sudden clinical onset.
learned that, in addition to the acute exsanguination/
• A demonstrated risk factor for ALI/ARDS.
reperfusion injury, type 2 alveolar cell proliferation
• Poor gas exchange measures (e.g., PAO2/FIO2
caused by the toxic effects of high inspired oxygen
ratio of 200 regardless of PEEP level).
concentrations increased the barrier to oxygen diffu-
• Diffuse bilateral infiltrates on frontal chest X-ray.
sion at the alveolar capillary membrane. This created a
• A pulmonary capillary wedge pressure of 18
vicious cycle of increasing respiratory failure and death.
mm Hg.
In the intervening years, it has been learned that
the primary injury is to the alveolar-capillary interface; Conditions that mimic ALI/ARDS are pneumonia,
alveolar leaks permit the exudation of blood and acute pulmonary embolism, pulmonary edema second-
plasma and the flooding of the alveolar space. Further, ary to cardiac disease, and acute exacerbation of
there are many other predisposing conditions of this chronic lung disease. These conditions must be ruled
syndrome unrelated to exsanguination injury (see out before making the diagnosis of ALI.16
Table 12-2). These conditions all have in common Although the routine chest X-ray is not reliable for
acute injury to the alveolar-capillary interface with telling whether the pulmonary edema is secondary to
hemorrhagic atelectasis. ALI/ARDS or to cardiac origin, the chest radiograph is
Spotlight
On
ARDS
A National Institute of Health (NIH) research study optimal PEEP is the pressure associated with
entitled ARDSnet Protocol vs. Open Lung Approach the best oxygenation or compliance during
in ARDS is trying to determine whether the addition the decremental trial.
of a decremental PEEP trial after a recruitment • Then performing the recruitment maneuver
maneuver improves patient outcomes during low again and setting the PEEP 2 cm H2O above
tidal volume ventilation. the optimal PEEP identified in the decremen-
The recruitment maneuver involves: tal PEEP trial.
• Change FIO2 to the lowest level that main-
• Sedating the patient,
tains PO2 in the target range.
• Preoxygenating the patient for 5–10 minutes
and ventilating via pressure or volume venti- The study started in January 2007 and is expected
lation with small VT (4–6 mL/kg). to conclude in March 2013. Visit the ARDSnet
• Increasing the PEEP to 30 cm H2O for Web site (http://www.ardsnet.org/) for additional
30–40 seconds. information and updates (ARDSnet Protocol vs.
• Lowering the PEEP by 2 cm H2O every Open Lung Approach in ARDS. available at http://
5–20 minutes while oxygenation (SPO2) or clinicaltrials.gov/ct2/show/NCT00431158).
compliance is monitored (SPO2 increases
as PEEP decreases, and then decreases or Kacmarek RM, Kallet RH. Should recruitment maneuvers be used in
plateaus as PEEP is further decreased). The the management of ALI and ARDS? Resp Care. 2007;52,5:622–635.
one of the primary methods used to support the mechanism of pulmonary edema. The pulmonary
diagnosis of ARDS.16 An additional complicating factor capillary wedge pressure (PCWP) is less than 18 mm
of using the chest X-ray as a diagnostic tool for ALI/ Hg in the patient with ALI/ARDS, except in patients
ARDS is that the X-rays may vary with different mecha- with underlying cardiac disease. This type of pulmo-
nisms of injury (e.g., direct or indirect injury). The nary edema is known as noncardiogenic pulmonary
chest X-ray differences are described as diffuse, bilateral edema or increased permeability edema (Table 12-3).
pulmonary infiltrates with greater density in the In the patient with pulmonary edema secondary to
dependent areas of the lung. The infiltrates predomi- cardiac disease, the PCWP is more than 18 mm Hg.
nately involve the peripheral lung areas. An air-bron- This edema is called cardiogenic pulmonary edema or
chogram may be visible, and the heart size is usually hydrostatic pulmonary edema.16
normal. Laboratory analysis of edema fluid that is extracted
Hemodynamic changes using the pulmonary artery from the respiratory tract and that reveals an edema/
flow-directed catheter are helpful in differentiating the plasma ratio (protein levels) greater than 0.7 indicates
TABLE 12-3 Clinical features of noncardiogenic pulmonary edema (ALI/ARDS)

and cardiogenic pulmonary edema
Feature Noncardiogenic Pulmonary Edema Cardiogenic Pulmonary Edema
Occurance of hypoxemia Early Late
Radiographic findings Bilateral infiltrates on frontal x-ray, Patchy, hilar and basilar, with
without Kerley B lines Kerley B lines
Pulmonary capillary wedge 18 mm Hg or no clinical evidence 18 mm Hg
pressure of left atrial hypertension
Ratio of total protein of edema 0.7 0.5
fluid to total protein of plasma
Common clinical risk factors Sepsis, trauma, multiple transfusions, Coronary artery disease, acute myocar-
pneumonia dial infarction, congestive heart failure
ARDS or noncardiogenic pulmonary edema. Protein cardiac output directly or use variations in the mixed
levels less than 0.5 are indicative of hydrostatic or venous PO2 to adjust the PEEP pressures up or down to
cardiogenic pulmonary edema. In ALI/ARDS, the achieve normal FRC and optimal oxygen delivery.
protein concentration of the alveolar edema fluid is Another way to determine optimal PEEP is to create a
similar to that of plasma because the mechanism of no-flow condition with the ventilator. Then, with the
pulmonary edema in ARDS is increased capillary ratio of volume and pressure, determine “ventilator”
permeability caused by capillary endothelial injury. The static compliance. When resting lung volume is
alveolar capillary membrane is severely injured and increased toward normal FRC, the compliance
allows free seepage of inflammatory cells, capillary increases. When optimal ventilating lung volume is
plasma, and red blood cells into the alveolar space.16 exceeded, compliance drops off, and the PEEP should
be reduced.
Patients with acute lung injury are critically ill and
CLINICAL PRESENTATION OF ALI/ARDS need to be treated in an ICU setting. They are likely to
be on ventilators and need extensive cardiac and
The clinical appearance of ALI/ARDS is time related. respiratory monitoring. Fluid and blood products are
The early signs and symptoms occur within hours of given to maintain BP and intravascular volume, being
the causative event. The inciting clinical cause may mindful of the fact that overtransfusion or giving excess
result in one or more of the following early clinical fluids can make pulmonary edema worse. Diuretics are
manifestations of ARDS.16 often given if the patient is not hypotensive. Vasopres-
• Tachypnea out of proportion to the blood gas sors to maintain blood pressure are often needed. The
changes underlying cause of the illness must be determined and
• Progressive hypoxemia treated promptly, whether it is shock, an undrained
• Few early radiological changes abdominal abscess, or unrecognized ruptured viscus.
• Decreasing vital capacity Note: The use of corticosteroids in this syndrome
for their anti-inflammatory effect is controversial in
In the ensuing 24–48 hours, the chest X-ray begins to recent years and has been largely discounted.
reveal diffuse infiltrates, and the patient is increasingly
dyspneic. Arterial oxygenation continues to decrease
and is no longer responsive (is refractory) to increasing
FIO2. A low ventilation/perfusion ratio (shunt effect) Summary
and atelectasis are the primary causes of oxygenation Pulmonary edema is a condition caused by excess fluid
problems. The patient’s deteriorating lung function in the lungs. This fluid collects in the interstitial spaces
results in acute oxygenation failure and eventual and may enter the alveolar space, interfering with
ventilatory failure, both of which require mechanical ventilation and gas exchange. In most cases, cardiac
ventilation. problems cause pulmonary edema. Fluid can accumu-
The earlier this syndrome can be recognized, the late for other reasons, including pneumonia, exposure
earlier treatment can be started and the better the to certain toxins and medications, exercising, or living
outcome will be. The goal is to oxygenate the patient at high elevations and malnutrition. Treatment for
without causing further injury to the lung from oxygen pulmonary edema varies depending on the cause
toxicity and to allow the lung to heal. Early measures but generally includes supplemental oxygen and
to more effectively ventilate a stiff low volume lung medications.
with loss of functional residual capacity (FRC) is to use Cardiogenic pulmonary edema—also known as
positive airway pressure throughout the respiratory congestive heart failure—occurs when the diseased or
cycle (PEEP or CPAP), thus enhancing the recruitment overworked left ventricle can not effectively pump out
of alveoli, decreasing compliance, and increasing FRC. the blood it receives from your lungs. As a result,
As oxygenation improves, the FIO2 can be gradually pressure increases inside the left atrium and then in the
lowered to 40% to preclude further injury. High pulmonary veins and capillaries, causing fluid to be
inflation pressures and high PEEP pressures are associ- pushed through the capillary walls into the interstitial
ated with barotrauma to the lung, resulting in pneu- spaces and alveoli.
mothorax, pneumomediastinum, and increased If not treated, pulmonary edema can raise pressure
sensitivity to the toxic effects of oxygen. in the pulmonary artery, and eventually the right
To determine the optimal—or “best”—PEEP, the ventricle will begin to fail. The increased pressure backs
clinician makes use of the fact that cardiac output is up into the right atrium and then into various parts of
optimal at FRC and lower at extremes of lung volume. your body. When not treated, acute pulmonary edema
Most patients in this degree of respiratory failure have can be fatal. In some instances it may be fatal even if
pulmonary artery catheters, so one can monitor the you receive treatment. Oxygen administration is the
first step in the treatment for pulmonary edema. It may d. prolonged hospitalization with coma.
be necessary to assist ventilation mechanically. e. fracture of the tibia with prolonged immobili-
Diseases of the lung can cause right heart disease zation in a plaster cast.
and subsequently right heart failure (cor pulmonale). 2. What is the cause of hypoxemia in acute pulmo-
Although other conditions can cause hypertrophy of nary embolism?
the right ventricle associated with cor pulmonale, very a. alveolar-capillary block
often it is caused by chronic obstructive pulmonary b. interstitial edema
disease. c. dead space ventilation
Embolization of the pulmonary vasculature is d. L-sided heart failure
generally the result of blood clots (thrombi) in the e. lymphatic engorgement
lower extremities. When emboli form in the lungs, they
3. Typical vital signs and lab values for a patient with
block venous circulation to distal alveoli, resulting in
acute pulmonary embolism are:
dead space ventilation. Obstruction of the pulmonary
a. T 102F, BP 150/95, P 120, RR 12, PO2 95,
vascular bed greater than 50% can be catastrophic. The
PCO2 34, and pH 7.50.
goals of treatment for pulmonary embolism are to
b. T 99.2F, BP 105/70, P 120, RR 20, PO2 72,
maintain oxygenation, and prevent new thrombus
PCO2 34, and pH 7.50.
formation and further extension of the embolus until
c. T 102F, BP 150/95, P 78, RR 12, PO2 95,
fibrinolysis can occur.
PCO2 55, and pH 7.34.
In ARDS, structural changes occur: alveolar and
d. T 99.2F, BP 105/70, P 78, RR 12, PO2 95,
interstitial edema, alveolar consolidation, loss of pulmo-
PCO2 40, and pH 7.40.
nary surfactant, and atelectasis. The general management
e. T 98.6F, BP 120/80, P 78, RR 20, PO2 105,
of ARDS requires modalities such as oxygen therapy,
PCO2 55, and ph 7.50.
mechanical ventilation using a lung protective strategy
and techniques to reinflate collapsed alveoli. 4. In acute pulmonary embolism, the most common
finding on a chest X-ray is:
a. normal chest X-ray
b. Westermark’s sign
Study Questions c. large pleural effusion
d. Hampton’s Hump
REVIEW QUESTIONS
e. enlarged heart
1. List the differences between hemodynamic pulmo- 5. Findings in acute pulmonary embolism include all
nary edema and edema associated with acute lung of the following except:
injury. a. hypoxemia.
2. Name several mechanisms by which patients b. pleural friction rub.
develop pulmonary hypertension. c. cough and sputum production.
3. Describe the pathophysiology of the various forms d. pleuritic chest pain and dyspnea.
of pulmonary edema. e. hemoptysis.
4. Explain the various ventilation/perfusion imbal- 6. Direct causes of ARDS include:
ances associated with acute pulmonary embolism a. sepsis.
and the mechanism of restoring balance as the clot b. hemorrhagic shock.
dissipates and blood flow is restored. c. pancreatitis.
d. pulmonary contusion.
5. Discuss the hypoxemia that occurs by means of many
different mechanisms in heart and lung disease. 7. The primary mechanism of hypoxemia in the
patient with ARDS is:
a. hypoventilation.
MULTIPLE-CHOICE QUESTIONS b. dead space ventilation.
c. intrapulmonary shunting.
1. Causes of deep venous thrombosis include all of
d. histotoxic hypoxia.
the following except:
a. a long bus ride across the United States from 8. The first recognition of ARDS appeared in patients
New York to San Francisco. with:
b. pelvic malignancy with spreading to the a. hemorrhagic shock.
posterior pelvic wall. b. overwhelming infection.
c. prolonged use of excessive amounts of the drug c. viral pneumonia.
Viagra. d. chest trauma.
9. What are edema fluid differences between cardio- prospective trial of bilevel versus continuous
genic and noncardiogenic pulmonary edema? positive airway pressure in acute pulmonary
a. the presence of neutrophils in the cardiogenic edema. Crit Care Med. 1997;25,4:620–628.
edema fluid and eosinophils in the noncardio- 6. Peinado VI, Pizarro S, Barbera JA. Pulmonary
genic edema vascular involvement in COPD. Chest.
b. the presence of more protein in the edema fluid 2008;134,4:808–814.
from patients with noncardiogenic edema 7. Vizza CD, Lynch JP, Ochoa LL, Richardson G,
c. the presence of blood in the edema fluid from Trulock EP. Right and left ventricular dysfunction
patients with cardiogenic pulmonary edema in patients with severe pulmonary disease. Chest.
d. no difference in the fluid characteristics 1998;113,3:576–583.
between the two types of pulmonary edema 8. Weitzenblum E. Chronic cor pulmonale. Heart.
10. What are primary causes of cor pulmonale? 2003;89,2:225–230.
a. left heart failure 9. McGoon M, Gutterman D, Steen V, Barst R, McCrory
b. primary pulmonary hypertension DC, Fortin TA, et al. Screening, early detection, and
c. chronic lung diseases diagnosis of pulmonary arterial hypertension: ACCP
d. autoimmune diseases evidence-based clinical practice guidelines. Chest
Supp. 2004;126,1:14S–34S.
CRITICAL-THINKING QUESTIONS 10. Kawut SM, Taichman DB, Archer-Chicko CL,
Palevsky HI, Kimmel SE. Hemodynamics and
1. How does ARDS result in decreased lung survival in patients with pulmonary arterial
compliance? hypertension related to systemic sclerosis. Chest.
2. What is the mechanism for the development of 2003;123,2:344–350.
pulmonary edema concomitant with malnutrition? 11. Elliott CG, Pulmonary physiology during
3. What is the mechanism for the pulmonary edema pulmonary embolism. Chest. Supp.
that might result from mitral valve stenosis? 1992;101,4:163S–171S.
12. Fedullo PF, Tapson VF. Clinical practice. The
evaluation of suspected pulmonary embolism.
References N Engl J Med. 2003;349,13:1247–1256.
1. Fishman A.P. Pulmonary edema. The water- 13. Weiss CR, Scatarige JC, Diette GB, Haponik EF,
exchanging function of the lung. Circulation. Merriman B, Fishman EK. CT pulmonary
1972;46,2:390–408. angiography is the first-line imaging test for acute
2. Nunn JF, Aaron S. Nunn’s Applied Respiratory pulmonary embolism: a survey of US clinicians.
Physiology (Fourth Edition). Critical Care Med. Acad Radial. 2006;13,4:434–446.
1995;23,10:1794. 14. Hudson L, Milberg J, Canard D, Maunder R.
3. Parmley WW. Pathophysiology and current therapy Clinical risks for development of the acute
of congestive heart failure. J Am Coll Cardiol. 1989. respiratory distress syndrome. Am Review Respir
13,4:771–785. Crit Care Med. 1995;151:293–301.
4. Connors Jr AF, Speroff T, Dawson NV, Thomas C, 15. Garber BG, Hebert PC, Yelled J.-D, Hotter RV.
Harrell Jr FE, Wagner D, et al. The effectiveness of Adult respiratory distress syndrome: a systematic
right heart catheterization in the initial care of overview of incidence and risk factors. Crit Care
critically ill patients. SUPPORT Investigators. Med. 1996;24,4:687–695.
JAMA, 1996;276,11:889–897. 16. Marino PL. Acute respiratory distress syndrome,
5. Mehta S, Jay GD, Woolard RH, Hipona RA, 3rd edition. In: The ICU Book. Philadelphia:
Connolly EM, Cimini DM, et al. Randomized, Lippincott Williams and Wilkins; 2007:419–435.
SECTION III
Essential Diagnostics
CHAPTER 13
Comprehensive History, Assessment,

and Documentation
William F. Clark
OBJECTIVES
• Recognize the need for clear and complete understanding during a patient interview.
• Describe the general guidelines and techniques for interviewing a patient.
• Describe the basic structure and parts of a complete history of an adult patient.
• Recognize the differences between an adult history and a pediatric history.
• Perform a clinical evaluation of an adult patient.
• Perform inspection, palpation, percussion, and auscultation on an adult patient.
• Perform the collection of vital signs on an adult patient.
• Recognize the need for confidentiality when dealing with patient data.
• Document a history and physical of an adult patient using the problem-oriented medical record technique.
CHAPTER OUTLINE
Patient History: The Interview Documentation and the Medical Record
General Guidelines for Interviewing Confidentiality
Basic Interviewing Techniques Legibility
Structure of the Interview Computerized Medical Records
The Comprehensive History Problem-Oriented Medical Record
Patient Behavior During the Interview Pathways
Assessment Care Plans or Protocols
Physical Examination Techniques Legal Requirements
Physical Examination of the Adult
301
302 SECTION III ■ Essential Diagnostics
KEY TERMS
active listening lordosis scoliosis
adventitious breath sounds murmur SOAP
auscultation palpation social space
bradycardia pectus carinatum source-oriented charting
bradypnea pectus excavatum method
central cyanosis percussion sphygmomanometer
fremitus peripheral cyanosis tachycardia
gallop rhythm personal space tachypnea
inspection physical examination voice sounds
intimate space problem-oriented medical
kyphoscoliosis record (POMR)
kyphosis pulse pressure
F
or many years, respiratory therapists have been health care provider must also respond to the patient’s
the acknowledged experts in cardiopulmonary emotions and develop rapport. Illness arouses different
care. They are taught to perform a thorough, emotions in patients. How the health care provider
focused pulmonary history and physical. responds to these emotions determines the type of
Through the use of clinical simulations, the profession rapport established with the patient and family.
has increased its effectiveness in the area of focused Without good rapport and trust, the health care
cardiopulmonary care. Health care is changing, how- provider cannot hope to elicit accurate information.
ever, and the profession must change with it. Respira- Finally, the health care provider must also use this time
tory therapists of the future must be able to address the to provide patient education and motivation. As the
patient as a whole, not just the patient’s pulmonary patient and the family understand the illness better,
status. they have greater motivation to adhere to the medical
As health care changes, the need for respiratory plan developed for the patient.1
therapists to be multicompetent is more important
than ever. One such competency is the ability to
perform an extensive history and physical on a patient. GENERAL GUIDELINES FOR INTERVIEWING
The American Association for Respiratory Care (AARC) Many factors affect the interview process, some of
offers a course on physical assessment. As more and which are impossible to control. Internal factors such
more practitioners start working in alternative sites and as previous experiences, attitudes, values, cultural
become case managers for health care organizations, heritage, religious beliefs, self-concept, listening habits,
the ability to perform a complete history and physical preoccupations, and the feelings of both the inter-
becomes even more vital to their success in alternate viewer and the patient are impossible to control.
site positions. However, many factors are controllable. Thus, the
interview environment is important.
The correct use of space helps establish rapport
Patient History: The Interview with the patient. Introduce yourself, making sure the
A complete patient history, an extremely important but patient can hear and see you. Move toward the patient
underused procedure, is as important as any lab test or until the patient recognizes you, usually when the
diagnostic procedure in determining a patient’s health distance between you is 4–12 feet, also known as
status. Asking the correct questions in a manner social space. The social space is where initial rapport
designed to collect the appropriate information ensures with the patient is established and where general,
that the subsequent laboratory tests and diagnostic nonpersonal questions can be asked. Once the initial
procedures confirm a suspected diagnosis instead of rapport has been established, the health care provider
uncovering a new condition. may enter the personal space, but only after receiving
The health care provider must be able to elicit the patient’s verbal or nonverbal consent. As shown in
enough information from a patient to understand the Figure 13-1, in the personal space (11/2–4 feet), the
problem. Although gathering data efficiently is neces- health care provider is close enough to ask questions
sary, a good interview takes time and effort. The without being overheard by others in the room. The
CHAPTER 13 ■ Comprehensive History, Assessment, and Documentation 303
CASE STUDY 13-1

William Smith is a 35-year-old male who has
come to the clinic and who has been waiting for
over 2 hours. Mr. Smith is finally called into a
treatment room, and the practitioner enters to
start the history and physical. As the practitioner
enters the room, she observes an anxious Cauca-
sian male sitting on a chair. The patient looks up
as the practitioner approaches. (Note: Mr. Smith
will be the patient throughout most of the
chapter. For simplicity and clarity, the patient
in the text will be assumed to be male, the
FIGURE 13-1 The patient interview. practitioner female.)
Questions
final area, intimate space (less than 11/2 feet), is where
1. How far away should the practitioner be
the actual physical examination is performed.2 It
when she makes her initial introduction?
should be noted that personal and intimate space is
greatly influenced by culture and ethnicity. The 2. When can the practitioner move into the
patient’s privacy should be honored at all times. room and enter the personal space?
In addition to space, other environmental factors 3. What should the practitioner do to make the
influence the interview. Room lighting, noise, and environment more comfortable for the
temperature can be controlled to provide the best patient?
interview conditions. The room should be well lit so
that the health care provider and the patient can see
each another clearly. All extraneous noise should be
kept to a minimum to allow for complete attention.
Keep interruptions to a minimum to allow for the free Questioning a patient can be stressful to both the
flow of information and to prevent having to repeat practitioner and the patient. To put the patient at ease
information. and to help reduce the stress felt during the interview,
Another key factor is communication style. Verbal the practitioner should be careful how the questions
barriers, such as the use of jargon, should be kept to a are asked. The tone of voice can speak volumes, even
minimum. The interviewer should also choose words for a simple response such as “oh.” Practice asking all
and voice tone that minimizes patient anxiety, stress, questions and making statements in a neutral tone so
and fear. Likewise, the interviewer should use appropri- as not to offend, scare, or anger the patient. Volume is
ate nonverbal communication such as body move- closely related to tone. Because volume can send subtle
ment, facial expressions, and dress to ease the messages, the practitioner should practice speaking at a
communication pathway. Finally, the interviewer level that the patient can hear but that does not convey
should always act professionally and show warmth and a personal judgment or opinion.3
interest during the interview process. Every interview should begin with open-ended
questions, which need more than a yes or no or other-
wise limited response. A typical open-ended question
BASIC INTERVIEWING TECHNIQUES is, “What brought you into the hospital?” To be less
Interviewing is not a science but an art that must be threatening to the patient, open-ended questions can
practiced and developed over time. The bulk of the be reworded as indirect statements that elicit informa-
interview consists of asking questions to elicit information but do not make the patient feel as if he or she is
tion. The kinds of questions asked, how those ques- being questioned. Direct questions can be used to focus
tions are framed, and proper probing for information the patient; these guide the patient to give more
all make the interview a success. Just as vital as the information in the areas of interest to the interviewer.
questions asked are active listening skills, which are To pinpoint a specific item, the interviewer should use
verbal and nonverbal techniques to indicate interest closed questions, that is, questions that can be answered
and comprehension. During the interview, the inter- with a simple yes or no. When asking probing closed
viewer should observe the manner of the patient and questions always keep in mind the four Ws and the
how the patient reacts to different questions. one H: what, when, where, why, and how. Table 13-1
TABLE 13-1 Verbal interviewing techniques

Skill Reason for Use Example
Open-ended questioning Starts flow of information What brought you into the hospital?
Direct questioning Guides patient to area of interest to interviewer What kind of pain are you experiencing?
Closed questioning Usually a yes or no question addressing a Do you have asthma?
specific area
Indirect questioning Between an open-ended and a direct question; Tell me about your problems.
usually less threatening to patient
Facilitating Helps keep the patient talking during open- Phrases such as “Yes” or “Go on” or
ended questioning repeating the last words said by the patient.
Checking or restating Checks the accuracy of information received Let me see if I understand you correctly.
You said . . .
Surveying Ensures that there is nothing else wrong What else is bothering you?
Clarifying Checks your understanding of ambiguous words What do you mean by the words a cold?
Summarizing A short summary of what the practitioner heard You said you have had a fever for 4 days
and been coughing up yellow sputum.
Empathizing Indicates you care about the patient’s problems; “That must have been difficult for you,” or,
can be used as a bridge to another type of “I can only imagine how that must have
question felt.”
Interpreting Keeps the focus of the interview on the patient Patient: “Before I was sick, I could help
while elaborating on patient’s statements (The other people. Now I just sit around and
practitioner should always give the patient do nothing.”
a chance to either confirm or deny the Practitioner: “I understand you to say
interpretation, since the practitioner can only that your illness has limited you. Is it
guess what the patient is feeling.) possible that you are feeling lonely since
you cannot help other people?”
Patient: “You could be right. I miss
being needed.”
Reflecting Communicates that the practitioner observes I can see that you’re upset at the
feeling or emotion from the patient moment.
Legitimizing or validating Communicates acceptance and validation of I understand why you are so upset.
an emotional experience
Supporting Communicates that the practitioner can help Please let me know what I can do to
the patient (must be honest) help you.
Partnering Communicates that the practitioner wants to After we have finished this interview,
promote a partnership in the treatment of maybe we can discuss some solutions
the patient for your problems.
Respecting Communicates that the professional has I am impressed by the way you have
respect for the patient’s problems (similar been able to cope with this problem.
to empathy)
illustrates the different types of verbal techniques that of communications: showing anger, responding to
can be used in an interview to elicit information. emotions inappropriately, giving advice, giving false
No one interviewing method is better than reassurance, moralizing, defending, arguing, or
another; the practitioner should be familiar and belittling. Finally, do not be afraid to use silence.
comfortable with all techniques. Changing tech- Silence is counterproductive when it creates tension
niques in an interview can be a very effective method between the patient and the practitioner, but it
of keeping the patient at ease and maintaining can be used effectively to signal the patient to con-
rapport. Avoid any behavior that can block the flow tinue talking or to elaborate. It also eliminates the
TABLE 13-2 Active listening techniques The powers of observation are also an important
Nonverbal Techniques aspect of an effective interview. During the introduc-
tion, the practitioner should be aware of any nonverbal
Maintaining eye contact as much as possible
messages the patient may be sending. When
Using supportive gestures such as nodding your approached, does the patient look down dejectedly or
head to indicate understanding or leaning forward look up expectantly? Watch for subtle messages sent by
toward the patient the patient that indicate whether rapport is being
Taking notes (if the patient is comfortable with the established. Watch for body movement, facial expres-
note taking) sions, and the tone and manner of answering questions
Listening with an open mind for indications of the patient’s emotional status. The
practitioner’s ability to observe these messages can
Listening to the content rather than the delivery
furnish further meaning to the words of the patient.
Keeping facial expressions neutral or supportive
Verbal Techniques
STRUCTURE OF THE INTERVIEW
Keeping the tone of your statements neutral
The structure of the interview is the agenda the practitio-
Using facilitating statements such as “Go on” or
ner has in conducting it. Nothing is gained by a
“And what else did you feel?”
stream-of-consciousness, free-ranging discussion with
Using checking statements such as “Is this what you no structure or reason; a free-for-all interview confuses
are telling me, . . .” the patient and usually wastes the practitioner’s time.
Paraphrasing the basic message and giving the Each practitioner should form a structure for each
patient a chance to confirm or deny the message interview and develop a checklist so that nothing is
Soliciting the patient’s reactions to your missed. However, the practitioner needs to remember
interpretation not to force the patient to respond. The practitioner
should also not be afraid to stray from the structure if a
Clarifying any vague or incomplete ideas
topic not on the list seems to need discussion.
The Opening. Every interview starts with the opening.

The opening consists of the introduction, establishing
possibility of sending the wrong signals about what
the goals of the interview, obtaining consent for the
the practitioner wants to hear.
interview, establishing the initial rapport, and ensuring
Always end the interview by asking whether the
of the patient’s comfort.
patient wants to discuss or needs anything else. This
Legally, all health care providers must introduce
final surveying of the patient allows for final reflections
themselves to the patient, including their name and
or further information.1,3–6
department. They should call the patient by name and
Just as important as interviewing techniques are
identify the patient as the person to be interviewed.
the listening skills that an interviewer uses to indicate
The introduction should be started when the practitio-
active listening. Table 13-2 lists nonverbal and verbal
ner is in the social space and continue as the practitio-
techniques that indicate that the practitioner is
ner moves into the personal space. Although a
listening.
handshake is usually a good rapport builder, be aware
The practitioner needs to understand what is being
that some cultures frown on touching in this manner.
said and to ascertain the accuracy and validity of the
Next, the practitioner should give the patient a short
information. The listener must be open to all the
explanation of the purpose of the visit, making clear
information being given. Because of past experience,
the interview’s purpose and the practitioner’s expecta-
the listener might fail to hear, being “certain” of what is
tions. Then the practitioner is legally bound to obtain
going to be said. This failure occurs because the
the patient’s consent for the interview. Most patients
interviewer’s frame of mind distorts the meaning of the
want to talk to you, but verbal consent is necessary for
words to fit the personal ideas instead of being open to
the interview to continue. Here is an opening that has
different interpretations. Active listening also requires
all these elements:
the listener’s undivided attention. If there are constant
interruptions or if the senses become overloaded, active Good morning, my name is Jane Simons, and I am
listening cannot take place. The interview must take a Respiratory Therapist from the respiratory care
place in an environment that limits interruptions or department. You are Mr. William Smith? Dr.
sensory overload. Finding such an environment in a Agrwal has asked me to interview you and take
hospital setting is difficult, but care should be taken to your medical history. Would you be willing to talk
limit distractions. to me for a few minutes?
TABLE 13-3 Patient history

CASE STUDY 13-2 Date
It is 7:00 p.m., and the practitioner (Jane Simons) Time

has entered the treatment room and introduced Identifying Data
herself to William Smith. She then establishes Name
initial rapport and moves toward the patient. She Address
closes the curtain to give herself and Mr. Smith Age
some privacy and sits down across from him. She Gender
begins the interview by explaining what she is Marital status
going to do and asks permission to continue. Occupation
Mr. Smith answers that he came here directly Source of history (patient, parent, child, friend, etc.)
from work and is very upset that it took over Chief complaint(s) (presenting problem)
2 hours to get to see anyone. As Jane Simons
prepares her papers and equipment, Mr. Smith History of the Present Illness
sits in the chair fidgeting and muttering. When Symptoms (location, duration, quality, quantity
Ms. Simons begins to ask her first question, or severity, associated aggravating factors and
Mr. Smith stands up and starts to pace back alleviating factors)
and forth in the small room. Negative symptoms
Past Health History
Questions Childhood illnesses and immunizations
1. What active listening skills should Jane Adult illnesses
Simons use to help put Mr. Smith at ease? Obstetric or gynecologic history (if relevant)
2. What verbal interviewing techniques should Psychiatric illnesses
she have used before starting to ask Injuries
questions? Blood transfusions
Surgical history
3. What patient mannerisms should have Hospitalizations
warned the practitioner not to begin
immediately asking questions? Current Health Status
Current medications
4. Does Jane Simons have the right to continue Allergies
with the interview? Tobacco use (type, amount, and duration of use)
Alcohol use
Drug or related substance use
Diet
THE COMPREHENSIVE HISTORY Screening tests (dates and results)
Immunization status (date of each vaccine)
The items of a comprehensive history vary depending
Sleep habits
on the age, sex, and illness of a patient; however, the
Exercise/leisure
practitioner must have an exhaustive checklist avail-
Environmental hazards
able. Time and the goals of the interview dictate how
Safety measures
many of the items are covered and in what detail. A
comprehensive history includes essentially two parts. Family History (note age and health of all living mem-
bers and cause of death of all deceased members)
• The first part is the patient history, described in
Social History
Table 13-3.
Educational level
• The second part (Table 13-4) is a comprehensive
Home environment
review of systems.
Significant others
Pediatric histories are different and are discussed later
in the chapter. clear and put it in chronological order, but the infor-
The history of the present illness and the past health mation must come from the patient. The history of the
history of the patient are documented before the review present illness section should include all of the princi-
of the systems is conducted. The chief complaint pal symptoms, described in detail as to location,
should be directly quoted in the patient’s words when duration, quality, and quantity or severity. It should
possible. When documenting the present illness, the also include any associated factors such as aggravating
practitioner should be sure to make the information factors and alleviating factors. Also included should be
TABLE 13-4 Review of systems

General
Patient’s perception of general state of health at the present, difference from usual state, vitality and energy levels
Psychological
Irritability, nervousness, tension, increased stress, difficulty concentrating, mood changes, suicidal thoughts, depression
Integumentary System
Rashes, itching, changes in skin pigmentation, black and blue marks (ecchymoses), change in color or size of mole,
sores, lumps, change in skin texture, odors, excessive sweating, acne, loss of hair (alopecia), excessive growth of hair
or growth of hair in unusual locations (hirsutism), change in nails, amount of time spent in the sun
Eyes
Blurred vision, change in visual acuity, glasses, contacts, sensitivity to light (photophobia), excessive tearing, night
blindness, double vision (diplopia), drainage, bloodshot eyes, pain, blind spots, flashing lights, halos around objects,
glaucoma, cataracts
Ears
Hearing deficits, hearing aid, pain, discharge, lightheadedness (vertigo), ringing in the ears (tinnitus), earaches, infection
Nose and Sinuses
Frequent colds, discharge, itching, hay fever, postnasal drip, stuffiness, sinus pain, polyps, obstruction, nosebleed
(epistaxis), change in sense of smell
Mouth
Toothache, tooth abscess, dentures, bleeding/swollen gums, difficulty chewing, sore tongue, change in taste, lesions,
change in salivation, bad breath
Throat/Neck
Hoarseness, change in voice, frequent sore throats, difficulty swallowing, pain/stiffness, enlarged thyroid (goiter)
Respiratory System
Shortness of breath (dyspnea), shortness of breath on exertion, phlegm (sputum), cough, sneezing, wheezing, cough-
ing up blood (hemoptysis), frequent upper respiratory tract infections, pneumonia, emphysema, asthma, tuberculosis
Cardiovascular System
Shortness of breath that wakes you up in the night (paroxysmal nocturnal dyspnea), chest pain, heart murmur, pal-
pitations, fainting (syncope), sleep on pillows to breathe better (orthopnea; state number of pillows used), swelling
(edema), cold hands/feet, leg cramps, myocardial infarction, hypertension, valvular disease, pain in calf when walk-
ing (intermittent claudication), varicose veins, inflammation of a vein (thrombophlebitis), blood clot in leg (deep vein
thrombosis), anemia
Breasts
Pain, tenderness, discharge, lumps, change in size, dimpling
Gastrointestinal System
Change in appetite, nausea, vomiting, diarrhea, constipation, change in bowel habits, black tarry stools (melena),
vomiting blood (hematemesis), change in stool color, excessive gas (flatulence), belching, regurgitation, heartburn,
difficulty swallowing (dysphagia), abdominal pain, jaundice, hemorrhoids, hepatitis, peptic ulcers, gallstones
Urinary System
Change in urine color, change in voiding habits, painful urination (dysuria), hesitancy, urgency, frequency, excessive
urination at night (nocturia), increased urine volume (polyuria), dribbling, loss in force of stream, bedwetting, change
in urine volume, incontinence, pain in lower abdomen (suprapubic pain), kidney stones, urinary tract infections
Musculoskeletal System
Joint stiffness, muscle pain, back pain, limitation of movement, redness, swelling, weakness, bony deformity, broken
bones, dislocations, sprains, gout, arthritis, osteoporosis, herniated disc
Neurological System
Headache, change in balance, incoordination, loss of movement, change in sensory perception/feeling in an extremity,
change in speech, change in smell, fainting (syncope), loss of memory, tremors, involuntary movement, loss of con-
sciousness, seizures, weakness, head injury
(continues)
TABLE 13-4 Review of systems (continued)

Female Reproductive System
Vaginal discharge; change in libido; infertility; pain during intercourse; menses: last menstrual period (LMP), age
period started (menarche), regularity, duration, amount of bleeding, prementrual symptoms, intermenstrual bleeding,
painful periods (dysmenorrhea); menopause: age of onset, duration, symptoms, bleeding; obstetric: number of preg-
nancies, number of miscarriages/abortions, number of children, type of delivery, complications, type of birth control,
estrogen therapy
Male Reproductive System
Change in libido, infertility, sterility, impotence, pain during intercourse, age at onset of puberty, testicular pain,
penile discharge, change in erectile function, emissions, hernias, enlarged prostate, type of birth control
Endocrine System
Bulging eyes; fatigue; change in size of head, hands, or feet; weight change; heat/cold intolerances; excessive sweating;
increased thirst; increased hunger; change in body hair distribution; swelling in the anterior neck; diabetes mellitus
any negative symptoms (for example, “no urinary prob- In the social history section, the patient’s home
lems”) that may help in differentiating the diagnosis. environment and significant others are documented.
The past health history should include any child- The review of systems (Table 13-4) should be done
hood and adult illnesses. Childhood illnesses should carefully, starting from the head and working down.
be listed as well as any immunizations for chickenpox, The practitioner should follow the same method every
measles, mumps, and polio. Adult illnesses should time to develop a personalized system. When asking
include medical problems such as high blood pressure, about general health, the practitioner should focus on
diabetes, asthma, chronic bronchitis, emphysema, general changes in the patient’s health, either recently
tuberculosis, and HIV disease. Any surgical and obstet- or in the past. For each system, the practitioner should
ric procedures or history should be documented as well try to use open-ended questions first and then direct
as any accidents or injuries, especially if they resulted questioning, clarifying, and surveying to ensure that all
in transfusions. Hospitalizations and psychiatric illness aspects of the system are reviewed. Finally, the practi-
should also be documented. tioner should summarize to allow the patient to correct
In current health status, the practitioner documents any misunderstandings. Refer to Table 13-4 for a list of
the patient’s current lifestyle: some of the problems that a patient may experience in
each of the systems. The list is by no means complete;
• Current medications being taken and any
it is provided to help the practitioner with areas that
allergies
may need closed questions.
• Use of tobacco, drugs, alcohol, or related
Most respiratory therapists do a focused review of
substances
systems that may not be as complete as the one in
• Diet along with any restrictions
Table 13-4; however, as the practitioners move out of
• Current immunizations such as tetanus, influ-
the hospital into alternative settings, they should be
enza, or hepatitis B
able to do a complete review of the systems if necessary.
• Recent screening tests such as mammograms,
The practitioner should start each system with an
Pap smears, tuberculin tests, or cholesterol tests
• Lifestyle information such as sleep habits,
exercise, environmental hazards, and safety
issues Best Practice
This information is especially vital if there is a possible
exposure to harmful substances. If the patient is Pack-Years History
retired, ask about his or her occupation because some
Cigarette smoking should be documented in
exposures such as asbestos can take many years to
pack-years, that is, the total number of years
affect the body.4
smoking times the highest number of packs ever
In the family history section, the practitioner should
smoked per day. For example, a patient who
document:
has smoked two packs a day for 30 years has
• Any health- or age-related problems of each a 60-pack-year history. If the patient has quit
immediate family member. smoking, document how long ago the patient
• The cause of death of any deceased immediate quit.
family member.
CASE STUDY 13-3

Mr. Smith becomes calmer and sits down in the asthma 3 years ago. Mr. Smith’s father and mother
chair in the treatment room. The practitioner (Jane are both living, and he has no brothers or sisters.
Simons) pulls out the chart that has been started on His father has been diagnosed with coronary artery
Mr. Smith. She sees that the face sheet lists him as disease and had bypass surgery 2 years ago. His
a 35-year-old male factory worker who is at the mother also has some heart problems and suffered
clinic because of occasional chest pain. She starts a heart attack last year. He says that all other family
interviewing Mr. Smith, who gives her the following members are deceased, but he cannot remember
information when asked what has brought him to what they died from.
the clinic. Mr. Smith says he works in a sheet metal
factory and graduated from high school. His hob-
There are times when I find it hard to breathe.
bies include working on classic cars and watching
I also sometimes have a pain in the center of
television.
my chest. It’s not all the time, but it’s been
bothering me for about 2 to 3 weeks and more Questions
lately. I’m having trouble walking up stairs.
1. Does the practitioner record the identifying data
As the practitioner continues the interview, as written on the face sheet or as given by the
Mr. Smith relates that he had allergies when he was patient?
young. He takes only aspirin and cold medicine. He 2. How would the practitioner write the chief
says that he had all the normal childhood diseases complaint?
and had very few medical problems until 3 or 4
3. What kind of interviewing technique would the
months ago. He has had no serious injuries and has
practitioner use to clarify the type of chest pain
had his tonsils removed. He smokes up to two packs
and the shortness of breath?
of cigarettes a day, and he started smoking at
age 15. He drinks socially two to three beers a night 4. What are the principal symptoms the practitio-
and denies any drug or substance abuse. He cannot ner would list for this patient?
remember any immunizations other than the usual 5. How could the practitioner further clarify the
childhood shots, but he had a tetanus shot 3 years symptoms to better understand what is
ago when he cut himself with a knife at work. happening?
Mr. Smith also relates that he has had cold- and 6. What other questions would be appropriate to
flulike symptoms for over 3 months, but the clarify the present illness, the past health
symptoms have been mild and he has not felt the history, the current health status, and the social
need to seek medical attention until now. history?
Mr. Smith says that he lives at home with his
7. How should the practitioner use the information
wife and one child, age 7. The wife seems to be in
about the flulike symptoms for over 3 months
good health, but the boy was diagnosed with
other than recording them in the chart?
open-ended question such as, “Please describe to me The problem with checking and probing is that they
any respiratory problems you may have had.” This is can be stressful to the patient. Likewise, the practitioner
now a open-ended inquiry. Once the flow of informa- must understand that an ill patient may not be able to
tion from this type of question starts to slow down, communicate well and may feel threatened. The
however, the practitioner should also ask about other practitioner must understand the possible perceived
specific ailments to find out whether there is a negative threats (Table 13-5), which can cause stress to a
response or if the patient just forgot to mention them. patient, because even normal responses may be
clouded by them.
A patient’s normal reaction to stress is to lapse into
PATIENT BEHAVIOR DURING THE INTERVIEW denial, regression, suppression, repression, anxiety,
The practitioner must frequently employ checking, as anger, and sadness. These emotions color patients’
described in Table 13-1, to ensure that the information responses to questions and even affect their ability to
is correct. While surveying a list of problems, the answer. The practitioner should keep the influence of
practitioner often has to probe to ensure completeness. stress in mind when conducting an interview.
CASE STUDY 13-4

The practitioner (Jane Simons) continues inter- The chest pain he feels is a pressing type of pain
viewing Mr. Smith with the review of systems. that is near the center of his chest. It does not
When asked how he usually feels, Mr. Smith radiate out to the arm or jaw. He denies any other
states that he usually feels fine but that he has cardiac problems. No gastrointestinal or urinary
felt as if he had the flu for over 3 months. He problems are elicited. He says he eats normally
denies any weight changes, fatigue except when and has been watching his diet since his mother’s
climbing stairs, and fever. He admits that he has heart attack. He admits that he has some coolness
had some weakness in the legs and arms lately. in the fingers at times and weakness of the legs
He admits to getting headaches at work but and arms. All other systems are normal according
denies any other problems with his head. He to the patient’s responses.
states that his eyes and ears are normal but
admits that he has a runny nose quite often and Questions
sometimes blows his nose so forcefully that it 1. What aspects of the review of systems are
bleeds. The patient states that his mouth and important and should be noted in the chart?
neck are normal. He states that his chest is 2. Would it be appropriate to list the negative
normal but admits to coughing up small amounts responses in the chart?
of thick white sputum, especially in the morning.
3. Which system areas need to be emphasized
He relates that he feels short of breath when he
when doing a physical examination?
exercises but not at rest. He says that he some-
times has shortness of breath after eating, but 4. On the basis of the patient’s answers, should
that it is not bad. He does not know if he wheezes the practitioner suspect the problem is respira-
but denies that he has any respiratory problems. tory or cardiac in nature? Why?
TABLE 13-5 Stress of illness

Threats Patient Manifestation of the Threat
Threat to efficiency Illness saps a person’s ability to deal with normal events. Patient must cope with
loss of ability to cope with normal aspects of life and the accompanying loss of
esteem.
Threat of separation Hospitalization induces the fear of being separated from family or loved ones. Even
the most independent person has a basic fear of separation.
Threat of loss of love Many patients fear that illness will make them unattractive or unloved by people
around them.
Threat of loss of bodily function Especially for hospitalized patients, this fear is the greatest. Incontinence makes a
person feel helpless to control even the simplest bodily functions.
Threat of loss of bodily parts This can be either a physical or a psychological reality. Some illnesses result in
physical loss, and some patients fear they will lose use of some of their body parts.
Threat of loss of rationality or Some patients dread the possibility of losing control or the ability to communicate.
cognitive function
Threat of pain Most patients do not want to feel pain or to suffer.
Threat of loss of privacy Most of the usual privacy people enjoy at home is lost in the hospital.
Threat of loss of home Many people find it difficult to sleep or relax in a strange environment. The hospital-
ized patient is forced to live in a strange and unnatural environment.
Threat of loss of independence This is the hardest for many patients. Hospitals force patients to do things by the
hospital’s schedule.
Compiled from Cohen-Cole SA. The Medical Interview: The Three-Function Approach. St. Louis: Mosby-Yearbook; 1991:101–103; and Purtilo R, Haddad A.
Health Professional and Patient Interaction. 5th ed. Philadelphia: W.B. Saunders Co; 1996:119–128.
Patient History of a Child
In addition to the information obtained in an adult Growth and development history
history, the following must be ascertained for a child. Physical growth (actual or approximate weight
and length at birth and beyond; any slow or
Identifying data
fast gains or losses)
Date and place of birth
Developmental milestones
Nickname
Age patient held up head in prone position
First name of parents (and last names,
Age rolled over from front to back and back
if different)
to front
Parents’ occupations and where they can be
Age sat with support and then alone
reached during work hours
Age said first words, combinations of
Chief complaint(s) (making clear whether it is a words, and sentences
patient concern, a parent concern, or both) Age tied own shoes
Age dressed without help
History of the present illness (include thoughts of
Age of tooth growth and loss pattern
family members concerning symptoms)
Growth according to growth chart
Past health history Social development
Birth history (important in first 2 years of life) Sleep
Prenatal history (maternal health and Toileting
substance abuse during pregnancy) Speech
Natal history (nature of labor and delivery) Personality
Neonatal history (any problems at birth and Discipline
gestational age) Schooling
Illnesses (any recent exposures to childhood Sexuality
illnesses)
Family history (age and health of individuals
Feeding history (important in first 2 years of life) who live in the child’s home)
Infancy (method of feeding and problems Source: Adapted from Bickley LS, Hoekelman RA. Bates’ Guide
with or parental concerns about growth) to Physical Examination and History Taking. 7th ed. Philadelphia:
Childhood (eating habits, amount, and types of JB Lippincott Co; 1999:39–42.
food eaten)
Not every patient behaves normally during an legitimizing can usually break the mood enough
interview. The practitioner’s ability to understand for the patient to answer questions. If the
abnormal responses and employing effective coping depression is too deep to penetrate, the patient
strategies can mean the difference between a successful requires psychiatric help.
interview and a trying experience for both the practitio- • A third type of maladaptive patient suffers from
ner and the patient. severe anxiety. This patient is liable to suddenly
• One type of maladaptive patient is the persistently become anxious that he or she has the diseases
angry patient. These patients lash out with every you are listing during a review of systems. He or
response. Sometimes it is helpful to allow angry she can also become severely agitated when
patients to vent their feelings and then to try to questioned. If the practitioner can maintain a
continue. Another coping mechanism is to calm and controlled demeanor during an inter-
legitimize the feeling (Table 13-1). If the anger view with this patient, he or she may respond.
persists, continuing the interview is not advis- However, if his or her mood is intractable,
able; instead, have another person try or seek psychiatric evaluation should be encouraged.
psychiatric help for the patient. Other types of patients that a practitioner may
• A second type of maladaptive patient is the one encounter are those who are compulsive, dependent,
who is in a major depression. Empathizing and histrionic, masochistic, narcissistic, psychotic, delirious,
or demented. Practitioners should be aware of these can provide important opportunities for health educa-
patients and be prepared to deal with them.1 tion, baseline data for future encounters, and opportu-
nities to find minor problems before they become
Barriers to Communication. In addition to major.
emotions and personality disorders, cultural and The physical examination techniques are inspection,
language differences may act as major barriers to palpation, percussion, and auscultation. Seeing, feeling,
communication. Every culture has its own customs and hearing still form the backbone of the complete
and traditions that affect how the patient responds physical examination. The practitioner can use the sense
to questions and touching by the practitioner. of smell. Odors sometimes help the practitioner make
Although learning all the different cultural influences clinical judgments, because distinctive odors provide
is impossible, the practitioner should be well aware clues to the diagnosis of certain conditions.
of varying traditions and watch for verbal and
nonverbal clues as to how the patient is tolerating Inspection. Inspection is the process of observing a
the interview and subsequent physical examination. patient’s outward appearance for positive and nega-
In this area, the family may be able to help the tive signs and symptoms. The practitioner must
respiratory therapist understand their cultural observe as much as possible. Inspection as part of the
practices and their expectations of the health care physical examination starts even before the history is
experience. In some cases, an interpreter may be taken. The patient’s demeanor, which can reveal
needed to ensure that the information gathered is emotional and mental status, can be observed at the
accurate and complete. beginning of the interview during the introduction.
The patient should also be observed during the
Interviewing a Child. A pediatric history is more interview for any changes in demeanor or mental
challenging because it may be coming from the parent status. Likewise, the practitioner should watch for
or guardian rather than from the patient. Whenever changes during the interview, such as shortness of
possible, engage the patient in the process unless the breath, patient posture, and whether the patient must
child is too young to be able to respond. stop talking after a few words or sentences. The
practitioner should inspect each part of the body
Assessment under direct light to reveal any changes, discolor-
ation, or textures. Tangential or indirect light can also
A physical examination is a thorough assessment of a be useful for seeing any lumps, bumps, or distortions
patient for all positive and negative medical condi- of the skin.4,7,8
tions. The physical examination requires keen observa-
tional and analytical skills. The practitioner must be
Palpation. Palpation is using touch to perform a
able to interact with a patient in such a way that he or
physical examination. There are two types of palpation:
she trusts the practitioner. Because the physical usually
follows the history, the rapport built during the history • Shallow, light, or superficial palpation is pressure to
can be used as a vehicle for the physical examination. about 1 cm deep, which is done to feel surface
Along with the history, a complete and comprehensive abnormalities (see Figure 13-2).
physical often leads a practitioner to a diagnosis • Deep palpation is pressure to about 4 cm deep,
without the use of expensive and often invasive clinical which is done to feel abnormalities deep
tests. The clinical tests can then be ordered to confirm beneath the surface and to detect tenderness or
the suspected diagnosis. guarding (see Figure 13-3).
As shown in Figure 13-4, different parts of the hand are
PHYSICAL EXAMINATION TECHNIQUES used for palpation. To palpate abnormalities, whether
A practitioner should follow some general guidelines superficial or deep, the practitioner should use finger-
to make the physical examination as easy and as pads. Therefore, fingernails should be cut short so as
nontraumatic as possible. The physical examination not to injure the patient. To palpate fremitus (vibra-
environment should ensure the patient’s privacy at all tions transmitted through the skin), the practitioner
times. In the hospital, privacy curtains should always can use the fingerpads or the ulnar (front) surface of
be drawn. At other sites, a private, quiet room should the hands. To palpate temperature, the practitioner
be used. The room should be well lit, and the tempera- should use the dorsal (back) surface of the hand.
ture should be comfortable for the patient. The practi- Vocal fremitus is performed to detect changes in the
tioner should schedule enough time to be able to transmission of vibrations through the tracheobron-
complete the exam without interruption. A complete chial tree. Have the patient repeat the number 99
physical does more than reassure a healthy person; it while systematically palpating the chest with the ball
FIGURE 13-2 Light palpation. FIGURE 13-3 Deep palpation.
Fingertip
Finger pad Fingertips
Metacarpo-
phalangeal
joints
(vibration)
Finger pads Ball of

assess: hand
Fine tactile (vibration) Dorsal surface
discrimination Back of
Moisture, Texture hand
Masses, (temperature)
Palmar surface
Pulsations,
Edema,
Crepitation,
Organ size,
shape,
position, mobility
and consistency
Palmar surface Dorsal surface
Ulnar surface
(vibration)
Ulnar surface
FIGURE 13-4 Parts of the hand used in palpation.
or the ulnar surface of the hand and comparing areas capacity as with emphysema. Increased vocal fremitus,
of the chest bilaterally. Vocal fremitus can indicate or increased vibration transmission, can be caused by
areas of pulmonary complications. Decreased vocal pneumonia, atelectasis, consolidation, pulmonary
fremitus, or the lack of vibration transmission, can be edema, and lung masses. Figure 13-5 indicates the
caused by fluid or air in the pleural space, complete pathways to be used to palpate tactile or vocal fremitus
obstruction of the airways, or changes in residual of the chest.
1 1 1
1
2 2 2 2
3 3
4 4 3 3
4 4
A. Anterior thorax
B. Posterior thorax
1 1
2
3
3
C. Right lateral thorax D. Left lateral thorax
FIGURE 13-5 Patterns for vocal or tactile fremitus.
Percussion. Percussion is the process the Proper percussion technique is essential. Perform the
practitioner uses to assess areas of the patient with percussion indirectly by tapping the finger of one hand
gentle tapping to produce vibrations. Percussion while it is resting against the patient’s skin. Figure 13-6
works by sending sound waves to areas 4–6 cm below shows the proper percussion technique, and Figure 13-7
the surface of the skin. The tone or intensity of the shows the proper positioning of the hands for percussion.
percussion note is determined by the density of the Be sure that the passive hand (the one being tapped) is
substance through which the sound waves travel. The placed firmly on the surface to be percussed. Separate
quieter the sound is, the denser is the substance the fingers of the passive hand so that the vibrations
transmitting the vibrations. Air transmits a loud are transmitted to the patient and not dampened by the
sound, whereas tissue transmits a soft sound. The adjoining fingers. Do not move your entire hand when
intensity and quality of the sound also indicate the percussing. Instead, tap by moving only the finger that is
type of substance. Table 13-6 indicates the type of percussing. Use the tip of your finger when percussing,
substance being percussed according to the intensity, not the pad. Perform percussion systematically and
duration, pitch, and quality of the sound using the bilaterally to ascertain any differences from right to left.
following terms for tones: flatness, dullness, Figure 13-8 shows a recommended path for percussion of
resonance, hyper-resonance, and tympany. the chest to determine bilateral differences.
TABLE 13-6 Characteristics of percussion sounds

Normal Abnormal
Sound Intensity Duration Pitch Quality Location Location Density
Flatness Soft Short High Flat Muscle (thigh) Lungs (severe Most dense
or one b pneumonia)
Dullness Moderate Moderate High Thud Organs (liver) Lungs
(atelectasis)
Resonance Loud Moderate Low Hollow Normal lungs No abnormal
to ong l location
Hyperresonance Very loud Long Very low Boom No normal Lungs
location (emphysema)
Tympany Loud Long High Drum Gastric air Lungs (large Least dense
bubble pneumothorax)
(A) (B) (C)
FIGURE 13-6 Percussion technique: (A) Hyperextend the middle finger of the nondominant hand
and press the distal phalanx and joint firmly on the surface to be percussed. (B) Cock the hand
upward, with the middle finger partially flexed and poised to strike. (C) Strike the middle finger of
the nondominant hand with the tip of the middle finger of the dominant hand.
A. Position of hands B. Percussion strike

FIGURE 13-7 Posterior thorax percussion.
1 2
1 2
3 4 3 4
5 6 6
5
7
8
8
7
9 10
9 10
12
11
A. Anterior thorax
B. Posterior thorax
1 1
2 2
3
3
4 4
C. Right lateral thorax D. Left lateral thorax
FIGURE 13-8 Percussion patterns.
Auscultation. Listening for sounds with a stetho- patient’s chest by positioning the chestpiece of the
scope, called auscultation, requires a quiet environ- stethoscope between your index and middle finger
ment. As shown in Figure 13-9, the typical stetho- and using your hand to stabilize the chestpiece
scope consists of an earpiece, binaurals, a tension against the skin (Figure 13-10). Disinfect the chest-
bar, rubber or plastic tubing, and the chestpiece. piece with alcohol and warm it before placing it
The chestpiece has two parts. The bell is for hear- against the patient’s chest. Be sure, especially when
ing low-pitched sounds, such as heart sounds. The listening for breath sounds, to auscultate over bare
diaphragm is for hearing high-pitched sounds, such as skin, not through the patient’s clothing. Cloth can
breath sounds. The chestpiece can be rotated so that mask sounds or vibrate against the chestpiece. Chest
either the bell or the diaphragm is positioned over hair also causes noise that can mask breath sounds;
the listening hole. To test which side of the chestpiece minimize these effects by dampening the hair. When
is operable, place the earpiece in your ears, and then auscultating the chest, use a systematic bilateral
gently tap the diaphragm or the bell. You will hear the technique, following the same pattern for auscultation
sound through the earpiece. as for percussion (see Figure 13-8); however, with
When using the stethoscope to listen to breath auscultation, start the pattern at the bases and work
sounds, be careful to stabilize it firmly against the upward.4,8
Earpiece entire process is presented here, with a focus on the

chest and cardiovascular system.
Binaurals
Mental Status. Upon approaching the patient and
engaging him in conversation, the practitioner starts
checking the patient’s mental status and continues to
observe his appearance and behavior during the interview.
• Assess the level of consciousness. Is the patient
alert and responsive to verbal stimuli, or is he
Tension bar lethargic, obtunded, stuporous, or comatose?
• Assess the patient’s posture and motor behavior,
observing the range, characteristics, and appro-
priateness of the patient’s movements. Are these
normal, or is the patient restless, agitated, or
Rubber or
plastic immobile? The patient may also exhibit bizarre
tubing postures or involuntary movements.
• While the patient is answering questions, assess
his speech and language patterns, noting the
clarity, loudness, quantity, and rate of speech.
These observations can indicate conditions such
as aphasia, dysphonia, or dysarthria.
Bell
(low pitch) • Finally, assess the patient’s mood, noting, for
Diaphragm
example, elation, depression, anxiety, anger, or
(high pitch) indifference.4
Another part of evaluating mental status is assess-
ing the patient’s thought processes and perceptions. By
FIGURE 13-9 Acoustic stethoscope.
listening to the patient’s answers, the practitioner can
assess coherence.
• Carefully probe any unusual or unpleasant
thoughts introduced by the patient, being careful
not to agitate him.
• Ask about any unusual perceptions the patient
might have, such as illusions or hallucinations.
Finally, establish the patient’s orientation, attention,
and memory.
A patient oriented to time, place, and person is said
to be “oriented times three” (written 3). If not
oriented times three, the patient is said to be “disori-
ented.” The Glasgow Coma Scale is the gold standard

for assessing a patient’s level of consciousness, especially
if the patient is recovering from a coma or lapsing into
a comatose state, has suffered head trauma, or has been
sedated or received anesthesia.9 Table 13-7 shows the
Glasgow Coma Scale.
FIGURE 13-10 Correct way to hold a stethoscope. Attention is established by assessing digit span,
serial sevens, or spelling backward.
• Digit span is tested by having the patient repeat
PHYSICAL EXAMINATION OF THE ADULT forward and backward a seven-digit phone
Presenting a total physical examination of the adult number spoken by the practitioner.
patient is not possible in this chapter because the • Serial sevens tests the patient’s ability to subtract
process is complex and each finding leads to another. seven repeatedly from a starting number of 100.
The combination of all the findings can help in • Spelling backward a five-letter word such as world
determining a diagnosis. Therefore, an overview of the is another test of attention.
TABLE 13-7 Glasgow Coma Scale sure that pressure does not impede the flow of blood to
the brain and that the carotid sinus is not stimulated
Eye-opening response Spontaneous opening 4
(stimulating the carotid sinus can result in bradycar-
To verbal response 3
dia). Evaluate the pulse for strength, rhythm, and rate.
To pain 2
None 1 • The strength of the pulse is the pulse pressure, the
Most appropriate verbal Oriented 5 difference between the systolic and diastolic blood
response* Confused 4 pressures. A weak pulse can be an early indication
Inappropriate words 3 of the compromise of systemic blood pressure.
Incoherent 2 • The rhythm should be regular (see Figure 13-11
None 1 for common abnormal pulse patterns).
• The rate should fall within the normal range for
Most integrated motor Obeys commands 5
the patient’s age. A heart rate above the normal
response Localizes pain 4
range is called tachycardia, and one below it is
Flexion to pain 3
called bradycardia. Table 13-8 gives the normal
Extension to pain 2
ranges for vital signs by age.
None 1
Normal consciousness is a score of 14, and coma is a The respiratory rate should be counted for at least
score of 3. 30 seconds as well. Because a patient can become
self-conscious when someone is directly watching
*Intubated patients cannot speak, so their scores are modified as 3 through his or her chest, observe the respiratory rate, rhythm or
10, with 10 as normal consciousness. pattern, and depth indirectly. Once the pulse has been
taken, the practitioner should keep her fingers on the
pulse point but, out of the corner of her eye, observe
• Memory is tested by asking the patient to answer the rise and fall of the patient’s chest. Respiratory
questions such as the current date, his or her rates above the normal range are called tachypnea.
birth date, the name of the president, or his or Rates below the normal range are called bradypnea.
her high school. Questions such as these test The pattern of breathing should also be observed.
short-term and long-term memory. Table 13-9 describes some common abnormal breath-
• Recent memory can be tested by asking the person ing patterns. Additionally, during the interview process,
about his or her activities for the past 24 hours. count the number of words a patient can say before
Poor performance on any of those tests is common in a stopping to breathe. This is a sensitive test for respira-
delirious or demented patient; however, it can also be a tory abnormalities and can be done without the patient
result of language or educational barriers or of learning noticing. Patients with respiratory problems tend to
disorders.
General Appearance. After observing the patient’s

mental status: Best Practice
• Observe the patient’s general state of
health, height, weight, build, and sexual Pulse
development. The pulse rate can be different from the heart
• Generally inspect the patient for odors, groom- rate. If an electrocardiogram (ECG) monitor is
ing, and personal hygiene, especially in home used to establish the heart rate, the vital sign
care or nonhospital settings. should be documented as a heart rate, not as a
• Assess motor activity, facial expressions, and pulse. By designating “pulse” on the chart, the
reactions. practitioner indicates that she actually felt for
• Observe and note skin color, signs of distress, a pulse and counted it for at least 30 seconds.
and posture.10 Because of some cardiac anomalies, not every
heartbeat on the ECG results in a pulse. Also,
Vital Signs. Typically, four vital signs are recorded as pulse oximeters are not as accurate as the prac-
part of the comprehensive physical examination: pulse, titioner’s own fingers in establishing what is a
respiratory rate, blood pressure, and temperature. pulse and what could be artifact. So the practi-
Pulse is measured by placing the fingers on a pulse tioner must take an actual pulse when perform-
point and counting the pulse for at least 30 seconds. ing vital signs and not rely solely on electronic
Common pulse points are the radial artery, the brachial devices.
artery, and the carotid artery. If using the carotid, make
FIGURE 13-11 Normal and abnormal pulse patterns.

TABLE 13-8 Normal vital sign ranges by age

Age Pulse (beats/min) Respiration (breaths/min) Blood Pressure
Newborn 130–160 30–60 50–52/25–30 mm Hg
Child 80–120 18–30 95–118/62–75 mm Hg
Adult 60–80 12–20 ⬍140/⬍89 mm Hg
TABLE 13-9 Abnormal breathing patterns

Abnormality Description Pathology
Kussmaul Rapid deep breathing Metabolic acidosis, anxiety
Cheyne-Stokes* Periods of deep breathing with periods of apnea Heart failure, cerebral damage
Ataxia Unpredictable irregularity; breathing may be Respiratory depression, medullary
deep or shallow with apnea brain damage
Biots Irregular breathing with long periods of apnea Increased intracranial pressure
Obstructive pattern Prolonged exhalation Asthma, emphysema
Retractions and bulging Skin at apices and in intercostal areas Severe airflow obstruction and large
retracts inward during inhalation or bulges swings in pleural pressures
outward on exhalation
Abdominal paradox Abdomen sinks inward during inhalation Diaphragmatic fatigue or paralysis
Respiratory alternans Periods of only diaphragmatic breathing Diaphragmatic fatigue or significant
alternating with only chest wall breathing inspiratory muscle fatigue
Orthopnea Shortness of breath that starts or increases Suggestive of left ventricular failure or
as patient lies flat mitral stenosis but may accompany
obstructive lung disease
Platypnea Shortness of breath increases in the upright Suggestive of right to left intracardiac
position shunt
Paroxysmal nocturnal Sudden onset of shortness of breath and Suggestive of left ventricular failure or
dyspnea orthopnea that awakens patient after a period mitral stenosis and may be mimicked by
of sleep nocturnal asthma attacks
Compiled from Bickley LS, Hoekelman RA. Bates’ Guide to Physical Examination and History Taking. 7th ed, Philadelphia: J.B. Lippincott Co; 1999:269; and
Wilkins RL. Physical Examination of the Patient with Cardiopulmonary Disease. In: Wilkins RL, Krider SJ, Sheldon RL, eds. Clinical Assessment in Respiratory
Care. 3rd ed. St. Louis: Mosby-Yearbook; 1995:38.
*This pattern can be normal in young children or in aging people during sleep.
breathe more often when expending energy by speak- A sphygmomanometer is a device used to measure
ing: the more serious the problem, the fewer the blood pressures. Using the correct cuff size when measur-
number of words between breaths. ing blood pressure is important. A cuff that is too wide
Blood pressure is the force of the blood exerted gives erroneously low values, and too small a cuff gives
against the walls of the arteries as it moves through erroneously high values. A small cuff often causes
them and is an important diagnostic measure of erroneously high readings in obese and very muscular
circulatory function. A blood pressure measurement patients. The bladder of the cuff should be a width of
contains two numbers: a systolic pressure and a 40% of the arm circumference and a length of 80% of the
diastolic pressure. It is reported as the systolic arm circumference.4 To accurately measure blood pres-
pressure over the diastolic pressure. The systolic sure, center the bladder of the cuff over the brachial artery,
pressure measures the peak force of contraction of with the lower border of the cuff at least 1 inch above the
the left ventricle. The diastolic pressure measures the antecubital crease. The cuff should be snug enough on the
blood pressure when the heart is at rest. The pulse arm to stay in place but not too snug. A cuff that is too
pressure is the difference between these two loose does not exert sufficient pressure when inflated. Too
measurements. snug a cuff can mask the diastolic pressure sounds.
The most effective sequence for accurately measur- Although a high normal alone is not a problem,
ing blood pressure is as follows: if combined with other risk factors such as
First, establish the palpable systolic blood pressure. smoking, overweight, and high cholesterol
Place the fingers of one hand over the brachial or radial values, high normal blood pressure can indicate
artery. pending cardiovascular problems.
• Hypertension is rated as Stage One (mild,
1. Rapidly inflate the cuff until the pulse is no
140–159/90–99 mm Hg), Stage Two (moderate,
longer felt.
160–179/100–109), and Stage Three (severe, 180
2. Then inflate 20–30 mm Hg above that point.
or above/110 or above).
3. Deflate the cuff slowly at a rate of 2–3 mm Hg per
second until you feel at least two beats of the Finally, critically ill patients often suffer from
brachial pulse. This is the palpable systolic blood shock, which produces very low blood pressures.
pressure. Deflate the cuff immediately. Hearing systolic and diastolic sounds may be impos-
sible, especially if the pulse pressure is lower than
Next, establish the diastolic and systolic pressures.
30 mm Hg. In these cases, only a palpable blood
1. Place the bell of the stethoscope over the brachial pressure is reported. Palpable blood pressure is reported
artery. as the systolic number only, with the word “palpable”
2. Pause for 30 seconds. after it to designate how the pressure was obtained.
3. Then inflate the cuff until it is 20–30 mm Hg Temperature is the fourth vital sign usually reported.
above the palpable systolic pressure. A patient’s temperature can be taken in four ways: oral,
4. Deflate the cuff slowly, while listening for the rectal, axillary, and aural. Each method has its restric-
following sounds: tions and usefulness; however, with the newer, more
accurate tympanic thermometers, the aural route has
• Two consecutive beats indicate the systolic
become the avenue of choice. The aural method usually
pressure and the beginning of the Korotkoff
registers almost one degree higher than the oral
sounds.
method and is very close to the reading of the rectal
• In some cases, the Korotkoff sounds are heard,
method, which is considered the closest to the patient’s
then disappear, and reappear when the cuff
core temperature. Normal adult oral and rectal tem-
pressure has decreased 10–15 mm Hg. This is
peratures are between 37° and 38°C or 98.6° and
the ausculatory gap, which can occur in
100.5°F. Temperature fluctuates during the day; it is
patients with systolic hypertension or severe
lower in the morning upon awakening and slowly rises
aortic regurgitation. Not being aware of the
throughout the day until late afternoon. Hypothermia,
possibility of this gap can cause misreading.
or low temperature, is relatively common and usually
• The Korotkoff sounds change from crisp to
results in the hypothalamus initiating shivering to
muffled. This is the first diastolic sound,
generate energy and vasoconstriction to conserve body
believed to be the closest to the actual dia-
heat.9
stolic arterial pressure. This sound signals the
imminent disappearance of Korotkoff sounds
Face and Skin. The next segment of the physical
(not to be confused with ausculatory gap).
examination consists of examining the patient’s face
• Note the point at which sounds disappear
and skin. With the patient sitting on the edge of the
completely. This is the second diastolic sound.
bed or on an examining table, stand in front of the
The American Heart Association recommends patient to examine the face for any discoloration,
recording systolic and both diastolic readings (for lesions, or injuries, noting their location, size, type,
example, 110/80/72). If only two values are recorded, color, and number. Study the patient’s head, scalp, and
they should be the systolic and the second diastolic.7
Normal values for blood pressure change with age;
however, the Seventh Report of the Joint National Best Practice
Committee on Detection, Evaluation, and Treatment of
High Blood Pressure established the following guide- Temperature
lines in 2004.
Hyperthermia, or fever, in a patient is vital to as-
• For adults over age 18, optimal blood pressure is sess, especially for respiratory patients, because
a systolic of less than 120 mm Hg and a diastolic oxygen consumption and carbon dioxide produc-
of less than 80 mm Hg. tion increase approximately 10% for each 1°C
• The high normal range is a systolic of 120– rise in body temperature above normal.
129 mm Hg and a diastolic of 80–84 mm Hg.
hair for any problems. Examine the patient’s hands and Eyes, Ears, Nose, and Throat. After inspecting the
nails for any discoloration, pallor, or temperature hair, scalp, skull, face, and skin, the practitioner
difference, all of which can indicate inadequate examines the patient’s eyes, ears, nose, and throat.
peripheral circulation. Examine the eyes for acuity and for position,
Also note the presence of any cyanosis or clubbing, alignment, and the ability to follow a moving object
and assess capillary refill. Cyanosis, a bluish discolor- (accommodation). Inspect the eyelids, sclera, and
ation of the skin, exists when the hemoglobin is conjunctiva of each eye. Compare the pupils, and test
reduced by 1.5 volume percent or more.8 Two types of their reaction to light. The abbreviation PERRLA is used
cyanosis can be discovered: to indicate “pupils equal, round, and reactive to light
and accommodation.”
• Peripheral cyanosis is the blueing of the fingers
Next, inspect the ears, including the auricles,
or nailbeds. It indicates peripheral venous
canals, and eardrums, noting any structural irregu-
obstruction or a decreased blood flow because of
larities, inflammation, discharge, or presence of wax
circulation problems.
or foreign objects. Then examine the outside of the
• Central cyanosis is the blueing of the lips and
nose, and, with a light, inspect the inside: nasal
mucus membranes. It indicates advanced lung
mucosa, septum, and the turbinates. Palpate the
disease, congenital heart problems, or abnormal
nose and the frontal and maxillary sinuses for
hemoglobin.4 In most cases, central cyanosis
tenderness.
indicates a lack of oxygenation.
Next, examine the mouth and throat with a
Clubbing is a condition in which the ends of the light. Inspect the lips, oral mucosa, gums, teeth,
fingers enlarge and the fingernail loses its angle. In tongue, palate, tonsils, and pharynx for swelling,
advanced stages, the ends of the fingers begin to look ulceration, discoloration, or irritation. The tongue
like clubs, with the ends larger than the fingers them- should also be inspected for texture, color, and
selves. Figure 13-12 illustrates early clubbing compared any nodules.
with a normal finger. Clubbing takes years to develop,
but it can be determined in the early stages by palpat- Neck. The neck should be inspected and palpated for
ing the base of the nails, which take on a spongy any masses, swollen lymph nodes, or unusual pulsa-
feeling. Clubbing is found in patients with chronic tions. Gently tracing the trachea with the index and
pulmonary disease such as emphysema and cystic middle finger on either side from the chin down to the
fibrosis, bronchogenic carcinoma, and chronic cardio- sternal angle allows a practitioner to assess whether the
vascular disease.8 trachea is midline or has shifted.
Capillary refill is the time it takes for capillary blood Because jugular venous pressure (JVP) reflects right
flow to return to an area and indicates the adequacy or atrial pressure, assess the jugular veins for distention.
inadequacy of peripheral circulation. To assess capillary As shown in Figure 13-13, raise the head of the bed or
refill, gently press and release a place on one of the examination table to higher than 45 degrees above
patient’s extremities, such as a fingernail or a toenail, or horizontal. At 60 degrees the top of the visible jugular
on the back of the hand or top of the foot. Observe veins should not be more than 3–4 cm above the
how long it takes for the nail or skin to return to its sternal angle. If the top is above 4 cm, jugular venous
normal or original color. With normal refill, the color distention (JVD) is present. This most likely indicates
returns within 3 seconds. A refill time of greater than right-side heart failure, which can be caused by chronic
3 seconds can indicate a lack of adequate peripheral hypoxemia or pulmonary hypertension; it can also be
circulation. secondary to left-side heart failure.
Curved nail
variant
Normal nail angle of normal Early clubbing
FIGURE 13-12 Nail angles.

the surface landmarks that mark the various internal

organs to be examined. Figure 13-14 shows the loca-
tion of the tracheal bifurcation, and Figure 13-16
Highest level shows the lobes of the lung. Figure 13-17 shows the
of pulsation
Venous pressure location of lung fissures.
Sternal angle Inspect the anterior and posterior chest for any
deformities or asymmetry. Observe any abnormal
retractions of the supraclavicular area or intercostal
External
spaces, note chest symmetry, and compare the chest
jugular vein
Internal
anterior-posterior (A-P) diameter with the lateral
jugular vein diameter. A normal chest has a larger lateral than
Common A-P diameter (see Figure 13-18). A person with an A-P
carotid artery
diameter equal to the lateral diameter is classified as
having a “barrel chest.” Other thoracic abnormalities
FIGURE 13-13 Inspection of jugular venous pressure. are pectus carinatum (sternal protrusion) and pectus
excavatum (sternal depression). While examining the
posterior view of the thorax, observe for spinal defor-
Respiration/Thorax. After examining the neck, exam- mities such as (see Figure 13-19):
ine the thorax. Knowing the basic anatomy of the chest
is essential for accurately assessing the respiratory • Kyphosis—abnormal anteroposterior curvature.
system. Figure 13-14 shows the pathway of the respira- • Scoliosis—abnormal lateral curvature.
tory tract. When examining the chest and documenting • Kyphoscoliosis—combination of kyphosis and
the results, use as reference points the standard surface scoliosis.
landmarks, as shown in Figure 13-15. Also remember • Lordosis—abnormal posteroanterior curvature.
Nasopharynx
Oropharynx
Nasal cavity
Laryngopharynx
Nose
Parietal pleura Rib Esophagus
Visceral pleura
Pleural cavity Epiglottis
Intercostal
Larynx
muscle Lung
Trachea
Main
Mainstem bronchus
bronchus
Secondary
bronchus
Tertiary
bronchus
Terminal
bronchiole
Alveoli
Alveolar
Diaphragm Mediastinum duct
Respiratory
bronchiole
Alveolar sacs
FIGURE 13-14 Pathway of the respiratory tract.

Right midclavicular line Left midclavicular line Left scapular line Right scapular line
Right anterior Left anterior

axillary line axillary line
Midspinal
or vertebral
line
Midsternal
line
Left Right
posterior posterior
axillary line axillary line
A. Anterior view
B. Posterior view
Anterior
Anterior
axillary line
axillary line
Midaxillary line Midaxillary line
Posterior
Posterior axillary line
axillary line
D. Left lateral view

C. Right lateral view
FIGURE 13-15 Thoracic surface landmarks.
Apex
Cardiac notch
Clavicle
LUL RUL
RUL
LUL
RML LLL
RLL
RLL T10
LLL
(expiration)
Base T12
(inspiration)
A. Anterior view
B. Posterior view
FIGURE 13-16 Lobes of the lungs. RUL ⫽ right upper lobe; RML ⫽ right middle lobe; RLL ⫽ right lower lobe; LUL ⫽ left
upper lobe; LLL
4th rib at Spinous process of T3

Horizontal fissure right sternal border
5th rib at
midaxillary line
Left oblique LUL RUL Right oblique

Right RUL fissure
5th rib at fissure
oblique LUL
fissure midaxillary line
RML Left oblique
RLL LLL LLL RLL
fissure
6th rib at
midclavicular line
A. Anterior view
B. Posterior view
Spinous Spinous
process Right oblique Left oblique process
of T3 fissure fissure of T3
RUL
Right
horizontal fissure
5th rib at 6th rib at LUL
4th rib
midaxillary line RML midclavicular
line LLL
RLL
6th rib at
midclavicular
line
C. Right lateral view D. Left lateral view
FIGURE 13-17 Fissures of the lungs. RUL ⫽ right upper lobe; RML ⫽ right middle lobe; RLL ⫽ right lower lobe; LUL ⫽
left upper lobe; LLL ⫽ left lower lobe.
After examining and observing the exterior of the thumb should move from the midspinal line equally
thorax, assess the interior structures. Using superficial about 3–5 cm. Bilateral reduction of chest expansion can
palpation, the examiner palpates the anterior and be caused by such problems as neuromuscular diseases
posterior chest for any tenderness or abnormalities in and respiratory diseases that result in severe hyperinfla-
the skin and chest wall, such as subcutaneous emphy- tion or air trapping (for example, emphysema or a
sema or lesions. To palpate the patient’s chest wall severe asthma attack). Unilateral reduction in chest wall
expansion, the practitioner places her thumbs posteri- expansion suggests lobar consolidation, atelectasis,
orly at approximately the eighth thoracic vertebra with pleural effusion, pneumothorax, or unilateral dia-
her fingers extended toward the midaxillary lines. phragmatic paralysis. During this part of the examina-
Anteriorly, she places her thumbs at the xyphoid tion, the practitioner should also palpate anteriorly
process and extends her fingers laterally along the ribs and posteriorly for changes in vocal fremitus.4,8
toward the midaxillary lines. Figure 13-20 shows After chest palpation, percussion should be
anterior and posterior hand placement. At full exhala- performed on both the anterior and posterior chest.
tion, she places the thumbs so that they are together, Because percussing over bone is not diagnostic, it
and then asks the patient to take a deep breath. Each should be done on the intercostal spaces and away
x
x
2x x
1:2 ratio 1:1 ratio

A. Normal adult B. Barrel chest
Protrusion Depression
C. Pectus carinatum D. Pectus excavatum
FIGURE 13-18 Chest configurations.
A. Kyphosis B. Scoliosis C. Kyphoscoliosis D. Lordosis
FIGURE 13-19 Abnormalities of the spine.

A. Anterior
FIGURE 13-21 Assessment of diaphragmatic position.
should work quickly so that the patient does not

become short of breath.) Normal diaphragmatic
movement is approximately 5–7 cm during a deep
breath. Although percussion can give only an approxi-
mate position of the diaphragm and its movement,
any decrease in movement bilaterally or unilaterally
can help in the diagnosis of respiratory problems.
Figure 13-21 shows the assessment of diaphragmatic
position.
After palpation and percussion, the next step
is assessing respiration through auscultation.
Using auscultation to distinguish between normal
and abnormal breath sounds is one of the most
B. Posterior important aspects of the physical examination of the
FIGURE 13-20 Hand placement for palpating chest wall chest. Auscultation must be performed in a quiet
expansion. environment with care being taken to auscultate all
areas of the lung.
To understand abnormal and adventitious breath
sounds (sounds not usually heard in the lungs, such as
from the scapulae. Percussion may have limited
wheezing and crackles), a practitioner must be able to
diagnostic value in patients who are obese or overly
identify normal breath sounds. The three types of
muscular. However, the practitioner can assess many
normal breath sounds are tracheal or bronchial breath
abnormalities with percussion. For example, it is useful
sounds, vesicular or normal breath sounds, and
for assessing diaphragmatic excursion. As the patient
bronchovesicular breath sounds.
fully exhales, the practitioner percusses the posterior
chest downward until a dull note is heard. This is the • Tracheal or bronchial breath sounds, normally
level of the diaphragm, and a line is drawn on the heard over the trachea, are high-pitched, loud
patient’s skin at this point. The patient takes a deep sounds, with the expiratory component equal to
breath and holds it. The practitioner then percusses the inspiratory component.
from the line down until the dull note is heard again • Vesicular or normal breath sounds, heard over the
and draws another line. The process is repeated on the peripheral areas of the lungs, are low-pitched,
other side of the posterior chest. (The practitioner soft sounds, with only a minimal expiratory
component. Bronchial breath sounds have been Adventitious breath sounds also indicate abnormal
described as the sound of air passing through a lung process. The American Thoracic Society and the
tunnel, and vesicular breath sounds have been American College of Chest Physicians recommend
described as the rustling of leaves in a gentle standardized descriptions and terminology for adventi-
breeze. tious breath sounds, described in Table 13-10. Adventi-
• Bronchovesicular breath sounds, normally heard over tious sounds are characterized as discontinuous (fine or
the main bronchi, have characteristics of both course crackles) or continuous (wheeze or rhonchi).
bronchial and vesicular breath sounds and occur Voice sounds, or vibrations of spoken letters or
when auscultating in a location, such as near the words heard via auscultation, are useful if other
scapulae, where both sounds can be heard. examination techniques suggest a respiratory abnor-
mality. These sounds are egophony, bronchophony,
In addition to these normal breath sounds, abnor-
and whispered pectoriloquy.
mal sounds may be heard.
• Egophony exists when the patient says the letter
• Abnormal breath sounds include normal breath
“e” and the practitioner hears the letter “a” over
sounds heard in abnormal areas of the chest. For
the peripheral chest wall. This difference suggests
example, bronchial or bronchovesicular breath
compressed lung tissue, usually identified only
sounds heard in the peripheral areas of the chest
above a pleural effusion.
can indicate consolidation or atelectasis that is
• Bronchophony is when spoken sounds increase in
in communication with the large airways and
clarity and intensity, indicating increased lung
transmitting the harsher sounds to the periphery
tissue density. Bronchophony is usually easier to
of the lung.
detect if it is unilateral and suggests consolida-
• Other abnormal breath sounds are those that are
tion of lobar pneumonia.
either diminished in one area or diminished
• Whispered pectoriloquy describes the selective
throughout the chest. Unilateral diminished breath
transmission of high-pitched sounds. When a
sounds suggest either a blocked bronchial tube,
patient whispers “one, two, three,” normal lung
such as a large mucus plug, or a space-occupying
tissue filters out most of the high-pitched sounds.
mass in the pleural space, such as a pleural
The practitioner hears a very faint, low-pitched
effusion or pneumothorax. Bilateral diminished
whispering through the stethoscope on the
breath sounds indicate hyperinflation or severe air
peripheral chest wall. Areas of selective lung
trapping such as in a patient who has emphy-
consolidation transmit the sounds clearly to the
sema or is having a severe asthma attack.
peripheral chest wall, and the practitioner hears
• The final adventitious sound is a pleural friction
the sounds clearly over the affected lung area.8
rub, which occurs if the pleural surface becomes
inflamed or loses its lubricating fluid. The sound The total examination of the thorax can suggest
is continuous throughout inhalation and many pulmonary disorders. Table 13-11 describes some
exhalation, resembling the sound of Velcro being of these disorders as well as the corresponding inspec-
pulled apart. tion, palpation, percussion, and auscultation results.
TABLE 13-10 Lung sounds

Type Sound Name Pathology
Discontinuous High-pitched, low amplitude, Fine crackles Atelectatic alveoli opening; does not
short duration at end of clear with cough
inspiration
Low-pitched, high amplitude, Coarse crackles Sudden opening of proximal bronchi
long duration during inspiration as in chronic bronchitis; unaffected
by cough
Continuous High-pitched, musical; heard Wheeze Polyphonic—small airway obstruction;
only or loudest during exhalation monophonic—large airway obstruction
Low-pitched, coarse sound; heard Rhonchi Thick mucus in trachea and large
most often continuously during airway; usually clears with cough
both inhalation and exhalation
Adapted from Seidel HM, Ball JW, Dains JE, Benedict GW. Mosby’s Guide to Physical Examination. 4th ed. St. Louis: Mosby-Yearbook; 1999:381–382.
TABLE 13-11 Possible physical findings associated with common respiratory conditions
Condition Inspection Palpation Percussion Auscultation
Asthma Tachypnea, dyspnea Tachycardia, diminished Occasional hyper- Prolonged exhalation,
fremitus resonance, occasional wheezes, diminished
diaphragm at lower lung sounds
level and limited
movement
Atelectasis Diminished chest wall Diminished fremitus, Dullness over Wheezes, rhonchi,
movement, respiratory apical cardiac impulse, affected lung and crackles in varying
lag, narrowed inter- and trachea shifted amounts, depending
costal spaces on toward affected side on extent of collapse
affected side, tachypnea
Bronchiectasis Tachypnea, respiratory Few, if any, consistent No unusual findings A variety of crackles,
distress, hyperinflation findings if no other pulmonary usually coarse, rhonchi,
problems sometimes disappearing
with cough
Chronic Respiratory distress, Limited diaphragm Occasional Diminished breath
obstructive audible wheezing, mobility, diminished hyperresonance sounds, rhonchi,
lung disease cyanosis, neck vein vocal fremitus wheezing, and fine
distention, peripheral crackles
edema in presence of
right-sided heart failure
Emphysema Tachypnea, prolonged Apical impulse may Hyperresonance, Diminished breath
exhalation, pursed-lip not be felt, liver edge limited diaphragmatic and voice sounds,
breathing, barrel chest, displaced downward, movement, dullness, diminished heart
thin, underweight diminished fremitus liver pushed sounds, occasional
downward adventitious sounds
Pleural effusion Diminished chest wall Unilateral diminished Dull note over Diminished to absent
and/or movement and chest wall movement affected area breath sounds over
thickening respiratory lag on or lag, cardiac api- affected area, bron-
affected side cal pulse and trachea chophony, whispered
shifted away from pectoriloquy, and
affected side, diminished egophony in area
fremitus over affected superior to effusion,
area, tachycardia occasional pleural rub
Pneumonia Tachypnea, shallow Increased fremitus Dullness if A variety of crackles
breathing, occasional in presence of consolidation and occasional rhonchi,
cyanosis, splinting and consolidation, decreased is large enough bronchial breath sounds,
limited motion on fremitus in presence of egophony, bronchophony,
affected side concomitant empysema and whispered
or pleural effusion, pectoriloquy
tachycardia
Pneumothorax Tachypnea, cyanosis, Cardiac apical pulse, Hyperresonance Diminished to absent
respiratory distress, mediastinal and breath sounds,
bulging intercostal tracheal shift away succussion splash
spaces (if tension from affected side, audible if air and fluid
pneumothorax), respira- diminished to absent mix, sternal and
tory lag on affected side, tactile fremitus over precordial clicks and
tracheal deviation away affected area, crackling if air underlies
from affected side tachycardia sternal area, diminished
to absent voice sounds
Courtesy of Seidel HM, Ball JW, Dains JE, Benedict GW. Mosby’s Guide to Physical Examination. 4th ed. St. Louis: Mosby-Yearbook; 1999:392–393.
pulmonary problem. The closure of the pulmonic

valve usually cannot be palpated; vibrations felt at the
left sternal border between the second and third ribs
suggest pulmonary hypertension.
After inspection and palpation of the chest,
auscultation is performed. Auscultation of the heart
requires that the practitioner understand and be able to
identify normal heart sounds: S1, Ej, and S2.
• S1, the first heart sound, is the closure of the
mitral valve during systole and ventricular
contraction. As the left ventricular pressure rises,
it exceeds the afterload pressure in the aorta, and
A P the aortic valve opens, accompanied by the early
E systolic ejection sound, or Ej.
• The second heart sound, S2, is the sound of the
T
M
aortic valve closing (also referred to as A2), when
the ventricles have finished contracting and the
ventricular pressure drops below the aortic
pressure. Normally, there is a long pause
between S2 and the next S1, reflecting the
diastole of the heart. During S2, the pulmonic
FIGURE 13-22 Cardiac landmarks: A ⫽ aortic area;
valve also closes, but this sound, referred to as
P ⫽ pulmonic area; E ⫽ Erb’s point; T ⫽ tricuspid area; P2, is usually masked by the louder aortic valve
M ⫽ mitral area. sound. If right heart enlargement and pulmo-
nary hypertension exist, the pressure closing the
pulmonic valve may be enough to make it as
loud as the aortic valve sound. This is referred to
Cardiovascular System. As with the respiratory as a loud P2 and is a common finding in cor
system, the practitioner must know the underlying pulmonale.
anatomy of the cardiovascular system before perform-
ing an examination. The heart lies between the lungs During inhalation, these two sounds sometimes
slightly on its side, with the right atrium inferior to the separate slightly and become audible; this separation is
left atrium and the right ventricle anterior to the left called splitting of the heart sounds. The mitral valve
ventricle. The apex of the heart consists of the ventricles opening is usually a silent event unless there is mitral
and extends slightly downward and into the left chest stenosis or prolapse, in which case the practitioner
almost to the midclavicular line. The base of the heart might hear a snap right after S2.
consists of both atria and lies beneath the body of the Two other sounds may be heard:
sternum. Figure 13-22 shows the anatomical position • A thrill-like sound that occurs after the opening
of the heart as well as the positions for auscultating of the mitral valve is the rapid filling of the
the valves. ventricles. This sound, normal in children and
While inspecting and palpating the chest, the young adults, is called the S3 sound.
practitioner should also inspect and palpate the area • The final sound, not usually heard in adults, is
around the heart. While inspecting the anterior chest, S4, or atrial contraction.
the practitioner, in some cases, is able to visualize the
apical impulse in the left intercostal space between Abnormal heart sounds, such as diastolic and
the fifth and sixth ribs near the midclavicular line. The systolic murmurs and gallop rhythms, can also be
apical pulse, the pulsation of the ventricles when they auscultated.
contract, can usually be palpated and is called the A murmur is caused by rapid blood flow across a
point of maximal impulse (PMI). The PMI is difficult to normal valve, the backflow of blood through an
assess on patients with emphysema because the unclosed valve, or blood flow through a stenotic valve.
increase in A-P diameter moves the apex of the heart A murmur should be described by the practitioner
away from the chest wall or, if it is felt at all, the PMI according to its location, timing, shape, pitch, and
may shift inferiorly owing to the diaphragm’s having intensity. Where the murmur is heard can indicate the
a lower resting point. Shift of the PMI also occurs location of the affected valve. For example, a mitral
when the mediastinum is shifted because of some valve murmur is most likely to be heard at the fifth
intercostal space at the left midclavicular line. Timing is Abdomen and Legs. The next segment of the physical
the next part of a murmur to assess. examination is the abdomen and legs. With the patient
in the supine position, the practitioner should inspect,
• If the murmur occurs between S1 and S2, it is a
palpate, and auscultate the abdomen for most of the
systolic murmur.
abdominal examination.
• If it occurs between S2 and the next S1, it is a
diastolic murmur. • First inspect the abdomen for any scars, rashes,
or lesions. Examine the contour of the abdomen
These types of murmurs can be further classified:
for any distention, protrusions, or bulges.
• A systolic murmur that is loudest in the middle Observe the abdomen for normal aortic pulsa-
of the S1 and S2, with breaks between the S tions at the epigastrium.
sounds and the murmur, is referred to as a • Next, palpate superficially for any tenderness,
midsystolic murmur. muscular resistance, and palpable masses.
• If there are no gaps and the sound is constant, Perform deep palpation to delineate any masses
the murmur is referred to as a pansystolic murmur. and to assess tenderness.
• A late systolic murmur occurs after the midpoint • Finally, auscultate the abdomen, listening for
between S1 and S2 and persists up to S2. active bowel sounds (clicks or gurgles occurring
• Diastolic murmurs are either early, midway, or late approximately 5–34 times per minute). If a
depending on when they occur during S2 and patient has high blood pressure, bruits—vascular
the next S1. sounds that resemble a murmur—may be heard.
Bruits in the upper quadrant and epigastrium
The shape refers to the pattern of sound over time
may indicate renal artery stenosis.
and can be:
Examine the legs, assessing the peripheral vascular
• Crescendo (goes from soft to loud).
system, the musculoskeletal system, and the neurologi-
• Decrescendo (goes from loud to soft).
cal system.
• Crescendo-decrescendo (louder in the middle).
• Plateau (has the same pattern throughout). • Note any swelling, discoloration, or ulcers.
• Palpate for edema, noting whether it is pitting or
Pitch is whether the sound can be classified as high,
nonpitting edema. With pitting edema, when the
medium, or low. It can be reported descriptively as
practitioner gently pushes in on the skin, the
blowing, harsh, rumbling, and musical.
indentation remains. In nonpitting edema, the skin
Murmurs are also graded by intensity, with six
returns to its previous shape, with no indentation.
grades of loudness from very faint to very loud.
• Palpate and evaluate the dorsalis pedis, posterior
Table 13-12 gives the grades of murmur intensities.
tibial, and femoral pulses.
A gallop rhythm is an abnormal heart sound with
• When examining the musculoskeletal system,
S3, S4, or both present. The sequence of sounds suggests
note any joint enlargement or deformity, and
the gallop of a horse. A gallop rhythm suggests ven-
check the range of motion if indicated.
tricular distention during diastole as would occur after
a myocardial infarction, ventricular disease, a left-to- Finally, examine the neurological system of the legs
right shunt, or ventricular failure.8 to ascertain any abnormal movements or neurological
deficit. This examination has three components.
• Test the patellar and Achilles reflexes with a
TABLE 13-12 Grading heart murmurs rubber hammer and note whether the reflexes
Grade Characteristics are normal or deficient.
• Ascertain movement and the patient’s ability to
I Very faint; heard only after a period of
follow commands. Ask the patient to flex the
concentration
foot up and down and wiggle the toes.
II Faint; heard immediately • Assess sensation by asking the patient to close his
III Moderate intensity eyes. Then, touching the end of the rubber
IV Loud; may be associated with a trill hammer to various points on the legs, have the
patient indicate when he can feel touch. Assess-
V Loud; stethoscope must remain in contact
ing sensation also includes determining whether
with the chest wall in order to hear; trill
the patient can distinguish between a sharp and a
palpable
dull stimulus. Most hammers have a tool on the
VI Very loud; heard with stethoscope off of chest end to perform this assessment. Do not use a
wall; trill palpable safety pin or other object that can pierce the skin.
CASE STUDY 13-5

Mr. Smith consents to a physical examination. The Vocal fremitus seems equal bilaterally. Percussion
practitioner (Jane Simons) asks him to remove his reveals slightly hyper-resonant tone bilaterally, and
shirt and put on a gown. She leaves and comes the posterior diaphragmatic excursion is less than
back in a few minutes to find Mr. Smith still pacing 5 cm. Upon auscultation, the practitioner hears
about the room. He appears to be in generally good bilateral diminished breath sounds, as well as faint
health, weighs 220 pounds, and is 6 feet 2 inches polyphonic wheezes during exhalation. Voice sounds
tall, with a generally stocky build. Mr. Smith are diminished but otherwise normal.
exhibits good grooming and personal hygiene. He is While inspecting and palpating the chest, the
frowning and looks a little anxious. His arms are practitioner notices nothing remarkable about the
crossed across his chest, and he is watching cardiac system. Upon auscultation, the practitioner
Ms. Simons closely. notes a grade II, medium-pitched, late-systolic
The practitioner approaches Mr. Smith and plateau murmur. There are no other abnormal
explains that she wants to take his vital signs. heart sounds.
Mr. Smith consents and sits down, but on the edge The abdomen shows no rashes or lesions, and it
of his seat. The practitioner records the following seems normal to palpation, with no tenderness or
vital signs: guarding. Bowel sounds are normal, and there are
no abnormal findings.
Pulse 110
Examination of the legs reveals no swelling,
Respirations 25
discoloration, edema, or ulcers. The pedal pulses
Blood pressure 150/95
seem a little weak, and there is some peripheral
Temperature 37°C (aurally)
cyanosis and temperature deficit of the feet. The legs
While taking Mr. Smith’s vital signs, the practi- seem to show a little bilateral neurological deficit.
tioner notices the following. His pulse is strong but
exhibits some pulsus paradoxus. Respirations are Questions
shallow, and there seems to be some obstruction to 1. Should the practitioner do anything before
flow. Owing to the muscular chest wall, retractions starting the physical examination after returning
are not observed. to the room?
A general examination of the face, extremities, 2. How would the practitioner classify the vital
and skin reveals no lesions, discoloration, clubbing, signs?
or injuries. There is some peripheral cyanosis, and
3. What does the examination of the patient’s
capillary refill is about 5 seconds. There seems to
extremities indicate to the practitioner?
be some bilateral weakness in his arms and grip.
Eyes, ears, nose, and throat are unremarkable. 4. What should the practitioner suspect after the
Neck is supple, and the lymph nodes are of examination of the chest and abdomen?
normal size. The trachea is midline, and there is no 5. Why is this patient experiencing shortness of
jugular venous distention. breath and chest pain?
The patient’s chest is of normal configuration, 6. Should any other questions be asked to help
and there are no spinal abnormalities. Chest expan- distinguish the diagnosis?
sion is bilaterally equal but seems less than normal.
Documentation and the injury; other episodes are less critical, such as routine
physical examinations. Many practitioners contribute
Medical Record to this overall medical record, and each practitioner
Whenever the practitioner comes into contact with a must recognize the importance of each record and
patient professionally, the results of the encounter make sure to document every encounter with the
must be documented. Documentation chronicles the patient accurately and clearly. Each institution has its
patient’s medical history from birth through death. own method for recording medical documentation;
Over the patient’s lifetime, distinct episodes focus on however, the formal medical record must be docu-
the illness of that moment, such as an acute illness or mented accurately and kept confidential.
TABLE 13-13 Confidentiality

1. Keep all client records secure.
Physical Examination of the 2. Consider carefully the content to be entered into
the record.
Child or Infant
3. Release information only with the patient’s written
Most of the techniques used to perform the adult consent and full discussion of the information to be
examination are applicable to both infants and shared, except when release is required by law.
children. However, when performing a physical
examination of a child or an infant, the practi- 4. Use professional judgment deliberately regarding
tioner should be aware of the need to alter the confidentiality when the client is a danger to self
examination to meet the patient’s special needs. or others.
Infants are the most difficult to examine be- 5. Use professional judgment deliberately when
cause of their inability to follow directions or to deciding how to maintain the confidentiality of a
keep still. The parent can be helpful in holding minor. The rights of the parent or guardian must
the infant and keeping his attention while the also be considered.
practitioner performs the examination. A unique 6. Disguise clinical material when used professionally
approach to examining a child or an infant is to for teaching and writing.
perform painful or distressing maneuvers out of
sequence, at the end of the physical examina-
tion. Auscultating the lungs and heart should
be done early, whereas examining the ears and
mouth and palpating the abdomen should be LEGIBILITY
done last. There may be some resistance to the Everyone knows the jokes about physicians’ handwrit-
examination, and the child may be crying or ing. The problem is that illegible handwriting can
screaming during the exam. The practitioner result in medical errors and confusion concerning treat-
should understand and not show anger or frustra- ment. Likewise, if the medical record is used as a
tion but allow time for the child to adapt to the document in a legal matter, illegible handwriting can
surroundings and the situation. Flexibility in the put the writer in jeopardy. When documenting any-
exam process and in the order of the physical thing in the medical record, take time to write the
exam is necessary to focus on what is important, entry clearly to prevent any misunderstandings among
particularly if the time for the examination is practitioners.
limited. Although abbreviations allow the practitioner to
chart quickly, they can also lead to confusion. For the
most part, avoid abbreviations if possible, or use only
those approved by the institution (the list is usually
CONFIDENTIALITY maintained by the medical records department).
The patient’s medical record, whether written or entered Consult with medical records before writing any
into a computer system, is a legal document indicating abbreviations in the patient’s chart.
exactly what was done to the patient and what hap-
pened as a result. Patients expect this document to be
kept confidential, and anyone not directly involved in COMPUTERIZED MEDICAL RECORDS
their care should refrain from violating this confidence.
To decrease the incidences of illegible handwriting and
Likewise, practitioners directly involved with the patient
to facilitate access to medical records, many institutions
should ensure at all costs that the patient’s right to
have converted to a computerized system. Computer-
privacy is respected. As stated in the Hippocratic Oath,
ized medical records have many advantages.
“What I may see or hear in the course of treatment or
even outside of treatment in regard to the life of men, • The record is always available wherever a com-
which on no account must be noised abroad, I will puter terminal is available. Even if the patient is
keep to myself holding such things shameful to be in one department for care, the medical record is
spoken about.” All health care practitioners are subject available simultaneously to the practitioner
to the same ethical code. Table 13-13 details the treating the patient, to the doctor who is respon-
fundamental elements of confidentiality. Failure to sible for the patient, and to other practitioners
maintain confidentially violates the Health Insurance who may need to see the patient at a later time,
Portability and Accountability Act (HIPAA) of 1995 and even if they are in different departments or even
may carry significant legal penalties. See Chapter 2. outside the institutional walls.
• The computerized medical record is legible and practitioner (source) had a separate section of the
current because what is entered is immediately patient chart in which to record information. This
available and in printable form. method hindered communication among disciplines
• Computer systems act as checklists for practitio- because each discipline had to read the entire chart to
ners by providing a preplanned charting system get a complete picture of the patient. Everything in the
that includes all the elements to be included in chart was organized in chronological order or, in some
the record. institutions, in reverse chronological order (i.e., the
• Results of tests can be attached directly to the most recent note was first in each section). The source-
computerized patient record at the point of oriented method made it difficult to treat the patient in
practice rather than being printed out and then the new multidisciplinary environment, and no two
placed on the paper chart later. institutions used the same organizational structure.
• Departments can list commonly used terms and Because of the need to standardize medical records,
then preprogram them into the computer. The most institutions have adopted the problem-oriented
terms can be accessed by a single key code, bar medical record (POMR). As medicine becomes more
code, or touch screen. dependent on teamwork and a multidisciplinary
• Finally, the record is complete, and no page is approach to treating patients, the POMR system helps
missing, as can happen with a paper chart. ensure accurate documentation. The POMR consists of
the database, the problem list, the problem-related
Some of these advantages are also disadvantages.
plans, flowcharts, and the progress notes.
• Because of instant access, people who understand
computer systems could get unauthorized access Database. The practitioner should list all aspects of the
to the patient record without too much trouble. health history and record the patient’s answers to the
Each institution tries to minimize this possibility questions as well as the practitioner’s observations. All
by establishing security barriers. The most elemen- negatives should also be recorded to indicate that they
tary barrier is the practitioner’s password. How- are negatives and that they were not overlooked. If the
ever, in most institutions the number of people practitioner who takes the first history does a complete
who need and who are legally authorized to access job, it does not have to be redone each time the patient
patient records is staggering. These people must is seen. The next practitioner just has to confirm aspects
remember and keep confidential their personal of the history and then “fill in” the time since the last
passwords. And, unless passwords are changed history. The physical examination also should be
frequently, the possibility of someone else getting recorded accurately by the practitioner performing it.
a practitioner’s password increases, making the With an accurate and complete history and physical,
system vulnerable to breakins. the practitioner can construct a complete problem list
• Preprogramming commonly used terms increases on the patient.
charting compliance, but the quality of the
charted notes may be less comprehensive than if Problem List. The problem list is the fundamental part
the practitioners compose the notes themselves. of the POMR. After taking the history and performing
• Even though computer records work well, many the physical exam, the practitioner should list all the
institutions do not plan well enough for when the problems that were uncovered. This initial master prob-
computer system malfunctions. Inevitably, systems lem list is placed in the front of the chart. As another
fail. The practitioner should be thoroughly problem is discovered or a problem is solved, it is
familiar with the paper back-up system to be used either added to or deleted from the list. Each problem
until the electronic system is restored. As computer is listed in order of importance or acuity, with the date
systems become more complex and more compre- it was entered on the list, not the date the patient first
hensive, the need to periodically review the discovered it. In time, the problem list is divided into
back-up procedures becomes more acute. Also, at two categories: active problems, which require action,
times, the system may not be available because of and inactive problems, which do not require action but
routine maintenance. At these times, the paper may be important for other practitioners to know. The
back-up system must be used for any of the tasks problems can be established diagnoses, physical signs
that the computer usually performs. and symptoms, laboratory tests, areas uncovered during
the history, or special risk factors.
Next to the problem list, a differential diagnosis
PROBLEM-ORIENTED MEDICAL RECORD list should be established. As each problem is investi-
In the past, hospitals and other medical institutions gated and the diagnosis is refined, the list includes
organized the patient chart according to the source- monitor or treatment lists to indicate how the problem
oriented charting method. Each department or is being handled.
CASE STUDY 13-6

The following documentation includes information Injuries: Small cut to hand by knife 3 years ago
gathered from follow-ups suggested by questions in Blood transfusions: No transfusions
preceding case studies.
Surgical history: Tonsillectomy, 1981
Patient History: Hospitalizations: No other hospitalizations
Date: 12/17/11 1900 hours
Current Health Status:
William Smith, 35-year-old male, married
Address: 1 Main St., Morris Plains, NJ Current medications: Aspirin and cold medicines
DOB: 10/2/76 Allergies: Allergy to mold, pollen, dust, and
Sheet metal factory worker grass as child; treated with desensitizing shots
Source of history: Patient until age of 12; shots discontinued because
Chief complaints: (1) Shortness of breath, symptoms stopped
(2) chest pain, (3) weakness of extremities Tobacco use: 40-pack-year history—still smoking
History of the Present Illness: Alcohol/drug use: 2–3 beers per day, no other
1. Shortness of breath: Started 2–3 weeks ago substance abuse
and is getting worse. Now has trouble Diet: No restrictions. Diet is high fat and
walking up stairs. Shortness of breath worse patient does not restrict intake of salt.
at end of workweek, better by end of Screening tests: None remembered
weekend. Also can occur after eating.
Immunization status: Tetanus 3 years ago
2. Chest pain: Noticed for the last 3 weeks.
Sleep habits: Normal with no nocturnal dyspnea
Nonradiating pressure to center of the chest
getting worse over the 3-week period. Exercise/leisure: Relatively sedentary lifestyle
Pressing-type pain. Associated with the with no regular exercise program; never
shortness of breath. traveled abroad
3. Weakness of the extremities: Noticed by Environmental hazards: Work hazards of fumes
patient for the last 3 days. Associated with and metal dust; at home, some paint fumes
weakness of grip and in legs. Safety measures: Patient uses seatbelt.
Patient had episode today that brought him to Family History:
the clinic. Episode involved not being able to Father: 60, alive (bypass surgery 2005)
walk up one flight of stairs without resting.
Mother: 58, alive (MI, 2006)
Shortness of breath, chest pain, and weakness
seemed worse at time, getting better since Wife: 35, alive and well
leaving work area. Son: 7, alive (asthma)
Past Health History: No brothers or sisters. Grandparents deceased,
causes unknown
Patient feels he is in general good health, with
some recent problems with breathing, chest No family history of TB
pain, and weakness. Social History:
Childhood illnesses: Patient remembers having A 35-year-old sheet metal factory worker
chickenpox, measles, and mumps as a child. who recently moved to a smaller work area
No history of diphtheria, whooping cough. where metal is being cut with torches.
Childhood immunizations: Remembers having Exposed to fumes and metal dust in poorly
“the usual shots.” Salk vaccine for polio. No ventilated room. Married to housewife who
adverse reactions. also works at home as a freelance sign
painter. Father of one 7-year-old boy who
Adult illnesses: No past history of adult ill-
was diagnosed 3 years ago as having asth-
nesses. Flulike symptoms for 3 months sub-
ma. Live together in house in suburbs with
sided about 2 weeks ago.
large lawn. One dog, which is usually kept
Psychiatric illnesses: No history of psychiatric outside.
problems
(continues)
Educational History: to questions quickly but seems agitated and

The patient has a high school diploma and 1 year anxious. His appearance is well groomed and
of community college. Mother has 2 years of neat. His color is good, and he sits and lies
college. Father dropped out of high school after without discomfort. When answering questions,
grade 11 but plans to complete GED and start shows some trouble breathing, with some use of
community college part time. accessory muscles. Breathlessness seems to
increase agitation.
Systems Review:
Vital signs: Pulse: 110 regular with some
General: No weight change, appetite normal, paradoxical pulse
flulike symptoms for over 3 months Respirations: 25/min and shallow
Psychological: No indication of illness BP: 150/95 right arm lying down; no
Integumentary system: No rashes or lesions, no appreciable difference in left arm
varicose veins, no edema or swelling, some Temperature: 37°C (aurally)
peripheral cyanosis Skin: Palms cool and dry; normal color and
Eyes: Normal vision texture; no visible lesions; some peripheral
cyanosis and prolonged capillary refill; no
Ears: Hearing good with no tinnitus, vertigo, or
clubbing; some temperature deficit in fingers;
infections
some cyanosis with no edema or varicose veins;
Runny nose sometimes yellow mucus; some no calf tenderness; feet cool to touch; scattered
nosebleeds with blowing of nose. Some superficial burn scars on hands and lower arms
postnasal drip noticed.
Head: Hair, scalp, skull, and face appear normal.
Mouth: Normal; last dentist visit over 3 years ago
Eyes: Vision 20/20 in each eye; no contact lenses
Throat/Neck: No lumps, goiter, or pain or eyeglasses; field of vision full by confrontation;
Respiratory system: Progressively worsening PERRLA; extraocular movement intact
shortness of breath. Morning cough with small Ears: Ear canals clear, and drums intact; acuity
amounts of thick white sputum. No hemoptysis. good to whispered voice
Exertional dyspnea and some shortness of
Nose: Nose intact, mucosa slightly inflamed,
breath after eating.
septum midline; some sinus tenderness
Cardiovascular system: Nonradiating chest pain
Mouth: Lips and mucosa pink, some irritation
associated with shortness of breath; no orthop-
noted in back of throat; teeth in good repair;
nea, palpations, edema, or nocturnal dyspnea;
tongue midline; tonsils absent
some exertional dyspnea
Neck: Supple, with no lymphadenopathy;
Breasts: No dimplings on inspection; no pain,
trachea midline; no JVD
tenderness, or lumps on palpation
Chest: Normal configuration, and no spinal
Gastrointestinal system: Good appetite; no
abnormalities; no masses palpated; decreased
nausea, vomiting, indigestion; bowel movements
bilateral chest expansion; hyper-resonant
normal about once daily; no diarrhea or bleeding;
percussion note bilaterally, with decreased
no pain, jaundice, gallbladder, or liver trouble
diaphragmatic excursion; diminished breath
Urinary system: No dysuria, hematuria, or nocturia sounds bilaterally, with faint bilateral polyphon-
Musculoskeletal system: No back pain or ic wheezes on exhalation; diminished bilateral
joint pain voice sounds
Neurological system: Some poor balance and Cardiovascular system: Good carotid pulses; no
weakness of grip; no fainting, seizures, or S3 or S4; grade II/VI medium-pitched late
trouble swallowing; memory good; headaches systolic plateau murmur at 2nd right inter-
associated with workplace; no head injuries space—does not radiate to the neck; diastole
Endocrine system: No known thyroid problems, clear; apical impulse absent due to muscular
temperature intolerance; sweating average; no chest.
symptoms or history of diabetes Abdomen: No rashes or lesions; slightly en-
Physical Examination: larged but normal to palpations and percussion;
normal bowel sounds; liver normal span but
General appearance: Mr. Smith is a tall, stocky displaced inferiorly; no bruits noted
male who walks and moves easily. He responds
Pulses:
Radial Femoral Popliteal Dorsalis Pedis Posterior Tibial
RT N(paradoxical) N ↓ ↓ ↓
LT N(paradoxical) N ↓ ↓ ↓
Musculoskeletal system: No deformities, no swollen or tender joints; good range of motion in hands, wrist,
elbows, shoulders, spine
Neurological system: Mental status: tense, agitated, alert, and anxious but cooperative; thought coherent;
oriented ⫻3; cognitive testing not done; cranial nerves intact.
Motor: Some flaccidity noted in extremities; muscle strength rated 4/5; some weakness of grip; gait normal
with some hesitation and unsteadiness
Sensory: Intact; reflexes: 2⫹, no ptosis
Problem List
Date Problem
Entered No. Active Problem Inactive Problem
12/17/11 1 Shortness of breath
12/17/11 2 Chest pain
12/17/11 3 Weakness of extremities
12/17/11 4 Exertional dyspnea
12/17/11 5 Grade II murmur
12/17/11 6 Morning cough
12/17/11 7 Headaches
12/17/11 8 Runny nose
12/17/11 9 Peripheral cyanosis
12/17/11 10 Flulike symptoms
12/17/11 11 Paradoxical pulses
12/17/11 12 Allergies
12/17/11 13 Smoking
12/17/11 14 Possible high blood pressure
12/17/11 15 Environmental hazards
12/17/11 16 Diet high in calories, fat, and salt
12/17/11 17 Sedentary lifestyle
(continues)
Patient Record Note [in part]:

Diagnosis: Asthma and possible bronchial challenge testing and/or
Assessment: Supporting this diagnosis are allergy testing. Therapeutic: Inhaled bronchodilator
tachypnea, shallow respirations, paradoxical treatment now and continue until peak flows
pulses, hyper-resonant lung percussion note improve. Education: Discuss nature of asthma,
bilaterally, bilateral inferior diaphragm placement, need for avoidance of environmental hazards, need
and decreased diaphragmatic exertion, polyphonic for smoking cessation.
wheezes bilaterally, childhood history of allergies,
Questions
nonradiating pressing pressure in middle of chest,
use of accessory muscles, and bilateral diminished 1. Does any aspect of the documentation need to be
breath and voice sounds. Possible occupational expanded?
asthma evidenced by timing of incidents. 2. Write an assessment and plan for the problems
Plan: Diagnostic: Pre- and postbedside spirometry in the problem list that were not covered in the
if possible, pre- and postpeak flow measurement. asthma notes.
Eosinophil count. Chest X-ray. Schedule for full 3. In your opinion, can this patient be sent home, or
pulmonary workup with pulmonary function testing should he be admitted? Explain your reasoning.
Initial Problem-Related Plan. As each initial problem the SOAP method of documentation: subjective,
is listed, a problem-related plan is developed. The plan objective, assessment, and plan.
includes any diagnostic tests needed, any monitoring
• The subjective part of the progress notes should
tests needed, what treatments are being prescribed, and
indicate (in the patient’s own words when
what education is necessary for the patient and family.
possible) what the patient is feeling or the
Each problem must have a plan, even if it is a simple
problem the patient is expressing.
plan such as “monitor patient until other signs or
• The objective part of the note records any physical
symptoms occur.” The plan is updated with each
signs, diagnostic or clinical tests, and physical
updated problem list. Once a disease or condition has
findings that may result from a treatment or
been resolved and moved to the inactive list, an arrow
changes that may affect the problem list and
is used to indicate the observations showing that the
plan for the patient.
disease or condition has been resolved and what
• The assessment should include whether the
follow-up may be needed.
practitioner feels that the subjective and objec-
tive data confirm the plan or alter it according to
Flowcharts. The POMR lends itself naturally to
assessment of the data.
flowcharts to show the patient’s progress. Clinical,
• Finally, the plan indicates what the practitioner
diagnostic, and monitoring tests and observations are
will do after making the assessment. Any modifi-
often done and repeated during the course of an
cation to the problem list and plan for the
illness. A flow sheet is a convenient way to keep a
patient should be documented here and on the
record of these tests, and the flowchart makes it easy for
problem list as well.
the practitioner to determine trends in the values of the
various tests. A perfect example is the vital signs
flowchart that most hospitals use for each patient. As
the practitioner takes the vital signs, the numbers are PATHWAYS
recorded on a sheet, accompanied in most cases with a Medicine, particularly the large health maintenance
graphic display. At a glance, every practitioner who organization (HMO), has embraced the use of clinical
comes into contact with the patient can assess quickly or critical pathways as a way to standardize treatment
the latest vital signs and whether the patient is stable, across the United States. Pathways are interdisciplinary
getting better, or getting worse. flowcharts that show what tests, treatments, counseling,
and interventions should be done to a typical patient
Progress Notes. The progress notes record the day-to- with a certain diagnosis. They are “plans of care that
day progress of the patient. Each practitioner should outline the optimal sequencing and timing of interven-
make a progress note every time she interacts with the tions for patients with a particular diagnosis, proce-
patient. The note should be brief and succinct, and it dure, or symptoms.”11 All pathways should contain
should focus on what was performed or on the change four aspects: patient outcomes, a timeline for the
being documented. The progress note should follow pathway, collaboration among disciplines, and
comprehensive care of the patient. Pathways sequence cases, an extensive history and physical exam decreases
naturally into case management of diseases because of the need for invasive testing and accurately indicates
a standardized plan for the disease management. what tests are necessary. Also, as respiratory therapists
are called on to do more and more, the ability to
perform a complete history and physical may help the
CARE PLANS OR PROTOCOLS practitioner perform in alternative sites.
Care plans are the disciplinary part of the pathways. Once information has been gathered, the ability to
Based on an accepted standard of care, care plans share it with other health care providers is essential for
sequence the patient’s treatment, based on the problem a seamless continuum of care. Documentation must be
list. Every problem listed in the active part of the done in a way that facilitates the dissemination of
problem list usually has an initial care plan to address information. Clear, concise, complete documentation
the problem. Most care plans or protocols are patient is the key to multidisciplinary care of the patient.
driven in that the patient’s signs and symptoms
generate the sequencing of the care plan.
Study Questions
LEGAL REQUIREMENTS REVIEW QUESTIONS
No discussion of medical records would be complete 1. Why is clear and complete understanding needed
without a discussion of the legal issues involving the during a patient interview?
records. Medical records are legal documents and
2. What are the general guidelines and techniques for
frequently requested by attorneys representing patients
interviewing a patient?
or their survivors to serve as evidence in malpractice
cases, real or perceived. What is in the record or not in 3. What are the basic areas covered in the patient
the record is often a key element in the legal processes history of an adult patient?
during medical malpractice, workers’ compensation, 4. What are the areas covered in the review of systems
and personal injury cases. RTs must record completely of an adult patient?
their actions and patient outcomes to all therapy 5. Why is it necessary to perform inspection, palpa-
interventions. Recording vital signs before and after tion, percussion, and auscultation on a patient?
therapy, recording ventilator settings before and after
6. What are the vital signs collected on an adult?
making adjustments, and noting patent conditions
before and after treatments are all important parts of 7. Why is confidentiality necessary when dealing with
patient care. The medical-legal axiom is, “If it isn’t patient data?
recorded, it wasn’t done.” The corollary is, “If it was 8. What is the basic structure of a problem-oriented
done, it should be recorded.” medical record?
Experience tells us that respiratory therapists are
increasingly being named in lawsuits as defendants in
medical malpractice cases. These cases include hospital, MULTIPLE-CHOICE QUESTIONS
long-term care sites, and home care practice. Therapists 1. Recognition is usually established in which of the
are being held responsible for their actions, their following?
misactions, and their inactions. The importance of a a. general space
complete and accurate medical record cannot be b. social space
overstated. RTs may be asked to remember that patient c. personal space
they took care of three years ago on Wednesday the d. intimate space
twenty-third at 6:50 p.m. Odds are they will not be
2. The interview is usually performed in which of the
able to cite the activities and actions they took with any
following?
degree of clarity, unless the medical record is complete
a. general space
and accurate. Therapists may not assume that someone
b. social space
else will record their activity.
c. personal space
d. intimate space
3. Most of the physical examination must be per-
Summary formed in which of the following?
A health care professional must act like a detective to a. general space
determine what is wrong with a patient. Thorough b. social space
questioning and an in-depth examination of the c. personal space
patient should reveal any medical problems. In most d. intimate space
4. To elicit a free flow of information, the interviewer 11. When the practitioner is checking the past
should use which of the following? health history, which of the following is not
a. open-ended questions included?
b. direct questions a. tobacco use
c. closed questions b. medical problems
d. surveying c. accidents or injuries
5. To focus the patient on specific information, the d. childhood illnesses
interviewer should use which of the following? 12. When performing a review of the systems, the
a. open-ended questions practitioner should begin with:
b. direct questions a. questions concerning the head.
c. closed questions b. questions concerning the eyes, ears, nose,
d. surveying and throat.
6. To pinpoint a specific piece of information, the c. questions concerning the skin.
interviewer should use which of the following? d. questions concerning general health.
a. open-ended questions 13. Some of the barriers to communication include
b. direct questions which of the following?
c. closed questions I. emotions
d. surveying II. language problems
7. To ensure that all information has been collected, III. cultural differences
the interviewer should use which of the following IV. personality disorders
at the end of each set of questions? a. I, II, III, and IV
a. open-ended questions b. I, III, and IV only
b. direct questions c. I, II, and III only
c. closed questions d. I, II, and IV only
d. surveying 14. Which of the following are required to perform a
8. Which of the following are nonverbal active physical exam?
listening techniques? I. privacy
I. taking notes II. soft dim lighting
II. maintaining eye contact III. comfortable temperature
III. listening to how the patient is speaking rather IV. no interruptions
than to what is being said a. I, II, III, and IV
IV. using supportive gestures to indicate under- b. I, III, and IV only
standing and support c. I, II, and III only
a. I, II, III, and IV d. I, II, and IV only
b. I, III, and IV only 15. According to the Glasgow Coma Scale, a score of 3
c. I, II, and III only is considered
d. I, II, and IV only a. obtunded.
9. Which of the following are verbal active listening b. confused.
techniques? c. coma.
I. keeping your voice tones neutral d. normal.
II. accepting vague and incomplete statements 16. Which of the following pulse patterns are
III. using checking statements to summarize what associated with decreased compliance of the
is being said aortic wall?
IV. using facilitating statements such as “Go on” a. weak pulse
a. I, II, III, and IV b. bounding pulse
b. I, III, and IV only c. pulses alternans
c. I, II, and III only d. paradoxical pulse
d. I, II, and IV only 17. Which of the following pulse patterns
10. Which of the following is not part of the history of are associated with obstructive lung
the present illness? disease?
a. location a. weak pulse
b. quality b. bounding pulse
c. age c. pulses alternans
d. timing d. paradoxical pulse
18. Which of the following pulse patterns are associ- 27. Which grade of murmur is considered quiet but
ated with left ventricular failure? can be heard immediately after placing the
a. weak pulse stethoscope on the chest?
b. bounding pulse a. grade II
c. pulses alternans b. grade III
d. paradoxical pulse c. grade IV
19. Which of the following is the range for child’s a d. grade VI
normal pulse rate? 28. Which of the following are considered part of
a. 130–160 confidentiality?
b. 80–120 I. All records should be kept secure.
c. 60–80 II. Information can be released with verbal
d. 40–60 consent.
20. Which of the following is considered bradycardia III. A practitioner should consider carefully what is
for an adult? to be entered into the record.
a. 130–160 IV. Material should be disguised if used for
b. 80–120 teaching and writing.
c. 60–80 a. I, II, III, and IV
d. 40–60 b. I, III, and IV only
c. I, II, and III only
21. Which range of respiratory rates is considered
d. I, II, and IV only
normal for a newborn?
a. 30–60 29. Which of the following is not an aspect of problem-
b. 18–30 oriented medical record keeping?
c. 12–20 a. the problem list of all past and present patient
d. 80–120 problems
b. the database of all findings, both positive and
22. With age, the blood pressure normally
negative, of the history and physical exam
a. decreases.
c. a subjective statement of the patient’s illness in
b. increases.
the patient’s own words
c. stays the same.
d. flowcharts that show the progress of the
d. decreases and then increases.
patient
23. Which of the following breathing patterns is
associated with asthma?
a. Kussmaul CRITICAL-THINKING QUESTIONS
b. ataxia
1. What could hinder a practitioner from gathering
c. biots
adequate information from a patient?
d. obstructive
2. Why is it necessary for a respiratory therapist to
understand the entire history and physical exam
associated with increased intracranial pressure?
rather than concentrating only on the respiratory
a. Kussmaul
history and physical exam?
b. ataxia
c. biots 3. Where in the entire process of dealing with the
d. obstructive patient could confidentiality be compromised?
How would you go about preventing the loss of
confidentiality?
associated with diaphragmatic fatigue?
a. retractions
b. abdominal paradox
c. ataxia References
d. orthopnea 1. Cohen-Cole SA. The Medical Interview: The Three-
26. Which of the following breathing patterns is Function Approach. 2nd ed. St. Louis, MO: Mosby-
associated with respiratory depression? Yearbook; 2000.
a. retractions 2. Wilkins RL. Preparing for the patient encounter. In:
b. abdominal paradox Wilkins RL, Krider SJ, Sheldon RL, eds. Clinical
c. ataxia Assessment in Respiratory Care. 6th ed. St. Louis, MO:
d. orthopnea Mosby-Yearbook; 2009.
3. Purtilo R, Haddad A. Health Professional and Patient 10. Estes MEZ. Health Assessment & Physical Examina-
Interaction. 7th ed. Philadelphia: WB Saunders Co; tion. 3rd ed. Clifton Park; NY: Delmar Cengage
2007. Learning; 2006.
4. Bickley LS. Bates’ Pocket Guide to Physical Examina- 11. Ignatavicus DD, Hausman KA. Clinical Pathways for
tion and History Taking. 6th ed. Philadelphia: JB Collaborative Practice. Philadelphia: WB Saunders
Lippincott Co; 2009. Co; 1995:10.
5. Tamparo CD, Lindh WQ. Therapeutic Communica-
tions for Health Professionals. 3rd. ed. Clifton Park,
NY: Delmar Cengage Learning; 2007.
6. Wilkins RL, Hodgkin JE. History and physical
Suggested Reading
examination of the respiratory patient. In: Chan PD, Winkle PJ. History and Physical Examination in
Burton GG, Hodgkin JE, Ward JJ, eds. Respiratory Medicine. 10th ed. Laguna Hills, CA: Current Clinical
Care: A Guide to Clinical Practice. 4th ed. Strategies Publishing; 2002.
Philadelphia: JB Lippincott Co; 1997. Edge RS, Groves JR. Ethics of Health Care: A Guide for
7. Seidel HM, Ball JW, Dains JE, Benedict GW. Mosby’s Clinical Practice. 3rd. ed. Clifton Park, NY: Delmar
Guide to Physical Examination. 7th ed. St. Louis, Cengage Learning; 2005.
MO: Mosby-Yearbook; 2010. Epstein O, Perkin GD, de Bono DP, Cookson J. Clinical
8. Wilkins RL. Physical examination of the patient Examination. 4th ed. London: Mosby-Yearbook
with cardiopulmonary disease. In: Wilkins RL, Europe; 2008.
Krider SJ, Sheldon RL, eds. Clinical Assessment in Lindh WQ, Pooler MS, Tamparo CD, Cerrato JU, eds.
Respiratory Care. 6th ed. St. Louis, MO: Mosby- Clinical Medical Assisting. 4th ed. Clifton Park, NY:
Yearbook; 2009. Delmar Cengage Learning; 2010.
9. Krider SJ. Vital signs. In: Wilkins RL, Krider SJ, Swartz MH. Pocket Companion to Textbook of Physical
Sheldon RL, eds. Clinical Assessment in Respiratory Diagnosis. 3rd. ed. Philadelphia: WB Saunders Co;
Care. 6th ed. St. Louis, MO: Mosby-Yearbook; 2009. 1998.
CHAPTER 14
Radiology for the Respiratory Therapist

Glendon G. Cox and Paul J. Mathews
OBJECTIVES
• Discuss why a respiratory therapist should be able to identify major abnormalities on chest radiographs.
• List the various types of radiological studies.
• Discuss the rationale for ordering specific radiological studies.
• Explain the principles of various radiological studies.
• Differentiate between a regular and a portable chest X-ray.
• Describe a sequence for systematically reviewing a chest radiograph.
• Discuss the diagnostic values of various types of radiographic studies.
• Given a list of conditions, select the appropriate studies for their evaluation and justify the choices.
• Identify common abnormalities on a chest film.
CHAPTER OUTLINE
Why Should a Respiratory Therapist Radiation Safety
Learn Radiology? How to Interpret Studies
How Can This Knowledge Be Gained? Preanalysis
Body Planes and Directional Terminology Review of the Study
Types of Radiological Studies Comparison with Previous Studies
Chest Radiography Correlation of Findings with Clinical Situation
Radiographic Studies Using Contrast Materials Final Interpretation
Fluoroscopy Example Cases
Computerized Tomography Normal Chest
Magnetic Resonance Imaging Emphysema and Bulbous Lung Disease
Ultrasound Lobar Pneumonia
Nuclear Medicine Studies Bronchopneumonia
(continues)
343
(continued)
Alveolar (Air-Space) Infiltrates and Device Positioning

Air Bronchograms Endotracheal Tubes
Lobar Atelectasis Swan-Ganz Catheters
Lung Cancer Nasogastric Tubes and Feeding Tubes
Tuberculosis Chest Tubes
Congestive Heart Failure, Pulmonary Edema, Aortic Balloon Pumps
and Pleural Effusion
Internal Cardiac Pacemakers and Defibrillators
Pneumothorax
Chest Trauma
Tension Pneumothorax
Flail Chest
Pneumoperitoneum
Subcutaneous Emphysema
Aortic Aneurysm, Aortic Dissection, and Traumatic
Aortic Injuries Penetrating Chest Wounds
Pulmonary Thromboembolism Foreign Body
Adult Respiratory Distress Syndrome
KEY TERMS
air bronchogram echocardiography radiodensity
angiogram flail chest radiograph
arteriography fluoroscopy radiology
atelectasis hemothorax radiopaque
barotrauma hot-lighting subcutaneous emphysema
bullae lateral decubitus Swan-Ganz catheter
computerized (axial) magnetic resonance transducer
tomography imaging (MRI) ultrasound
contrast positron emission ventilation/perfusion
Doppler sonography tomography (PET) (V⭈/Q⭈ ) scan
R
espiratory therapists can enhance their limitations in diagnosing the cause of a patient’s
contribution to the care of their patients and cardiopulmonary complaints. In many cases, lungs
their value to the clinical care team if they really are simply better seen than heard.
have a basic knowledge of chest radiology.
Radiology is the use of X-rays and other forms of
energy to generate images of the internal structures of
the chest in the diagnosis and treatment of disease).
Why Should a Respiratory
Almost all hospital patients requiring an evaluation of Therapist Learn Radiology?
their pulmonary function or treatment for pulmonary
A respiratory therapist should learn some basic radiol-
disease or whose care involves services by respiratory
ogy to develop the ability to:
therapy undergo diagnostic imaging studies. Such
studies are ordered because they allow the treating • Get information not available by physical
physician or the respiratory therapist to learn things examination.
about patients’ internal structure and function that are • Identify conditions that require respiratory care
not readily available through observation, physical or emergent treatment.
examination, history taking, or laboratory testing. Even • Assess a patient’s response to respiratory care.
a tool as important as breath sounds has significant • Identify complications of respiratory care.
CHAPTER 14 ■ Radiology for the Respiratory Therapist 345
• Conduct a preliminary assessment of radio- learning how to verify the proper placement of these
graphs when radiologists and physicians are devices using chest radiographs.
not available.
• Confirm proper positioning of devices, tubes,
and monitor leads.
How Can This Knowledge
Radiological studies of the chest, typically chest
radiographs, are often the primary means by which Be Gained?
physicians and therapists identify the diseases or Reading this chapter is the first step toward becoming
processes that are responsible for a patient’s shortness comfortable viewing and doing basic analysis of chest
of breath or chest pain. These diseases range from radiographs. The key to becoming proficient, however,
conditions that are relatively easy to manage, such as is practice. The more radiographic studies respiratory
atelectasis, to more severe, sometimes life-threatening therapists look at and analyze, the better they become
conditions, such as pneumonia, adult respiratory at distinguishing what is normal from what is not and
distress, or tension pneumothorax. Radiographs can be the more conditions they learn to recognize. Respira-
used in judging the response to a variety of medical tory therapists should make a habit of examining as
and surgical treatments, including responses to antibi- many radiographic studies as possible. Examining
otics, diuretics, therapeutic bronchoscopy, and chest radiographs is easy to do in intensive care areas, which
tube or artificial airway placement. Chest radiographs often have display systems or digital access to the
are used to screen for complications of respiratory care complete image files of all of the patients in the unit.
procedures including barotrauma (damage caused by Increasingly, the review of radiographs of any inpatient
excessive pressure during mechanical ventilation), and most outpatients can also be accomplished either
misplaced lines and tubes, or volume loss (atelectasis, at specialized display consoles or on appropriately
or airlessness of a pulmonary segment, a lobe, or an configured personal computers. Also, a number of
entire lung). Web-based resources that are dedicated to chest
A respiratory therapist (RT) should have some radiology and imaging can be accessed by a simple
basic skills in analyzing radiographs because many Internet search. These sites are invaluable as learning
studies are done and available for review only when tools for even the most seasoned respiratory therapist.
the radiologist or treating physician is at another In addition to viewing and studying radiographs,
hospital, at home, or otherwise unavailable. A respira- the RT should take advantage of every opportunity to
tory therapist who can identify a pneumothorax or a draw information from others who have more experi-
misplaced endotracheal tube before the physician ence and knowledge and who can explain and point
makes rounds or the radiologist interprets a study can, out findings. A respiratory therapist who works in a
by notifying appropriate personnel, prevent complica- teaching hospital should try to attend the daily X-ray
tions and in some cases save a life. rounds with the attending physicians or radiologists.
Today’s “X-rays” are more likely to be viewed and Asking the attending or covering physician to discuss a
stored in a digital format or as digitalized images film is an excellent way to build rapport with the
rather than as films. In fact, the images in this physician and simultaneously to build expertise in this
chapter are mostly from digital sources. However, the important skill. In a short time, quite a bit of profi-
term “film” is still used because it is a useful cogni- ciency can be gained in this way. Respiratory therapists
tive aid for learners and because films still exist and who work in non-teaching hospitals should approach
are still frequently encountered when comparisons staff physicians, the medical director, the emergency
to older imaging studies are required. With increased room doctors, and on-call radiologist about teaching
use of digital radiography, physicians with appropri- them the fundamental skills. Remember that physi-
ately designed computer systems have access to the cians learn by teaching other physicians and medical
results of radiographic studies in their offices or at students. They are often happy to pass on their
their homes 24 hours a day. As teleradiology, the knowledge.
interpretation of medical imaging studies at sites
remote from the hospital or imaging facility, evolves
and expands, remote reading and analysis of radio-
graphic images, especially images that require Body Planes and Directional
subspecialty expertise, will become commonplace.
Respiratory therapists who are trained to insert or Terminology
maintain artificial airways or to manage pulmonary To ensure accurate communications and the reproduc-
artery or umbilical catheters can help prevent com- ibility of imaging studies, clinicians must use common
plications of these therapeutic interventions by frames of reference with regard to anatomic positions
and projections. Locations of structures are often Sagittal plane

referred to in relation to the body surface. For example:
• A structure close to the surface is said to be Coronla plane
superficial to structures or organs lying farther
from the skin surface. Obviously, structures lying
farther from the body surface are referred to as
Transversal plane
deep. Using this convention, the muscles of the
chest wall are deep to the skin and subcutaneous
fat layers.
• The front of the body is referred to as anterior or
ventral, and the back of the body is posterior or
dorsal.
• The right and left sides of the patient’s body are
right lateral and left lateral, respectively.
• Locations of structures or body parts can also be
referred to in terms of their relationships to the
body’s center of mass. Structures located farther
away from the central mass than an arbitrary
reference point or landmark are said to be distal
to that landmark, and structures that are nearer FIGURE 14-1 The three primary planes of the body.
the center of mass are proximal. For example, the
wrist is distal to the elbow, and the hip is
proximal to the knee.
• The transverse (or axial) plane divides the body
• Another frame of reference identifies the relative
into cranial and caudal portions. In a standing
position of two structures in relation to the
human, the transverse plane is parallel to the
midline of the body. A structure located farther
ground.
from the midline than an arbitrary landmark is
said to be lateral to the landmark, and a second Figure 14-1 illustrates these three primary planes of
structure located closer to the midline is said to reference. Each primary anatomic plane defines an
be medial. In the standard anatomic projection, infinite set of parallel planes along which the body can
with the palms facing forward, the thumbs are be imaged. More generally, the transverse, or axial,
lateral to the little fingers, and the little fingers plane is perpendicular to the longitudinal, craniocau-
are medial to the thumbs. dal axis. Any sectional set of images is described based
• Finally, the relative locations of landmarks may on the primary anatomic plane to which the planes of
be specified in terms of their relationships to the section of the images are parallel. For example, many
head or tail (in Latin, cauda is the word for of the computerized tomography (CT) images gener-
“tail”) or feet (in the case of tail-less humans). If ated by examinations of the chest and abdomen are in
you were to draw a line starting from the top of planes perpendicular to the longitudinal axis of the
the sternum to the pubis, the direction that you body, parallel to the primary transverse plane; they are
would move your pen would be craniocaudal— referred to as axial images. In fact, early CT scanners
from the head, toward the tail or feet. could generate only images in transverse, hence an
obsolete term for CT scanning was computerized axial
Many modern imaging systems produce cross-sectional
tomography, or CAT.
images of the body. The planes of section are described
The use of standard terminology is essential in
in relation to three primary, orthogonal (mutually
describing the exact position or direction of the organs
perpendicular) planes:
and anatomic structures, medical instrumentation and
• The sagittal plane lies in the midline of the body implants, or foreign objects that may be found in the
and divides its right and left sides. The sagittal body. The terminology is also necessary to ensure
suture of the skull takes its name from the accurate communication between physicians and
sagittal plane. radiologic technologists in prescribing examinations
• The coronal plane is perpendicular to the sagittal and positioning patients.
plane and divides the body into anterior and In radiology, as in many areas of life, the need for
posterior portions. The coronal suture that the rapid and accurate transmission of data has led
separates the frontal and parietal bones of the to the adoption of specialized terms, abbreviations,
skill lies in the coronal plane. and nicknames for procedures. For example, a chest

Use of Abbreviations Radiograph Formats
The use of abbreviations may confuse communi- In some countries and for certain specialized
cations because many abbreviations have several clinical applications, the images are viewed in a
meanings. For example, PA can refer either to black-on-white format in which low-density areas
a posterior-anterior radiographic projection (the are white instead of black.
direction of the X-ray beam as it passes through
the body) or to the pulmonary artery. Abbrevia-
tions are often specific to a discipline, with the
same abbreviation having different meanings Radiographs are the most simple, inexpensive, and
in different fields of practice. Even when used available studies. They are most useful when the tissues
in context, these phrases and others like them being studied have density differences sufficient to
can be confusing. Consequently, current best show the details needed for the purpose intended.
practices and accreditation criteria require that Radiographs of the chest rely on the different densities
the use of abbreviations in communications be of aerated and nonaerated lung tissue, bones, the heart,
restricted or eliminated. and other mediastinal structures, as well as the many
artificial devices such as endotracheal or chest tubes or
venous catheters.
Figure 14-2A is a normal chest radiograph showing
radiograph may be referred to as a CXR, a chest film, the four basic densities in plain film radiography: bone,
a picture, a radiograph, or a “X-ray.” A computed soft tissue, fat, and air. Figure 14-2B is the correspond-
tomographic study may be referred to as a CT (or, ing normal left lateral view of the chest in which the
archaically, as a CAT scan). Magnetic resonance studies patient’s left side of the chest is placed against the X-ray
are often referred to as MRs or MRIs. detector or film cassette. Lateral views are helpful in
identifying fluid accumulations, such as pleural
Types of Radiological Studies effusions. Alternatively, lateral decubitus views can be
used to detect small amounts of pleural fluid. To
Many types of radiological studies are encountered in obtain a lateral decubitus view, the patient is placed on
clinical practice, and more are added as the science a table or cart, lying with the affected side down. This
advances. Respiratory therapists should be familiar allows any fluid present in the pleural space to layer
with the types of studies available at the institution along the dependent (lowest) portion of the parietal
where they work. pleural. The image is obtained by shooting the X-ray
beam parallel to the table top.
CHEST RADIOGRAPHY
Chest radiographs, often referred to as chest films in a Correct Orientation for Viewing Chest Radiographs.
nod to the passing era when chest radiographs were By convention, all chest X-rays, whether PA or anterior-
produced and stored on 14⫻17-inch films, are among posterior (AP, from front to back), are displayed as if
the most commonly performed imaging studies. They the observer (reader) were facing the patient; the
are the type of X-rays most people are familiar with. patient’s left is to the observer’s right. Normal chest
The patient’s chest is placed between an X-ray detector, images in the PA view should show the heart, specifi-
historically a sheet of X-ray film, and a source of X-ray cally the cardiac apex, on the patient’s left, or your right
energy. The “shadows” cast on the film after a short when viewing the image. The right diaphragm is
exposure to the X-rays are recorded. The “colors” white, normally slightly higher than the left by about 1–2 cm
black, and grays on the film are determined by the (about ½–1 inch). Gas in the upper portion of the
relative ability of various tissues, devices, and sub- stomach—the gastric bubble—is usually readily appar-
stances to block the X-rays from reaching the film. By ent under the left diaphragm.
convention, the images are viewed in a white-on-black When the PA radiograph is obtained, the patient’s
format. Black areas represent low-density substances, arms should be raised or the shoulders rotated upward
such as air, that do not block X-rays very effectively. and forward toward the cassette, thereby elevating the
White areas represent high-density substances, such as clavicles (collar bones) and moving the scapulae
metal or bone, that are more efficient in blocking the forward and laterally so that they are projected as much
X-rays. Materials that have densities lying between as possible away from the lungs. The lengths of the
these two extremes appear as various shades of gray. collar bones should appear to be equal and their
(A) (B)
FIGURE 14-2 (A) Normal inspiratory PA view: This illustrates the relative radiodensities of bone,
soft tissues, fat, and air. Note the wide intercostal spaces (ICS), long thin heart, and relatively flat
diaphragms bilaterally. Also note the presence of a gastric air bubble below the left diaphragm. (B) A
normal inspiratory left lateral view with the left side of the patient’s chest near the X-ray detector.
proximal ends should lie equidistant from the poste- horizontally oriented. In a comparison of
rior spinal processes of the upper thoracic vertebra, inspiratory and expiratory films on the same
which are used as marker of the midline on the PA or patient, the lower lung zones appear more dense
AP radiograph. The trachea and mediastinum should and the vessels in the lower lobes are crowded
also lie near the midline under the sternum; otherwise together.
the patient may be rotated into an oblique position or
there may be a disease process resulting in tracheal or
Portable Versus Nonportable Studies. Chest radio-
mediastinal shift.
graphs can be made using either fixed equipment in
the radiology department or portable equipment in
Inspiratory versus Expiratory Studies. The reader of
intensive care units, emergency departments, or other
chest X-rays has to be able to distinguish between
settings. Portable studies are most frequently used
inspiratory and expiratory radiographs. Ideally, chest
when patients are difficult or impossible to move
radiographs are taken at full inspiration. (“Take in a
deep breath and hold it.”) Occasionally, expiratory
views are taken in special situations, such as attempting
to demonstrate small pneumothoraces or to look for
evidence of bronchial obstruction or air trapping. With
practice, RTs can recognize the differences between
inspiratory and expiratory chest radiographs based on
their different characteristics—some subtle, some
obvious.
• Inspiratory films (Figure 14-3) show wide
intercostal spaces (ICS) with increased transverse
(side-to-side) and AP diameters, and a flattened
diaphragm. The heart appears relatively vertical

and narrow in the standard upright inspiratory
chest film.
• Expiratory films (Figure 14-4), on the other
hand, have narrow intercostal spaces and the
diaphragm is upwardly domed. The AP and FIGURE 14-3 Normal inspiratory PA view: Note the wide
transverse diameters of the chest are shorter, and ICS, increased side to side and front to back diameters.
the heart appears somewhat broader and more Note the flattened diaphragms and elongated narrow heart.
FIGURE 14-4 Normal expiratory film: Note the narrow ICS,
domed diaphragm, thickened lower lobes, and decreased FIGURE 14-6 A portable radiograph, usually an AP view:
AP and transverse diameters with a relatively wider and The patient is normally on his or her back or sometimes
shortened heart image. propped up in bed in a seated or semirecumbent position.
Note the magnification effect caused by the shorter focal
length of the X-rays and the increased distance from the
chest wall to the heart.
because of either their condition or equipment
(ventilators, chest tubes, and so on). The quality of
portable studies is frequently limited, however, owing
to nonstandard positioning, nonstandard distance, and detector or film cassette. The X-ray tube is positioned
other factors. Chest radiographs done in the radiology 6 feet behind the patient. The PA designation indicates
department are almost always of better quality than the direction of the X-ray beam as it traverses the body
those done with portable techniques. The portable from back (posterior) to front (anterior). The patient’s
studies can be useful, however, provided the interpreter arms are either raised or the shoulders are rolled
is aware that (1) the study was obtained using a forward toward the detector or cassette, stretching the
portable unit and (2) portable techniques have certain thoracic cage while spreading and raising the scapulae.
limitations. Portable radiographs are usually taken with the
In standard chest radiography obtained in a PA patient in a semirecumbent or recumbent position
projection (Figure 14-5), the patient stands upright (Figure 14-6). In these positions, the arms are not
with the anterior chest wall against the imaging raised over the head and the chest wall is not elevated
and elongated. These films are commonly shot from
front to back, hence the AP designation. Unlike PA
radiographs where the tube-to-receptor distance is
standardized at 72 inches, the tube-to-receptor distance
for portable AP chest radiographs is generally no more
than 48 inches, and it is often as short as 36 inches.
Due to the combined effect of the shorter tube-to-
receptor distance and the fact that the heart is farther
away from the receptor in the AP projection, the
shadow of the heart (the cardiac silhouette) is magnified
compared to its appearance in PA.
Best Practice
AP versus PA Radiographs
FIGURE 14-5 Posterior-anterior (PA) view, sometimes
Observers who are unaware of this single differ-
called a standard view: These films are taken in an X-ray ence between AP and PA radiographs find them-
or radiology lab. The patient’s front chest wall is posi- selves erroneously diagnosing enlargement of the
tioned against the image detector. The patient is normally heart (cardiomegaly) in their patients.
standing (erect). Note the raised arms.
Radiographic Studies Using its location and shape. Fluoroscopy is frequently used
during bronchoscopic procedures, such as transbron-
Contrast Materials chial biopsies, to verify that the forceps got to the area
Standard radiographic techniques are not very useful of pathology and that it is not on the pleural surface
when the structures of interest are surrounded by other (so as to prevent a pneumothorax).
structures of the same or very similar density. For
example, an X-ray of the chest does not show the aorta
or esophagus as distinct structures in the mediastinum COMPUTERIZED TOMOGRAPHY
because they are both of soft tissue density, the same as In computerized (axial) tomography (CT or CAT), a
the density of all the surrounding structures in the thin beam of X-radiation is projected through the
central portion of the chest. To demonstrate these patient in an axial plane to produce a scan. Rings of
structures, contrast materials must be used; contrast detectors surrounding the patient continuously mea-
materials have the ability to significantly block the sure the amount of the transmitted X-ray radiation. A
passage of X-rays and thereby alter the radiodensities of computer processes these measurements to produce a
the structures into which they are introduced. For two-dimensional image of the patient. Normal and
example, in arteriography, the technique used to visualize pathological anatomy is displayed as if the patient were
arteries on radiographs, a liquid contrast agent that cut into cross sections (hence the term “tomography”—
contains atoms of iodine bound to organic ring mol- to create a picture of a cut surface or slice).
ecules is injected into an artery while images are To assure that the region of interest is appropriately
obtained. The contrast agent mixes with the arterial included on the scan, a scout image—a digital radio-
blood, making the blood radiopaque (i.e., capable of graph produced by the CT scanner—is used to create
blocking a greater proportion of the X-ray beam). As a the CT exam prescription. The exam prescription
result, the artery is opacified, that is, its density is specifies the locations, thicknesses, and spacing of the
increased to show the interior of the vessel. Similarly, in cross-sectional images as well as the amount of X-ray
performing a study of the esophagus and stomach, energy to be used. Figure 14-7A is an example of a
commonly referred to as an esophogram and upper GI, CT scout image. The scout image is annotated with
either a barium sulfate suspension or Gastrographin superimposed lines that identify the start and end
(another water-soluble, iodine-based liquid contrast positions of the scan and the locations of proposed
agent) is ingested to fill the esophagus and stomach, so-called cuts; examining it ensures the completeness
allowing the internal features of these structures to be of the examination. Figure 14-7B shows the same scout
seen. Contrast agents, particularly intravascular contrast image view annotated with slice location data.
agents, are also useful in CT scanning to distinguish The thickness of the slices used to create an image
pathological abnormalities, such as tumors, abnormally set can be varied depending on the degree of detail and
enlarged lymph nodes, or blood clots from normal the size of the structures of interest for a particular
vascular structures. examination. A typical slice thickness ranges from
1.5 to 10 mm.
When studying CT images, the contrast and
FLUOROSCOPY brightness are adjusted to best display the anatomic
In fluoroscopy (or fluoro), an image intensifier attached structures of interest. These adjustments are performed
to a video system is used to generate and record the X-ray by changing the:
images. Unlike radiography, in which a single image—a
• Window width, or range of different gray values
snapshot—is obtained, fluoroscopy generates a series of
displayed.
radiographic images, closely spaced in time, creating a
• Window center (level), or position of the center
kind of movie or video of internal organs such as the
value of the window width along the range of
heart, blood vessels, esophagus, or stomach as they
possible gray values.
function. The resulting video files allow the reader to see
moving pictures instead of still images. Figure 14-8A is an example of a chest CT with intravas-
Fluoroscopy is useful in guiding a catheter, needle, cular contrast using a mediastinal window accentuating
or biopsy forceps to a particular point inside a patient. the differing radiographic densities of the major
It is also helpful in clarifying whether a nodule that structures such as the heart, aorta, and pulmonary
projects over the lung on a plain film is within the lung artery. By adjusting the window width and level, the
parenchyma or attached to the chest wall. This distinc- same image can be modified to display the internal
tion is made by rotating the patient under fluoroscopy structures of the lungs (Figure 14-8B).
as the nodule is viewed; the movement of the nodule By obtaining thin CT slices and changing how the
can be compared with the movement of structures computer processes the data, radiologists can obtain
behind or in front of it to get a better appreciation of very detailed, sharp images of small structures in the
(A)
(A)
(B)
(B)
FIGURE 14-7 (A) A scout image of a computerized
tomography (CT) scan: This is used to determine the
slice locations for a full CT study. (B) The same scout
image: The image now includes the cut location data. (C)
FIGURE 14-8 (A) A chest CT with intervascular contrast
highlighting the mediastinal structures using a
parenchyma of the lung. This technique is commonly
mediastinal window. (B) The same patient with the
referred to as high-resolution computed tomography
window expanded to study the internal lung structures.
(HRCT). Figure 14-8C is an example of an image from (C) A high-resolution CT: The HRCT enhances the
small peripheral structure of the scanned area—in
this case the lung. Note the superb detail.
Best Practice
an HRCT of the lung showing the exquisite detail of the
CT Settings small vascular and bronchiolar structures achievable
Because simultaneously displaying bone, me- using this technique.
diastinal (soft tissue), and lung at their optimal Though the basic CT data set is used to generate a set
window and level values is impossible, a com- of “stacked” axial images, the computer can reconstruct
plete review of a chest CT involves looking at slices in any desired plane without having to rescan the
each image using several different window and patient. Three-dimensional (3-D) images of structures can
level settings. also be generated. By combining basic CT techniques
with the use of intravascular contrast and applying some
X-ray beam, magnetic resonance imaging (MRI)

creates cross-sectional images based on the behavior of
hydrogen nuclei (protons) in a magnetic field. To
understand the basic physics of MRI, think of the single
protons in the hydrogen nuclei as tiny bar magnets
(magnetic dipoles), similar to the needle in a compass.
A powerful magnet is used to cause the dipoles of the
hydrogen nuclei to align with the external magnetic
field. Radio frequency pulses are then used to excite, or
tip, the dipoles out of alignment with the external field.
Once the exciting radio frequency pulse is turned off,
the protons relax back to the ground state in which
they align again parallel to the external field. As the
protons realign, the scanner “listens” for a radio
frequency signal emitted from the body. The computer
© Delmar/Cengage Learning system of the MR scanner then processes the emitted
signals to form the images. MRI, unlike CT and radiog-
raphy, uses no ionizing (X-ray) radiation. As a result,
numerous closely spaced images in several different
planes can be generated with excellent detail and tissue
FIGURE 14-9 An image of a 3-D reconstruction of a CT
differentiation without the risk of overexposure to
angiogram of the abdominal aorta and its subdivisions. radiation, which is a growing concern in CT imaging.
An MRI study involves putting the patient in a
small tunnel, and some patients experience feelings of
of the special imaging-processing capabilities of modern claustrophobia. Recently, open, or C-shaped, MRI
CT systems, technicians can create 3-D images of many scanners have allowed even claustrophobic patients to
vascular structures. Figure14-9 is an example of a 3-D undergo MRI procedures. Because it can take several
reconstruction of a CT angiogram of the abdominal seconds to obtain the data for each standard MR data
aorta and its major branches. set, imaging moving objects, such as the heart, was
For patients with pulmonary problems, CT scans difficult. However, specialized fast scanning techniques
are frequently used to determine the nature and that allow imaging of the heart and great vessels are
location of various infiltrates or masses. Computerized now widely available.
tomography is the most sensitive means of detecting The appearance of an MR image depends on how
bronchectosis and is very sensitive for detecting and the radiofrequency data are obtained. The amount of
quantifying pleural fluid (effusion), pleural thickening time between the radiofrequency pulses used to excite
(plaques), or pneumothorax. It can also be used to the protons is referred to as TR. The amount of time
guide needle biopsies (i.e., a tissue sample usually between an exciting pulse at the time at which the
obtained by an invasive method) and to allow for scanner is listening for the radiofrequency signal, or
precise placement of catheters to drain abscesses or echo, is called the TE. By systematically varying TR and
other localized fluid collections. The most advanced CT TE, one can accentuate the differences between tissues
scanners currently in wide clinical use acquire up to 64 and translate these differences into differences in
channels of attenuation data simultaneously as the brightness, or contrast, in the MR images. Figure 14-10A
table moves the patient continuously through the X-ray is an axial (transverse) image of the brain using a
beam. This technique, commonly referred to as spiral short TR/short TE, or T1-weighted pulse sequence.
CT, creates a data set with no gaps between adjacent (By convention, axial images are oriented so that the
slices, making it possible to create exquisitely detailed patient is facing up and the patient’s right is to your
images of the human body. These systems make it left.) On T1-weighted images:
possible to image structures as small as the coronary • Water and similar materials produce the lowest
arteries or peripheral branches of the pulmonary artery signal and appear dark, as illustrated by the
and to diagnose coronary artery stenosis or pulmonary cerebrospinal fluid (CSF) in the ventricular
emboli with high specificity and sensitivity. system.
• Solid materials, such as the gray-and-white
MAGNETIC RESONANCE IMAGING structures of the cerebral hemispheres, show
Whereas CT creates images based on differences in the signals of intermediate intensity and show up
abilities of various tissues to block, or attenuate, an as various shades of gray.
coronal or sagittal images can be generated directly by

Best Practice changing how the radio frequency signal is detected.
Figure 14-10C shows a T2-weighted midline, sagittal
MRIs and Magnets image of the head and cervical spine. Here the conven-
tion is to display the image as if the patient were
Because of the strength of the magnets used
facing to the reader’s left. Figure 14-10D is a coronal,
in MRI, patients with certain metallic implants
T1-weighted image of the brain.
or electronic devices, such as pacemakers or
MRI currently has relatively limited clinical appli-
cochlear implants, cannot be imaged. In addition,
cations with regard to the lungs, though a variety of
patients with metallic foreign bodies, especially
possible uses are being actively investigated. Most
in the eye or orbit, should not be imaged because
patients who require MRI while under the care of a
there is a danger of displacing magnetic metals.
respiratory therapist are imaged for neurological
MRI can also erase computer disks or credit cards
conditions.
brought into the MRI suite. Because of these
dangers, most mechanical ventilators and many
monitors cannot be used near an MRI scanner.
However, specially designed and fabricated ULTRASOUND
systems are becoming available to allow scans Ultrasound, or sonography, uses high-frequency
of critically ill patients. Until these new devices sound waves to generate cross-sectional images of the
become available, these patients may have to be body. Various tissues differ in their abilities to transmit,
manually ventilated while they are being scanned. absorb, or reflect high-frequency sound waves. To
Also, furniture, gas cylinders, medical devices, or generate an ultrasound image, a transducer (a device
other objects containing ferrous materials (iron that can convert one form of energy to another and
compounds) or other magnetic metals are banned back again) is placed against the surface of the body.
in MRI suites. Additionally, pagers, cell phones, The transducer converts an electronic signal into a
PDAs, watches, jewelry (especially piercings), pulse of high-frequency sound waves that is transmit-
and medical/dental implants may contain ferrous ted into the body. This acoustic pulse passes through
compounds. These objects can be pulled into the some tissues (usually liquids) very well, but soft tissues
bore of the magnet at high velocities, posing the absorb some of the acoustic energy. Some energy is
risk of serious bodily injury to patients and staff, scattered away from the transducer, and some is
not to mention significant damage to the very reflected back toward it from the interfaces where two
expensive MRI equipment. tissues of slightly different acoustic properties touch
one another. Once the transducer has generated and
transmitted the initial pulse, it “listens” for the echo of
sound reflected back from the patient’s internal organs.
• Finally, fat in the subcutaneous tissues and in
In the listening mode, the transducer converts the
the marrow space between the inner and outer
acoustic energy of the reflected ultrasound pulse to a
layers of the skull show the highest signal and
series of electronic signals. The computer of the
appear as white.
ultrasound unit uses data about the strength and
Compare this image with Figure 14-10B, an image timing of the reflected sound waves to create an image.
obtained using a long TR/long TE, or T2-weighted pulse The frequency of the sound waves used for most
sequence. medical imaging is 3.5–10 million cycles per second
(MHz), far above the range of human hearing.
• The highest signal is emitted from the CSF in
Ultrasound is a minimally invasive method that
the ventricular system, which appears as white.
does not use either ionizing or nonionizing radiation.
• The gray-and-white matter of the cerebral
The sound transmission and reflection characteristics of
hemispheres emit signals of lower intensity and
a tissue are completely different from the properties
appear as dark gray.
that contribute to radiodensity or MR tissue contrast.
• The signal emitted by fat is of intermediate
Consequently, ultrasound differentiates tissues in ways
intensity between those of CSF and soft tissue.
completely unlike conventional radiography, computed
A third commonly used pulse sequence is the long tomography, or MRI.
TR/short TE, which produces spin density: the signal is Ultrasound images may be recorded as two-
weighted in proportion to the number of protons per dimensional images, frozen at a particular point in
unit volume in a given area. time, or they can be stored and viewed as real-time
In addition to modifying the tissue contrast by video or movie files. Although most ultrasound
changing how an MR signal is obtained and processed, imaging is rendered as two-dimensional cross sections,
(A) © Delmar/Cengage Learning
(B)
(C) (D)
FIGURE 14-10 (A) an example of an axial (transverse) image of the brain using a short TR/
short TE, or T1-weighted pulse sequence. (B) An image obtained using a long TR/long TE, or
T2-weighted pulse sequence. (C) A T2-weighted midline, sagittal image of the head and
cervical spine (the image is displayed as if the patient were facing to the reader’s left).
(D) A coronal, T1-weighted image of the brain.
a number of available systems can generate three- for imaging structures near the surface of the body.
dimensional, real-time images. Furthermore, some substances, such as bone or air,
When imaging the chest, several factors limit the block the transmission of ultrasound waves into the
use of ultrasound as compared to CT or MR. First, the underlying tissues, making it impossible to image
ability of the sound waves to penetrate and therefore to structures in the aerated lung or directly beneath the
image the human body decreases with their frequency. ribs or scapulae.
On the other hand, the ability of ultrasound to demon- In imaging of the chest, ultrasound is commonly
strate small structures increases as the frequency of the used to evaluate pleural effusions and to guide drain-
beam increases. Consequently, ultrasound works best age of effusions (thoracentesis) or other pleural or
(A) (B)
FIGURE 14-11 (A) A 2-D grayscale sonographic image of the right common femoral vein
showing a nonocclusive clot (thrombus) against a black background due to the absence of
reflected echoes from the blood flowing around the clot. (B) A color Doppler image of the
same area: The ultrasound unit has been adjusted to detect signals reflected from the
moving red cells in the vein and to translate them to a blue color. In this image, the clot
is seen as a gray structure partially surrounded by the blue color representing nonclotted,
flowing blood.
pericardial fluid collections. More common applica- technologically advanced systems, ultrasound devices
tions for ultrasound are: are being used in surgery, in emergency room ICUs,
and sometimes on patient floors.
• Imaging abdominal or pelvic organs, including
the prenatal evaluation of fetal growth and
development. NUCLEAR MEDICINE STUDIES
• Imaging the arteries and veins of the extremities
Nuclear medicine studies involve administering a small
and neck.
amount of a radioactive material (called a radiotracer,
• Echocardiography, a specialized form of
tracer, radioisotope, or isotope) to the patient. Imaging is
ultrasound used to image the heart in motion.
performed by placing the patient under a camera that
Doppler sonography is useful for documenting blood detects the photons of energy emitted by the tracer as
flow and measuring the degree of narrowing, or the isotope with which it is labeled decays. The radio-
stenosis, in diseased vessels. In the intensive care unit, isotope tracer is carried to and accumulated by the
where patients are at increased risk of developing deep tissues and organs of interest by a number of different
venous thrombosis and pulmonary embolism, Doppler mechanisms in the areas of interest. For instance, in a
sonography can detect clots in the deep veins of the perfusion lung scan, particles of a material called
lower extremities. Figure 14-11A is a 2-D grayscale macro-aggregated albumin are tagged with a radioac-
sonographic image of the right common femoral vein tive isotope of technetium and injected into the
showing a nonocclusive clot (thrombus) against a patient’s vein. Due to the size of the albumin particles,
black background due to the absence of reflected they and the isotope they carry become trapped in
echoes from the blood flowing around the clot. pulmonary capillaries in the perfused parts of the lung.
Figure 14-11B is the color Doppler image of the same When the patient is placed under a camera, the image
area. The ultrasound unit has been adjusted to detect (Figure 14-12A) is a map of the perfused parts of the
signals reflected from the moving red cells in the vein lungs. Similarly, ventilation can be mapped by having
and to translate them to a blue color. In this image, the the patient breathe either a radioactive gas, usually an
clot is seen as a gray structure partially surrounded by isotope of xenon (Figure 14-12B), or a radioactive aero-
the blue color representing nonclotted, flowing blood. sol. The two images make up a ventilation/perfusion
With the advent of smaller, lightweight, and more (V⭈ /Q⭈ ) scan for the patient. By comparing the images
(A)
(B)
FIGURE 14-12 (A) A perfusion lung scan, showing the trapped isotopes in the pulmo-
nary capillaries in the perfused parts of the lung. (B) Mapping of ventilation when the
patient breathes a radioactive gas, usually an isotope of xenon.
and looking for areas of the lung that are ventilated bloodstream. White blood cells are naturally attracted
but not perfused, to the reader can detect pulmonary to areas of infection or inflammation. Consequently
emboli. when radio-labeled WBCs are injected, they and the
Another example of nuclear medicine imaging is isotope are concentrated in any sites of active inflam-
the use of indium-labeled white blood cell scans to mation. Such scans are sometimes used to detect
localize infectious or inflammatory processes. In this occult (hidden) abscesses or other inflammatory
type of study, white blood cells (WBCs) labeled processes when other diagnostic tests have been
with radioactive indium111 are injected into the unsuccessful.
Still another common type of nuclear medicine

imaging is the use of the radioisotope thallium201 to
evaluate the blood flow to the heart in patients
suspected of having myocardial ischemia (angina
pectoris).
Positron emission tomography (PET) is yet
another application of nuclear medicine imaging. In
this technique, chemical compounds, such as glucose
or other sugars, are labeled with positron-emitting
isotopes. These compounds are actively taken up by
cells during their metabolism. A positron is a unique
particle in that, when a single positron collides with an
electron, both particles disappear in a phenomenon
called annihilation. Positron annihilation results in the
emission of two high-energy photons that travel in
opposite directions along a straight line. The photons
can be detected using a special scanner that can
identify the “coincident” photon pairs and map their
locations in the body with much greater accuracy than
is achievable with a standard nuclear medicine camera.
By assigning different colors, or grayscale values, to
various levels of activity of tracer uptake, one can
actually see the accumulation and concentration of the
labeled materials. Because the radio-labeled com-
pounds used for PET imaging are actively taken up by
living cells during metabolism, groups of actively
growing and dividing cells appear as foci of increased
activity—so called hot spots—on PET images.
FIGURE 14-13 A typical coronal projection PET scan image
PET can be used to image infectious or inflamma- in a patient who has a history of cancer of the urinary
tory processes. However, it is most widely used for bladder treated by cystectomy and who has developed
assessing the growth and spread (metastasis) of metastases to the left hilar lymph nodes.
malignant tumors. For example, using a glucose
derivative labeled with the positron-emitting isotope
fluorine18 (F-18 fluorodeoxyglucose, or FDG), PET
scanning can detect malignancies such as lung cancer
because many cancers are metabolically active and tend
to accumulate the modified glucose molecules to a
greater degree than normal tissues. Figure 14-13
presents a typical coronal projection PET scan image in
a patient with a history of cancer of the urinary bladder
treated by cystectomy; the patient has developed
metastases to the left hilar lymph nodes.

Often, PET images are combined with CT or MR
images (a process sometimes referred to a fusion
imaging) to allow physicians to localize lesions ana-
tomically with greater confidence than is possible using
PET images alone. Figure 14-14 is an example of a FIGURE 14-14 An example of a PET-CT fusion image in a
PET-CT fusion image in a patient with a left hilar lung patient with a left hilar lung cancer.
cancer. The colored PET data are mapped over the
grayscale CT data for an axial image at the level of
the tumor. radiologists, physicians who have completed at least four
The formal interpretation of imaging studies years of training after medical school. Although the
requires knowledge and skills that can be fully acquired formal interpretation of medical imaging studies is
only through years of medical education. In the beyond the scope of this chapter and not a part of
hospital setting, the final interpretations of radio- respiratory therapy practice, RTs need to understand the
graphic studies are usually performed by diagnostic range of imaging techniques that can be brought to
bear when evaluating lung structure and function, and How to Interpret Studies
they should have a general understanding of the types
of abnormalities commonly encountered in clinical In interpreting (reading) radiology studies, the reader
practice. must fully understand the context in which the study
was obtained. Before a study is interpreted and man-
agement decisions are made based on the findings, the
Radiation Safety images should be reviewed for technical adequacy in
light of the following questions:
Respiratory therapists and other health care professionals
managing unstable patients are sometimes required • Does the examination obtained match the
to tend to their patients when imaging studies are examination that was ordered?
performed. Occupational exposure to ionizing radiation • Is the patient clearly identified by markings or
while caring for patients undergoing radiography, annotations that are either a part of the images
computed tomography, and nuclear medicine examina- or permanently linked to the study in the
tions is a legitimate concern. However, the levels of electronic medical record (EMR)?
occupational exposure are tightly regulated, and the risks • Are the date and time of the image also included
can be minimized by following a few simple rules. on the images or linked to the study in the EMR?
• Is the position of the patient clearly indicated
• An individual’s exposure is directly related to the (upright, supine, decubitus, or oblique)?
level of exposure used to generate the images • Is the view or projection (PA, AP) clearly indi-
and to the duration of the exposure. Technolo- cated on the images?
gists are trained to use the lowest possible dose • Is the region of interest completely included on
of radiation necessary to produce technically the images?
adequate images, thus minimizing the dose to • Are the exposure factors adequate?
the patient and they exposure to personnel due • Was the X-ray beam of sufficient energy, and was
to scatter radiation. the length of exposure sufficiently long to
• The respiratory therapist can further limit produce an image of diagnostic quality?
exposure by minimizing the time spent in a • Was a sufficient amount of X-ray attenuation
room while a study is being obtained. data collected to generate CT images that are of
• The RT who must be in the room during an diagnostic quality?
exposure should ask the technologist for appro- • Were an adequate number of photons counted
priate shielding equipment, such as lead aprons to generate nuclear medicine images that can be
or screens. confidently interpreted?
• Radiation dose varies inversely with the square • Did the way in which the image was acquired
of the distance from the source (the inverse either create artifacts or degrade the image?
square law, Chapter 3). So increasing the • Were all garments, jewelry, overlying devices
distance from the source of exposure, typically (lines, tubes, etc.), surgical instruments, and
the patient rather than the imaging device other foreign bodies removed? If not, does their
itself, significantly decreases exposure. Increas- presence compromise or limit the diagnostic
ing the distance to the patient’s bedside from quality of the examination?
1 to 2 feet, reduces the scatter dose by a • Are the images degraded by patient movement
factor of 4. (breathing, cardiac motion, changes in
• Finally, if the RT is in a position that requires position)?
regular attendance during imaging examinations,
the facility’s safety office should provide a
personal dosimeter to monitor the cumulative PREANALYSIS
exposure over time.
In addition to knowing the type of study being read,
Ultrasound and MR examinations do not entail the reader must know how the patients were prepared
exposure hazards. However, MR does present signifi- and positioned for examinations. For example, one
cant physical hazards due to the effect of the power- needs to know whether a chest radiograph was
ful magnetic fields on certain metal objects such as obtained in the upright or supine position. Depending
chairs, gas canisters, and medical devices. Also, on the position, a suspected pleural effusion shows up
personnel and patients with medical devices such as either as a blunting of the costophrenic angle in the
pacemakers or cochlear implants should not enter upright position or as generalized increase in the
the MR suite without first checking with the MR density of the involved lung (hemithorax) due to the
supervisory staff. fluid lying behind the lung in the supine position.
Best Practice
Exposure of the Chest
Radiograph
As a general rule, in a radiograph of the chest,
the penetration and exposure should be such
that the intervertebral spaces in the thoracic
spine are just visible.
One must also be certain that the region of interest
is completely and appropriately imaged. For example,
if the concern is for a pneumothorax, a radiograph (A)
performed in a supine position or one that clips
(does not include) the lung apices, is inadequate.
The overall quality of the film must also be
assessed. When a chest radiograph is too dark (overex-
posed), a pneumothorax, which is also dark on a plain
film, is difficult to detect. Using intense back lighting
(called hot-lighting or spot lighting) details can be
enhanced in overexposed (dark) films. If the radiograph
is too light (underexposed), important mediastinal
landmarks or the tips of devices, such as endotracheal
tubes, central venous lines, or a Swan-Ganz catheter,
may not be visible.
Cardiac or respiratory motion can blur the images
of medical devices, particularly those in or near the
heart and great vessels, such as Swan-Ganz catheters or
internal cardiac pacemakers. Artifacts or foreign objects (B)
on an image may confuse the reader. For example, FIGURE 14-15 Two radiographs taken before (A) and
consider a portable chest X-ray obtained while a after (B) surgery: Note the endotracheal tube (ET), a
patient is in the operating room that shows a surgical Swan-Ganz (pulmonary arterial) catheter, a left thoracos-
clamp overlying the left lung. Without additional tomy tube, and several additional sternal wires that were
information or additional lateral or oblique views, placed as a part of the patient’s coronary artery bypass
the reader cannot determine absolutely whether the surgery.
clamp is inside the patient’s chest or lying on the
surgical drapes covering the chest wall. Finally, at some details can prevent adverse events such as the retention
point during the review of every examination, the of surgical drains, sponges or instruments—events that
reader should locate and identify all foreign objects are considered completely avoidable and inexcusable
and devices and compare them with previous examina- by patients and their families.
tions to determine whether there are any new devices
or lines or any of the previously noted devices and REVIEW OF THE STUDY
lines have changed significantly in their positions.
Be systematic! Always look at images and examinations
As an exercise, take a look at the two images in
in a consistent and systematic way. The order in which
Figure 14-15, which were obtained immediately before
an image is reviewed is not critical, as long as the
(A) and after (B) a trip to the operating room. Even a
method or sequence used is logical to the reader. The
relatively cursory comparison of the two images shows
method should ensure that the entire image, including
an endotracheal tube (ET), a Swan-Ganz (pulmonary
all edges, corners, and image annotations, are exam-
arterial) catheter, a left thoracostomy tube, and several
ined. Consider a commonly used sequence for evaluat-
additional sternal wires that were placed as a part of
ing a chest radiograph by reviewing Figure 14-16:
the patient’s coronary artery bypass surgery. Although it
is easy to become lackadaisical in the checking routine 1. Check the identity of the patient.
postsurgical tubes, drains, and lines, attention to these 2. Check the date and time of the study.
including the superior mediastinum (e.g., a shift

of the mediastinum, mass, aneurysm, abnormal
calcification).
14. Evaluate the trachea and central bronchi (e.g.,
masses, foreign bodies).
Be careful to review the entire image. A radiograph of
the chest can reveal a critical abnormality in the abdo-
men, or an abdominal film might identify something
critical in the chest. In many cases, an additional study
may be required to completely evaluate the incidentally
identified abnormality. However, do not make the
mistake of ignoring free gas in the abdomen beneath the
diaphragm or similar “incidental findings” on an
otherwise normal chest radiograph just because a chest
X-ray rather than an abdominal study was obtained.
The image used for this exercise (Figure 14-16) is
essentially normal. Nevertheless, the patient’s first ribs
are asymmetric and small, particularly on the patient’s
left. This happens to be an incidental finding or normal
variant, but it is still a good test of an RT’s observa-
FIGURE 14-16 Review of the chest radiograph.
tional skills.
For purposes of publication, the patient identifying

COMPARISON WITH PREVIOUS STUDIES
information and date and time of the study are
suppressed. This information is generally recorded or Always compare the current study with the most recent
displayed as image annotations at the corners of the studies of the same anatomic region to detect new
image. abnormalities and to reduce the tendency to mistake
3. Identify the type of study (know what was

ordered, what was done, position, view). Best Practice
4. Evaluate the technical quality of the image.
5. Identify any and all artifacts.
6. Identify all foreign objects (e.g., tubes, lines,
Systematic Review
devices). Having a systematic process of reviewing films
7 Evaluate extrathoracic soft tissues (e.g., subcuta- is helpful. RTs should follow the same sequence
neous emphysema, foreign material). every time they review a film to prevent miss-
8. Evaluate bony structures and joints (e.g., ing important facts. Sometimes changing your
fractures, dislocations, normal variations, perspective by moving around the film - go to the
abnormal densities). left - to the right - go forward and go backwards.
9. Evaluate the pleura, including the apices and Changing your point of view can help you “find”
costophrenic angles (e.g., a pneumothorax, variations in the film.
pleural effusion).
10. Evaluate the upper, middle, and lower zones of
the lungs, using the corresponding regions of the
opposite lung to improve your sensitivity to focal
abnormalities (e.g., masses, nodules, infiltrates,
cavities). Pay particular attention to the areas Minimizing Patient Movement
beneath the clavicles and first ribs, behind the Infants, small children, patients who are con-
heart, and beneath the domes of the diaphragm. fused or combative, and patients with Parkinson’s
11. Evaluate the right and left hilum, again using the disease, seizure disorders, or tremor-producing
opposite hilum for comparison (e.g., enlargement disorders may be very difficult to X-ray or perform
of one as compared to the other). scans on. If X-rays or scans are critically impor-
12. Assess the size and configuration of the heart tant, either such patients must be physically or
(e.g., cardiomegaly, abnormal shape). chemically restrained, or the practitioner has to
13. Evaluate the aorta, main pulmonary artery, settle for a poorer-quality film and analysis.
and other mediastinal soft tissue landmarks,
important and mention any so-called pertinent nega-

Best Practice tives. For example, in a patient with a resolving pneu-
monia, the final interpretation might be, “The lobar
Image Verification consolidation noted on the previous study has now
resolved, and there are no new areas of consolidation.”
The reader must verify that the image set is of
The reader then reports an impression that, as
the correct patient and was taken at the cor-
concisely as possible, explains possible reasons for the
rect time. An image or study that is not properly
observations. Consider, for example, a chest radiograph
labeled should be interpreted with caution, if at
obtained following drainage of a moderate left pleural
all. Critical errors in patient management can be
effusion. The image shows a patchy, air-space infiltrate
made if someone accidentally reads a study of a
in the left lower lobe (the description of your major
wrong patient or from last year while assuming
finding), a small residual left pleural effusion, and no
that the image represents the patient in question
evidence of a pneumothorax (a pertinent negative in a
today.
patient who has just undergone a procedure that may
be complicated by the development of a pneumotho-
rax). The patient’s morning examination indicates that
stable lesions or normal variants as pathological she has a productive cough, a fever, and an elevated
findings. The comparison is also helpful in the assess- white blood cell count. The explanation of the radio-
ment of the rate of change of new lesions or of lesions graphic findings could be that the patient has a left
appropriate for radiographic follow-up rather than lower lobe pneumonia associated with a parapneu-
biopsy or surgical removal. A single study is only a monic effusion.
snapshot in time; without comparing it to older Note: The impression should reflect and can be
studies, the reader cannot tell whether a process is influenced by all of the information known about the
improving, worsening, stable, or chronic. As a general patient (e.g., a productive cough, fever, and elevated
rule, a lesion, such as a lung nodule, can be considered white count). However, the observation and descrip-
benign if it shows no change in size or border contour tion of findings should reflect only the findings
over a two-year period. However, even relatively minor revealed by the images and should not be influenced
changes in the size or border features of a nodule are (biased) by other available clinical information.
cause for concern because certain lung cancers, particu-
larly those arising in regions where the parenchyma is
scarred, can evolve relatively slowly. Example Cases
The cases and commentaries in this section illustrate
how a variety of clinical conditions and disease pro-
CORRELATION OF FINDINGS WITH
cesses manifest themselves radiographically. A number
CLINICAL SITUATION
of technical and clinical factors related to the radio-
Accuracy in interpreting a radiograph improves greatly graphic findings are also discussed.
when the radiographic findings are compared with what
is known about the patient’s clinical presentation and
clinical course. The reader is not only more likely to NORMAL CHEST
look for information that is pertinent to the patient’s The normal PA chest radiograph (Figure 14-17) may
situation, but also more likely to correctly identify the show many features that reflect anatomic variations
pathology. For example, a diffuse infiltrate in an ICU among individuals.
patient could represent pulmonary edema, acute
respiratory distress, pneumonia, or pulmonary hemor- • Common variations are in the thickness of the
rhage, among many other conditions. The clinician is soft tissues of the chest wall, the shape of the
much more likely to correctly identify pulmonary heart, and the heights of the domes of the
hemorrhage as the underlying cause of the infiltrates if diaphragm.
he or she is aware that the nurse has reported significant • In Figure 14-17, note the symmetric soft tissue
hemoptysis and that the morning laboratory findings densities overlying the lower lungs due to the
show a significant drop in the patient’s hemoglobin or a normal breast shadows in this female patient.
marked prolongation of the patient’s bleeding time. • Another common normal finding related to both
the male and the female breast is the presence
of unilateral or bilateral solitary soft tissue
FINAL INTERPRETATION “nodules” over the lower lobes. On careful
The final interpretation of a radiological study should review, though sometimes only after a repeated
describe all observations that are believed to be examination with radiopaque markers placed on
© Delmar/Cengage Learning (A)
FIGURE 14-17 The normal chest.
the nipples, these are shown to be false nodules

due to the soft tissue of the nipples.
• Other normal variants are the presence of
additional ribs associated with the lowest
cervical vertebra, the absence or hypoplasia of
the last thoracic ribs, and deformities of the
sternum and anterior ribs such as pectus excava-
tum (sunken chest) or pectus carinatum (pigeon
breast).
Only through practice and experience does one become
proficient in recognizing normal variations and (B)
distinguishing normal and normal variant anatomy FIGURE 14-18 Emphysema and bulbous lung disease:
from pathological findings. (A) Radiograph. (B) CT.
EMPHYSEMA AND BULBOUS LUNG DISEASE

Emphysema is an irreversible enlargement of the of air in the chest cavity is a pneumothorax in the
airspaces (alveoli) in the lung with destruction of the pleural space or an air-filled bulla in the substance
alveolar walls. The resulting cystic airspaces may (parenchyma) of the lung itself. The radiograph in
become large enough to see with the naked eye and are Figure 14-18A and the CT scan in Figure 14-18B are
called bullae. Because air does not move efficiently out from a patient with marked changes of emphysema
of these abnormal air cysts, over time the size of the with bulbous disease. Note the increased lucency of the
bullae and of the lungs themselves tend to increase, lungs and the flattening of the diaphragm illustrated by
resulting in increased diameters of the chest and a the chest X-ray. The CT also shows the loss of normal
flattening of the diaphragm. The vessels in the most lung markings, the hyperlucency, and the formation of
involved regions tend to be reduced in number, innumerable bulla that displace and stretch the
smaller in caliber, and stretched lengthwise due to remaining vascular and septal structures. Making the
the increased volume of the diseased pulmonary distinction between a bulla and a pneumothorax is
parenchyma. critical. Placing a chest tube into a bulla on the mis-
In extreme cases, the structural elements of the taken impression that it is a large pneumothorax can
lung, including the blood vessels, are very diminished lead to severe complications, such as a persistent air
in number. It is difficult to tell whether a collection leak and chronic pneumothorax. Occasionally, bullae
may become infected or filled with fluid, in which

case air-fluid levels may be seen on upright chest
radiographs or on CT.
LOBAR PNEUMONIA
Infection in the lung is called pneumonia. Infections can
involve the air spaces (alveoli), the conducting airways
(bronchi and bronchioles), the walls and supporting
elements of the lung (interstitium), or any combina-
tion of these. Interstitial pneumonias, often caused by
viruses, produce an increase in the linear markings in
the lung and a thickening of the interlobular septa,
similar to the pattern seen in interstitial pulmonary
edema (discussed in Congestive Heart Failure,
Pulmonary Edema, and Pleural Effusion on page 368).
Infections of the alveoli or conducting airways produce
a focal area of increased density in the lung paren-
chyma that can be identified on chest X-ray, but their (A)
appearance differs in ways that can suggest one caus-
ative bacterium over another.
Pneumonia developing at the level of the alveolus
often presents as a lobar process—a condition that
involves much or all of one or more of the anatomic
lobes of the lung. To identify lobar diseases, the reader
must have a knowledge of the basic lobar anatomy of
the lung. The right lung normally has three lobes
(upper, middle, and lower), and the left lung has only
two (upper and lower). The lobes are separated from
one another by the interlobar fissures: two on the right
(the major and minor fissures) and one on the left (the
major fissure). The fissures separating lobes are not
especially prominent on a chest radiograph, but they
can become much more evident should fluid accumu-
late in the fissure or should a lobar infiltrate develop in
the adjacent lung.
Lobar processes tend to produce a relatively
uniform, often quite dense, opacification of the (B)
involved portions of the lung. Figure 14-19 is an
FIGURE 14-19 Lobar pneumonia: (A) PA projection show-
example of a lobar pneumonia involving portions ing the right minor fissure sharply defining the inferior
of the right upper lobe. On the PA projection border of the infiltrate, indicating involvement of the
(Figure 14-19A), the right minor fissure sharply defines anterior segment of the right upper lobe. (B) Lateral view
the inferior border of the infiltrate, indicating involve- showing an area of consolidation partially delineated by
ment of the anterior segment of the right upper lobe. the cephalad portion of the right major fissure, which
However, the lateral view (Figure 14-19B) is somewhat normally defines one border of the posterior segment of
confusing because the area of consolidation is also the right upper lobe.
partially delineated by the cephalad portion of the
right major fissure, which normally defines one border caused by Streptococcus pneumoniae, though many other
of the posterior segment of the right upper lobe. This bacteria can produce this pattern of disease.
unusual appearance is due to the involvement of
portions of both the anterior and posterior segments of
the right upper lobe while sparing the apical segment. BRONCHOPNEUMONIA
This pattern of involvement is sometimes referred to as Bronchopneumonia is a second common pattern of
pneumonia of the axillary segment, based on reports of pneumonia produced by bacterial and, less commonly,
a normal variant axillary bronchus supplying these viral or mycoplasmal (fungal) infections of the lung.
regions of the lung. Classically, lobar pneumonia is The classic agent is Staphylococcus aureus. In this case,
(A)
FIGURE 14-20 The typical, patchy, inhomogeneous

appearance of the infiltrates of a bronchopneumonia
involving all lobes in a patient infected with Mycoplasma
pneumoniae.
the initial focus of infection is in the airways, and the

infectious agent can be passed relatively freely from
one area to another as secretions are transported
centrally and the patient coughs. The infection starts
with the bronchioles and bronchi, and then the alveoli
supplied by the affected airways become involved.
Unlike lobar pneumonias, no anatomic barriers, such
as the fissures, act as barriers to the spread of the
process. Consequently a bronchopneumonia often
involves more than one lobe, and in many cases both
lungs are affected. Figure 14-20 illustrates the typical,
patchy, inhomogeneous appearance of the infiltrates of
a bronchopneumonia involving all lobes in a patient
infected with Mycoplasma pneumoniae. (B)
FIGURE 14-21 (A) Air bronchograms against a background
ALVEOLAR (AIR-SPACE) INFILTRATES of extensive alveolar consolidation in a patient with over-
AND AIR BRONCHOGRAMS whelming sepsis and diffuse alveolar damage. (B) A num-
Lobar pneumonia is one example of a whole range of ber of branching lucencies radiating from the left hilum
conditions that result in alveolar, or air-space. consoli- and extending well into the periphery of the left lung.
dation (infiltrates). Air-space disease starts peripherally
and progresses centripetally (toward the center),
displacing the air from the lung parenchyma. Because becomes clearly defined as a linear or cylindrical lucency
the central airways have more effective ways of clearing in the area of consolidation. These lucencies are
mucus and debris than do the peripheral air-spaces, referred to as air bronchograms. Figure 14-21 illus-
they tend to remain filled with air. As the lung sur- trates air bronchograms against a background of
rounding the air-filled bronchus becomes more extensive alveolar consolidation (Figure 14-21A) in a
radio-dense due to the accumulation of fluid, cells, patient with overwhelming sepsis and diffuse alveolar
bacteria, pus, or blood in the airspaces, the bronchus damage. This radiograph (Figure 14-21B), on careful
examination, shows a number of branching lucencies also result in the displacement of the hilum and the
radiating from the left hilum and extending well into elevation of the diaphragm on the involved side.
the periphery of the left lung. This is an extreme Because an airless lobe can be very small, changes of
example of air bronchograms. An air bronchogram is complete lobar atelectasis can be easily overlooked,
said to be present if airways can be followed to their particularly on a single view of the chest. Figure 14-22
segmental or subsegmental branches in a lobe (roughly illustrates the radiographic appearance of complete
three or four generations of branching from the atelectasis of the right middle lobe. Figure 14-22A is a
carina). The clinical settings in which alveolar infil- PA radiograph of a patient with complete atelectasis of
trates are common include lobar pneumonia, the adult the right middle lobe, showing only subtle loss of the
respiratory distress syndrome, neonatal hyaline mem- definition of the right heart border. The corresponding
brane disease (infantile respiratory distress syndrome), lateral view (Figure 14-22B) shows the atelectatic right
and pulmonary edema or pulmonary hemorrhage middle lobe as the thin band of soft tissue projected
(see Chapter 8). obliquely over the cardiac silhouette.
Figure 14-23 is a second example of complete
LOBAR ATELECTASIS lobar atelectasis.
Atelectasis is the technical term for volume loss or the • Figure 14-23A shows a radiograph of some soft
collapse of a portion of the lung. If the air is removed tissue fullness overlying the area between the
from the lung parenchyma, the volume of the remain- aortic arch and the main pulmonary artery (the
ing soft tissue is quite small. Lobar atelectasis, or aorticopulmonary window), hyperlucency of the
airlessness and volume loss of an entire lobe, typically upper portion of the left hemithorax, and
occurs when a central airway is blocked and the air stretching and splaying of the vessels in the
distal to the blockage is absorbed into the blood- upper portion of the left lung.
stream. As a result, the lobe supplied by the obstructed • The lateral view (Figure 14-23B) shows a thin
bronchus becomes smaller and more radio-dense. band of soft tissue density against the anterior
Atelectasis results in the displacement or bowing of wall of the hemithorax, increasing the density of
adjacent fissures toward the involved lobe, and it may the normally radiolucent retrosternal clear space.
(A) (B)
FIGURE 14-22 (A) A PA radiograph of a patient with complete atelectasis of the right middle lobe showing
only subtle loss of the definition of the right heart border. (B) The corresponding lateral view shows the
atelectatic right middle lobe as the thin band of soft tissue projected obliquely over the cardiac silhouette.
(A) (B)
(C) (D)
FIGURE 14-23 (A) The PA radiograph shows some soft tissue fullness overlying the area between the aortic arch
and the main pulmonary artery (the aorticopulmonary window), hyperlucency of the upper portion of the left
hemithorax, and stretching and splaying of the vessels in the upper portion of the left lung. (B) The lateral
view shows a thin band of soft tissue density against the anterior wall of the hemithorax, increasing the density
of the normally radiolucent retrosternal clear space. (C) The CT image shows a wedge-shaped area of soft
tissue density closely applied to the left anterior mediastinal and anterior-medial chest wall with a posterior
border that is bowed inward, toward the density. (D) A representative image from the patient’s PET/CT, show-
ing intense focal uptake of the F-18 labeled FDG in red.
• The CT image (Figure 14-23C) shows a wedge- • Figure 14-23D is a representative image from the
shaped area of soft tissue density closely applied patient’s PET/CT, showing intense focal uptake
to the left anterior mediastinal and anterior- of the F-18 labeled FDG in red.
medial chest wall with a posterior border that is
Both of these cases demonstrate, with atelectasis,
bowed inward, toward the density. This patient
that there is always a loss of volume in the affected area
had a complete obstruction of the left upper
and that other structures—other segments or lobes,
lobe bronchus due to lung cancer, resulting in
fissures, the heart, and/or mediastinum—are pulled
complete atelectasis of the left upper lobe.
(A) (B) (C)
FIGURE 14-24 (A) A thin-walled cavitary lesion that was initially thought to be infectious or inflammatory in origin. (B) The
follow-up study showing a significant increase in the thickness and irregularity of the wall of the cavity—changes highly
suggestive of malignancy. (C) A CT scan, acquired on a lung window setting, that confirmed the aggressive, irregular,
nodular wall of the lesion, one of the common presentations of the squamous cell type of bronchogenic carcinoma.
toward the area of atelectasis. In the most extreme inflammatory or infectious in origin. The patient
cases, when the right or left main bronchus is in Figure 14-24 presented for an annual physical
obstructed—for instance, by tumor—the entire lung on examination with a new, thin-walled cavitary lesion
the involved side collapses, and the heart and mediasti- (Figure 14-24A) that was initially thought to be
num shift toward the involved side, resulting in infectious or inflammatory in origin. However, a slight
complete opacification (white-out) on the side of the irregularity of the wall was noted; so the patient had a
lesion and hyperexpansion of the uninvolved lung on follow-up chest X-ray to see whether the cavity resolved
the opposite side. or progressed. The follow-up study (Figure 14-24B)
showed a significant increase in the thickness and
irregularity of the wall of the cavity—changes highly
LUNG CANCER suggestive of malignancy. The CT scan in Figure 14-24C
Respiratory therapists frequently are called on to was acquired on a lung window setting and obtained
evaluate and help manage patients with lung cancer, or to evaluate the patient’s hilar and mediastinal nodes
bronchogenic carcinoma. The radiographic appearance before removal of the lung. It confirmed the aggressive,
of primary malignancies of the lung is highly variable, irregular, nodular wall of the lesion, one of the
ranging from solitary pulmonary nodules or masses common presentations of the squamous cell type
with more or less well-defined margins, through of bronchogenic carcinoma.
irregularly marginated masses and cavities, to ill-
defined masses and infiltrates or diffuse infiltrates
resembling lobar or bronchopneumonia. Other TUBERCULOSIS
patients present with no abnormalities in the lungs but Tuberculosis (TB), an infection caused by Mycobacterium
have mediastinal or hilar masses due to disease spread- tuberculosis, was once relatively well controlled in the
ing to the lymph nodes. Still others, like the patient in United States, but it has experienced a resurgence due
Figure 14-23, present primarily with atelectasis. Finally, to the prevalence of HIV/AIDS and to the expanding
unfortunately, for many patients, their tumors produce use of immunosuppressive therapies for a variety of
no detectable radiographic abnormalities; their cancers malignant and nonmalignant conditions. Two forms
are radiographically occult. of tuberculosis are generally described: primary and
When a lung cancer presents as a mass or nodule, postprimary (reactivation).
the lesion shows growth over time. Typically, lung Primary tuberculosis occurs on an individual’s first
cancers double in volume within 6 weeks to 6 months. exposure to the bacillus and often goes undetected
(For spheres, only a 25% increase in diameter produces clinically or radiologically. If a patient happens to have
a two-fold increase in volume.) Lesions with volume a chest X-ray during the initial infection, the appear-
doubling times longer than 6 months tend to be ance is one of a nondescript focal infiltrate and/or hilar
benign, such as granulomas or hamartomas (benign adenopathy, especially in children. In most individuals,
tumors containing several different types of tissue); the infection is contained, and the X-ray shows little or
lesions that double in less than 6 weeks tend to be no detectable residual abnormality. In some patients,
(A) (B)
FIGURE 14-25 (A) A chest X-ray illustrates bilateral patchy apical inflitrates with nodules typical of early
reactivation TB. (B) The CT scan shows the same patient’s pathology depicting patchy areas of alveolar
consolidation in the apices of both lungs.
the healed focus of infection can be seen as a soft tissue miliary TB because the nodules are generally 1–3 mm
nodule, called a granuloma, which may calcify over in size, comparable in size to millet seeds.
time. Some patients with healed primary tuberculosis
also show calcifications in hilar or mediastinal lymph
nodes.
CONGESTIVE HEART FAILURE, PULMONARY
Postprimary, or reactivation, tuberculosis occurs in
EDEMA, AND PLEURAL EFFUSION
patients with a previously contained primary infection. Patients with congestive heart failure due to chronic
In such patients, alterations in the ability to fight coronary artery insufficiency, previous myocardial
infection due to the weakening of the immune system infarctions, or chronic cardiomyopathy frequently have
allow the bacillus to reemerge. The radiographic cardiomegaly. The cardiothoracic ratio cannot be used
changes are those of patchy consolidation (broncho- to assess cardiomegaly on AP or supine radiographs
pneumonia), often involving the apical segment of the because the heart is magnified to a greater degree than
upper lobe or superior segment of the lower lobe in on the PA projection.
one or both lungs. Figure 14-25A is a chest X-ray of a In congestive heart failure, the progression of
patient with early reactivation TB showing patchy, changes in the pulmonary vascular anatomy, intersti-
nodular infiltrates in the apices of the lungs. Figure tium, and airspaces is relatively predictable based on
14-25B is the patient’s CT scan showing patchy areas of the severity of the left ventricular dysfunction and the
alveolar consolidation in the apical segments of both resulting elevation in left atrial, pulmonary venous,
upper lobes. The early changes of postprimary disease and pulmonary capillary pressure.
often progress to cavitation, the radiographic hallmark • Early in the course of progression, the pulmo-
of reactivation TB. In many patients, the infection is nary venous pressure increases, resulting in an
ultimately contained by host responses or by treatment equalization of the sizes of the upper and lower
with specific drugs. However, even in patients who
recover from reactivation TB, the involved areas often
become fibrotic and scarred, resulting in bronchial Best Practice
dilatation and volume loss in the affected lobes.
In severely immunocompromised patients, TB is
less likely to have the characteristic apical distribution The Cardiothoracic Ratio
or cavitation. Instead, the disease demonstrates a On upright PA chest radiography, the ratio of
pneumonialike pattern similar to that seen in primary the width of the cardiac silhouette to the widest
tuberculosis. In some patients, the tuberculosis bacillus diameter of the thorax between the inner cortical
spreads through the bloodstream, seeding the intersti- margins of the ribs (the cardiothoracic ratio) is
tial spaces of the lungs and producing a pattern of fine normally less than 0.5.
nodularity throughout the lungs—a pattern called
lobe pulmonary veins. (Remember that, in the

normal upright patient, the upper lobe veins are
smaller in caliber due to the hydrostatic pressure
gradient between the upper and lower lung
zones.)
• With further deterioration in left ventricular
function and the resulting increases in left atrial
and pulmonary venous pressures, fluid begins to
leak from the intravascular space into the
pulmonary interstitium. This results in the
thickening of the septal structures in the lung,
particularly the interlobular septa.
• The thickening of the interlobular septae results
in an increase in the linear markings in the
lungs, which is easily appreciated in the periph-
eries of the lower lobes. A pattern of short, 1- to
2-cm-long lines perpendicular to the visceral
FIGURE 14-26 This patient demonstrates radiographic
pleura (Kerly B lines) may be seen.
evidence of congestive heart failure (CHF) and interstitial
• The accumulation of interstitial fluid may also
pulmonary edema: increased upper lobe vascular mark-
appear as a thickening of the fissures and of the ings, increased interstitial markings in the perihilar area,
peribronchial soft tissues (peribronchial cuffing). and many Kerly B lines.
• Finally, with the most marked elevations of left
atrial pressure, fluid begins to fill the airspaces,
resulting in alveolar consolidation, often in a blunting of the costophrenic angles laterally or posteri-
perihilar (batwing or butterfly) distribution. orly (see Chapter 13).
Figure 14-27 illustrates a common sequence of
Figure 14-26 illustrates the increased prominence of
radiographic changes in a patient with an acute
the upper lobe veins, increased linear (interstitial)
myocardial infarction (a heart attack).
markings in the central (perihilar) zones, and numer-
ous Kerley B lines in a patient with congestive heart • Figure 14-27A was taken at the time of the
failure and interstitial pulmonary edema. If the patient’s admission to the emergency depart-
patient’s congestive heart failure can be effectively ment and shows bilateral air-space infiltrates due
treated, these findings may resolve relatively rapidly. to acute, alveolar pulmonary edema.
Patients with congestive heart failure also often develop • Figure 14-27B shows partial clearing of the
pleural effusions, indicated by a rounding off or edema but development of bilateral blunting of
(A) (B) (C)

FIGURE 14-27 (A) The first of three films documenting the sequence of radiographic changes in a patient admitted to the
ER with a heart attack (myocardial infarction, MI): This first film shows bilateral air-space infiltrates due to acute alevolar
pulmonary edema. (B) The partial clearing of the acute pulmonary edema, but development of bilateral blunting of the
costophrenic angle, which is most apparent on the right due to development of pleural effusion. (C) The clearing of the
pulmonary edema and pleural effusions in response to treatment: However, there is a residual cardiomegaly (increased
size of the heart).
the costophrenic angles, more apparent on the shows a moderate left pneumothorax. The detection of
patient’s right, due to the development of pleural a pneumothorax may be difficult due to its size or the
effusions. presence of other conditions, particularly the presence
• Figure 14-27C demonstrates the resolution of of air in the chest wall, a condition called subcutane-
the pulmonary edema and pleural effusions with ous emphysema. Careful examination of Figure 14-29
residual cardiomegaly as the patient responded reveals that, in addition to the moderate right pneumo-
to treatment. thorax, there is a striped, or striated, pattern of alternat-
ing bands of density and lucency, best seen over the
Pulmonary edema due to heart disease is usually
right costophrenic angle. This striated appearance
associated with cardiac enlargement. However, some con-
is one of the radiographic signs of subcutaneous
ditions, such as acute mitral valve insufficiency (as can be
emphysema.
seen in rupture of a papillary muscle) or acute cardiomy-
The identification of pneumothoraces on supine
opathy resulting from viral myocarditis can result in
radiographs is also problematic unless the reader
pulmonary vascular congestion, pulmonary edema, and
searches for specific features. A classic indicator in a
pleural effusions with a normal heart size on chest X-ray.
supine image is the deep sulcus sign—the extension of
In chronic mitral valvular disease, an enlarged left atrium
the pneumothorax into the nondependent portions
is frequently seen in association with the changes of
of the costophrenic sulcus, resulting in a deep and
vascular congestion and pulmonary edema.
more radiolucent costophrenic angle on the involved
side. Figure 14-30 illustrates a deep sulcus sign in
PNEUMOTHORAX the left costophrenic angle in a patient who suffered
A pneumothorax occurs when air enters the pleural a small-caliber gunshot wound to the left chest.
space, allowing the lung on the affected side to col- Another, often very subtle, finding is increased
lapse. Pneumothoraces, particularly small ones, are lucency either in the region of the diaphragm on the
easy to miss on a chest X-ray if the study is not carefully involved side or along the heart border or adjacent to
reviewed. The signs of a pneumothorax are the pres- the mediastinum.
ence of a radio-dense visceral pleural line that separates It is easy to underestimate the size of a pneumo-
the lung, with its normal vascular and interstitial thorax if the reader considers only the distance between
marking from the air-containing pleural space. Obvi- the edge of the lung and the chest wall. Significant
ously, the air in the pleural space lacks the vascular and portions of the pneumothorax may be located anterior
interstitial markings and soft tissue components of a or posterior to the lung, and they may not be well
normal lung. So it appears more radiolucent than the appreciated on a single AP or PA view. The lateral view
adjacent lung, as illustrated by Figure 14-28, which of a chest radiograph, if available, should also be used
FIGURE 14-29 A right pneumothorax of moderate size and

what appears to be subcutaneous emphysema over the
right costophrenic angle (appearing as a striped light and
FIGURE 14-28 A moderate left pneumothorax. dark pattern).
expiration, the tissues surrounding the wound draw

together, closing the defect and preventing air from
leaving the pleural space. Over multiple respiratory
cycles, air progressively accumulates, intrapleural and
intrathoracic pressures progressively increase, and a
tension pneumothorax evolves.
Another common setting for tension pneumotho-
rax is in ventilated patients who require significant
positive pressures to maintain oxygenation. Tension
pneumothoraces tend to result in the kinking and/or
compression of the superior and inferior vena cava,
leading to decreased venous return to the heart,
decreased cardiac output, shock, and, in untreated
cases, death.
Whenever pneumothorax is identified on imaging,
the interpretation should include a comment on
whether there is evidence of tension. Signs of a tension
FIGURE 14-30 A supine view of a patient who was shot in pneumothorax (Figure 14-31A) include flattening or
the left chest with a small-caliber gun. Note the promi-
nent costophrenic angle on the left side as compared to
the right side, illustrating a pneumothorax.
in estimating the size and location of a pneumothorax.

CT scanning is much more sensitive at identifying and
estimating the volume of a pneumothorax than is a
radiograph. CT should be used in questionable cases
and when the severity of the patient’s clinical condition
is disproportionate to the apparent size of the pneumo-
thorax on the radiograph.
TENSION PNEUMOTHORAX
In a tension pneumothorax (see Chapter 11), the air in
the pleural space results in an increase in enough (A)
intrapleural and/or intrathoracic pressure to affect the
function of other organs, particularly the heart. They
can occur from a variety of injuries to the lung or chest
wall, but they are particularly common in penetrating
trauma, such as stab wounds. Wounds of this type
often result in a one-way, or flap, valve at the tissue
defect. During inspiration, air is pulled into the pleural
space by the negative intrathoracic pressure, but on
Best Practice
Pneumothorax
A pneumothorax should be assumed to exist until (B)
proved otherwise in any patient in whom subcu- FIGURE 14-31 (A) A patient with a tension pneumothorax: The
taneous emphysema (air under the skin) is seen film exhibits a tracheal, cardiac, and mediastinal shift toward
or in whom abnormal lucencies (clear areas) are the unaffected (contralateral) lung. (B) The treatment of a
seen overlying the lung or mediastinum. pneumothorax with the insertion of a chest tube: This film
shows the almost complete reexpansion of the lung.
relatively limited collapse of the lung. In patients

with underlying lung disease, even small pneu-
mothoraces can lead to a life-threatening
elevation in intrathoracic pressure.
• In those uncommon cases of bilateral tension
pneumothoraces, the heart tends to be small and
the diaphragm is pushed down far below its
normal position. However, the mediastinum
may or may not be shifted, depending on the
relative pressures in the two pleura.
PNEUMOPERITONEUM
A pneumoperitoneum (Figure 14-33) is air in the abdom-
inal cavity outside the stomach or bowel. Air tends to
rise to the nondependent portions of the abdomen; so
this condition is typically diagnosed on an upright
abdominal or chest radiograph, appearing as increased
radiolucency due to gas between the diaphragm and
liver or other upper abdominal organs. In these cases,
FIGURE 14-32 A right tension pneumothorax with marked the diaphragm appears as a thin, soft tissue density arc
widening of the ICSs and bulging of the parital pleura separated from the liver and other organs by a lucent
between the ribs: Note the shift of the heart, mediastinal crescent representing the free gas. As with pneumotho-
structures, and the trachea to the right. races, the identification of a pneumoperitoneum on a
supine radiograph is problematic. Consequently, in
patients who cannot stand or sit upright, it may be
necessary to resort to lateral decubitus views, with the
even inversion of the diaphragm on the side of the patient lying on the side and the X-ray beam parallel to
pneumothorax and a shift of the trachea, mediastinum, the exam table, to evaluate for the presence or absence
and heart away from the side of the pneumothorax. of free gas.
Other findings of a tension pneumothorax are illus-
trated in Figure 14-32, the radiograph of a patient with
a right pneumothorax. Note the marked widening of
the intercostal spaces and bulging of the parietal pleura
between the ribs in addition to the shift of the trachea,
mediastinum, and heart from right to left.
A tension pneumothorax is treated by the prompt
placement of a chest tube (thoracostomy) (Figure 14-31B),
which generally results in rapid resolution of the
hemodynamic instability attributable to increased
intrathoracic pressure. In Figure 14-31B, note the
marked decrease in the size of the pneumothorax
and the nearly complete reexpansion of the collapsed
left lung.
Two final notes about tension pneumothoraces:
• Be aware that the degree of collapse of the lung

on the involved side has no reliable correlation
to the degree of elevation of the intrapleural
pressure, especially in ventilated patients or
those with underlying lung disease. Pulmonary
edema, fibrosis, and other conditions decrease FIGURE 14-33 An upright abdominal pneumoperitoneum
the tendency of the lung to collapse completely, caused by free gas or air in the abdominal cavity: The
and the positive ventilatory pressure tends to preferred technique for these pictures are either an
keep the lung inflated, leading to the paradoxical upright abdominal or chest X-ray. Note the increased
situation of a tension pneumothorax with lucency of the film due to the presence of gas.
on a patient with a dissection of the ascending thoracic

aorta showing the thin, soft-tissue lucency of the
so-called intimal flap outlined by the opacified blood
in the true and false lumens of the dissection.
Aneurysms and dissections are two distinct patho-
logic entities, but they frequently coexist. Both are
often related to underlying atherosclerosis. Clinically,
aortic aneurysms are often silent and discovered in the
course of a workup for other conditions, particularly
coronary artery disease. In contrast, aortic dissections
often present as severe, acute chest pain. The radio-
graphic findings in both conditions are often relatively
unimpressive, particularly in the case of aortic dissec-
tion where aortic dilatation may not be a feature.
Although large aneurysms may appear as a dilatation
of the involved segment of the thoracic aorta, many
small, though clinically significant, aneurysms may
produce no apparent radiographic changes.
FIGURE 14-34 Enlargement of the thoracic aortic arch
indicating a thoracic aortic aneurysm.
High-speed trauma or crush injuries of the chest
may produce a range of traumatic aortic injuries, includ-
ing intimal laceration, traumatic dissections, transmu-
AORTIC ANEURYSM, AORTIC DISSECTION, ral lacerations (tears), and posttraumatic aortic
AND TRAUMATIC AORTIC INJURIES pseudoaneurysms.
An aortic aneurysm is an abnormal dilatation, or • Intimal lacerations are focal defects in the inner
ballooning, of the aorta. The wall of the aneurysm lining of the aorta that are usually radiographi-
includes all three histological layers—tunica intima, cally occult, though they can be symptomatic
tunica media, and tunica adventitia—that normally particularly if they are associated with local
make up the wall of the aorta. Figure 14-34 is a chest thrombosis and arterial occlusion.
radiograph on a patient with a thoracic aortic • Traumatic dissections are simply separations of the
aneurysm showing the abnormal enlargement of the intima from the media by a false lumen in the
aortic arch. setting of trauma.
An aortic dissection is a separation of the inner layer • Transmural lacerations are tears of the wall of the
of the aortic wall (the intima) from the other two layers aorta that involve all three layers.
(media and adventitia) by a false channel of flowing or • Aortic pseudoaneurysms are formed when a
clotted blood. Figure 14-35 is an image from a CT scan traumatic laceration or other through-and-
through injury of the aortic wall is contained by
the surrounding mediastinal soft tissues and
hematoma (Figure 14-36).
Chest radiographs in patients with traumatic

aortic injuries are usually unimpressive, but some
show a widening of the superior mediastinum and the
loss of definition of the aortic arch (Figure 14-36A).
CT scanning has now become the gold standard for
the initial diagnosis of traumatic aortic injuries. It is
capable of demonstrating the full range of findings
from relatively subtle, isolated intimal injuries to
obvious complete lacerations of the aorta with their

associated hematomas and pseudoaneurysms.
Figure 14-36B is an image from the CT scan obtained
on the patient with the widened mediastinum illus-
trated in Figure 14-36A, showing contrast filling a
FIGURE 14-35 A CT scan of a patient with a dissecting saccular pseudoaneurysm anterior to the proximal
ascending thoracic aorta aneurysm. These conditions can descending aorta surrounded by the soft-tissue density
rapidly become life-threatening. of the associated hematoma. Many thoracic surgeons
(A) (B) (C)
FIGURE 14-36 (A) Chest X-rays of patients with traumatic aortic injury may not always show clear evidence of those inju-
ries. But in all cases of high-velocity or crush trauma, they must be considered unless proven otherwise. (B) A contrast
CT of the patient shown in the previous figure: The CT shows contrast media filling a sacklike pseudoaneurysm in front
of the proximal descending thoracic aorta. The hazy area around the sack is a hematoma for the aortic leak. (C) A single
frame of the associated thoracic aortogram: The aneurysm shown in “C” (right upper darkness at the top of the long
tube-like structure is the pseudoaneurysm. In “B” it shows as the white projection in the right side of the chest – note
the light gray chicken leg shaped object.
have become accustomed to taking patients directly to

surgery based on the CT diagnosis of a traumatic
aortic injury. However, aortography, which can show
the detail of intimal injuries, dissections, and pseudo-
aneurysms, still has a role, particularly in patients
who are candidates for endovascular stent grafting—a
relatively new technique that involves placing tubular
grafts in the lumen of the aorta via a catheter placed
in the femoral artery and advanced to the site of
the injury. Figure 14-36C is a single frame from a
thoracic aortogram that demonstrates the pseudo-
aneurysm initially diagnosed on the CT image
(Figure 14-36B).
(A)
Best Practice
Thoracic Trauma
Traumatic aortic injuries, particularly aortic
tears and pseudoaneurysms, are life-threatening
conditions with exceptionally high mortality rates
if they are undiagnosed. The vast majority of
patients who are undiagnosed and/or untreated
are dead within 7–10 days of their trauma.
Occasionally, patients beat these odds and

survive for extended periods, as illustrated by the
patient whose CT (Figure 14-37A) and aortogram
(Figure 14-37B) shows a chronic pseudoaneu-
rysm nearly 5 years after his chest injury. Trau-
matic aortic injuries should be suspected in all (B)
cases of significant chest trauma, especially in FIGURE 14-37 A 5-year follow-up of the patient from
moderate- to high-speed motor vehicle collisions. Figures 14-36A–C. (A) The follow-up CT. (B) The 5-year
post–chest trauma single frame of his aortogram.
PULMONARY THROMBOEMBOLISM remains relatively normal while the perfusion images

In pulmonary thromboembolism, or more simply pulmo- show one or more areas of decreased activity in the
nary embolism (PE), blood clots that have formed in a pulmonary segments that are deprived of blood flow
peripheral vein break free and migrate through the by the blockages in their arterial supply. Figure 14-38A
right atrium and right ventricle to lodge in one or more is the ventilation study from a patient with proven
branches of the pulmonary artery. Risk factors for the acute pulmonary emboli showing the preservation
development of pulmonary emboli include prolonged of normal distribution of the inhaled xenon gas.
bed rest and immobilization. Patients with acute Figure 14-38B is the perfusion study from the same
pulmonary emboli often present with chest pain, patient showing numerous areas of little or no activity
shortness of breath, and rapid breathing. Pulse in the portions of the lungs where blood flow has
oximetry or arterial blood gas analysis generally been cut off by clots that occlude branches of the
shows significantly decreased levels of arterial oxygen pulmonary arteries.
(hypoxemia). The development of multidetector, helical, or spiral
The most common site of origin of pulmonary CT scanning has significantly altered the radiologic
emboli is in the deep veins of the legs. Although workup of patients with suspected pulmonary emboli.
preventive measures, such as early mobilization after So-called CT angiograms can now be prepared that are
surgery, the use of compression stockings or pneumatic of sufficient quality to detect emboli directly. In
compression devices, and/or the use of anticoagulants addition, the CT study for pulmonary embolism takes
such as heparin, are widely used in high-risk patients, significantly less time than that required for preparing
⭈ ⭈
pulmonary embolism is a significant, often prevent- and administering the radioisotopes in V/Q scanning.
able, cause of increased morbidity and mortality A CT pulmonary angiogram is obtained by scanning
among hospitalized patients. the patient while a bolus of intravenous contrast is
The most common radiographic presentation of an injected. The scan is timed in such a way as to obtain
acute pulmonary embolism is a normal chest X-ray. images during peak opacification of the pulmonary
However, other types of medical imaging play a central arteries. On CT angiography, pulmonary emboli appear
role in the diagnosis of this condition. Until recently, as low-attenuation (darker) filling defects outlined by
the primary diagnostic imaging technique was the more attenuating (lighter) contrast containing
ventilation/perfusion lung scanning. In patients with blood in the pulmonary arterial bed. Figure 14-38C is
pulmonary emboli, the ventilation portion of the study an axial CT image in a patient with a large, acute
(A)
FIGURE 14-38 (A) The ventilation scan of a patient with a known history of pulmonary
emboli: The radioactive gas distribution appears normal. (continues)
(C)
(B) (D)
FIGURE 14-38 (B) The perfusion study of the same patient: Areas of the lung show very poor perfusion
secondary to the emboli blocking branches of the pulmonary circulation. A comparison of the two images
⭈ ⭈
reveals areas of V /Q mismatch. (C) An axial CT image of a bilateral pulmonary artery emboli. (D) A coronal
CT image of the left pulmonary artery portion of the emboli described in C.
pulmonary embolus that involves both the right and are severe shortness of breath, tachypnea, refractory
left pulmonary arteries. Figure 14-38D is a coronal CT hypoxemia, and more-or-less diffuse pulmonary
image of the same patient showing the branching infiltrates on the chest X-ray. ARDS inflicts diffuse
embolus in the left pulmonary artery. damage at the alveolar level in the lung parenchyma.
As a result of the damage to the alveolar wall, the
airspaces in the early stage of development are flooded
ADULT RESPIRATORY DISTRESS SYNDROME with fluid (alveolar edema). Shortly thereafter, areas of
The adult respiratory distress syndrome (ARDS) is alveolar hemorrhage and hyaline membrane formation
commonly encountered in critically ill patients. can be seen on microscopic examination.
Virtually any systemic insult can result in the develop- Should the patient survive the initial period of
ment of ARDS, common ones being trauma, shock, respiratory failure, the lung attempts to heal itself.
sepsis, aspiration, or pneumonia. The clinical features However, for reasons that are not clearly understood,
FIGURE 14-39 The ground glass appearance of a patient (A)
with early stage acute respiratory distress syndrome
(ARDS) 48 hours after the initial symptoms were noted.
the reparative process is unchecked and the involved

portions of the lung develop fibrosis and scarring. The
fibrotic stage of the disease can be severe enough to
result in permanent impairment lung function.
Figure 14-39 shows the diffuse, so-called ground-glass
infiltrates of the earliest stage of ARDS in a trauma
patient that, over the course of the first 48 hours in the
intensive care unit, developed progressive and refrac-
tory hypoxemia, ultimately requiring intubation.
Device Positioning
The chest radiographs and CT scans in this section
demonstrate the positions of thoracic tubes, lines,
(B)
catheters, and medical or surgical appliances or devices.
Some of these illustrate correct positioning and FIGURE 14-40 (A) A misplaced endotracheal tube: This
placement; others show misplaced or dislodged is a right mainstem bronchus. The left lung is not being
devices. ventilated. (B) The same patient after the endotracheal
tube has been repositioned to the correct position.
ENDOTRACHEAL TUBES
Radiographs are two-dimensional representations of than the left bronchus due to its more vertical course
three-dimensional structures. Do not assume that an from the carina. Figure 14-40A shows misplacement of
endotracheal tube overlying the trachea is actually in an endotracheal (ET) tube with intubation of the right
the trachea. Normally, the esophagus lies just behind bronchus, resulting in atelectasis of the unventilated
the trachea, and an esophageal intubation can be left lung. Figure 14-40B shows the same patient after
missed on an AP radiograph. A lateral view is diagnos- repositioning of the ET tube so that its tip is at an
tic because it shows an appropriately positioned appropriate level in the trachea with nearly complete
endotracheal tube overlying the air filled cervical resolution of the atelectasis on the left. These images
segment of the airway, whereas a tube in the esophagus were obtained 15 minutes apart, illustrating the
lies posterior to the trachea. Frequently, the initial transitory nature of atelectasis when the cause of the
placement of an endotracheal tube is too deep, result- volume loss is identified and treated.
ing in intubation of one of the main bronchi. In these In some patients, usually those undergoing cardiac
cases, the tube tends to be directed into the right rather or pulmonary surgery, the lungs need to be ventilated
or necrosis is the bulging of the contour of the cuff

beyond the margins of the tracheal air-shadow. The
occurrence of this complication has been reduced by the
use of endotracheal tubes designed with low-pressure
cuffs. In patients with a history of prolonged intuba-
tion, tracheal stenosis may be apparent as a narrowing
or tapering of the subglottic tracheal air-shadow.
SWAN-GANZ CATHETERS
A Swan-Ganz catheter is a specialized type of intravas-
cular catheter used to monitor pulmonary arterial
pressure (PAP) and the pulmonary capillary wedge
pressure (PCWP). The catheter is typically placed via a
subclavian venous puncture and passed sequentially
through the innominate vein, superior vena cava, right
atrium, right ventricle, pulmonary outflow tract, and
pulmonary artery. The unwedged catheter may be left
in place for several hours or days as a means of assess-

ing how much the pulmonary edema is due to cardiac
failure (elevated pulmonary capillary wedge pressure)
or to noncardiac factors (normal wedge pressure).
When the wedge pressure is measured, the tip of
FIGURE 14-41 A double lumen endotracheal tube, which is the catheter is advanced, often with the assistance of a
used when it is desirable to either isolate one lung or to floatation balloon incorporated into the distal portion
ventilate one lung independently from the other. of the catheter, until the tip of the catheter occludes a
small pulmonary artery branch and a relatively flat,
nonpulsatile pressure tracing, characteristic of the capil-
independently. In these instances, a special, dual- lary wedge pressure, is obtained. Once the capillary
lumen endotracheal tube is placed with its tip in one pressure is obtained, the catheter is withdrawn so that
of the main bronchi and the side port of the second its tip is in the more proximal pulmonary artery. In the
lumen above the carina. By occluding one of the parked position, the tip of the catheter should be no
lumens, one lung can be intentionally collapsed while more than 2–4 cm beyond the margin of the hilum.
maintaining ventilation to the contralateral lung, Figure 14-42 shows a Swan-Ganz catheter placed, via
allowing improved surgical exposure to the structures the right jugular vein, passing:
on the side of the collapsed lung. Figure 14-41 shows
a double-lumen endotracheal tube with its tip in the • Caudally to the level of the right atrium.
left main bronchus. • Across the tricuspid valve and out the pulmonary
When using cuffed endotracheal tubes, pay atten- outflow tract.
tion to the tube cuff. If cuff inflation is maintained • Through the pulmonic valve and main pulmo-
with too great a pressure, erosion or necrosis of the nary artery into the right pulmonary artery.
tracheal wall can occur. A sign that suggests overinflation • Parked with its tip projected over the right
hilum.
Best Practice NASOGASTRIC TUBES AND FEEDING TUBES

Nasogastric (NG) tubes should be positioned so that
Endotracheal Tube Placement their tips and all side holes are below the gastroesopha-
Ideally, the distal tip of an endotracheal tube geal junction. A nasogastric tube with its tip or one or
should be at least 1–2 cm above the carina. If more of its side holes in the esophagus does nothing to
the carina cannot be visualized, the top of the alleviate symptoms related to gastroesophageal reflux
aortic arch or between the fourth and sixth tho- or to lessen the risk of aspiration. Feeding tubes are
racic vertebra are good landmarks for placement positioned with their tips either in the stomach or
of the tip in adults. duodenum, depending on the particular medications
or feeding solutions.
Best Practice
Placement of the Swan-Ganz Catheter
Failure to park the catheter in a more proximal posi- or a pulmonary artery aneurysm can occur.
tion can result in thrombosis of a branch artery to a Figure 14-44 is a CT image from a patient with
portion of the lung and pulmonary infarction. acute hemoptysis following removal of a peripherally
Figure 14-43 demonstrates a Swan-Ganz catheter inflated Swan-Ganz catheter; it shows opacification
with its tip parked in too peripheral a location. Note of a pulmonary artery pseudoaneurysm in the medial
also the unusual course of the catheter due to the right lower lobe, surrounded by an area of consoli-
patient having a left-sided superior vena cava. If dation due to pulmonary hemorrhage. On the other
the catheter is inserted too far or if the balloon is hand, pulling the catheter so far back that its tip is
inflated while the catheter is in its wedged position, in the right ventricle may cause arrhythmias, injury,
pulmonary artery perforations, pulmonary hemorrhage, or even perforation of the right ventricular wall.
FIGURE 14-42 A Swan-Ganz catheter placed in the right jugular vein and threaded through the
heart into the right pulmonary artery.
FIGURE 14-43 A Swan-Ganz catheter that was advanced FIGURE 14-44 A CT of a pulmonary artery pseudo
too far: Note the abnormal position of the superior vena aneurysm following a Swan-Ganz catheter being placed
cava, which is on the left rather than on the right. too far into the pulmonary artery.

Placement of a Nasogastric Placement of a Chest Tube
Tube The placement of a chest tube should always be
Radiographic confirmation of appropriate NG or checked by chest X-ray. Figure 14-46 shows a
feeding tube placement is important because left chest tube in a patient treated for a left
occasionally the tube is inadvertently placed in tension pneumothorax. Note the extensive
the trachea or advanced into a more peripheral subcutaneous emphysema.
bronchus.
position of the tube tip since a final location in the

upper portion (apex) of the pleural space is advanta-
Misplacements are generally easy to identify by
geous for the evacuation of a pneumothorax. On the
chest radiography. Failure to confirm appropriate
other hand, a position in the posterior, lower pleural
placement, especially of tubes being used for feeding or
space or costophrenic angle aids in the drainage of
medication, can result in iatrogenic (resulting from
fluid.
medical care) aspiration pneumonia. Figure 14-45 is a
radiograph that demonstrates both appropriate posi-
tioning of a nasogastric tube, which loops in the gastric AORTIC BALLOON PUMPS
fundus, and inappropriate positioning of a feeding
Intra-aortic balloon pumps are specialized balloon
tube, which is directed into the right lower lobe
catheters that are placed from a femoral artery
bronchus.
approach and positioned in the descending thoracic
aorta. The inflation of the balloon is timed to occur
CHEST TUBES during diastole, when the aortic valve is closed, to
decrease the amount of pressure that the left ventricle
Chest (thoracostomy) tubes are inserted to drain and
must work against while improving diastolic perfusion
remove fluids and gases from the pleural space. During
of the coronary arteries. A radiopaque, metallic marker
their placement, an attempt may be made to direct the
is embedded in the tip of the catheter and should be
positioned in the proximal descending aorta, just
below the aortic notch. On chest X-rays obtained
during diastole, the inflated balloon can be seen
as a cylindrical lucency within the descending aorta
(Figure 14-47).
B A
FIGURE 14-46 A chest drainage tube in the left chest: The

FIGURE 14-45 A: A correctly positioned nasogastric (NG) patient is being treated for a left tension pneumothorax.
tube. B: An incorrectly placed feeding tube. Note the Note the position of the tube relative to the patient’s
feeding tube is in the right lower lobe bronchus. anatomy and the large area of subcutaneous emphysema.
defibrillators are programmed to shock the heart back

into a regular rhythm when the normal electrical
signals controlling the heartbeat become disorganized,
as in ventricular fibrillation. The leads for these devices
are generally threaded from the subclavian vein,
through the superior vena cava and into the right
atrium. Depending on the condition being treated, the
tips of one or more electrodes may be placed in the
right atrium, right ventricle, and/or coronary sinus (for
left ventricular pacing). Internal defibrillators generally
have two leads that are distinguished from simple
pacemaker leads by additional coils along segments of
the atrial and ventricular leads. These units are powered
and controlled by a battery and microchip contained in
a battery pack that is implanted in the subcutaneous
tissues of the chest wall. Today, many of these
devices combine the functions of a pacemaker and
a defibrillator.
Chest radiographs are routinely used to confirm
the placement of the electrodes and to evaluate for
broken leads in patients who experience implant

failures. One of the possible pitfalls in the interpreta-
tion of chest films of patients with pacemakers or
defibrillators is that portions of the lung are obscured
by their battery packs. Consequently, the reader could
miss subtle or slowly developing lesions in the lung
FIGURE 14-47 An aortic balloon pump catheter with its tip
beneath the battery packs. Such a case is shown in
properly placed distal to the aortic notch: These devices
Figure 14-48. The initial chest X-ray (Figure 14-48A)
are also known as ventricular assist devices.
shows four electrodes: one defibrillator electrode each
in the right atrium and the right ventricle, an addi-
INTERNAL CARDIAC PACEMAKERS tional right ventricular pacemaker electrode, and a
AND DEFIBRILLATORS pacemaker electrode in the coronary sinus. The battery
Internally placed cardiac pacemakers and defibrillators pack is overlying the left upper lobe. The study other-
are among the most common implanted devices wise looks essentially normal, but several coarse bands
encountered in the outpatient setting. Pacemakers are of soft-tissue density extend toward the area of the
used to control the rhythm of the heart. Internal lung obscured by the battery pack. However, due to his
(A) (B) (C)

FIGURE 14-48 (A) The chest X-ray shows 4 electrodes: 2 defibrillator electrodes in the right atrium and right ventricle,
1 pacemaker electrode in the right ventricle, and another pacemaker electrode in the coronary sinus. The pacemaker’s
battery pack is also imaged on this view. The film was assessed as being essentially normal. (B) A repeat chest X-ray,
done 6 months later: Note the large soft tissue mass that was obscured by the battery pack in the previous study. (C) A
CT scan performed still later, confirming the findings of a left upper lobe bronchiogenic carcinoma hidden by the power
pack in the first study.
persistent cough, the patient returned to see his

physician 6 months later and had a repeat chest X-ray.
The study in Figure 14-48B showed a large, soft-tissue
mass extending from the hidden portion of the lung
toward the left hilum. The CT (Figure 14-48C),
obtained after the second chest radiograph, confirmed
the presence of a left upper lobe bronchogenic
carcinoma that had been obscured on the initial
radiograph.
Chest Trauma
Radiology is extremely important in the assessment
and diagnosis of damage done by various forms of
chest trauma. Common injuries range from fractures of
the ribs, sternum, spine, or clavicles to injuries of the
FIGURE 14-49 A patient with multiple fracture of the ribs
lung, bronchi, pulmonary vessels, or pleura. The bilaterally in ribs 2–9; many of the ribs have several frac-
resulting conditions can be pulmonary contusion, tures: The film also illustrates bilateral pneumothoraces
pulmonary hemorrhage, pneumothorax, pneumomedi- and large areas of subcutaneous emphysema. Note the
astinum, pneumopericardium, or hemothorax (blood positions of the bilateral chest tubes.
in the pleural space). Other possible injuries are to the
heart or great vessels, resulting in hemopericardium,
atrial or ventricular perforation, traumatic aortic Complaints of chest wall pain on inspiration,
injuries, or mediastinal hematomas. Knowledge of the bruising patterns on the chest, chest wall movement
mechanism of injury provides important diagnostic that lags on one side, or paradoxical movements of the
clues to the potential injuries. chest are all indicative of the need to look for fractured
ribs or sternum. The presence of downward diagonal
bruising on the chest wall indicates seat belt injuries:
FLAIL CHEST left to right for driver-side occupants, right to left for
passenger-side occupants. These bruising patterns are
A flail chest results from multiple fractures of adjacent often clues to rib fractures and chest wall muscular
ribs. The precise number of ribs involved to qualify as a injuries.
flail chest varies based on the experts questioned. Some
say as few as two adjacent ribs with two or more
fractures each is a sufficient criterion. In practice, the
diagnosis of flail chest is based largely on the clinical Best Practice
observation of paradoxical motion of any portion of
the chest wall as the patient breathes. In other words,
the involved segment moves inward on inspiration and
Rib Fractures
outward on expiration—the opposite of the normal Chest radiography is a relatively insensitive
movements. These asynchronous motions affect method for identifying fractures, especially non-
pressure gradients in the thorax, reducing the efficiency displaced fractures. Nearly 50% of rib fractures
of ventilation. The depth and rate of respiration are may be missing on the initial chest radiographs
also affected because pain responses result in shallow, obtained in the trauma suite. In the care of
rapid breathing. Obviously, the observation of para- trauma patients, therefore, a good practice is to
doxical motion can be made only prior to intubation closely examine each rib, the sternum, the spine,
and mechanical ventilation of the trauma victim. and the clavicles for the presence of fractures.
Figure 14-49 is a chest radiograph of a patient with a Also keep in mind the fact that single-view chest
bilateral flail chest due to multiple segmental fractures radiographs are relatively insensitive to even
of the right and left second–ninth ribs, bilateral major injuries of the chest wall, great vessels,
pneumothoraces, and extensive subcutaneous emphy- or heart. Consequently, CT examinations are
sema. The right chest tube is appropriately positioned, routinely used in the evaluation of individuals
but the left chest tube is kinked and does not enter the presenting with chest injuries.
pleural space.
FIGURE 14-50 A trauma victim with subcutaneous emphy- FIGURE 14-51 A dental cap that was loosened and
sema: Findings of subcutaneous emphysema in trauma aspirated during an endotracheal intubation: The dental
patients are commonly associated with injury to the cap can be seen beside the ET tube in the trachea.
chest, heart, and trachea.
effusion). Blunt trauma with fractured ribs can also

SUBCUTANEOUS EMPHYSEMA lead to injury to the lung or abdominal contents,
leading to pneumothorax, hemothorax, or a lacerated
Subcutaneous emphysema presents as palpable
liver or spleen.
bubbles of air under the skin. These bubbles have a
classic feel referred to as crepitus; the feeling has been
described as resembling the feeling of popping Rice FOREIGN BODIES
Krispies® or bubble wrap. In a trauma patient, subcu-
Inspect all chest X-rays, particularly those of trauma
taneous emphysema (Figure 14-50) almost always
patients, for evidence of foreign bodies in the chest
indicates a pulmonary, tracheal, or bronchial injury
wall, lungs, mediastinum, or airway. Frequently, teeth
and is almost always associated with a pneumothorax
or dental appliances are dislodged during a traumatic
injury or a pneumothorax. Intubated, tracheosto-
event or, less often, during the intubation of an unsta-
mized, and ventilated patients are at increased risk of
ble patient. Figure 14-51 demonstrates a metallic dental
subcutaneous emphysema due to tracheal wall punc-
cap that was inadvertently dislodged during intubation
ture, false passage intubation, and the increased
and aspirated into the trachea, where it now lies
pressure gradients that result from positive pressure
alongside the endotracheal tube.
ventilation, either mechanical or manual. These
injuries often cut through other tissues in the head,
neck, and chest, leaving subcutaneous air in these
locations. The build-up of gas pressure can lead to CASE STUDY 14-1
vascular resistance and deceased perfusion to the
affected areas. Figure 14-52 shows the chest film of a man who
had unsuccessfully attempted suicide by hang-
ing. The chest X-ray was taken at the same time
PENETRATING CHEST WOUNDS as a cervical spine film that showed only soft
Penetrating wounds from knives, especially stab tissue injury—no neck fracture (fx).
wounds (as opposed to slash injuries), are more likely
to lead to a tension pneumothorax than a gunshot
Questions
wound. A knife entrance wound allows air to leak into 1. What could account for this rather startling
the pleural space from a punctured lung but does not chest film?
provide a way for air to leave the pleural space as 2. What is the probable cause of the pulmonary
would a gunshot wound. Penetrating trauma frequently edema?
leads to a hemothorax (which looks like a pleural
Summary
A respiratory therapist should be able to effectively
review and analyze radiographic studies, should know
how various imaging modalities can contribute to a
patient’s diagnosis and treatment, and should be able
to use the information obtained from medical imaging
to improve patient care. Such a knowledgeable RT is an
asset to patients, to other health care workers, and to
the health care facilities at which they work. To prop-
erly use medical imaging information, a respiratory
therapist must understand the basic principles of how
the study is created and how to systematically evaluate
studies for their technical quality and meaning.
Proficiency can be obtained and maintained only
through frequent practice and learning from mentors
and teachers.
FIGURE 14-52 Supine portable chest indicating diffuse Study Questions

pulmonary edema: This film was taken contemporaneously
with a C-spine film of a patient who attempted suicide by REVIEW QUESTIONS
hanging. The neck was not fractured, but the associated 1. Why should a respiratory therapist be able to read
soft tissue swelling and airway narrowing of the trachea
and interpret chest radiographs?
indicate mechanical asphyxiation by strangulation.
(Courtesy of Glendon Cox, M.D., University of 2. What are the major types of radiological studies?
Kansas Medical Center) 3. What factors influence the ordering of specific
radiology studies?
4. Explain the principles of various radiological studies.
5. Differentiate between a regular and a portable
chest X-ray.
6. List a sequence for systematically reviewing a chest
Best Practice radiograph.
7. Identify common abnormalities on a chest film.
Safety Practices
Respiratory therapists are often involved in
supporting ventilation during the application
of ionizing radiation, for either diagnostic or 1. Which of the following is characteristic of a
treatment purposes. They are typically given portable chest film?
lead aprons and lead shields to protect the a. high quality
gonads and thymus while in the procedure b. low visibility of spine
room. If RT is supporting the patient’s c. prominent spinal column
head or neck, wearing lead-lined gloves is d. erect position
appropriate. 2. Your patient, Mrs. J, is having difficulty breathing
It is far less common for respiratory thera- and diminished breath sounds in the right base
pists to wear radiation dose meters (dosimeters), and is complaining of “pain in my lower right
which provide an ongoing and cumulative record chest when I inhale.” Which of the following
of radiation exposure over time. RTs who are sta- radiographic examinations would be most sensi-
tioned in the ICU or ER or who frequent transport tive to rule out a small (⬍50 mL) right pleural
and support procedures in the radiology depart- effusion?
ment should wear a dosimeter. If they are not a. a right lateral oblique
provided with a dosimeter, they should request b. a left lateral decubitus
one. c. an AP lateral
d. a bronchogram with contrast
3. Mr. P’s PA chest radiograph shows that his right clavicle 8. Which of the following techniques should be
and ribs appear larger than do those on his left. Which employed to reduce heart magnification in chest
of the following is a probable cause of this effect? X-rays (CXRs)?
a. Mr. Plump is rotated so that his left anterior I. Have CXR shot during expiration.
chest wall is closer to the imaging cassette. II. Have CXR done in radiology department.
b. Mr. Plump has a growth disorder, causing the III. Have CXR done as a portable study.
right side to develop more than the left. IV. Use the PA view.
c. The X-ray machine was partially set on the a. I, II, and III
magnify setting. b. I and II only
d. The film was a left lateral radiograph, and this c. II and IV
result is normal for that view. d. IV only
4. A patient is suspected of having an obstructive 9. Which of the following is not an appropriate safety
lesion, and the lesion’s size, shape, and location precaution for reducing the respiratory therapist’s
have to be precisely delineated. Which of the occupational exposure to radiation?
following radiological tests would you suggest? I. Wear a dosimeter and be enrolled in a monitor-
I. plain chest film ing program.
II. a lateral decubitus chest film II. Avoid caring for persons likely to need radio-
III. MRI scan logical procedures.
IV. CT scan III. Wear a lead apron and shield when exposure
V. V⭈/Q⭈ scan is necessary.
a. I only IV. Limit exposure as appropriate.
b. II and IV a. I, III, and IV
c. I and V b. II and IV only
d. III and VI c. II, III, and IV
5. Which of the following radiographic features d. I only
would be expected in a CT scan of an untreated 10. Which of the following statements is true regarding
tension pneumothorax? radiological procedures in chest trauma?
I. mediastinal shift away from the pneumothorax a. Owing to their complexity, CT scans are often
II. mediastinal shift toward the pneumothorax inappropriate for use in trauma.
III. extra pulmonary air in the contralateral chest cavity b. Prone and lateral positions are the most
IV. air-fluid level valuable when assessing chest trauma.
V. foreign object in the chest cavity c. Upright, PA films are seldom the view of choice
a. I, II, and V in severe chest trauma.
b. I only d. Supine AP and lateral films are likely to be
c. II, IV, and V useful for initial diagnosis in chest trauma.
d. III and IV only
6. In a thoracic CT scan of an acute hemopneumo-
thorax that is not under tension, which of the
following is likely? 1. What variations should a reader expect to see a
I. mediastinal shift toward the lesion standard, plain chest radiograph were compared
II. mediastinal shift away from the lesion with a portable one taken a few minutes apart on
III. foreign object in the chest cavity the same patient?
IV. air in the contralateral chest cavity 2. What are the limitations of X-rays when it comes to
V. air-fluid level in the ipsilateral (affected-side) making a diagnosis of pulmonary diseases?
pleural space
3. Is it necessary that just about every patient who
a. II and V
comes into the hospital have a chest X-ray? Explain
b. I only
your answer.
c. II, IV, and V
d. III and IV only 4. Mr. K is a 2-day postcode patient who remains on
a ventilator with increasingly high pressures.
7. Which of the following is indicative of an expira-
Observation of the patient reveals that his face and
tory portable CXR?
neck appear to be bloated. What are the possible
a. wide intercostal space
reasons for this observation?
b. depressed sternum
c. AP view
d. domed diaphragm
Suggested Readings Society of Thoracic Radiology Cardiac Resources,

http://education.thoracicrad.org/cardiac_
and Web Resources imaging.htm.
Fraser RS, Colman N, Muller NL, Pare PD. Synopsis of University of Virginia ICU Chest Radiology,
Diseases of the Chest. 3rd ed. Philadelphia: Saunders/ http://www.med-ed.virginia.edu/courses/rad/chest/
Elsevier; 2005. University of Miami Interactive Chest Radiology,
Goodman L. Felson’s Principles of Chest Roentgenology: A http://www.med.miami.edu/articulate/Rad_
Programmed Text. 3rd ed. Philadelphia: Saunders/ INTERACCXR/CXR0413.html.
Elsevier; 2007. Webb WR, Higgins CB. Thoracic Imaging: Pulmonary and
Muller NL, Silva IS. Imaging of the Chest, Vols. I and II. Cardiovascular Radiology. Philadelphia: Lippincott
Philadelphia: Saunders/Elsevier; 2008. Williams & Wilkins; 2005.
Society of Thoracic Radiology Pulmonary Resources,
http://education.thoracicrad.org/pulmonary_
imaging.htm.
CHAPTER 15
Clinical Laboratory Studies

Ingo S. Kampa
OBJECTIVES
• Explain the functions of electrolytes and the causes and consequences of alterations in their concentration.
• Be able to describe the chemical concepts of analyzing electrolytes.
• Describe the causes of various acid-base disturbances and typical laboratory findings.
• Understand the importance of ionized magnesium and calcium ions.
• Identify the current biochemical markers for acute myocardial infarction.
• Outline the statistical methods used to validate analytical assay runs.
CHAPTER OUTLINE
Body Fluids and Electrolytes Laboratory Methods for Determining Arterial
Water Blood pH, Carbon Dioxide Pressure, and
Oxygen Pressure
Sodium
Potassium Laboratory Methods for Analyzing Carbon Dioxide
and Chloride
Chloride
Laboratory Findings in Acid-Base Disturbance
Bicarbonate
Laboratory Findings in Metabolic Acidosis
Calcium
Laboratory Findings in Metabolic Alkalosis
Ionized Calcium
Laboratory Findings in Respiratory Acidosis
Phosphorus
Laboratory Findings in Respiratory Alkalosis
Magnesium
Current Biochemical Markers in Acute
Ionized Magnesium
Myocardial Infarction
Laboratory Methods for Determining Electrolytes
Statistical Quality Control
Flame Photometry and Indirect
Establishing Precision Goals
Ion-Specific Electrodes
Monitoring the Analytical Precision of a Test
Ion-Specific Electrodes
Conducting Interlaboratory Comparisons
Biosensor Technology
Determining the Accuracy of an Analytical Assay
387
KEY TERMS
coefficient of variance (CV) ionized calcium osmolality
coulometric-amperometric ionized magnesium standard deviation (SD)
titration method ion-specific electrode (ISE)
electrolyte Leland Clark electrode
E
lectrolytes consist of anions (negatively samples, which represent a small compartment, or
charged particles) and cations (positively portion, of body fluids, and interpretation must be
charged particles). The major cations in a related to the total body fluid compartments. There-
physiological system are sodium (Na⫹), fore, the disease status must be considered along with
potassium (K⫹), calcium (Ca2⫹), and magnesium the clinical status of the patient. Also, laboratory
(Mg2⫹). The major anions are chloride (Cl⫺), bicarbon- electrolytes are reported in concentration units and
ate (HCO3⫺), HPO4⫺, dibasic phosphate (HPO42⫺), may not represent the total amount of electrolytes in
and sulfur dioxide (SO42⫺).1 Electrolytes have numer- the plasma.
ous functions in the body. Essentially all metabolic
reactions are controlled or influenced by electrolytes.
In addition, electrolytes regulate water movement,
osmotic pressure, pH, and numerous other factors. As Body Fluids and Electrolytes
a result, the accurate determination of electrolytes is Body fluid is distributed in three separate compart-
important in the diagnosis and treatment of many ments: the plasma, the interstitial fluid (ISF), and the
disorders. extracellular fluid (ECF). The fluids in these compart-
Body fluids contain large quantities of inorganic ments are not homogeneous but consist of subcom-
electrolytes. The large concentrations of sodium partments containing varying concentrations of
(largely confined to the extracellular space) and electrolytes.2
potassium (found in the intracellular space) have a The electrolytes consist of cations (positive charge)
major influence on both the distribution and retention and anions (negative charge).1 The important cations
of body fluids. Because water is freely diffusible, are sodium (Na⫹), potassium (K⫹), calcium (Ca2⫹),
changes are influenced to a large extent by sodium and inorganic phosphorus, and magnesium (Mg2⫹).
potassium concentrations in the various compart- Important anions discussed in this chapter are chloride
ments. Both electrolytes have a significant effect on (Cl⫺) and bicarbonate (HCO3⫺) (Figure 15-1).
osmolality, which in turn determines the flow of water
between extra- and intracellular compartments.
Increased electrolyte dehydration can occur during
periods of water restriction or when the rate of water
loss exceeds the rate of electrolyte loss. This difference Extracellular Fluid Intracellular Fluid
in loss rates can result in intracellular dehydration Anions Cations Anions Cations
because the compensatory mechanism shifts water
from the cells to the extracellular space. Typical symp-
toms of this condition include severe thirst and
possibly nausea and vomiting. Excess ingestion of
electrolyte-free water as a response to the depletion of Cl- Na+ HPO4-- K+
both water and electrolytes results in an extracellular
electrolyte dilution or deficit. The result is intracellular
edema because water passes into the cells from the
extracellular compartment.
Mg++
Monitoring body water disturbances and their K+
effects on acid-base and metabolic disturbances HCO3- Ca++ HCO3- Na+
requires accurate measurement of electrolytes. How- HPO4-- Mg++ Cl- Ca++
ever, several factors should be kept in mind in the
evaluation of fluid and electrolyte status. Laboratory
measurements are made on plasma or serum and urine FIGURE 15-1 Anions and cations in body fluid.
CHAPTER 15 ■ Clinical Laboratory Studies 389
fluid (ECF). The fluid within individual cells is rela-

tively constant; thus, cellular fluid in the numerous
separate cells can be referred to as a single compart-
ment. Extracellular fluid is a more heterogeneous
mixture that consists mainly of plasma, interstitial
fluid, and transcellular fluids.
Water is constantly lost from the body through
Cellular 40% water vapor from lungs, perspiration through the
Intracellular skin, urine via the kidney, and feces via the intestine
(Figure 15-3). Water loss by urine can be measured
easily and is called sensible water loss. The water loss
that cannot be measured (exhaled, in feces, and
Interstitial 15% through perspiration) is called insensible water loss.
Extracellular The amount of insensible water loss is substantial,
ranging between 1500 and 2000 mL daily by an adult.
Plasma 5%
NORMAL SODIUM
Fluid Percent of Body Weight
Sodium, the most plentiful electrolyte, is found in high
FIGURE 15-2 Body fluid compartments. concentration in extracellular fluid and in low concen-
tration in intracellular fluid (Figure 15-1). (The normal
plasma sodium value is 135–145 mmol/L.) Sodium is
WATER involved in the maintenance of intracellular and total
The most abundant compound in a human living body body fluid volumes, the maintenance of osmolality,
is water, representing 65–90% of the total weight of an neuromuscular excitation processes, and hydrogen ion
individual (Figure 15-2). Water is contained in indi- metabolism. Potassium concentration is the opposite
vidual cellular compartments, usually referred to as of sodium concentration; that is, it is high in the
intracellular fluid (ICF), and outside of cells; water intracellular compartment and low in the extracellular
outside cells is collectively referred to as extracellular compartment. Cell membranes maintain these
Intake
Liquid 1000–1200 mL
Food 800–1000 mL
Oxidation of food 200–300 mL
Output
Lungs 400–500 mL
Skin 300–500 mL
Urine 1000–1500 mL
Feces 100 mL
Total Total
2000–2500 mL 1800–2600 mL
FIGURE 15-3 Normal pattern of water intake and loss.
concentration differences. Maintaining these differ- gradient. This task requires energy and is accomplished
ences in concentration requires the movement of by the action of the Na⫹, K⫹-ATPase pump. Potassium
sodium from the intracellular compartment to the is important in maintaining ionic gradients required
extracellular compartment. for nerve impulse transmission and contractility of
The cell must continuously expend energy to both cardiac and skeletal muscles.
preserve these ionic conditions against the concentration The daily dietary requirement of potassium is
gradient. These conditions are preserved by the Na⫹, approximately 50–150 mmol/day. Potassium is rapidly
K⫹-ATPase system, which is activated by the high-energy absorbed in the gastrointestinal tract. The cellular
compound adenosine 59-triphosphate (ATP). Because uptake is relatively small. As a result, nearly all of the
sodium has a high concentration in the blood, it is the dietary potassium is excreted in the urine, and the
source of over half of the inorganic ions that produce urine output generally reflects the dietary intake of
the plasma osmolality. The average daily sodium potassium. Other factors affecting or regulating potas-
consumption of 8–15 g is almost entirely absorbed by sium secretion are plasma levels of aldosterone and
the gut. Daily sodium requirements are only 1–2 mmol/ acid-base balance. Aldosterone enhances potassium
day. The kidneys excrete the vast excess of sodium. secretion, whereas acidosis affects renal regulation of
Elevated plasma sodium concentrations potassium secretion. High levels of potassium result in
(hypernatremia) may result if the body’s water storage weakness and numbness. Cardiac arrest and death may
is depleted. Other causes may be: be the consequences as potassium concentrations
exceed 7.0 mmol/L.
• Increased mineralocorticoid production.
Excessive plasma potassium levels (hyperkalemia) are
• Decreased antidiuretic hormone (ADH)
often the result of later stages of renal disease, as a result
production.
of damage to cells, hemolytic anemia, and the excessive
• Decreased renal tubular sensitivity to the
use of dietary supplements containing potassium.
antidiuretic hormone.
Addison’s disease increases potassium levels by causing
• Inappropriate administration of saline as a result
sodium depletion. Symptoms of hyperkalemia are
of parenteral therapy.
cardiac and central nervous system depression. Bradycar-
The kidney’s ability to concentrate urine in the dia, peripheral vascular collapse, and ultimately cardiac
presence of depleted water stores is limited. Insensible arrest are the consequences of severe hyperkalemia.
water losses through the lungs, skin, and stool aggra- Potassium levels of less than 3.0 mmol/L (hypoka-
vate the condition. In chronic water starvation, the lemia) are associated with neuromuscular abnormali-
kidney’s compensatory ability to increase sodium ties and indicate severe critical intracellular depletion.
excretion proportionally may be overwhelmed. Adrenal Low levels of plasma potassium are often the result of
tumors are a common cause of increased mineralocor- prolonged gastrointestinal loss through vomiting and
ticoids, resulting in increased tubular reabsorption of diarrhea, prolonged administration of laxatives,
sodium. A decrease in or an absence of antidiuretic diuretic therapy, and metabolic acidosis. The excretion
hormone, or diabetes insipidus, results in the decreased of potassium is also increased by excessive quantities
ability of retaining body water. of corticosteroids and corticotrophin; such an increase
Decreased plasma serum sodium levels (hyponatre- may result in a potassium deficit. Insulin therapy in
mia) are often caused by decreased intake of sodium diabetic hyperglycemia may also result in hypokalemia
and is exaggerated by vomiting and prolonged diar- owing to concomitant cellular uptake of potassium
rhea. Extracellular fluid expansion without a concomi- along with glucose.
tant increase in sodium, as seen in edema, is another
cause of hyponatremia. Inappropriate increased CHLORIDE
secretion of antidiuretic hormone can result in plasma
expansion without an increase in sodium levels. Chloride is maintained predominately in the extracellu-
Metabolic acidosis, as observed in ketoacidosis in lar fluid (Figure 15-1). (The normal plasma chloride
uncontrolled diabetes, results in the loss of sodium due concentration is 97–108 mmol/L.) Chloride plays a
to coexcretion with large amounts of organic anions. special function in the blood by maintaining electrical
neutrality. As bicarbonate ions diffuse out of the erythro-
cytes into the plasma, equimolar quantities of chloride
POTASSIUM enter the erythrocytes, in a process known as the chloride
Potassium, the most abundant of the intracellular shift. Chloride is obtained almost entirely as sodium
cations, is found in only small quantities in the chloride absorbed in the intestinal tract, and its intake
extracellular fluid (Figure 15-1). (The normal plasma and output are essentially inseparable from sodium.
potassium value is 3.5–5.0 mmol/L.) The intracellular Elevated chloride levels (hyperchloremia) are
concentration is maintained by actively transporting associated with metabolic acidosis, kidney dysfunction,
potassium into the cells against the concentration Cushing’s disease, hyperventilation, dehydration, and
salicylate intoxication. Decreased chloride levels ionized fraction, constituting approximately 40% of
(hypochloremia) are observed in diabetic ketoacidosis the total, is thought to be more important physiologi-
and excessive gastrointestinal losses through prolonged cally. Approximately 45% of the body’s calcium is
vomiting or diarrhea. Hypoventilation, heat exhaus- bound to proteins, and the remainder of the calcium
tion, and Addison’s disease also promote excessive complexes with bicarbonate, citrate, lactate, and
chloride excretion. phosphate. Calcium is important in the transmission
of nerve impulses, in the normal contractility of
BICARBONATE muscles, as a cofactor in certain enzyme reactions, and
in the coagulation of blood.
Carbon dioxide is a component of the most important
Calcium ions are absorbed in an active transport
buffer in plasma, referred to as bicarbonate (HCO3⫺)
process in the upper small intestine. Calcium
(Figure 15-1). (The normal plasma bicarbonate value is
uptake in the intestine is regulated by a metabolite
22–32 mmol/L.) It serves as the primary mechanism
(1,25-dihydroxycholecalciferol) of vitamin D. Its
for eliminating acids because lungs can readily dispose
synthesis in the kidney is in response to low plasma
of carbon dioxide. Laboratory methods for measuring
concentrations of ionized calcium (calcium that is not
carbon dioxide or bicarbonate usually consist of
bound to proteins or diffusible ligands). The body
measuring the bicarbonate ion (HCO3⫺) carbon
eliminates calcium through excretion in urine and feces.3
dioxide bound loosely to the amine group of proteins
Parathyroid hormone (PTH) regulates plasma
and carbonic acid.
calcium concentrations, operating as a typical feedback
Lung disease and impaired carbon dioxide
regulation. A hyperactive or adenomatous parathyroid
excretion (respiratory acidosis) result in decreased
gland results in a large accumulation of plasma cal-
blood pH. The loss of stomach content through
cium (12–22 mg/dL). In many cases of hyperparathy-
prolonged vomiting (metabolic alkalosis) results in
roidism, the total calcium is not elevated, but increases
decreased stomach acid content with an elevation
in ionized calcium levels are diagnostic of hyperpara-
of carbon dioxide. Overmedication with sodium
thyroidism. A low concentration of ionized calcium
bicarbonate or diuretics also results in an increase
stimulates the synthesis of PTH, which mobilizes
in carbon dioxide.
calcium from bone, increasing the renal reabsorption
During hyperventilation, carbon dioxide concen-
and the intestinal absorption of calcium.
trations commonly decrease and pH increases. Hyper-
ventilation can result from overstimulation of the
portion of the brain that controls breathing, often
caused by anxiety or intake of toxic substances. In
IONIZED CALCIUM
diabetic metabolic acidosis, both carbon dioxide and Many published studies attest to the importance of
pH are decreased. monitoring ionized calcium. It has been known for
some time that ionized (free) calcium determinations
are more useful than total calcium in critically ill
CALCIUM
patients. (The expected reference intervals for ionized
Calcium is present in the body in larger amounts than calcium levels are 1.15–1.35 mmol/L, or 4.6–5.4 mg/dL.)
any other mineral element. About 99% of body Critically ill patients undergoing major surgery, such as
calcium is found in the skeleton and teeth; only about cardiopulmonary bypass procedures, and receiving
1% circulates in the bloodstream. (The normal plasma citrated blood or platelets, heparin, and bicarbonates
calcium value is 8.5–10.0 mg/dL.) The unbound, or have high total calcium and often critically low ionized
calcium. These patients are likely to have abnormal
protein levels, along with alterations in blood pH and
Best Practice temperature. Measurements of free calcium levels in
patients receiving citrated blood platelets, intravenous
Carbon Dioxide Concentration solution of bicarbonate, calcium, or heparin are found
Changes in carbon dioxide concentration are to be more accurate than measurements of total
early signs of dysfunction of the acid-base status. calcium and provide better maintenance of cardiac
However, because the acid-base balance must function than does measurement of total calcium.
be maintained in a narrow range to sustain life, Monitoring free calcium levels, along with potassium
changes in plasma carbon dioxide concentration levels and blood gases, has benefited patients undergo-
may occur only after substantial damage has ing cardiopulmonary bypass. Ionized calcium determi-
already been incurred. Also, the nature of the nations have been important, also, in the diagnosis of
acid-base imbalance cannot be determined from hypercalcemia.
the carbon dioxide changes alone. A problem encountered with free calcium levels
is the instability of free calcium in blood samples.
MAGNESIUM
Best Practice Magnesium is one of the most important cations in the
body. (The plasma reference intervals for magnesium in a
Ionized Calcium normal individual are approximately 0.6–1.1 mmol/L.)
Patient preparation for the measurement of ion- Next to potassium, it is the most prevalent intracellular
ized calcium is important. The patient must be ion, involved in activating or catalyzing many enzymes.
relaxed, and the tourniquet application procedure It acts by binding to enzyme active sites, by binding to
must be as brief as possible. Bed rest is also ligands in enzymes that require ATP, and by promoting
important because it may elevate ionized calcium aggregation in multienzyme complexes.
levels into the abnormal range. The practice of Very high levels of magnesium (hypermagnesemia)
calculating ionized calcium from nomograms may result in the loss of sensations of touch,
using total calcium and albumin or proteins has temperature, and pain and even in cardiac arrest.
been shown to produce erroneous results. Increased magnesium levels can be expected in
Source: From National Committee for Laboratory Standards,
diabetic acidosis and Addison’s disease. Low plasma
Standardization of Sodium and Potassium Ion-Selective magnesium levels (hypomagnesemia) produce
Electrode Systems to the Flame Photometric Reference Method; impaired neuromuscular function, which, if not
Approved Standard C-29A. Wayne, PA: National Committee for
Laboratory Standards; 1995.
corrected, may result in prolonged involuntary
muscle spasm. Hypertension and atherosclerosis
have also been linked to low magnesium levels.
Magnesium is absorbed in the gastrointestinal tract.
Samples must be sealed completely after centrifugation The kidneys control plasma concentrations by
to prevent the loss of carbon dioxide from them. New regulating the excretion of magnesium.4
instrumentation and new studies have resulted in
increased interest in ionized calcium levels. Highly IONIZED MAGNESIUM
accurate instrumentation for measuring ionized
Magnesium exists in three forms in plasma. Ionized
calcium levels has become routinely available. It can
magnesium (iMg) is the physiologically active form
measure the pH of aerobically collected blood samples
and represents approximately 55% of the total plasma
and adjust the ionized calcium to a level at a pH of 7.4.
magnesium. (The whole blood reference intervals for
ionized magnesium in a normal individual range from
PHOSPHORUS approximately 0.45 to 0.60 mmol/L.) The other two
Phosphorus (inorganic or organic phosphate) is distrib- forms—protein-bound and ligand-complex—are
uted throughout the body. (The plasma reference interval unavailable for biological processes. The iMg is
for phosphorus in a normal individual is approximately believed to be in equilibrium with the intracellular
2.5–4.5 mg/dL.) The largest amount is combined with compartment and represents the biologically active
calcium in bones and is a major component of hydroxy- form. Ionized magnesium levels could change signifi-
apatite. Phosphorus is also a constituent in carbohy- cantly in critically ill patients without accompanying
drates, lipids, and proteins. It is an essential energy changes in the total plasma calcium.5
compound owing to the formation of the high-energy Changes in pH, acid-base status, and ligands can
phosphate bond in adenosine triphosphate (ATP). As a alter the iMg concentration. The bicarbonate ion,
result, phosphorus is involved in the regulation of sometimes administered during hypoxia (associated
carbohydrate, lipid, and protein metabolic pathways. with increased lactate levels), binds with iMg, reducing
This element is available in nearly all foods and is readily its concentration. A decrease in iMg in critically ill
absorbed in the intestine and excreted in urine. patients may have serious consequences because iMg is
Plasma phosphorus concentrations are normally essential for maintaining electrical integrity across cell
inversely related to the calcium levels. Thus, phospho- membranes.6 The Na⫹, K⫹-ATPase pump is iMg
rus levels are usually elevated in conditions causing dependent. This pump maintains high potassium and
hypocalcemia and decreased in hypercalcemia. low sodium cellular concentrations by pumping
Increased plasma phosphorus levels (hyperphosphatemia) potassium into the cell and removing sodium from it.
are commonly seen in renal disease and can be a A disruption of this process can disrupt electrolyte
prominent cause of acidosis in severe renal disease. gradients and have fatal consequences in a critically ill
Low plasma phosphate levels (hypophosphatemia) are patient. In addition, high intracellular sodium concen-
seen in certain malabsorption syndromes as well as in trations cause sodium-calcium exchange, resulting in
hyperparathyroidism and celiac disease. In most cases an increase of intracellular calcium concentrations.
of malabsorption, both plasma calcium and plasma The functions of anions and cations in the body
phosphorus levels are reduced. are summarized in Table 15-1.
TABLE 15-1 Electrolytes and their functions
Sodium Chloride Potassium Bicarbonate Calcium Phosphorus Magnesium
Neuromuscular • Transmission • Transmission and • Transmission of • Normal nerve • Transmits
and conduction of nerve nerve impulses and muscle neuromuscular
conduction impulses • Contraction of activity activity
of nerve • Contraction of skeletal muscles • Mediator of neural
impulses skeletal and smooth transmissions in
muscle CNS
Body fluids • Osmolality • Osmolality • Regulates osmolality
of vascular of vascular of intracellular fluids
fluids fluids
• Regulation • Regulation of
of body fluid body water
balance
Cellular • Sodium • Enzyme activity for • Maintenance • Forms high- • Carbohydrate
pump cellular energy of cellular energy and protein
• Enzyme production permeability compounds metabolism
activity • Deposits glycogen in • Coagulation of • Formation of red • Transports
liver cells blood blood cell sodium and
enzymes calcium across
• Utilization of cell membrane
B vitamins • Influences
• Transmits utilization of
hereditary traits potassium,
calcium, and
• Metabolizes
protein
carbohydrates,
fats, and proteins
Acid-base • Regulation • Regulation • Elimination • Maintains
levels of balance of balance of acids acid-base
• Acidity of balance in body
gastric juices fluids
Cardiac • Nerve conduction • Contraction of • Contraction of

and contraction of heart muscle heart muscle
the myocardium
Bones and • Formation of • Formation,
393
teeth bones and teeth strength, durability

Laboratory Methods for Spotlight

Determining Electrolytes On
A variety of specimen types can be used to measure
electrolytes. In the clinical laboratory, serum is still the
Measuring Electrolytes
most common type of specimen. However, the use of Analytical electrolyte (Na, K, Cl, and CO2) values
heparinized plasma samples and whole blood is differ among serum, plasma, and whole blood.
gaining popularity quickly because they eliminate the With the exception of potassium, these differences
time required for clotting and serum separation. are small and not clinically significant. The
potassium concentration in plasma is approxi-
mately 0.3 mmol/L less than that in serum.
FLAME PHOTOMETRY AND INDIRECT Potassium concentrations in whole blood are
ION-SPECIFIC ELECTRODES approximately 0.2 mmol/L greater than in serum.
For many decades, flame emission photometry was the Source: National Committee for Laboratory Standards, Standard-
most common procedure to quantitatively measure ization of Sodium and Potassium Ion-Selective Electrode Systems
to the Flame Photometric Reference Method; Approved Standard
sodium and potassium in body fluids. However, since C-29A. Wayne, Pa: National Committee for Laboratory Standards;
the mid-1990s flame emission photometry has rapidly 1995.
disappeared from the clinical laboratory and is no
longer used. These results are then compared to the
original results from flame photometry, which is still Flame photometry had always been plagued with
considered the reference method.7 problems. It was difficult to maintain a constant and
The basis for flame photometry is that many controlled supply of energy to the solution that
metallic elements, when supplied with sufficient energy, contained the analytes. Other problems were:
emit this energy at a wavelength that is characteristic for
the specific element. When energy is supplied to a • The danger of using gases to produce the flame.
solution of serum in the form of a hot flame, the • The continuous emissions caused by the burning
absorbed energy is released by both sodium and of nonionic products.
potassium in a characteristic spectrum for each element. • Signal enhancement (mutual excitation) caused
Sodium emits a visible yellow light, and potassium by high sodium concentrations in the sample.
emits a violet light. Specific wavelengths in the sodium
and potassium spectra that emit the largest amount of ION-SPECIFIC ELECTRODES
energy are selected and compared with the energy Today, sodium and potassium are measured with
emitted from a standard solution of sodium and ion-specific electrodes (ISEs), which consist of
potassium. The light intensity produced at a specific sodium electrodes with glass membranes and an
wavelength is directly proportional to the concentration electrode with a liquid ion-exchange membrane.
of atoms in the solution. The mathematical comparison Measuring the electron potential on a selective mem-
of the emitted spectra of the unknown sample with brane requires a complete electrical circuit. There are
those of the standard reveals the actual concentration of two electrodes: a reference and an ion-specific elec-
either sodium or potassium.7,8 Figure 15-4 shows a trode. The potential of the reference electrode is
typical schematic of a flame photometer. maintained constant and that of the ISE electrode
varies. As sodium ions penetrate the ion-exchange
membrane, a change in the membrane potential is
detected and then related to sodium concentration.
Potassium measurements are accomplished
similarly. The potassium ISE contains a valinomycin
membrane that excludes the large sodium ion while
allowing the smaller potassium ion to penetrate.
Flame Electrodes measuring total carbon dioxide consist
of a carbon dioxide–permeable membrane and a pH

Monochrometer Detector electrode. The bicarbonate ion and protein-bound
Atomizer or
Diffraction Gradient carbon dioxide are converted to carbon dioxide gas,
Slit Slit which can diffuse through the membrane to dissolve in
Aspirator
a bicarbonate buffer solution. The diffused carbon
dioxide causes a change in the pH, which is measured
FIGURE 15-4 Schematic of a flame photometer. with the pH electrode.
Spotlight Laboratory Methods for

On Determining Arterial Blood pH,
Ion-Specific Electrodes Carbon Dioxide Pressure, and
Ion-specific electrode methods can be divided Oxygen Pressure
into two types: the direct method and the The pH electrode consists of an Ag/AgCl electrode and
indirect method. In the indirect method, the a calomel electrode. The calomel electrode (the refer-
sample is diluted with a diluent of high ionic ence) consists of mercury covered by a thin layer of
strength before being presented to the electrode. HgCl2. The Ag/AgCl (indicator) electrode is surrounded
In the direct method, undiluted serum, plasma, by a glass membrane immersed in a reference solution.
or whole blood is introduced directly into the Hydrogen ions in the test solution penetrate the glass
ion-specific electrode. The latter approach allows membrane of the indicator electrode, effecting a change
the use of whole blood and thus is compatible in the reference solution. The potential charge differ-
with the simultaneous determination of blood ence between the test solution and the reference
gases. solution is calibrated into pH units. Figure 15-5
illustrates the components of a pH electrode.
The PCO2 (Stow-Seringham) electrode consists of a
glass pH electrode separated from the blood or plasma
BIOSENSOR TECHNOLOGY to be measured by a thin, gas-permeable membrane
Biosensors are devices that combine ion-specific consisting of Teflon, silicon rubber, or other material
electrodes, enzymatic methodology, and solid-phase that allows gas but not liquid to permeate. Blood,
technology to selectively recognize an element with a plasma, or gas is introduced into a temperature-
transducer. Thus, biosensors can be defined as devices controlled chamber that is separated from a compart-
in which an immobilized biochemical component ment containing bicarbonate buffer by a thin (0.001-in.)
reacts with an analyte, such as an ion, to produce a gas-permeable membrane. The membrane allows
signal. The signal is proportional to the quantity of uncharged particles such as carbon dioxide to permeate
the analyte.8–10 (Although the potassium electrode but prevents charged particles (nongaseous substances)
uses a biocomponent, valinomycin membrane, it is from penetrating. The diffused gas reacts with the
not considered a biosensor because the electrode does bicarbonate solution, resulting in the following reaction:
not incorporate biorecognition in its measuring CO2 ⫹ H2O ↔ H2CO3 ↔ H⫹ ⫹ HCO3⫺
process.)
The hydrogen ions produced penetrate the gas elec-
trode, and the Ag/AgCl internal electrode detects the
change in potential. Figure 15-6 illustrates the compo-
Spotlight nents of a PCO2 electrode.
On The PO2 electrode, also known as the Leland
Clark electrode, consists of a platinum cathode and
Biosensors an Ag/AgCl anode in a phosphate buffer. The platinum
electrode is separated from the test solution by a
The major manufacturers’ blood gas analyzers
gas-permeable membrane. When the cathode is set at
use direct ISE methods. Earlier ISEs using the
⫺0.65 V in the absence of oxygen, the current is zero.
indirect method consisted of a rather large
When oxygen diffuses across the membrane, it is
electrode surface, requiring a large volume to
reduced at the cathode, resulting in a current flow
cover the electrode. With the development of
between the two electrodes. The current flow is
smaller electrodes, smaller sample volumes have
eliminated the need for sample dilution.
Workable biosensors have been used for such Glass (Ag-AgCI)
analytes as creatinine, glucose, lactate, and urea Sample
nitrogen. Biosensors have also been developed for
H+ H+ H+
blood gases, heparin, homocysteine, and protein.
Some technical hurdles related to sensitiv-
ity and specificity have to be overcome before
Reference (Calomel)
biosensors are used commonly as routine
Electrodes Amplifier Recorder
measuring devices.
FIGURE 15-5 Components of a pH electrode.
Glass (Ag-AgCI) bicarbonate ion, is reacted with the substrate phospho-

enolpyruvate and the enzyme phosphoenolpyruvate
Sample CO2 CO2 carboxylase to form oxaloacetate. That is, in turn,
CO2 CO2 reacted with nicotinamide adenine dinucleotide
hydrogen (NADH) and malate dehydrogenase to form
CO2 CO2
malate and reduced nicotinamide adenine dinucleotide
(NAD⫹). The decrease in absorbance is measured at a
Reference (Calomel) wavelength of 340 nm and is used to quantitate the
Electrodes carbon dioxide concentration.
Membrane Amplifier Recorder Nearly all other methods in use today use a carbon
FIGURE 15-6 Components of a P CO2 electrode.
dioxide electrode. The carbon dioxide electrode consists
of a carbon dioxide gas–permeable membrane and a
pH electrode. The sample is acidified to convert all
bicarbonate, both free and protein bound, into carbon
Platinum dioxide gas. The liberated carbon dioxide diffuses
through a permeable membrane and dissolves in the
Sample O2 O2
internal filling solution. The dissolved carbon dioxide
O2 O2 in the internal filling solution causes a pH change in
O2 O2 the solution, which is measured by the pH electrode.
The magnitude of the pH change is a function of the
total carbon dioxide content of the sample and is
Gas Permeable Ag-AgCI converted to carbon dioxide concentration units.
Membrane Electrodes Amplifier Recorder Traditional methods for plasma chloride determi-
nations included photometric (use of a spectropho-
FIGURE 15-7 Components of a P O2 electrode.
tometer) and coulometric-amperometric titration
methods.11
• Coulometry is an electrochemical titration in
calibrated to the oxygen concentration in the test which the titrant is electrochemically generated
sample. A typical PO2 electrode is shown in Figure 15-7. and the end point is detected by amperometry.
Chapter 16 provides additional details on acid-base • Amperometry is the measurement of the current
and blood gas analysis. through an electrolyte solution.
A typical spectrophotometric analysis reacts mercuric
Laboratory Methods for Analyzing thiocyanide with chloride ions in plasma or serum to
form mercuric chloride and free thiocyanate ions. The
Carbon Dioxide and Chloride free thiocyanate ions are reacted with Fe3⫹ to form
Historically, numerous methods have been used to ferric thiocyanate, which is spectrophotometrically
measure carbon dioxide.1 One of the earlier and more quantitated at a wavelength of 480 nm.
reliable assays is the manometric method popularized Coulometric-amperometric titration methods for
by Samuel Natelson, known as the Natelson microgas- quantitating chloride levels are based on the generation
ometer. This method is based on the pressure resulting of silver ions at a constant rate from a silver electrode.
from the carbon dioxide released when acid is added to The generated silver ions react with chloride ions to
a solution in an enclosed system. After the barometric form insoluble silver chloride. When all of the chloride
pressure in the solution has been measured, the ions have been used in the formation of silver chloride,
mixture is treated with alkali, and the dissolved carbon the generation of silver from the silver electrode is
dioxide is absorbed into the solution. The barometric terminated. The time interval between the beginning
pressure of the resulting solution is measured, and the and end of the reaction is directly related to the
difference between the two measurements is estab- amount of chloride ion in the sample. Comparing the
lished. The difference in pressure, after correction for time of analysis of a known standard against the time
atmospheric pressure, is the basis for determining the of analysis of the unknown sample allows the quantita-
carbon dioxide concentration in the sample. tion of chloride in the sample.
In most laboratories, automated analytical assays Ion-specific electrodes (ISEs) have become the new
have replaced the microgasometer. One of the more methodology in measuring chloride concentration in
successful methods is an enzymatic assay. It requires the plasma, serum, and whole blood.12 Typically, a refer-
conversion of all forms of carbon dioxide to the ence electrode and an ion-specific electrode are used.
bicarbonate ion. The resulting solution, containing the The potential of the reference electrode remains
constant; that of the ISE varies depending on the levels, along with decreased blood pH, and increased
activity of the chloride ion across the membrane. The plasma chloride concentrations. Differential laboratory
change in potential is predicted by the Nernst equation tests require renal function tests.
and allows for the quantitation of the unknown Metabolic acidosis caused by increased lactic acid
chloride sample.7 The ISE electrode used for chloride can have a variety of causes, including anaerobic
measurements is a silver chloride membrane electrode, metabolism. Other causes are:
one of whose drawbacks is that therapeutic levels of
• Alcohol consumption.
bromide and iodide in blood can cause significant
• Diabetes mellitus.
errors in chloride levels. The silver chloride electrode
• Glycogen storage diseases.
selectively recognizes these halogens as compared with
• Tumors.
chloride. Thus, small therapeutic levels of bromide and
• Idiopathic causes.
iodide could result in falsely elevated chloride results.
• Vomiting and diarrhea, which can cause a signifi-
cant loss of bicarbonate ion and other conjugate
Laboratory Findings in bases.
• Inappropriate administration of hydrochloric
Acid-Base Disturbance acid and administration of ammonium chloride
As described in Chapter 4, acid-base disturbance due to during treatment procedures in medical settings.
changes in the bicarbonate levels in blood is of meta- The compensatory response to metabolic acidosis
bolic origin. Low blood bicarbonate levels without a is primarily neuromuscular and secondarily renal.
change in H2CO3 are defined as acidosis, and excess Increased alveolar ventilation results in rapidly
bicarbonate levels as alkalosis. Changes in CO2 as a decreasing PCO2 levels. Renal compensation also
result of altered ventilation are respiratory acidosis involves increasing the elimination of hydrogen ions
(increased CO2) or respiratory alkalosis (decreased by increasing the ammonium ion loss.
CO2).13
LABORATORY FINDINGS IN METABOLIC

LABORATORY FINDINGS IN METABOLIC ACIDOSIS ALKALOSIS
Metabolic acidosis is based on the loss of extracellular Common causes of metabolic alkalosis include exces-
buffers, the accumulation of fixed acids, or both. sive losses of noncarbonic acids from the upper
Common conditions causing metabolic acidosis gastrointestinal tract, diuretic therapies, and increases
include diabetic ketoacidosis, excess production of in corticosteroids.
lactic acids, uremia and chronic renal disease, diarrhea,
• Prolonged and excessive vomiting and gastric
and the administration of drugs.
suction in medical settings are the most com-
Diabetic ketoacidosis occurs in insulin-dependent
mon causes. The greater chloride concentration
diabetes mellitus (IDDM, type I) and in advanced stages
in the gastrointestinal fluid results in chloride
of non-insulin-dependent diabetes (NIDDM, type II).
depletion and excessive retention of the bicar-
In both cases, the severely abnormal carbohydrate and
bonate ion; these effects result in increases of
lipid metabolism results in large increases in the
plasma bicarbonate and decreases in plasma
production of keto-acids such as hydroxybutyric acid
chloride levels.
and acetoacetic acid.14 In this condition, an increased
• Diuretic therapy and laxatives cause impairment
anion gap is found [anion gap ⫽ Na⫹⫺(Cl⫺ ⫹ HCO3⫺)].
in the reabsorption of potassium ion and
Common laboratory findings are large increases in
increased excretion of hydrogen ions by the
blood glucose, increased chloride concentrations, and
kidney.
significant reductions in bicarbonate levels. An increase
• Hyperaldosteronism and steroid therapy are less
in urine ketone bodies and positive plasma acetone
common causes of metabolic alkalosis. Both of
levels is also expected. Blood gas findings include
these steroids cause increased secretion of
increases in hydrogen ion concentrations, as indicated
potassium and hydrogen ions.
by lower blood pH, and decreases in PCO2 levels.
The administration of insulin results in significant Laboratory findings in metabolic alkalosis show
improvements. increases of both dissolved carbon dioxide and bicar-
Renal tubular acidosis is characterized by the inap- bonate ion, resulting in an increase of PCO2. A
propriate reabsorption of bicarbonate ions by the decreased concentration of plasma chloride and
proximal tubules.15 The deficiency in the reabsorption potassium is common, and an elevation in plasma
of bicarbonate ion results in the increased reabsorption sodium is possible. Patients with potassium deficiency
of chloride ion. Laboratory data show decreased PCO2 show general weakness, decreases in tendon reflexes,
and, in more severe cases, tachycardia and cardiac decrease in the urine’s secretion of hydrogen ion and
arrhythmia. Compensatory mechanisms are not clearly decreased retention (increased excretion) of bicarbon-
understood and usually include decreased alveolar ate ion in an effort to lower blood pH.
ventilation. The primary laboratory findings in respiratory
alkalosis are reductions in PCO2 and dissolved carbon
dioxide, resulting in increased blood pH. Table 15-2
LABORATORY FINDINGS IN RESPIRATORY summarizes the lab values found relative to acid-base
ACIDOSIS disturbances.
Respiratory acidosis demonstrates an elevation of PCO2
(hypercapnia) and is caused by defects in the excretion
CURRENT BIOCHEMICAL MARKERS IN ACUTE
of bicarbonate ion. Defects in respiration include
MYOCARDIAL INFARCTION
obstructive lung disease and trauma to the respiratory
center, resulting in CNS depression. Chronic obstruc- Biochemical markers to diagnose acute myocardial
tive lung disease and the overuse of respiratory depres- infarction have been in use since the mid-1950s with
sant drugs are probably the most common causes of the initial use of aspartate aminotransferase (AST). Since
respiratory acidosis. Chronic bronchitis, emphysema,
pulmonary edema, and fibrosis are common condi-
tions resulting in chronic obstructive lung disease. TABLE 15-2 Lab Values of Acid-Base
CNS depression has multiple causes: inappropriately Disturbances
prescribed antidepression and narcotic drugs, self-
Acid-Base
administered narcotics, and overdoses of prescription
Disturbance Common Lab Values
drugs.
Laboratory findings before compensation show Metabolic • Large increases in blood glucose
high PCO2, decreases in PO2, and low pH levels. acidosis • Increased chloride concentrations
Renal compensation is the primary response to • Significant reductions in
respiratory acidosis. A decrease in arterial pH bicarbonate levels
(increased hydrogen ion concentration) and an • Increase in urine ketone bodies
increased PCO2 level are powerful stimuli for bicarbon- • Positive plasma acetone levels
ate ion reabsorption by the kidneys. The kidneys’ • Increase in hydrogen ion
response is not immediate, however; it takes 2–5 days concentrations
to fully develop. Laboratory findings after compensa- • Lower blood pH
tion show increases in the bicarbonate ion and total • Decreases in P CO2 levels
carbon dioxide levels. The ratio of bicarbonate ion to
Metabolic • Increases of both dissolved carbon
dissolved carbon dioxide is decreased, causing a further
alkalosis dioxide and bicarbonate ion
decrease in blood pH level.
• Increase of P CO2
• Decreased concentration of
plasma chloride and potassium
LABORATORY FINDINGS IN RESPIRATORY (common)
ALKALOSIS • Elevation in plasma sodium
Respiratory alkalosis is the result of excessive alveolar (possible)
ventilation, which leads to an excessive loss of carbon
dioxide, thereby lowering PCO2 levels. Alveolar hyper- Respiratory Before compensation:
ventilation that occurs repeatedly without apparent acidosis • High P CO2
reason is known as hyperventilation syndrome. Emotional • Decreases in P O2
states such as excitement, hysteria, and anxiety increase • Low pH levels
alveolar hyperventilation. Metabolic acidosis, pulmo- After compensation:
nary emboli, and mild restrictive lung diseases are • Increases in the bicarbonate ion
other causes of respiratory alkalosis. Subnormal levels and total carbon dioxide levels
of PO2 stimulate the respiratory center, resulting in • Decreased ratio of bicarbonate ion
increased breathing. A variety of drugs are also known to dissolved carbon dioxide
to cause alveolar hyperventilation. • Decrease in blood pH level
Normal and relatively rapid responses to respira-
Respiratory • Reductions in P CO2
tory alkalosis consist of buffering and intra- and
alkalosis • Dissolved carbon dioxide
extracellular ion shifts. Compensatory mechanisms in
• Increased blood pH
acute and prolonged respiratory alkalosis consist of a
then, other markers for acute myocardial infarction Statistical Quality Control
(AMI) that have been used are:
Good laboratory practice and the enactment of the
• Lactic dehydrogenase isoenzymes. Clinical Laboratory Improvement Amendments of
• Total creatine kinase (CK). 1988 (CLIA-88) require that all laboratory testing
• Creatine kinase isoenzymes by electrophoresis. processes be monitored using quality control speci-
• Creatine MB determinations by immunoassay mens and the appropriate use of statistical quality
techniques (CK-MB). control (QC) procedures.20
• Creatine kinase isoforms.
The difficulties with these markers included the ESTABLISHING PRECISION GOALS
lack of specificity and, in some cases, the length The analytical performance of an analyte needs to be
of the assay procedure. Since 1992, troponin T (cTnT) monitored in order to assess the performance of an
and soon thereafter troponin I (cTnI) have become analytical test method.21,22 Precision is a measure of
the predominant AMI markers. These later reproducibility and is determined by analyzing the
markers are: same material repeatedly over time. If the observed
• Highly specific for cardiac muscle injury. concentration of the control is plotted against the
• Have a high assay sensitivity. frequency of the occurrence of observed concentra-
• Appear very early after myocardial infarction. tions, a normal, or Gaussian, distribution is obtained
• Display prolonged elevation after myocardial (Figure 15-8). The same distribution curve of data can
injury.16,17 also be obtained by calculating the mean and standard
deviation of the data.
The striated muscle in the cardiac tissue contains a The mean is simply the average value of the data
protein complex consisting of three polypeptides that points and is calculated as follows:
are involved in calcium regulation. Two of these,
troponin I and troponin T, are considered highly _ ⌺x1 ⫹ x2 ⫹ x3 ⫹ . . . xn
x ⫽ ____________________
n
specific for cardiac muscle injury because they have not _
been demonstrated in other types of skeletal muscle.18 where x ⫽ mean; ⌺ ⫽ sum of all values; n ⫽ the
Troponin is elevated in 4–8 hours after an acute number of determinations.
myocardial infarction and thus is similar to CK-MB. Standard deviation (SD) is a measure of disper-
Unlike CK-MB, however, troponin T and troponin I are sion (the spread of the data around the mean). It is the
highly specific for striated muscle tissue and remain square root of the sum of the squares of the observed
elevated for several days. data minus the mean value of the observed data
In addition to the troponins and CK-MB, myoglobin
determinations are frequently used because of their
early increases in patients’ blood.19 Myoglobin
becomes abnormal within 2 hours after an acute
myocardial infarction and peaks within 6–9 hours. The
early elevations are of particular importance because
thrombolytic therapy for AMI patients is most effective
when used within the first 6 hours of an AMI. Because
myoglobin is an acute-phase reactant, however, its
elevation alone is not a confirmation of AMI. It must
be used along with electrocardiogram and clinical
evaluation.
Best Practice
Drug Overdoses 68.3%
95.55%
Salicylate overdose and excessive doses of ana-
bolic drugs, epinephrine, and progesterone are 99.7%
known to result in alveolar hyperventilation. –3s –2s –1s Mean +1s +2s +3s
Increased alveolar ventilation is a normal
response to metabolic acidosis.
FIGURE 15-8 Gaussian distribution of data.

Analyte Performance Standard Deviations
Analyzing control materials of various concentra- Standard deviations can be used to establish the
tions can monitor the performance of an analyte. upper and lower limits of a control material. Plus
Control materials are usually commercially pro- and minus 2 standard deviations (2 SD) from the
duced lyophilized serum products that contain mean are traditionally used as control limits.
analyte concentrations below, within, and above
reference intervals. The observed values are then
compared with acceptable upper and lower limits
for the specific analyte. An analytical assay run The coefficient of variation (CV) is more meaning-
is then evaluated as successful or unsuccessful ful than standard deviation because it expresses the
according to certain established criteria. standard deviation as a percentage of the mean.
Assume that two PCO2 controls have means of 55
and 110 mm Hg and standard deviations of 6 and
divided by the number of observations. It is calculated 8 mm Hg. The CV of the lower control is 10.91, and
as follows: that of the higher control is 7.27. The value obtained
__________
_
with the higher control is more precise even though it
⌺(xi ⫺ x )2
√
SD ⫽ _________
n
has a higher standard deviation.
where SD ⫽ standard deviation; xi ⫽ value of observed

_ MONITORING THE ANALYTICAL PRECISION
data points; x ⫽ mean value of observed data; and
OF A TEST
n ⫽ number of determinations.
As shown in Figure 15-8, the normal distribution of The two types of errors a laboratory needs to monitor
data can be divided into areas corresponding to ⫾1 SD, are random and systematic errors.
⫾2 SD, and ⫾3 SD. The percentages of values in these • Random errors are an indication of the precision
distinct areas are 68.3, 95.55, and 99.7, respectively. of a test method. They are observed by the
This range, however, may be too narrow for analytes, scatter of control data points around the mean
which have excellent precision and thus a very narrow of the control value. The scatter of control values
acceptable, perhaps unrealistic, range for controls. Also, should be randomly distributed above and
by statistical design, nearly 5% of the control assays fall below the mean.
outside the acceptable range. Using plus and minus 3 SD • On the other hand, systematic errors are reflec-
enlarges the range for acceptable controls to 99.7% of tions of the accuracy of the method. Accuracy has
the control samples. Observations (data) which falls been defined as the agreement between the best
outside the 3rd SD are also known as “outliers”. estimate of a quantity and its true value. These
Another approach to create reference intervals for can be detected by the comparison of laboratory
control values is to use a coefficient of variance (CV), data with those obtained from other laboratories
which is the standard deviation expressed as a percent- using the same methodology.
age of the mean. A CV of 5% is considered an accept-
able analytical performance. This requires that a Once a control material, along with the upper
theoretical standard deviation be calculated using the and lower control limits, has been established, the
mean and a CV of 5%. This is calculated as follows: performance of the assay needs to be monitored.
Control results are ideally distributed randomly around
100 ⫻
_ SD
CV ⫽ _________ the mean value of the control. The number of control
x
_ values outside control limits (i.e., out of control) in a
where CV ⫽ coefficient of variation, x ⫽ mean, and properly performing assay depends on the method
SD ⫽ standard deviation. used to determine the control limits. If ⫾2 standard
If we assume that a control for PCO2 has a mean deviations is used to establish the control limits, then
concentration of 55 mm Hg, then: 5%, or 1 out of 20, control values will be outside the
100 ⫻ SD control limits. At 3 SD, only 3 out of 1000 will fall
5 ⫽ _________
55 outside control limits. If a CV of 5%, is the basis for
100 SD ⫽ 275 setting control limits, then failure will depend on the
SD ⫽ 2.75 precision of the particular assay. If the precision of the
Thus, the reference interval for an acceptable control assay is at or near 5%, then a larger number of control
value is the mean ⫾2 SD, or 49.5–60.5 mm Hg. results will fall outside the limits. When an analytical
run is performed, a judgment needs to be made 114

whether a run is in control or out of control. If the run 112
110
is in control, then the patient results are acceptable for Mean +3SD
Control (concentration)
108
clinical interpretation. If the run is considered out of 106
104
control, patient values cannot be used, and corrective 102
actions need to be initiated. 100
98 Mean
Various criteria can be used to judge whether a run 96
is in or out of control. A common procedure used in 94
laboratories is the multirule procedure developed by 92
90
Westgard and coworkers.23 The multirule method is
88
86 Mean –3SD
often incorporated into instrument computer quality
84
control modules, into laboratory information systems 82
(LIS), and into hospital information systems (HIS). It 80
entails a simple approach to interpreting control values 0 2 4 6 8 10 12 14 16
Run Number
and determining the rejection or acceptance of an
analytical run. Table 15-3 outlines the rules. Clinical FIGURE 15-9 Levey-Jennings control chart: Control limits
laboratories extensively use the first three rules to are set at the mean ⫾3 SD.
evaluate the performance of their assays.
Other approaches include the use of Levey-Jennings
charts, as depicted in Figure 15-9.24 These charts are Best Practice
simple and convenient to use because laboratory and
hospital computer information systems can produce
them automatically. The Levey-Jennings charts can be
Trend Analysis
used to monitor internal quality control by the West- Trend analysis can be useful in monitoring the
gard multirule method and by trend analysis.25 deterioration of either the quality control mate-
rial or the calibration curve. Deviations of control
values from the mean over a period of time are
indications of trends, whereas sudden changes of
CONDUCTING INTERLABORATORY COMPARISONS control values involving a shift in either direction
Various manufacturers of quality control material often require immediate attention. A good labora-
conduct external laboratory quality assurance (QA) tory uses a variety of these methods to monitor
programs. Laboratories using the same lot number of quality control.
control samples submit their monthly quality control
TABLE 15-3 Westgard’s rules

12 SD The value of one control exceeds the mean by ⫹/–2 SD. Warning rule: further evaluation required
Evaluate rules 13 SD, 22 SD, R4 SD, 10X.
Accept the run if it passes these rules.
Reject the run if it fails any of these rules.
13 SD The value of one control exceeds the mean by ⫹/–3 SD. Reject the run.
22 SD The values of two consecutive controls exceed the mean by Reject the run.
⫹/–2 SD.
R4 SD The value of one control exceeds the mean by ⫹2 SD; Reject the run.
another exceeds the mean by –2 SD.
41 SD Four consecutive control values exceed the mean by ⫹1 SD Reject the run.
or –1 SD.
10x Ten consecutive control values fall above the mean, or Reject the run.
10 consecutive control values fall below the mean.
Source: From Westgard OJ, Klee GG. Quality management. In: Burtis CA, Ashwood ER, eds. Tietz Textbook of Clinical Chemistry. 3rd ed. Philadelphia: WB
Saunders Co; 1999; 384–418.
results, which consist of the mean and standard

deviation for each analyte tested. The submitted data Best Practice
are statistically compared with the data submitted by
other laboratories. A common statistical comparison is Interlaboratory Comparisons
the standard deviation interval (SDI), calculated as
Interlaboratory comparison data are available to
follows:
participants of group data comparison studies.
laboratory mean ⫺ group mean Such studies are conducted by companies that
SDI ⫽ ____________________________ sell quality-control material and organizations
group standard deviation
that provide quality control surveys, such as the
The group mean is the mean of values in analyses College of American Pathology (CAP).
of an analyte obtained from all participant laboratories
using an identical method. The group standard devia-
tion is a calculated standard deviation of the mean
values from all laboratories submitting data.
tions, the point of intersection should fall at 0.0. Data
The laboratory SDI value can then be used to
points drifting to the right are indications of propor-
evaluate the analyte performance of an individual
tional errors. Displacement of the point downward or
laboratory in the group. An SDI of less than ⫹2 SD
upward is an indication of a constant error or constant
or ⫺2 SD is an indication that the laboratory result
errors. The difficulties are the number of participating
is in good agreement with data submitted by
laboratories and the fact that a laboratory with bad
other laboratories using identical methods. A value
data can affect the group mean and the group standard
that exceeds ⫾2 SD is an indication of a lack of
deviation.
agreement.
SDI units can also be presented in a Youden plot
(Figure 15-10). This plot requires two control materials
DETERMINING THE ACCURACY
of different concentrations to be used. The SDI value of
OF AN ANALYTICAL ASSAY
control 1 is plotted on the y-axis, and the SDI value of
control 2 is plotted on the x-axis. Under ideal condi- Accuracy is a measure of truth or adherence to consen-
sus for an analytical test method. Ideally, a test method
in a clinical laboratory should be traceable to a refer-
3.0 ence material. The accuracy of a test method can be
Corrective action needed
ascertained by analyzing the recovery of a reference
material. Often, the unavailability or cost of obtaining
2.0
Marginal performance reference material makes this approach impractical.
Manufacturers of reagents use reference material as
1.0 their calibrators or have their calibrators traceable to
Acceptable reference materials. Thus, the laboratory is relying on
performance manufacturers for the accuracy of the laboratory
SDI of control 1
method.
A B C In addition, laboratories rely on regional quality
0.0 control programs and on government-mandated or
accrediting agency–mandated proficiency testing for
acceptable accuracy performance of their analytical
methods. In interlaboratory comparisons, the
laboratory results are evaluated against results
–1.0
obtained by other laboratories using the same
reagents and instrumentation. In mandatory profi-
–2.0 ciency testing for analyses monitored by the Centers

for Medicare & Medicaid Services (CMS, formerly the
Health Care Financing Administration (HCFA)I, the
–3.0
laboratory results are compared with the results
SDI of control 2 obtained by other laboratories or with methodolo-
gies considered to be accurate. Several professional
FIGURE 15-10 Representation of the Youden plot: Compar-
ing the standard deviation interval (SDI) values of two organizations and many individual states provide
control materials. All values on the x-axis are 0.0 SD. these surveys for a fee. The laboratory survey results
Coordinate for the observed mean of control 1 versus the are monitored by CMS, and an acceptable passing
observed mean of control 2. score must be obtained.
CASE STUDY 15-1 CASE STUDY 15-2

After completing the normal morning mainte- A 10x alert comes up on a sodium assay during a
nance on the blood gas analyzer, the laboratory daily quality control assay. The sodium quality-
technician analyzed three control samples and control results show that the sodium values of
obtained the following results (acceptable values the normal and high controls are 121 and
⫾2 SD; the variations in the normal ranges given 149 mmol/L, respectively. The control ranges
in parentheses are attributable to the lot number, (⫾2 SD) for these controls are 120–128 and
the manufacturer, and other factors): 148–154 mmol/L, respectively. A review of the
quality-control values for the past month reveals
Control 1:
that the control values for both sodium controls
pH ⫽ 7.320 (7.28–7.36) have been slowly drifting downward. All of the
PO2 ⫽ 98 mm Hg (95–105 mm Hg) other analytes produce acceptable results
PCO2 ⫽ 60 mm Hg (57–64 mm Hg) without error flags. The sodium methodology on
the analyzer is an ion-specific electrode, placed
Control 2: on the analyzer 6 months ago.
pH ⫽ 7.128 (7.132–7.184)
PO2 ⫽ 45 mm Hg (46–51 mm Hg) Questions
PCO2 ⫽ 35 mm Hg (35–41 mm Hg) 1. Determine which of the following actions to take:
a. No actions are required, both quality-
Control 3: control values are within acceptable limits.
pH ⫽ 7.456 (7.436–7.510) b. Perform maintenance and reanalyze
PO2 ⫽ 68 mm Hg (65–74 mm Hg) quality-control samples.
PCO2 ⫽ 75 mm Hg (71–79 mm Hg) c. Replace the sodium ISE electrode, perform
maintenance, and repeat quality-control
Questions samples.
1. After evaluating the quality control run, which d. Replace the reagents; they are probably
of the following should the technician do? deteriorating.
a. Report the results to the physician. 2. Why are quality controls essential to electrolyte
b. Recalibrate the analyzer and repeat the analysis?
controls.
c. Rerun the quality control material.
d. Follow the troubleshooting procedure for and cations in the body. Ionized calcium and ionized
the test on the analyzer. magnesium have been shown to be better indicators of
2. Why are controls essential to the operation cardiac function after cardiopulmonary bypass than the
and maintenance of a blood gas analyzer? total levels of calcium and magnesium, consisting of
both bound and free forms.
Respiratory therapists must be familiar with the
various cardiac markers and their release into the blood.
The understanding of basic quality control, along
Summary with basic concepts of measuring various analytes,
The respiratory therapist must have a basic understand- allows the respiratory therapist to monitor the accuracy
ing of chemistry and the various properties of atoms, of analytical results. Thus, proper and accurate infor-
bonds, and the atomic structure of biological mol- mation is provided to the physician or health care
ecules. This knowledge is necessary to understand how provider.
electrolytes influence and control metabolic reactions.
Both sodium in the intracellular space and potassium
in the extracellular space have a major influence on the Study Questions
distribution and retention of body fluids and on REVIEW QUESTIONS
osmolality. Thus, electrolytes and body fluids affect
changes in HCO3⫺, PCO2, and pH. 1. Describe how element 11 (Na) differs from ele-
Also helpful is an understanding of the various ment 19 (K), and describe how the two elements
factors that control the concentration of both anions are similar.
2. Biological molecules are usually classified into four 5. When you are calibrating pH, PCO2, and PO2 in a
groups: carbohydrates, lipids, proteins, and nucleic blood gas analyzer, it is not necessary to
acids. Which group is the most important source of a. control electrical drift.
energy? b. maintain the temperature at 37°C.
3. Identify some functions of electrolytes in the c. determine the barometric pressure and make
human body. necessary adjustments.
d. prime the instrument using a whole blood
4. List three methods of analyzing for electrolytes,
sample.
and indicate why one of these methods is now
used almost exclusively. 6. Ion-specific electrodes (ISEs) are based on the
principle of:
5. Diabetes mellitus is a common cause of metabolic
a. oxidation-reduction reactions.
acidosis. Detail the typical laboratory results seen
b. electrochemical reactions.
in this condition.
c. potentiation.
6. Explain the significance of measuring ionized d. coulometric-amperometric analysis.
magnesium levels in critically ill patients.
7. A number without units used to show
7. Explain why the measurement of myoglobin alone deviation regardless of the concentration
is not a reliable indicator for the diagnosis of of a control is:
myocardial infarction. a. standard deviation.
8. What are the statistical requirements to validate b. coefficient of variation.
and monitor an analytical assay? c. mean.
d. trend.
MULTIPLE-CHOICE QUESTIONS 8. Accuracy refers to the:
a. true value of an analyte.
1. Which of the following plasma analyses is the least b. precision of an analyte.
affected by hemolysis? c. standard deviation of a control value.
a. potassium d. reliability of the assay result.
b. chloride 9. The coefficient of variation is equal to:
c. lithium a. standard deviation ⫻ 100%.
d. sodium b. (mean/standard deviation) ⫻ 100%.
2. A principal cause of metabolic acidosis is the forma- c. (standard deviation ⫻ 100%)/mean.
tion of organic acids at a rate exceeding their break- d. standard deviation ⫻ mean ⫻ 100%.
down. In diabetic patients with uncontrolled diabetes 10. Which of the following statements about the PCO2
mellitus, there is an overproduction of organic acids electrode is not true?
such as acetoacetic acid and beta-hydroxybutyric acid, a. It measures the rate of change of the oxygen
which leads to metabolic acidosis. Another common concentration.
cause of metabolic acidosis is:
b. Oxygen diffuses across an O2-permeable
a. late stages of salicylate poisoning.
membrane.
b. fat loss due to vigorous exercising.
c. Silver is oxidized at the anode; oxygen is
c. severe hypothermia.
reduced at the platinum electrode.
d. moderate consumption of ethanol.
d. The CO2 gas diffuses through the membrane,
3. The following laboratory findings were obtained altering the pH of the bicarbonate solution.
pH ⫽ 7.24 11. The potassium electrode is different from the
PCO2 ⫽ 24 mm Hg sodium electrode in that it:
Total carbon dioxide ⫽ 18 mmol/L a. contains a valinomycin membrane.
These values are consistent with: b. contains a silver electrode.
a. respiratory alkalosis. c. consists of a double glass system.
b. respiratory acidosis. d. allows for a change in pH.
c. metabolic alkalosis. 12. “Chloride shift” refers to:
d. metabolic acidosis. a. the shift of plasma chloride to the red blood cells.
4. Bicarbonate diffuses from the red blood cells into b. an abnormally high concentration of plasma
the plasma through an exchange mechanism with: chloride.
a. sulfate. c. an abnormally low concentration of plasma
b. lipids. chloride.
c. chloride. d. the irreversible binding of chloride ions to
d. phosphate. plasma proteins.
13. The Teflon membrane on the PCO2 electrode The serum results were reported to the physician.
prevents the transition (diffusion) of: Because the Na level was now closer to the normal
a. oxygen. range (135–145 mmol/L), slight hemolysis was
b. hydrogen ion. considered the most likely cause of the elevated
c. dissolved CO2. Na. Determine the most likely cause for the
d. ionized magnesium ions. elevated sodium. Was it indeed a critical value, or
14. A state of elevated carbon dioxide in blood is was hemolysis or sample contamination the most
called: likely cause?
a. hypercalcemia. 2. A severely ill patient admitted in the emergency
b. hypocapnia. room had the following laboratory results
c. hypernatremia. (the normal reference interval is given in
d. hypercapnia. parentheses):
15. The most specific marker for myocardial infarction Na ⫽ 158 mmol/L (135–145)
(MI) is: K ⫽ 5.9 mmol/L (3.5–5.0)
a. myoglobin.
Cl ⫽ 124 mmol/L (97–108)
b. troponin T or troponin I.
c. creatine kinase MB. CO2 ⫽ 33 mmol/L (22–32)
d. lactic dehydrogenase (LD). Glucose ⫽ 340 mg/dL (70–110)
16. The extent to which the true value of an analyte Osmolality ⫽ 271 mOsm/kg (280–300)
agrees with the analytical measurement is iCa ⫽ 1.6 mmol/L (1.15–1.35)
known as:
iMg ⫽ 0.85 mmol/L (0.45–0.60)
a. reproducibility.
b. accuracy. Detect inconsistencies with respect to the values.
c. precision. Provide the reasons for these.
d. reliability. 3. Two blood gas analyzers are being considered for
possible purchase for the department. The goal is to
CRITICAL-THINKING QUESTIONS select the instrumentation with the better precision.
The evaluation is conducted by two respiratory
1. A whole blood sample was analyzed for therapists, each using a control material over a period
electrolytes (Na, K, Cl, CO2), iCa, and iMg. of 14 days. The following results of this evaluation are
The following results were obtained (the to be used to make a purchase decision:
normal reference interval is given in
parentheses): Data from Data from
Na ⫽ 209 mmol/L (135–145) Instrument 1 Instrument 2
K ⫽ 5.5 mmol/L (3.5–5.0) pH Mean 7.124 7.591
Cl ⫽ 104 mmol/L (97–108) SD 0.094 0.102
CV 1.26 1.34
CO2 ⫽ 29 mmol/L (22–32)
n 14 14
iCa ⫽ 1.4 mmol/L (1.15–1.35)
PCO2 Mean 55 mm Hg 99 mm Hg
iMg ⫽ 0.7 mmol/L (0.45–0.60) SD 4.02 5.03
The very high Na level required further investiga- CV 7.31 5.08
tion before the results could be reported. An n 14 14
examination of the whole blood specimen PO2 Mean 55 mm Hg 99 mm Hg
revealed slight hemolysis. A nonheparinized SD 0.094 0.102
sample was obtained and allowed to clot. CV 1.26 1.34
The resulting serum specimen was analyzed n 14 14
in the main laboratory with the following
Select an instrument, and provide reasons for your
results:
selection.
Na ⫽ 149 mmol/L
4. An arterial blood gas analysis is performed on a
K ⫽ 5.2 mmol/L patient with the following results:
Cl ⫽ 103 mmol/L pH ⫽ 7.38
CO2 ⫽ 26 mmol/L PO2 ⫽ 75 mm Hg
iCa ⫽ 1.4 mmol/L PCO2 ⫽ 49 mm Hg
iMg ⫽ 0.55 mmol/L HCO3⫺ ⫽ 25 mmol/L
The specimen has been recapped and refrigerated. common following cardiac surgery. J Cardiothorac
Two hours later, the physician questions the result Vasc Anesth. 1991;5:201–208.
and asks for a repeat analysis on the same sample. 7. D’Orazio P, Miller WG, Myers GL, et al. Standard-
The following results are obtained: ization of sodium and potassium ion-selective elec-
pH ⫽ 7.39 trode system to the flame photometric reference
method. Approved standard. 2nd ed. CLSI. 2000;
PO2 ⫽ 75 mm Hg
20:1–22.
PCO2 ⫽ 38 mm Hg 8. Durst RA, Siggaard-Anderson O. Electrochemistry.
HCO3⫺ ⫽ 41 mmol/L In: Burtis CA, Ashwood ER, eds. Tietz Textbook of
How would you explain the changes to the Clinical Chemistry. 3rd ed. Philadelphia: WB
physician? Saunders Co; 1999:133–149.
9. Freitag R. Biosensors in Analytical Biotechnology
5. A blood gas analysis is performed on an arterial
Austin, TX: RG Landis Co; 1995.
specimen, and the following results are obtained:
10. Wang J. Electro analysis and biosensors. Anal Chem.
pH ⫽ 7.35 1995;67:487R–492R.
PO2 ⫽ 98 mm Hg 11. Wrotnowski C. Biosensor technology advances.
PCO2 ⫽ 35 mm Hg Genet Eng News. 1998:18:132.
12. Karselis TC. The Pocket Guide to Clinical Laboratory
HCO3⫺ ⫽ 32 mmol/L
Instrumentation. Philadelphia: FA Davis Co; 1994.
Moderate hemolysis was also observed, which was 13. Oech U, Ammann D, Simon W. Ion-selective
noted on the report. membrane electrodes for clinical use. Clin Chem.
The physician requested some additional chemistry 1986;32:1448–1459.
tests on this specimen. The results were as follows 14. Heusel JW, Siggaard-Anderson O, Scott MG.
(normal reference intervals are given in parentheses): Physiology and disorders of water, electrolyte, and
Na ⫽ 144 mmol/L (135–145) acid-base metabolism. In: Burtis CA, Ashwood ER,
eds. Tietz Textbook of Clinical Chemistry. 3rd ed.
K ⫽ 7.1 mmol/L (3.5–5.0)
Philadelphia: WB Saunders Co; 1999:1095–1124.
Cl ⫽ 109 mmol/L (97–108) 15. Sacks DB. Carbohydrates. In: Burtis CA, Ashwood
CO2 ⫽ 31 mmol/L (22–32) ER, eds. Tietz Textbook of Clinical Chemistry. 3rd ed.
Glucose ⫽ 85 mg/dL (70–110) Philadelphia: WB Saunders Co; 1999;750–808.
16. Lash JP, Arruda JAL. Laboratory evaluation of renal
iCa ⫽ 1.33 mmol/L (1.15–1.35)
tubular acidosis. Clin Lab Med. 1993;13:117–129.
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CHAPTER 16
Arterial Blood Gases and Noninvasive

Monitoring of Oxygen and Carbon Dioxide
Paul J. Mathews and Larry Conway
OBJECTIVES
• List the normal measured and calculated values for arterial blood gases.
• Given examples, select blood gases that indicate abnormal conditions, such as respiratory acidosis, respiratory
alkalosis, metabolic acidosis, metabolic alkalosis, and mixed metabolic and respiratory conditions.
• Calculate and explain the significance of anion gap variations.
• Given a clinical scenario, choose the correct acid-base status of the patient.
• Supplied with adequate information, calculate projected blood gas values.
• Determine the oxygen-carrying capacity and content of blood.
• Differentiate between SaO2, SPO2, and O2 content.
• Determine whether the available information is sufficient to perform blood gas prediction equations.
• Define oxygen saturation, oxygen content, oxygen combining capacity, oxygen dissociation curve, pulse
oximetry, and buffer.
• Select and order the steps in blood gas sampling by arterial puncture, arterial line aspiration, and capillary-
sampling techniques.
• Discuss the principles of operation for transcutaneous and gas-sampling techniques.
• Identify the strengths and weaknesses of various types of invasive and noninvasive analysis techniques.
• Identify the indications and contraindications associated with various blood gas analysis and monitoring
techniques.
CHAPTER OUTLINE
Blood Gases Acid-Base Balance
What Are the Blood Gases? Ventilatory Buffering
The TCA Cycle Renal Buffering
Gas Transport in the Blood Intracellular Buffers
Extracellular Buffers
(continues)
408
CHAPTER 16 ■ Arterial Blood Gases and Noninvasive Monitoring of Oxygen and Carbon Dioxide 409
(continued)
Measurement of ABG and Acid-Base Results Analysis Techniques

Oxygen Saturation Arterial Blood Gas Analyzers
Nomenclature Pulse Oximeters
Homeostasis Co-Oximeters
Lungs End-Tidal CO2 Analyzers
Kidneys Transcutaneous Gas Analysis
Arterial Blood Gas Point of Care Testing
Collecting the ABG Sample Role of Hemoglobin and Its Variants in ABG Analysis
Indwelling Blood Gas Other Factors That Affect ABG Results
Analyzer Electrodes Anion Gap
Noninvasive Methods Used to Measure Sampling Errors
Oxygenation Status Analysis
Pulse Oximetry Quality Control, Quality Assurance, and
Tissue Oxygen Saturation (STO2) Performance Improvement
Transcutaneous Monitoring Quality Control
Gas Sampling Quality Assurance
Normal Values Performance Improvement
Measured Acid-Base Values Interpreting Blood Gas Analysis Results
Calculated Values Methods and Rules
Deviations from Normal Predicting and Estimating Changes in Blood
Acid-Base Variances Gas Values
Blood Gas Variances New and Emerging Technologies
KEY TERMS
Allen’s test (modified) conjugate pairs respiration
analyte co-oximetry spectrophotometry
anion gap (AG) dyshemoglobins SPO2
arterial blood gases (ABG) glycolysis tricarboxylic acid (TCA) cycle
capnogram metabolism ventilation
capnometer plethysmography
T
he goals of this chapter are to provide an window through which we can examine ventilation,
understanding of the principles of acid-base respiration, metabolism, and acid-base balance during
balance and the arterial blood gases as they health and disease. Arterial blood gas analysis is
apply to the body’s quest for homeostasis. perhaps the single most important diagnostic tool
Also discussed are the methods used to sample arterial in the treatment and diagnosis of respiratory and
blood gases and pH. The factors that affect the normal respiratory-related disease.
blood gases and those that can adversely affect the This chapter details the normal values of the
results of the analysis are examined. measured and calculated ABGs and the variations in
Arterial blood gases (ABGs) are the diagnostic these measures that signal disease states. Factors that
tests that best define the function of the lungs in their influence the arterial blood gases and acid-base balance
task of supplying oxygen to and removing carbon and the methods of estimating and measuring these
dioxide from the body. Arterial blood gases provide a values are discussed. The role of hemoglobin and its
structural and biochemical variations in oxygen produce energy. Carbon dioxide, water, other chemical
transport and ABG analysis are explained. The concept substances, and heat are by-products of this process.
and importance of anion gap are detailed. Sampling, The total process is called metabolism. The major
analysis, quality control, and possible error-causing pathway of metabolism is called the Krebs cycle.
factors are covered. In addition, some new and emerg- Figure 16-1 illustrates the major components of the
ing technologies to assess the blood gases are dis- TCA cycle.
cussed. Through the use of several case studies, the
information provided in this chapter is applied.
THE TCA CYCLE
The tricarboxylic acid (TCA) cycle is one of three
Blood Gases subpaths of metabolism (Figure 16-1). In the first,
The study of blood gases entails the study of gases glycolysis, two molecules of adenosine triphosphate
carried in the blood, in most cases, in the arterial (ATP) and heat are produced by the reaction of pyruvic
circulation. acid and glucose (C6H12O6). Enzymes in the body
break the glucose down into 2 units of pyruvic acid
WHAT ARE THE BLOOD GASES? [CH3, 4 hydrogen ions, and energy expressed as heat
(Δ)]. Chemical shorthand expresses this reaction in the
Blood gases are physiological indicators of the effi-
following formula:
ciency and effectiveness of internal and external

respiration and of ventilation. Respiration is the C6H12O6 → 2 CH3 O COOH 4H
movement of gases across biological membranes by glucose → pyruvic acid
diffusion. Ventilation is the gross movement of gas
CH3 CHOH COOH Δ
into and out of the lungs. In other words, ventilation is
→ lactic acid
an external process, and respiration is an internal
process. More precisely, ventilation is composed of at Because no oxygen is used, this reaction is known as
least three internal functions: pulmonary respiration, an oxidative or anaerobic (without oxygen) form of
tissue respiration, and cellular respiration. metabolism. Note in the formula that the original 6
Once the oxygen reaches the cell or tissue level, it oxygen molecules from the glucose are still present in
is drawn into the cells. There, it undergoes a chemical the 2 molecules of pyruvic acid that resulted from the
bonding with other substances in a process called reaction. At this point, the TCA cycle is activated in
oxidative phosphorylation, which is part of a complex aerobic situations, producing acetyl coenzyme A,
series of biochemical reactions that utilize oxygen to 2 hydrogen, and 2 carbon dioxide molecules, producing
Glucose (6-carbon)
2 ATP GLYCOLYSIS 2 H2
Oxygen
Lactic anaerobic 2 pyruvic
acid acid (3-carbon)
a 2 H2
e from NADH2 CYTOCHROME
r 6 H2O
o SYSTEM
b
i
c
acetyl CoA 2 CO2
TCA 34 ATP
Cycle
8 H2
2 ATP 4 CO2 from
NADH2
or
FADH2
FIGURE 16-1 The TCA cycle.

2 more ATP molecules, 8 H2 molecules, and 4 CO2 content of 43.9 mg/L3. Take the barometric pressure,
molecules: deduct the water vapor pressure, and then calculate the
partial pressure of each inspired gas by multiplying the
2 CH3 C COOH O2 → 2 H2 2 CO2 acetyl CoA
adjusted barometric pressure by its fractional concen-
pyruvic acid
tration (F). The result is the partial pressure (P) of each
If sufficient oxygen is available, the reaction proceeds gas in the mixture. For example, room air (RA) has the
to the third, or aerobic, subpathway—more formally following partial gas pressures under the assumed
called the cytochrome or oxidative phosphorylation system. conditions:
In this subsystem, oxygen and 10 H2 molecules enter
PB 760 mm Hg
the system and produce 6 H2O molecules and 34 ATP
molecules.1,2 PH2O 47 mm Hg
Figure 16-1 illustrates these three oxygen- and PB(adj) 713 mm Hg
glucose-consuming, energy-producing, and carbon
dioxide–producing systems. Note the glycogen and
PB(adj) FIO2 PaO2
glucose reaction is dynamic and reversible, indicating
that glycogen stores are conserved. Clearly, the body’s PB(adj) 0.2093 PaO2
ability to acquire and use oxygen and to eliminate 713 mm 0.2093 149.2309 mm Hg PaO2
carbon dioxide is a critical function. 713 mm 0.003 2.139 mm Hg PaCO2
The chapters on applied physics (Chapter 3) and
713 mm 0.78 556.14 mm Hg PaN
pulmonary anatomy and physiology (Chapter 6)
discussed how the body provides for the bulk move- 713 mm Hg 0.0077 5.4901 mm Hg Ptrace
ment of gases into and out of the lungs. In this chapter 713.00 mm Hg Ptotal
is a discussion of how these respiratory gases, mainly
After compensation for the water vapor pressure,
oxygen and carbon dioxide, are transported throughout
the partial pressures of the other gases equal 713 mm
the body. The first area of discussion is how the
Hg, with each gas having a pressure proportional to its
circulatory system carries these gases to the tissues and
fractional concentration (its percentage in the inspired
organs of the body.
gas) in the atmosphere. This fact holds true for all
altitudes to which an unaided human might travel. The
GAS TRANSPORT IN THE BLOOD PH2O changes only with changes in temperature. The
The respiratory gases are carried in the blood in one of pressure exerted by water in the gas is called its water
three ways. They may be: vapor pressure.
• Dissolved in the liquid (plasma) portion of the

blood. Acid-Base Balance
• Chemically bound to other substances.
In addition to blood gases, other factors govern the
• Attached to hemoglobin.
acidity (pH) of the blood. Acid-base balance is the
Each of these methods has different characteristics and dynamic equilibrium between the substances in the
affects gases in a different way. body that are proton donors and those that are proton
Gases that are dissolved in the plasma exert a acceptors (Chapter 4). This balance in the normal
partial pressure in response to Dalton’s law (see individual is such that the pH, or balance of alkalinity
Chapter 3). The partial pressure exerted is proportional and acidity, in the body remains stable within a very
to the fractional (percentage) concentration of the gas fine but slightly alkaline range of 7.35–7.45 pH.
in the inhaled gas volume. For example, room air is To restate this concept, acid-base balance is that
composed of 20.93% oxygen, 0.03% carbon dioxide, part of the homeostatic function of the body that
78% nitrogen, and small percentages of trace gases. maintains the fluids in the body in the correct acidity
For this example, assume a sea level normal range to promote optimum biological and chemical
barometric pressure (PB) of 760 mm Hg and an function. Not all body fluids are in that pH range, but,
ambient temperature in a range suitable for human life. on average, the normal human adult body is in that
Also assume that the well hydrated human body is range. Infants have slight differences in the acid-base
normally capable of warming (or cooling) the inhaled homeostasis (Chapter 29).
gas to a temperature of about 37°C and humidifying it The major systems that maintain optimal pH are
to 100% saturation by the time it reaches the carina. the respiratory system (by controlling carbon dioxide
As a result of this warming and addition of water levels) and the renal or urinary system [by controlling
vapor, the volume of gas now has a water vapor bicarbonate (HCO3)]. The balance between the
pressure (PH2O) of 47 mm Hg and a water vapor production and excretion of the two substances results
in a buffer system (Chapter 4). The buffer systems maintain the acid-base balance in homeostatic ranges
referred to in this chapter, in general, result from the as the plasma and blood proteins circulate in the body.
reactions of weak acids and weak bases. The particular
weak acid and weak base pair of interest is the weak
acid carbonic acid (H2CO3) and the weak base bicar- Measurement of ABG and
bonate (HCO3). The reversible reaction formed by Acid-Base Results
these substances is shown in the formula:
Arterial blood gases and acid-base balance are generally
H2CO3 ↔ H HCO3 measured simultaneously because they are interrelated
Weak acid Weak base and interdependent. Additionally, they can be mea-
sured using the same blood sample; the patient does
Such pairs of acids and bases, and others like them, are
not have to undergo another arterial needlestick and
called conjugate pairs (i.e., a weak base and its
the associated discomfort. The PaCO2 level is integral to
conjugate acid or a weak acid and its conjugate base).
the acid-base balance represented by the measured pH
The body has four types of H buffering: ventilatory,
value and the calculated bicarbonate (HCO3). An
renal, intracellular, and extracellular buffering.
acute change in the PaCO2 produces relatively immedi-
ate changes in the pH through the relationships of the
VENTILATORY BUFFERING major buffering systems described by the Henderson-
Carbon dioxide regulation (hyper- or hypoventilation) Hasselbalch (H-H) equation.
is the most rapid method the body has to alter and
control acid-base status. It is also very fatiguing and
produces metabolic acids, primarily lactic acid, as a Best Practice
result of the energy expenditure required.
Henderson-Hasselbalch
RENAL BUFFERING
Equation
The kidneys regulate H through blood filtering and
urine production. Renal buffering is energy sparing but The relationship of the weak acid H2CO3 and the
slow in effect. In addition, it puts a strain on the kidney weak base HCO3 is defined in the Henderson-
and at times on the heart and circulatory system. Hasselbalch equation:
[HCO3]
pH pK log ________
INTRACELLULAR BUFFERS [H2CO3]
Intracellular buffers include protein, phosphates, and In this equation, HCO3 represents the metabolic
hemoglobin (Hb). Carbon dioxide buffering by the red (kidney) component, and the H2CO3 represents
blood cells (RBCs) triggers a response that results in the respiratory (lung) component. H2CO3 can
the following transformation: be calculated from measured PaCO2 using the
constant factor 0.03. For a person with textbook
H Hb ↔ HHb
normal ventilation (PaCO2 40) and bicarbonate
The RBC buffering also assists the movement of (HCO3 24), the equation transforms to:
HCO3 out of the cell and the movement of chloride
[24]
ions (Cl) into the cell to balance cellular electrical pH pK log ____________
[40 0.03]
charges. This is known as the chloride shift.
[24]
Excess H moving into the cell causes the move- pK log _____
[1.2]
ment of both Na (sodium ions) and K (potassium
ions) out of the cells and into the circulating plasma in pK log [20]
order to retain the cell’s electrical neutrality. The Since pK is a constant with a value of 6.1, and the
increase in circulating sodium generally has little effect log of 20 is 1.3, the equation further resolves to:
owing to the already high concentration of plasma
sodium. The addition of small amounts of potassium pH 6.1 1.3
may have little effect because of its initial low concen- 7.4
tration, but it can have dramatic and sometimes lethal Thus, pH for a person with normal ventilation
effects if hyperkalemia ensues. (indicated by a normal concentration of CO2)
and bicarbonate levels is 7.40. The two primary
EXTRACELLULAR BUFFERS components in this buffering system are the
Bicarbonate and blood proteins have small but impor- lungs and the kidneys.
tant effects on acid-base balance. They stabilize and
Alternatively, the body’s most immediate response to A. PaCO2 pH

pH changes caused by other buffering systems is to
modify breathing patterns. The response is to alter
HCO 3–
the PaCO2:
• Either by increasing the minute volume of gas PaCO2 pH
reaching the alveoli (alveolar hyperventilating) B.
for increased PaCO2 or decreased pH.
• Or by reducing gas volumes per minute deliv- HCO 3–
ered to the alveoli (alveolar hypoventilation) for
FIGURE 16-2 Simple acid-base balance model: (A) The
decreased PaCO2 or increased pH. pivot point is at the HCO3. Therefore, if HCO3 is stable,
The minute volume change can be changed by chang- as PaCO2 rises, pH falls. If PaCO2 falls, pH rises. This is
ing either the frequency (rate) of ventilations, the tidal a respiratory-based change. (B) The pivot point is located
at the PaCO2, indicating that PaCO2 is the stable com-
volume of each breath, or both rate and volume. The
ponent: As HCO3 rises, pH also rises. If HCO3 falls,
general relationship between pH, PaCO2, and HCO3
pH also falls. This is a metabolic-based change. Actual
can be described with the illustration in Figure 16-2. clinical scenarios often include combinations in which,
First, consider the illustration to be a seesaw, for example, HCO3 has changed a lot and PaCO2 has
with the HCO3 as the unmoving pivot point. changed a little, causing a combined change on the pH.
(Figure 16-2A). When the PaCO2 falls, as in simple
hyperventilation, the pH rises. This rise produces
simple, uncompensated respiratory alkalemia. Alterna- curve (Figure 16-3). The shape and shift of this curve
tively, if the PaCO2 rises, as in simple hypoventilation, directly affect the loading, unloading, and transport
the pH falls. This fall produces uncompensated of oxygen in the lungs and at the tissues. Given the
respiratory acidemia. dramatic and direct relationships, ABGs and acid-base
Next, consider that the PaCO2 is the unchanging balance have to be addressed together.
pivot point of the line (Figure 16-2B). If the HCO3
falls, as in diabetic crisis, the pH is “pulled down” as
the center of the lever is lowered. This fall in pH
produces uncompensated metabolic acidemia. If the Oxygen Saturation
HCO3 rises, the lever is “pushed up,” and the pH Oxygen saturation (SO2) can be determined in several
rises, resulting in metabolic alkalemia. ways, leading to some confusion and misunderstand-
In addition to these interactions, the pH affects the ings about this variable. The most common method of
placement and shape of the oxyhemoglobin dissociation expressing the oxygen saturation (SO2) is as the SPO2,
100
90
80
% Hb saturation (SO2)
70
60
50
40
30
20
10
0
0 10 20 30 40 50 60 70 80 90 100 110 120 130 140 150 160
PO2 (mm Hg)
FIGURE 16-3 The oxyhemoglobin dissociation curve.

where the subscripted “P” indicates that this value is Nomenclature

determined by pulse oximetry (discussed in detail later
in this chapter). The SPO2 value is an expression of the There is widespread misapplication of certain terms
ratio of the hemoglobin with oxygen attached to the related to blood gases and acid-base balance. In general:
total amount of hemoglobin present in the circulation • Terms ending in “-ia” refer to conditions at the
that passed the pulse oximeter’s sensor during the tissue level (e.g., anoxia).
sampling period. The hemoglobin with oxygen • Terms ending in “-emia” refer to conditions in
attached is called saturated hemoglobin or oxyhemoglobin the blood (e.g., hypoxemia).
(HbO2). Hemoglobin without oxygen attached is
known as unsaturated, or reduced, hemoglobin (Hbr, Scientific and medical accuracy, both in communica-
RHb, or HbR). Recall that hemoglobin carries about tions and in application, demands that all personnel use
97% of the O2 circulating in the blood. correct and appropriate terminology in patient care,
The other 3% of the circulating O2 is dissolved in research, and oral or print communications. To do
the blood plasma and is readily available to the tissues otherwise invites error and chaos. Here are some
and their cells. This volume of O2 also has a saturation, confused or confusing terms and their correct meanings:
called the saturation of arterial oxygen (SaO2) or venous
• Acidemia—Blood pH less than 7.35
oxygen saturation (SVO2) depending on where the
• Acidotic—Having a lower than normal pH
sample was obtained. For the most part, the arterial
(less than 7.35)
value is reported as part of an arterial blood gas report.
• Alkalemia—Blood pH greater than 7.45
The SaO2 and SVO2 values represent the percentages of
• Alkalotic—A higher than normal pH (greater
the actual, as opposed to the potential, partial pres-
than 7.45)
sures of oxygen in the plasma. This concept is the same
• Anoxemia—The total lack or absence of oxygen
as that for expressing relative humidity, where the
in the blood
actual is compared to the potential water vapor pres-
• Anoxia—The total lack or absence of oxygen in
sure. Be aware that the SaO2 oxygen value is calculated,
the tissues
not measured. and that it represents only 3% of the
• Hypercapnea—A higher than normal PaCO2 (greater
circulating O2 mass. Also, SaO2 and SPO2 do not
than 45 mm Hg), caused by hypoventilation
represent the same data and should not be taken to be
• Hyperoxia—A higher than normal level of oxygen
interchangeable even though their values may at times
at the tissues
be similar.
• Hyperventilation—Alveolar ventilation sufficient
From the definition, clearly at least three factors
to lower PaCO2 to below normal (less than
influence oxygen saturation: the amount of oxygen
35 mm Hg)
available, the amount of hemoglobin available, and
• Hypocapnea—A lower than normal PaCO2
the ability of the hemoglobin to carry oxygen. When
(less than 35 mm Hg)
the partial pressure of oxygen in the arterial blood is
• Hypoventilation—Alveolar ventilation decreased
plotted against the %Hb saturation (SO2), the plot
sufficiently to cause a PaCO2 above normal
assumes a characteristic S-shaped, or sinusoidal,
(greater than 45 mm Hg)
curve (Figure 16-3). For more information on the
factors that affect the oxygen saturation curve, see Note: Hyper- and hypoventilation address changes
Chapter 6. in minute alveolar ventilation by changes in respiratory
rate, in volume, or in both. Breath-by-breath changes
may not result in hypo- or hyperventilation.
Best Practice • Hypoxemia—A lower than normal level of oxygen

in the blood
• Hypoxia—A lower than normal (but adequate)
Oxygen Saturation level of oxygen at the tissues
Oxygen saturation (SO2) is expressed as a per- • Metabolic—In blood gas interpretation, a condi-
centage of saturation, that is, the percentage of tion driven by the kidneys
the available hemoglobin (Hb) that is combined • Mixed—An acid-base condition in which the
with oxygen. Common abbreviations for this respiratory and metabolic systems (lungs and
value are SaO2, % SO2, SO2%, O2 Sat, and Sat. kidneys) are driving the pH variance in the same
This ratio does not indicate the total oxygen direction
content of the blood. It reports only the portion • Respiratory—In blood gas interpretation, a
of the oxygen bound to hemoglobin. condition driven by the respiratory system
(e.g., changes in PaCO2 of the lungs)
Homeostasis as sedation, the body limits the level to which the

PaCO2 rises to accomplish compensation for alkalosis.
The role of a buffer is to resist or diminish the level of
pH change in a system. A buffer system is a combina-
tion of a weak acid and a weak base that, together, KIDNEYS
absorb the introduction of a strong acid or base, The kidneys are an effective but much slower means to
resulting in a smaller change in acid-base balance. compensate for acid-base imbalances. Their response
Therefore, the effect of a buffer system is to moderate can take 24 hours or more to produce significant
changes in pH and to maintain homeostasis. impact. By retaining or excreting more HCO3, the
The purpose of buffering is to maintain a relatively kidneys can offset an acidemia or an alkalemia, effects
narrow balance of pH (normal 7.35–7.45). This that are commonly seen in chronic lung disease
dynamic balance, or equilibrium—called homeostasis— patients. Many of these patients live day to day with
represents the optimum pH for bodily functions. That relatively elevated PaCO2 levels, which cause lower pH
is the pH range where metabolic functions are most (acidemia). Over time, the kidneys retain more HCO3
efficient and most effective. By far the most important that “pushes up” on the center of the lever described in
buffering system in controlling pH is the bicarbonate Figure 16-2, raising the pH to a more normal level.
(bicarbonate–carbonic acid) system. Although this is a Likewise, the kidneys can compensate for acid-base
very poor chemical buffer system, it is an effective disturbances caused by other buffering systems by
physiological buffer. This system is all the more adjusting the level of HCO3 maintained in the body.
powerful because it is an open system; that is, one of
its constituent parts (CO2) can be added or removed
quickly.
Other, lesser buffering systems are nonbicarbonate
Arterial Blood Gas
systems and closed; that is, the constituent parts remain The most accurate and complete assessment of acid-
in the system. These are hemoglobin itself, proteins, base and gas status is the arterial blood gas. Analysis of
and phosphate. arterial blood not only gives direct measurement of
pH, PaCO2, and PaO2 but also derives values for
• Hemoglobin is quantitatively the most impor- HCO3, SaO2, and base excess (BE). Oxygen saturation
tant so-called chemical buffer in the red (SaO2) can also be measured directly by co-oximetry,
blood cell. which is also used to measure total hemoglobin and to
• Protein buffers (Pr/HPr) are the most impor- recognize and quantify dyshemoglobins. Dyshemo-
tant chemical buffers in the plasma, but they are globins are types or species of hemoglobin that do not
quantitatively less important than hemoglobin. readily attract, carry, or release oxygen (discussed later
• The phosphate buffer system (HPO4/H2PO4) in the chapter). Both the arterial blood gas and
is relatively unimportant as a body-buffering co-oximetry require an invasive puncture. Although
system. arterial blood gas analysis is more accurate than
noninvasive means, it is an isolated and static measure-
ment. It cannot reflect continuous changes in oxygen-
LUNGS ation status.
The lungs, through the adjustment of the PaCO2, are a
primary means of maintaining pH homeostasis in the
body. The placement of the H2CO3 in the Henderson- COLLECTING THE ABG SAMPLE
Hasselbalch equation indicates that PaCO2 and pH are ABG sampling requires a physician’s order or a patient
inversely related. In general, every 20-mm-Hg rise in care protocol that is established and approved by the
PaCO2 results in a decrease of 0.1 pH units; conversely institution. The first step of any analysis is collecting an
a 10-mm-Hg fall in PaCO2 causes an increase of 0.1 pH acceptable specimen. In the case of ABG/acid-base
units. The impact of the lungs on pH can be rapid, analysis, the sample is arterial blood. It must be
almost instantaneous. A patient’s maximal hyperventi- collected under aseptic conditions and maintained and
lation to lower the PaCO2 to offset the falling pH of transported in a way to avoid ambient air contamina-
diabetic ketoacidosis (DKA) dramatically demonstrates tion. Care must also be taken to prevent or diminish
the power of the lungs in this regard and the extent to the ongoing metabolism of the blood cells from
which the body goes to maintain pH homeostasis. significantly altering the values in the sample before
To a lesser extent, the body uses the lungs to analysis. Therefore, the sample must be obtained with a
compensate for elevated pH. Decreasing ventilation minimum of air bubbles in the sample, and the sample
and allowing the PaCO2 to rise lowers the pH some- must be either iced or analyzed within a very short
what. In general, in the absence of other factors, such time. The AARC clinical practice guidelines for arterial
blood gases state that the “sample should be immedi-

ately chilled or analyzed within 10–15 minutes if left at Age-Specific Competency
room temperature.”3 It is not always possible or desir-
able to ice the sample because icing can produce errors Sites for Arterial Puncture
if other analytes (substances being analyzed), such as The femoral artery is used in situations in which
electrolytes, are to be measured from the sample. the radial and the brachial arteries are not
Historically, acquiring samples for ABG/acid-base accessible. The dorsalis pedis and the temporal
analysis has been done in three ways: or superficial cranial arteries are sometimes used
• Single, separate arterial punctures at one of in neonates and children or in adults whose
several common sites primary preferred sites are unavailable.
• Capillary sampling
• Drawing blood from indwelling arterial lines.
Arterial Punctures. Standard arterial punctures to access, it is relatively shallow in the tissue, and the
(arteriotomies) to obtain arterial samples are relatively bone structure makes it fairly easy to limit movement
easy to perform once the technique is perfected. of the artery. Generally, the collateral blood supply is
However, they carry significantly higher risks than adequate should some arterial interruption occur, and
venipuncture. the site is generally easy to compress and to monitor
A number of sites are available for arterial punc- after the puncture. There remains controversy over
ture, as is shown in Figure 16-4. The most commonly which site, if any, has a clear advantage regarding the
used is the radial artery at the wrist. It is relatively easy risk of adverse outcomes.
A.
Brachial
C.
A. Inguinal
ligament
B.
Femoral
B. C.
Radial
Ulnar D.
Posterior
tibial
Dorsalis
pedis
D.
FIGURE 16-4 The four most common sites for arterial puncture: (A) The brachial artery.
(B) The radial artery. (C) The femoral artery. (D) The dorsalis pedis artery. Collateral
circulation for the radial artery is generally the greatest and most reliable, whereas
collateral circulation for the femoral artery is the least reliable, making the femoral the
least attractive site for puncture.
A sample procedure for arterial punctures is

Best Practice outlined in Procedure 16-1. Specifics regarding site
selection, modified Allen’s, the test use of ice, the size of
Dangers of Arterial Punctures sample, the use of adhesive bandages on puncture sites,
and the required label information can vary from
Greatest among the risks of arterial punctures is
facility to facility or depend on equipment require-
the possible interruption of blood flow distal to
ments.
the puncture site. In worst-case situations, fingers
or hands have been rendered useless or lost.
Capillary Sampling. Capillary sampling is a common
Patients must be assessed before puncture for
procedure in the care of neonatal patients. Capillary
conditions or medications that increase the risk of
sampling of blood is a fairly common technique that
prolonged bleeding, hematoma, and subsequent
involves heating the patient’s extremities to dilate the
blood-flow interruption. It is also critical that the
underlying vessels. This dilation promotes increased
puncture be assessed shortly after the procedure
blood flow to the warmed part. In capillary sampling
to ensure that blood flow has returned to normal.
for estimation of arterial values, the site is first warmed
in an attempt to arterialize the capillary bed beneath
the site by increasing arterial flow to the area. The
increased blood flow carries with it the increased
Best Practice arterial oxygen content and hence has higher oxygen
The Allen’s Test (modified)

The Allen’s test (Figure 16-5) is a clinical test
during which both the radial and ulna arteries
in the wrist of the sample site arm are occluded Best Practice
by manual pressure by the person doing the
arterial puncture. The patient is instructed to Use of Bandages
hold the sampling arm above heart level and to
The use of adhesive bandages and other dress-
“pump” the hand for 30 seconds to a minute.
ings that visually obscure the puncture site
The palm of the hand should blanch from the
should be avoided because they may prevent the
lack of arterial blood flow. At this point, the
timely notice of hematoma formation or continu-
caregiver releases pressure on only the ulnar site
ous bleeding from the site.
and observes for a return of color to the hand.
Color should return within 20 seconds of reliev-
ing the pressure. Failure to recolor is indicative
of reduced or absent collateral blood flow to
that hand. The respiratory therapist should then
select another puncture site.
A. B. C.
Ulnar Ulnar
artery artery
Radial Radial
artery artery
Thrombus
FIGURE 16-5 Modified Allen’s test: (A) Pallor is initiated by compressing the radial artery with the
fist clenched. (B) A patent ulnar artery reveals the return of palm perfusion despite radial artery
compression. (C) An occluded ulnar artery results in continued pallor of the hand while the radial
artery is still compressed.
PROCEDURE 16-1
Sample ABG Puncture Procedure
Equipment required (Figure 16-6): 17. Perform the puncture (Figure 16-7).
Arterial blood gas kit a. Insert the needle with the bevel up.
Biohazard plastic bag for sample
b. Insert at approximately 45-degree angle.
Gloves (nonsterile)
Equipment to anesthetize site (optional) c. Point syringe “upstream” relative to blood
Ice flow.
Disinfectant swab (e.g., Betadine) and alcohol d. Use smooth, consistent advancement of the
Face shield, mask, or goggles needle. If any redirection of the needle is
required, withdraw to just under the skin
Procedure: and then readvance. Avoid deep side-to-side
1. Assemble disposable blood gas kit according to movement of the needle.
manufacturer’s specifications. e. Watch for flash of blood in the hub of the
2. Obtain ice for the sample (if hospital policy). needle.
3. Verify physician’s order. f. Consistent with the type of syringe kit used,
4. Review chart for anticoagulant or bleeding allow blood to fill to an adequate sample size
disorder status. (often 2.5–3 cc for adults 0.5–1.0 cc for
infants and children) under arterial pressure.
5. Verify patient’s identity.
18. Remove the needle and apply pressure for 3–5
6. Maintain standard precautions.
minutes or until the site has stopped bleeding.
7. Explain the procedure to the patient.
19. Expel all air from the sample, remove the
8. Wash hands. needle, and cap the syringe. (Dispose of the
9. Don gloves. needle in an appropriate biohazard container.)
10. Select the site for the puncture. If it is the 20. Mix the blood thoroughly.
radial artery, perform a modified Allen’s test to 21. Label the sample (Figure 16-8): Name and
verify good collateral circulation. If adequate room number (required on all samples); ventila-
collateral circulation not present, follow hospi- tion parameters; FIO2; time; patient tempera-
tal policy to select an alternate site. ture; puncture site; doctor.
11. Maintain aseptic technique. 22. Place sample in ice and transport to the blood
12. If hospital policy, swab the site with a hospital- gas lab. (If the sample will be run within a few
approved cleanser or disinfectant, such as minutes of drawing, it is not necessary to use
Betadine. Follow the manufacturer’s instruc- ice to transport it.)
tions for use. 23. Assess the patient’s puncture site. Ensure that
13. If hospital policy, anesthetize the site. all bleeding has stopped. Check for distal pulse.
14. Localize the target artery using the fingers of Place adhesive bandage securely over puncture
the nondominant hand. site if required by facility protocol.
15. Inform the patient before the actual puncture. 24. Dispose of all waste, remove gloves, and wash
hands.
16. Swab puncture site with Betadine. Wipe clean
with alcohol. 25. Analyze the blood.
FIGURE 16-6 Equipment needed for arterial puncture:
alcohol, syringes, gauze, heparinized solution, and a FIGURE 16-9 Sites for capillary refill in an infant
cup of ice. (shaded area).
content than does venous blood; that is, the blood is

arterialized.
Capillary samples are typically obtained from
infants and neonates. Great care must be used in the
warming process to avoid burning the skin and under-
lying tissue, especially in neonates. Common sites for
capillary sampling are the heels of the feet or digits,
either fingers or toes.
Capillary gas values, especially the PaO2, should
not be taken as absolute equivalents of arterial values.
Capillary values should instead be considered approxi-
mations, assuming optimal site preparation and quick

collection free of room air contamination. Figure 16-9
shows capillary-sampling sites. Procedure 16-2 pro-
vides a sample procedure for capillary sampling.
FIGURE 16-7 Insert the needle with the bevel up at a Arterial Lines. For patients who are expected to require
45-degree angle. numerous ABG/acid-base analyses, indwelling arterial
Name
Capillary Sampling
Capillary sampling is not true arterial blood
Date Time sampling. It is an alternative for patients or in

Room No. Temp. situations in which a traditional arterial puncture
is not appropriate. Capillary sampling is used
FIO2 VT Puncture site
most often in the pediatric and neonatal settings,
Doctor partly to avoid the risk of injury to very small and
fragile arteries.
FIGURE 16-8 Sample ABG label.
PROCEDURE 16-2
Capillary Blood Sampling
Equipment required: 9. Don gloves.
Heel warmer (lab) or appropriate warming device 10. Firmly puncture area so that it forms drops of
Lancet/Accu-Jet blood rapidly. Do not squeeze, or “milk,” the
Betadine and alcohol wipes site to increase blood flow! If flow is inad-
Sterile gauze equate, another, more aggressive, puncture is
Gloves required.
Heparinized capillary tube
11. Fill the tube from the middle of the drop. Avoid
Capillary tube caps
admission of air. Keep the tip of the tube that
Ice
is in the blood drop slightly lower than the other
ID label
end to avoid air entry in the sample stream.
Metal mixing “fleas” (optional)
Magnet (optional) 12. (Optional) If it is departmental policy, insert
mixing “flea” in sample.
Procedure: 13. Cap the capillary tube with the cap provided.
1. Gather equipment and ice. 14. (Optional) If it is departmental policy, use the
2. Verify physician’s orders. magnet to move the “flea” throughout the
3. Observe standard precautions. sample to mix the heparin and blood.
4. Identify yourself to patient (or family). Verify the 15. Label the sample according to departmental
patient’s identity. policy.
5. Explain procedure and purpose. 16. Ice sample. (If the sample will be used
to determine electrolytes, icing may be
6. Wash hands.
inappropriate.)
7. Select the puncture site area, and use a heel
17. Tend to the puncture according to departmental
warmer or other appropriate device to establish
policy.
increased regional circulation.
18. Transport the sample and analyze it according
8. Swab site with Betadine and blot dry with
to departmental policy.
sterile gauze.
catheters (arterial lines) are generally placed to avoid flushing the line with heparin (an anticlotting medica-
subjecting the patient to multiple punctures. The lines tion) after each sampling.
also offer the advantage of providing a continuous Both heparin and a permanent line in the arterial
display of arterial blood pressure and heart rate. system carry risks.
Clotting of the blood in the line is prevented by • Indwelling lines carry an increased risk of
infection for the patient.
• The arterial line (A-line) could become
Best Practice disconnected and allow for significant blood
loss by the patient. Because the catheter is
in the arterial (high pressure) part of the
Squeezing the Sample Site circulatory system, blood loss can occur rapidly
Avoid “milking,” or squeezing, the capillary sam- and in large volumes. Careful attention is
pling site to increase the blood flow. Squeezing warranted when dealing with these indwelling
increases the venous component of the sample lines, especially in patients receiving anticoagu-
and causes decreased accuracy in reflecting the lants such as heparin. Their blood is slow or
true values. Therefore, an aggressive puncture unable to clot, compounding the bleeding
technique must be developed to avoid repeated problem.
discomfort from multiple ineffective attempts. • Clots can form around the line and then break
away to float in the circulation.
In some facilities, respiratory therapists Indwelling Blood Gas

are authorized to place arterial lines once a
prescribed course of training and competence Analyzer Electrodes
demonstrations have been completed. In other There has long been hope for indwelling electrodes or
facilities, placement of arterial lines remains the sensors that continually measure and display ABG
domain of physicians. values, making these parameters dynamic rather
The collection of a sample involves allowing the than snapshots of the clinical status of the patient.
heparin solution that fills the catheter between sam- Numerous designs for these sensors have been pro-
plings to empty so that a true unadulterated arterial posed and actually produced and utilized. In some
sample is collected. Procedure 16-3 presents a sample designs, the sensor actually is placed in the artery and
procedure for arterial line collection. transfers values to a display. In other designs, blood is
PROCEDURE 16-3
Arterial Line Sample Collection
Equipment required: also require reinfusion of “presample” blood
Arterial blood gas sample kit to minimize overall blood loss and the need
One 15-mL syringe (if drawing blood for labs) for transfusion.
Face shield or mask and goggles 11. Turn the stopcock halfway toward the sideport.
One 6- to 8-mL syringe (Caution: If stopcock is turned off to the
Sterile gloves sideport, blood is diluted with flush solution.)
Betadine swab
12. Attach the sterile 15-mL syringe. (ABG syringe
if only obtaining ABGs; if blood is drawn for
Procedure:
ABGs only, skip steps 12–15.)
1. Assemble the necessary equipment.
13. Turn the stopcock off to the transducer line.
2. Verify the orders.
14. Draw 12 mL of blood for the lab.
3. Explain the procedure to the patient (if the
patient is alert). 15. Return the stopcock halfway toward the
side port.
4. Wash hands.
16. Remove the syringe and attach the ABG
5. Don gloves and goggles.
syringe.
6. Swab the access port on the stopcock with
17. Turn the stopcock off to the transducer line.
Betadine swab and wait 3–4 minutes for the
antimicrobial effect. 18. Draw 2.5–3 mL of blood.
7. Note the patient’s temperature. If the patient is 19. Turn the stopcock off to the patient.
on an ETCO2 or SaO2 monitor, note the values 20. Flush the side port of the stopcock with flush
and record. solution. Be careful not to contaminate the
8. Change to sterile gloves. Use the wrapper to system by touching the port while clearing it.
form a sterile field under the access port. 21. Replace the deadhead cap.
9. Ensure adequate pressure on the IV pressure 22. Turn the stopcock off to the side port; flush the
bag. line thoroughly; remove all blood from the
10. Using aseptic technique and, with stopcock in catheter.
the off position to the access port, remove the 23. Remove all waste material from the patient’s
deadhead cap and replace with a 6-mL sterile bed.
syringe. Turn the stopcock off to the transducer 24. Discard the blood in an appropriate container.
line. For adults, draw 3 mL of blood from the
25. Remove the gloves and wash hands.
catheter and discard it. For babies and
neonates, institutional policy usually limits 26. Transport the blood to the lab and analyze it
the amount of blood withdrawn. Policy may according to procedure.
periodically withdrawn from the artery, analyzed, and

returned to the patient, eliminating blood loss. Unfor- Hb
tunately, most designs and sensor types have failed to HbO2
HbCO
demonstrate benefits that outweigh the risks and costs.
Absorbance
Several companies have introduced and marketed
versions of this technology but have failed to be
financially successful. As a result, these units are not in
widespread use today.
Noninvasive Methods Used to

500 520 540 560 580 600
Measure Oxygenation Status
A B C
Although noninvasive methods of monitoring oxygen- Wavelength (nm)
ation status may not be as accurate as arterial blood gas Point A – All three absorbances are equal
analysis, they have certain advantages. The most Point B – HbCO has the single greatest absorbance
Point C – HbO2 has the single greatest absorbance
obvious is patient comfort. Also, the risk of complica-
tions is minimal with noninvasive monitoring. Nonin-
vasive monitoring can provide the practitioner with a FIGURE 16-10 Principle of spectrophotometric oximetry:
continuous display of the patient’s oxygenation status, Various forms of hemoglobin absorb light differently at
different wavelengths. The relative proportion of each can
rather than isolated, static measurements. These
be measured by comparing points of equal absorbance
continuous measurements allow for the detection of
(isobestic points) between different pairs of hemoglobin
trends in real time and promote early interventions in species.
developing patient conditions. Reliable noninvasive
methods of assessing ABGs are an ultimate goal.
Noninvasive procedures are often considered less • The SPO2 cannot be directly related to the PaO2.
expensive than invasive alternatives. However, no single The shape and shift of the oxyhemoglobin
noninvasive method has been developed that can dissociation curve are not constant and are not
provide all the parameters of an ABG. When the cost of assessed by pulse oximetry.
all the current noninvasive procedures that are required • The oxyhemoglobin curve is relatively flat at
to provide information comparable to the ABG is PaO2s above 60 mm Hg. Therefore, SPO2 is
considered, it may actually be greater. Of course, not inaccurate in determining saturations below
every patient requires all the information that an ABG 80 mm Hg. SPO2 is a poor indicator of ventilation
provides, so clinical judgment and risk-benefit analysis status, so its use alone for patients with suspected
are vital. ventilator compromise is not sufficient.
Clinical applications of pulse oximetry include the
PULSE OXIMETRY following:
Pulse oximetry is the most commonly used noninva-
• Continuous monitoring of oxygenation during
sive method of assessing a portion of the ABG data:
anesthesia
oxygen saturation. Pulse oximetry uses the pulsate
• Adjusting FIO2 or titrating oxygen liter flow
nature of arterial flow to focus on arterial rather than
during oxygen therapy
on venous blood. It analyzes the absorption of certain
• Documenting SPO2 during long-term oxygen
light wavelengths and compares the absorption with
therapy for purposes of Medicare requirements
the known absorption of specific light wavelengths by
for reimbursement for disability
hemoglobin (Figure 16-10). Oxygen saturation deter-
• Continuous monitoring of oxygenation during
mined by pulse oximetry is referred to as SPO2. This
weaning from mechanical ventilation
technique provides information on the oxygen satura-
• Prevention of retinopathy of prematurity (ROP)
tion obtained by pulse oximetry (SPO2), not the arterial
in neonates (although transcutaneous monitor-
oxygen saturation (SaO2). The two values may not
ing is more sensitive)
always be the same. (The principles of operation of
• Monitoring oxygenation during diagnostic
pulse oximetry are discussed elsewhere in the chapter.)
procedures such as bronchoscopy, sleep studies,
Pulse oximetry has three shortcomings.
and exercise testing
• It is able to provide only an indirect measure of • With appropriate remote auditory alarms, serving
a single analyte available from ABGs; it does not as an alarm system in non-ICU situations such as
determine either pH or PaO2. long-term care or ventilator-weaning facilities.
TISSUE OXYGEN SATURATION (STO2)

Tissue oxygen saturation (STO2) is a new technology that
uses photo spectrometry to determine peripheral tissue
oxygenation. Infant Transcutaneous
Monitoring
Transcutaneous monitoring is the preferred meth-
TRANSCUTANEOUS MONITORING od of monitoring oxygenation status in infants
Transcutaneous monitoring is a measurement of the younger than 2 weeks of age. The skin compo-
partial pressures of the gases that diffuse through the sition is such that the correlation of TCO2 and
skin. The transcutaneous probe heats the skin to PaO2 is excellent. Transcutaneous monitoring is
increase the rate of diffusion, thus increasing the gas more sensitive than pulse oximetry. There is a
pressures at the transcutaneous sensor to more closely much wider range in PaO2 relative to SaO2. Pulse
mirror arterial levels. The transcutaneous partial oximetry is unable to reflect hyperoxia, because
pressures of both oxygen (TCO2) and carbon dioxide a large increase in PaO2 presents as only a small
(TCCO2) can be measured simultaneously by incorpo- increase in SaO2 above a PaO2 of 80 mm Hg.
rating into the same probe a Clark electrode for Transcutaneous monitoring is a great benefit
measuring PO2 and a Severinghaus electrode for in preventing conditions such as retinopathy of
measuring PaCO2. The probe is secured to the skin by prematurity (ROP), in which oxygenation should
an adhesive and connected to a monitor for continu- be monitored continuously.
ous readings. A heater and a thermistor inside the
probe are connected to an external heat source to
control skin temperature.
Transcutaneous oxygen monitors are typically used impeding ventilation. There are two major clinical
to monitor oxygenation status and oxygen therapy in reasons for gas sampling:
neonates and newborns. Transcutaneous monitoring is
much more sensitive than pulse oximetry in these • Analysis of exhaled carbon dioxide and oxygen
patients, and it is not affected by ambient light or for purposes of metabolic assessment (not
movement of the patient. It can also serve to reflect within the scope of this chapter and not
cardiopulmonary compromise. discussed here)
Transcutaneous oximetry has great potential but • Analysis of exhaled carbon dioxide through
has not fulfilled its promise. It is used mostly in capnometry
pediatric and neonatal patients. The two greatest A capnometer simply provides digital readings of
problems with this technique are the requirement of the carbon dioxide in respiratory gases during the
heating the site and the variability of the TCO2 relation- respiratory cycle. A capnogram, or capnograph, may or
ship with the PaO2. In neonates, and even pediatric and may not display the values but provides a graphic wave-
adult patients, the monitoring site must be moved form of the partial pressure of the exhaled carbon
frequently to avoid injury to the skin and underlying dioxide throughout the breathing cycle. Through
tissues. Also, it can be difficult to ensure correlation analyses of these waveforms, much complex informa-
between true arterial values and the transcutaneous tion can be derived.
values.
Additional types of transcutaneous monitors are
currently in development, in clinical testing, and Best Practice
available for patient care. Among these are monitors
that use technology similar to TCO2 monitors or to the
pulse oximetry. These devices can measure muscle O2
Transcutaneous Monitoring
and tissue O2 and some work has been done using Whenever the TCO2 is decreased, an arterial blood
these techniques to measure blood glucose and other gas should be drawn. If the PaO2 is normal, a
electrolytes. perfusion or circulatory impairment should be
suspected. The heating requirements for the
probe to alter the TCO2 toward PaO2 levels should
GAS SAMPLING be used to verify altered perfusion. Higher-power
At its simplest, gas sampling is merely the collection and (heat) requirements suggest lower blood flow.
analysis of exhaled gases. The complex part of this Decreases in both the TCO2 and the PaO2 reflect
process is the technology that allows the collection and pulmonary impairment.
analysis to occur rapidly and without significantly
By assessing the carbon dioxide levels, various

deflection points (places where there is a change in the Age-Specific Competency
direction of the waveform), and slopes (steepness) on
the capnogram, one can determine: Testing in Children
• Deadspace ventilation volume. Because children, especially those of a young
• The severity of pulmonary disease. age, either cannot or do not cooperate and give
• The response to therapy. voluntary best-effort spirometric attempts, tests
• The integrity of the ventilator circuit. that are highly cooperation- and effort-dependent
• The effects of esophageal versus tracheal are not suited for testing in this age group. Testing
intubation. methods that do not require a high level of effort
or cooperation should be encouraged and used to
Various studies have evaluated the usefulness of the provide high-quality and repeatable results.
capnogram in assessing bronchospasm. You and
coworkers found a strong correlation between spirom-
etry and the angle between the ascending and alveolar
phases.4 Yaron et al. reported that the plateau phase of
the capnogram is a rapid, effort-independent, noninva-
sive measure that indicates significant bronchospasm
Spotlight
in adult emergency room patients.5 They found that
On
this method is correlated well with the peak expiratory Capnograms in ARDS
flow rate (PEFR).
The potential for the use of a capnogram to assess Capnograms are also being evaluated for their
bronchospasm in children is especially exciting because value in predicting cardiac output changes and
the measurements from the capnogram are noninva- monitoring ventilatory disturbances in ARDS
sive and effort independent, as opposed to traditional patients. Capnography also may be a strong
pulmonary function studies. This benefit is of particular predictor of post resuscitation survival.
interest to persons studying lung function and asthma
in children, especially children who are too young to
understand and follow complex directions.
normal range. Table 16-1 shows both ranges on the
assumption that, if the first SD range is accepted, the
Normal Values health care provider becomes proactive at recognizing
and responding to alteration of the ABGs.
Normal values are generally cited as a numerical value
When analyzing, interpreting, and reporting ABGs
and an index of variability, usually the standard
and pH, remember that some of the values are directly
deviation (SD). Normal blood gas data are shown in
measured, whereas others are calculated from the
Table 16-1. These data are shown as the mean (aver-
measured values. The values generally measured for
age), data, and the first and second standard deviation
arterial blood gas analysis are:
(SD) ranges of the means. The first SD ranges encom-
pass nearly 68% of the population; the second SD • pH
ranges include about 95% of the population. Most • PO2
texts show second standard deviation ranges as the • PaCO2
TABLE 16-1 Normal blood gas values with 1-SD and 2-SD ranges
Arterial Venous
Value Units Mean 1-SD Range 2-SD Range Mean 1-SD Range 2-SD Range
PH 7.40 7.38–7.42 7.35–7.45 7.36 7.35–7.38 7.31–7.41
PaCO2 mm Hg 40 38–42 36–44 46 44–48 41–51
PaO2 mm Hg 97 94–99 80–104 33 35–38 25–40
HCO3 mEq/L 24 22–26 20–28 23 21–22 21–25
SaO2 % 97 95–98 93–99 75 65–85 70–80
BE/D mEq/L 0 –2.4–2.3 / 3.0 Same Same Same
Lactate mg/dL 9.45 4.5–14.4 NA 12.15 4.5–19.8 NA
Spotlight Best Practice

On
Normal Physiological Data Analyzers
The measured and calculated values may vary
Normal values for physiological data have been from analyzer to analyzer. Each year, more tests
determined through the efforts and talents of are being added both to the overall range of tests
many clinical and basic scientists. Many of the performed on the arterial blood sample and to
so-called “normal values” are the results of data the list of calculated and measured tests. Respi-
collected in the U.S. Army’s World War I and ratory therapists should know the capabilities of
World War II Selective Service physical examina- the analyzers used in their institutions.
tions. The values may not be normal for all
individuals or, for that matter, for all groups. In
fact, at this time, most normal values are biased
toward white males. The addition of studies and
data from other ethnic and racial groups and
from females is reducing this bias. Best Practice
Calculated Values
Respiratory therapists must know that calculated
Hemoglobin (Hgb) is measured in some ABG analyzers, values are not always the same as measured
as are serum electrolytes and lactate (a derivative of values. The discrepancies may be small, but they
lactic acid). may be nonetheless important in some cases.
The values generally calculated for arterial blood When in doubt, get measured values to confirm
gas analysis are: the results.
• HCO3
• Base excess/base deficit
• O2 saturation
adding it to a constant value for human blood (the
dissociation constant, 6.3).
MEASURED ACID-BASE VALUES The value of the concentration of carbon dioxide
The sole routinely measured acid-base value is pH. Note (CO2) can be calculated using a constant value and the
that the pH is dimensionless. The technique uses an measured PaCO2. The HCO3 value is calculated using
electrode based on pH-sensitive glass. The operation of algorithms in the analyzer based on this equation. An
the pH electrode is detailed elsewhere in this chapter. HCO3 value developed in this way cannot be used as
The measured blood gas values are generally the a test of the validity of the pH or PaCO2 measurement
PaO2 and the PaCO2. These are measured using the because the HCO3 is derived from the suspect data.
Clark and Severinghaus electrodes, respectively. The Base excess (sometimes called base deficit when its
operation of these electrodes is discussed elsewhere in value is negative) is a calculation intended to quantify
this chapter. the nonrespiratory acid-base status. It is sometimes
loosely defined as the excessive amount of base if the
pH were instantaneously corrected to 7.40.
CALCULATED VALUES
The calculated values are derived from the measured Blood Gases. The most often reported calculated
values by means of a series of mathematical equations blood gas value is oxygen saturation. It is calculated on
called regression equations or by means of algorithms the basis of the predicted slope of the oxyhemoglobin
within the microprocessors in the blood gas analyzer. dissociation curve, given a known measured pH,
temperature, PaCO2, and PaO2. However, not all labs
Acid-Base Balance. The most common calculated report calculated oxygen saturations. With the advent
acid-base values are HCO3 and base excess (or base of more blood gas analyzers with built-in co-oximetry,
deficit). The relationship between pH, PaCO2 (mea- actual measured oxygen saturation values, rather than
sured), and HCO3 (calculated) is defined in the calculated ones, are becoming more common. Co-
Henderson-Hasselbalch (H-H) equation. This equation oximeters are devices that measure the actual percent-
essentially calculates pH by determining the ratio of age of hemoglobin that is carrying (i.e., is saturated
H2CO3 to CO2, taking the logarithm of that ratio, and with) oxygen (discussed later in this chapter).
Deviations from Normal Best Practice

Because arterial blood gas analysis includes both the
determination of acid-base status and the analysis of Terminology
the functions of gas diffusion and transport, several
variations from normal are possible. In addition, In most clinical references, acidemia and
several of the quantities measured are not only interde- alkalemia are referred to as acidosis (acidotic)
pendent but may also change simultaneously. The and alkalosis (alkalotic), instead of by their more
usual method of interpreting arterial blood gas results proper names of acidemia or alkalemia.
is to begin with the acid-base status and then to
evaluate the gas exchange condition.
ACID-BASE VARIANCES The changes characteristic of these primary vari-

ances are displayed in Table 16-2.
The four primary types of acid-base variances, or
Not all variances are simply one of these primary
disturbances, are named according to their pH abnor-
types. There are also cases of mixed alkalemia and
mality and the primary system causing the variance:
acidemia. In a mixed variance, both the metabolic and
• Respiratory alkalemia respiratory systems are contributing to the pH displace-
• Respiratory acidemia ment, as displayed in Table 16-3.
• Metabolic alkalemia Once a variance has been going on long enough
• Metabolic acidemia for the body to attempt to return to homeostasis, the
result is always a mixed variance, referred to as compen-
The names are modified by stating whether the values
sated. The compensating system shifts in the direction
are compensated or uncompensated. Compensated
necessary to correct the pH toward normal. The
means that the body is responding to a change in the pH
compensation is generally not complete, so a slight pH
and has brought it back to normal (fully compensated)
shift remains in the direction of the primary variance,
or toward normal (partially compensated). Thus:
as detailed in Table 16-4.
• Respiratory alkalemia is an uncorrected, uncom-
pensated alkalemia (high blood pH) caused Metabolic Acidosis. In cases of metabolic acidosis,
by a decrease in the PaCO2 (respiratory). nonrespiratory acid levels increase relative to the
• Respiratory acidemia is an uncorrected, uncom- respiratory and metabolic bases and the respiratory
pensated acidemia (low blood pH) caused by acid. The PaCO2 represents respiratory acid. Metabolic
an increase in the PaCO2. acids are difficult to measure and are detected by
• Metabolic alkalemia is an uncorrected, uncom- decreased (more acid) pH, while PaCO2 remains
pensated alkalemia caused by an increase in the within its normal range; that is, they are detected by
HCO3 (metabolic system). exclusion. Various metabolic conditions can result in
• Metabolic acidemia is an uncorrected, uncom- metabolic acidosis, including anaerobic metabolic
pensated acidemia caused by an decrease in the states, diabetes, and the ingestion of alkalinizing
HCO3. substances.
TABLE 16-2 Primary acid-base variances

Imbalance pH HCO3ⴚ PaCO2 Base Excess
Respiratory alkalemia Increase No change Decrease Increase
Respiratory acidemia Decrease No change Increase Decrease
Metabolic alkalemia Increase Increase No change Increase
Metabolic acidemia Decrease Decrease No change Decrease
TABLE 16-3 Mixed acid-base variances (respiratory and metabolic)

Alkalemia Increase Increase Decrease Increase
Acidemia Decrease Decrease Increase Decrease
TABLE 16-4 Compensated variances

Respiratory alkalemia No change (slight alkalemia) Decrease Decrease (primary) No change
Respiratory acidemia No change (slight acidemia) Increase Increase (primary) No change
Metabolic alkalemia No change (slight alkalemia) Increase (primary) Decrease No change
Metabolic acidemia No change (slight acidemia) Decrease (primary) Increase No change
Respiratory Alkalosis. Respiratory alkalosis occurs and even the discomfort and anxiety associated
when arterial CO2 levels are abnormally low, causing with the drawing of the ABG are reasons for
pH to rise above 7.45. Respiratory alkalosis results hyperventilating. Trauma, certain drugs, and
when the patient is exhaling too much carbon diox- various psychological states can also lead to
ide. This condition often occurs when people are hyperventilation.
undergoing manual or mechanical ventilation with One of the most important results of hyperventila-
faster than normal rates or volumes or a combination tion is to reduce—some would say “blow off”—CO2,
of both. decreasing the PaCO2. The effect of the reduced PaCO2
Hyperventilation or, more properly, alveolar in the absence of corrective factors is to swing the pH
hyperventilation can rapidly decrease PaCO2. to a physiologic alkalotic state. Recall that the body is
Fear, exercise, mechanical ventilation, hypoxia, normally slightly alkalotic (pH 7.35 to 7.45), although,
from a chemical point of view, acidotic states begin
below pH 7.00, and alkalotic states begin above pH 7.00.
CASE STUDY 16-1

A. H. is a 34-year-old female who is confused and CASE STUDY 16-2
lethargic. She has had “flu” for 3 days and has not
eaten in that time. She is an insulin-dependent J. L. was seen in the postoperative recovery room
type I diabetic who missed her injections while ill. after relatively minor surgery under general
On 40% face mask, her ABGs are as follows (all anesthesia. He was having difficulty coming out
normal values are 2 SD normal ranges): of anesthesia and was being mechanically
pH 7.29 (normal 7.35–7.45) ventilated at high volumes and rates. His FIO2
PaCO2 34 mm Hg (normal 35–45 mm Hg) was 0.30. Arterial blood gases were obtained,
with the following results:
HCO3 12 mEq/L (normal 22–26 mEq/L)
pH 7.52
PaO2 198 mm Hg (normal 95–100 mm Hg
on 21% O2, >200 on 40%) PaCO2 23 mm Hg
SaO2 94% (normal 96–99%) PaO2 145 mm Hg
Serum glucose 690 mg/dL (normal <100 mg/dL; HCO3 26 mm Hg
diabetic normal <150 mg/dL) SaO2 99%
ABG interpretation. pH is acidotic; PaCO2 is Respiratory rate 35, respiratory volume
just below normal; HCO3 is very low (acidotic); 1.5 normal
PaO2 is high; SaO2 is low; and glucose is
The PaO2 and pH are high; HCO3 and PaCO2
extremely high.
are low.
Diagnosis: Acute metabolic acidosis (diabetic
ketoacidosis) with partial compensation and Questions
hyperoxia. Probable Kushmaul’s respirations if
1. With the low PaCO2 and HCO3 normal, and
not corrected.
in light of the pH, is this a metabolic or a
Question respiratory disorder?
1. Why is Ms. H.’s HCO3 so low? What result 2. What actions do you recommend to stabilize
of diabetes caused the decline in bicarbon- Mr. L.?
ate being delivered? 3. What is Mr. L.’s oxygenation status?
Respiratory Acidosis. Respiratory acidosis occurs when

the PaCO2 increases. The increased PaCO2 causes the Best Practice
pH to decrease and become more acidic. In the absence
of compensatory measures, the pH remains in a Organ Control
physiological acidotic range, and the blood becomes
PaCO2 can change rapidly, whereas HCO3
acidemic. PaCO2 increases because of alveolar hypoven-
changes slowly. The reason is that the principle
tilation, that is, a reduction in the gas entering the
organ controlling PaCO2 level is the lung, while
alveoli via the respiratory system. Causes of reduced
HCO3 depends on the slower-acting kidney for
alveolar ventilation include obstruction and neuromus-
its control.
cular and restrictive conditions.
For example, in an automobile accident victim,
chest wall and lung surface injuries may cause restriction
of inspiratory movement because of pain. The restriction Mixed Metabolic and Respiratory Acidosis. On
results in lower lung volumes. The patient tries to occasion, both metabolic and respiratory conditions
accommodate this condition by increasing respiratory occur, each of which would result in an acidotic
rate but is unable to compensate for the reduced alveolar condition. When they occur simultaneously, a mixed
ventilation. This is a classic differentiation of hypoventi- acidosis is evident. These mixed conditions are charac-
lation versus tachypnea. Do not confuse hypoventilation terized by HCO3 and PaCO2 values that would
(low alveolar ventilation) with bradypnea (low respira- individually result in a pH in the acidotic range. A
tory rate) or hyperventilation (excessive alveolar ventila- factor that may be involved is the anion gap.
tion) with tachypnea (rapid respiratory rate). The anion gap (AG) is the difference between
Respiratory acidosis occurs when the lungs are the serum anions and the serum cations. It represents
unable to excrete carbon dioxide owing to one or more the fixed or volatile acids generated as metabolic end
of three mechanisms: products. (The anion gap is discussed more fully later
• Diffusion problems at the alveolar capillary in the chapter.) Anions are negatively charged ions,
(a–c) membrane and cations are positively charged ions. Anions can
• The failure of the ventilatory pump to bring be produced from the breakdown of acids, and
sufficient gas flow to and from the alveoli and cations can be formed by the breakdown of alkaline,
other respiratory structures in the lungs or base, substances. For instance, the substance
• Failure of the circulation to reach the a–c H2SO4 (sulfuric acid) breaks down to 2 H
membrane (hydrogen) SO4 (sulfide) in a dynamic
equilibrium reaction
Often combinations of these mechanisms affect a
patient’s status. H2SO4 ↔ 2H SO4
CASE STUDY 16-3

M. J., a 16-year-old male automobile accident low normal range; PaO2 and O2 Sat are both mark-
victim, was admitted to the emergency room edly decreased.
with an ETT (endotracheal) tube in place, and he Diagnosis: Respiratory acidosis secondary to
was on 100% O2. He had a fractured pelvis and reduced tidal volume (VT), question of pleural
possibly internal bleeding and lung contusions. effusions, question of early acute respiratory
PE – P 130, BP 90/50, RR 36 – IVs 2. distress syndrome (ARDS), decreased compliance
ABGs were ordered, obtained, and reported as and increased WOB (work of breathing) secondary
follows: to abdominal injury. Probable stage II shock.
pH 7.25
Questions
PaCO2 65 mm Hg
1. What are the likely causes of the changes from
HCO3 23 mEq/L normal in the blood gases reported?
PaO2 55 mm Hg 2. What features of this blood gas indicate
SaO2 85% whether it is a chronic or an acute condition?
ABG interpretation: pH is in the acidic range, 3. How can we use the answer to the previous
<7.35; the PaCO2 is increased; the HCO3 is in the question to treat the pH abnormality?
From this breakdown, we derive an end product Metabolic Alkalosis. Metabolic alkalosis occurs when
acid (H) and its conjugate base (SO4). HCO3 (the base) rises in relation to PaCO2. The cause
Metabolic end products are substances that are may be a chronic condition, in which case the kidneys
created as the body performs its functions but that are reserve bicarbonate—a slow process. Or the cause may
not utilized. These include lactic and pyruvic acids, as be acute, such as the ingestion of a solution or sub-
well as more complex organic acids. To get a more stance high in bicarbonate that can cause metabolic
accurate picture of the total acid-base state, calculate changes in a short period of time. Finally, rapid loss of
the difference between the acid and base influences systemic acids can be reflected in an acid-base imbal-
on serum pH. The normal anion gap range is between ance. Prolonged vomiting and diarrhea are often
12 and 14 mmol/dL. associated with metabolic alkalosis.
CASE STUDY 16-4

I. S., a 69-year-old, 110 pack-year smoker was (metabolic alkalosis), indicating renal compensa-
readmitted to the intensive care unit on 2 Lpm of tion; SaO2 is low even on 2 Lpm O2 by nasal
oxygen by nasal cannula. Her chief complaint (CC) cannula.
on admission was, “I can’t breathe. Can I have a Diagnosis: Compensated respiratory acidosis
smoke?” Her admission ABGs were: and hypoxemia secondary to COPD and long-term
pH 7.36 tobacco addiction.
PaCO2 53 mm Hg
HCO3 32 mEq/L Questions
PaO2 68 mm Hg 1. What if any effect does Ms. S.’s pH have on her
oxygenation status?
SaO2 82%
2. Why is her pH within “normal limits”?
ABG interpretation: pH is low normal; PaCO2 is
very high (respiratory acidosis); HCO3 is very high
CASE STUDY 16-5

L. T. is a 24-year-old power company lineperson who The resuscitation efforts resulted in increased
was electrocuted 45 minutes ago. She arrived in the bicarbonate. It was not enough to offset the acido-
emergency room in full arrest. She was being sis that occurred secondary to the hypoxia during
manually ventilated via ET tube with 90% O2. the arrest and the production of lactic and other
Three ampoules of sodium bicarbonate had been organic acids that led to the anion gap (AG) while
given in the field, along with chest compression. CPR the patient was using anaerobic metabolism to
was started 1 minute postarrest. Arterial blood gases provide energy. The PaCO2, although high and in the
were drawn and analyzed, with the following results: acidosis-producing range, is not high enough to
pH 7.12 produce a pH of the level shown. Additional acids
must be causing this effect. These acids must come
PaCO2 56 mm Hg
from the metabolic processes. This effect is called
HCO3 26 mEq/L the anion gap.
PaO2 320 mm Hg
SaO2 99% Questions
Anion gap* 25 mmol/dL 1. What metabolic acid is the most likely cause of
ABG interpretation: pH is acidotic; PaCO2 is acidosis in the hypoxic individual, an d why is
very acidotic; HCO3 is slightly alkalotic; PO2 and your answer correct?
the anion gap are very high. 2. What is the compensation mechanism for
Diagnosis: Mixed acidosis secondary to high respiratory acidosis in patients with chronic
PaCO2 and unmeasured organic acids (lactic, lung disease?
pyruvic, etc.); hyperoxygenation.

Antacid Use Treatments and Drug Use
The overuse of antacids can also result in shifts Always question patients about all their drugs
of the pH into the alkalotic ranges. In cases of and treatments, whether prescribed, over-
chronic metabolic alkalosis, dietary habits and the-counter (OTC), or folk cures.
history should always be investigated during
the history and physical, as well as use of home
remedies. return the acid-base status to a normal or homeostatic
condition. The body’s goal is to maintain the pH at its
physiological optimum range of 7.35–7.45. To com-
During protracted vomiting and diarrhea, gastroin- pensate for metabolic alkalosis the body must conserve
testinal acids are purged from the body. This lowering respiratory acid (PaCO2). It can do this either by
of total body acid results in a downward shift of breathing more slowly, by breathing less deeply, or
hydrogen (H) ion concentration, resulting in a doing some combination of the two.
disturbance of the acid-base balance. The treatment of Some cases of metabolic alkalosis occur secondary
the diarrhea and vomiting, as well as reducing or to the use of folk remedies, such as eating clay to treat
ceasing antacid intake, should resolve the cases of the complications of the early stages of pregnancy such
metabolic alkalosis for these causes. as nausea. These cases illustrate not only a cause of
metabolic alkalosis but also that the use of folk rem-
Compensated Metabolic Alkalosis. Compensation edies, herbs, and other self-prescribed practices can have
occurs when the body takes action in an attempt to marked effects even on patients presenting for standard
scientific medical evaluation and treatment.
CASE STUDY 16-6

CASE STUDY 16-7
M. C. is a 67-year-old female who presented to
the emergency room complaining of “nausea and J. M. is a 72-year-old, long-term congestive heart
vomiting for 3 days.” She was diaphoretic and failure patient who was admitted to the critical
her vital signs were RR 16; pulse 124; care unit for “decompensation.” He was on the
BP 135/88. Arterial blood gas (ABG) analysis usual cardiac drugs, including Lasix and Atten-
revealed the following values: alol. He was on 2 Lpm O2 by nasal cannula. His
pH 7.51 ABGs revealed the following:
PaCO2 40 mm Hg pH 7.45
HCO3 33 mEq/L PaCO2 50 mm Hg
PaO2 92 mm Hg HCO3 33 mEq/L
SaO2 96% PaO2 74 mm Hg
ABG interpretation: pH is alkalotic (normal, SaO2 94%
7.35–7.45); PaCO2 is normal (35–45); HCO3 is RR 8 breaths per minute
high (22–6). Tidal volume 380 mL/breath (normal for Mr. M.
Diagnosis: Acute metabolic alkalosis; “acid would be 480–500 mL)
dumping” secondary to vomiting and possible ABG interpretation: pH is high normal;
antacid overuse. PaCO2 is high; HCO3 is high; PaO2 is within
Questions normal limits for his age.
Diagnosis: Compensated metabolic alkalosis
1. Will slowing this patient’s respirations and
secondary to long-term use of diuretics. Oxygena-
reducing alveolar hyperventilation, with no
tion is normal.
other treatment, reduce or increase the
alkalosis? Explain your answer. Questions
2. What would be the effect of increasing 1. Why is it necessary to correct this condition
respiratory rate and increasing alveolar if Mr. M. is able to compensate so well?
hyperventilation in this case with no other 2. Why is age a requirement for compensation
treatment? Explain your answer. of the PaO2 but not of the PaCO2?

Calculating Normal PaO2 L. T., the 24-year-old power company lineperson
Increased age brings a reduced normal range. from Case Study 16-6, is given 2 more amps of
The expected or normal PaO2 can be adjusted for bicarbonate and placed on a ventilator via an
age in patients over 60 years old by subtracting endotracheal tube. Her fraction of inhaled oxygen
60 from the patient’s age and then subtracting (FIO2) is 80%, and her tidal volume (VT) is
the remainder from 80 mm Hg. For example, the 600 mL. Her respiratory rate is 20 breaths per
expected, or age-adjusted, PaO2 for a 72-year-old minute, and she is on positive end-expiratory
patient is 68 mm Hg: pressure (PEEP) of 5 cm H2O. Her estimated
weight is 120 pounds. Gases are drawn
80 – (72 – 60) 68 20 minutes after the bicarbonate infusion with
the following values reported:
pH 7.56
PaCO2 28 mm Hg
Respiratory Alkalosis. Respiratory alkalosis results when HCO3 34 mEq/L
the PaCO2 (the acid) decreases in relation to the PaO2 240 mm Hg
HCO3. This situation can occur from alveolar hyper- SaO2 99%
ventilation or tachypnea or both. Some toxic sub-
AG 18 mmol/dL
stances such as methyl alcohol bind CO2 and can
essentially strip away dissolved CO2, reducing the CO2 ABG interpretation: pH is very alkalotic;
levels to extremely low values. Even in the short run, PaCO2 is very low; HCO3 is very high. The PaO2
the CO2-to-H2CO3 discrepancy in these cases can result is also very high; AG is stabilizing toward normal.
in a profound respiratory alkalosis. These blood gases can be interpreted as indicat-
Table 16-5 indicates the acid-base status for ing a metabolic and a respiratory alkalosis
nonmixed and uncompensated acid-base disorders, the occurring at the same time. The diagnosis is
problem, examples of their causes, and the usual mixed alkalosis secondary to overaggressive
treatments. ventilation and resuscitation drugs.
Mixed Respiratory and Metabolic Alkalosis. Some- Questions

times treatments and the body’s compensatory mecha- 1. Another scenario in which this condition is
nisms overlap, producing mixed states in which both likely to occur is that of the patient in kidney
respiratory and metabolic processes are occurring failure. What events might lead to such a
simultaneously. situation?
Mixed or combined alkalotic conditions are 2. Because the patient is in acute mixed
found when HCO3 increases and PaCO2 decreases alkalosis, what treatment strategies would be
simultaneously but not necessarily proportionally. In appropriate?
a patient on ventilation or undergoing resuscitation, a
combination of too much HCO3 administered over a
short period of time and overventilation (hyperventi-
lation) may set this condition into action. The HCO3 BLOOD GAS VARIANCES
cannot be processed and removed by the kidney Gas variances, as the term suggests, are changes not of
quickly enough, so it remains in the circulation. the acid-base components of the blood gases but rather
Overly enthusiastic manual or mechanical ventilation of the measured gas values. They are related to the PaO2
can blow off carbon dioxide. The result is two (oxyemia) and the PaCO2 (carbia).
approaches to alkalemia: The low CO2 works to
increase alkalinity while the high increased HCO3 Oxyemia. Oxyemias are conditions or states affected by
raises the base portion of the blood serum acid-base the amount of oxygen in the blood. The phrase gener-
balance, resulting in a mixed respiratory and meta- ally refers to the relative amount of oxygen that is
bolic alkalosis. dissolved in the plasma and that exerts a partial
Nonproportional changes in HCO3 and PaCO2 pressure. Therefore, to refer to a person as having an
lead to partial compensation; proportional changes altered oxyemia by virtue of oxygen saturation, as is
lead to full compensation. This fact bears repeating; the commonly done, is incorrect. The measurement of
speed of change depends on whether PaCO2 or HCO3 PaO2 is the proper analysis technique to determine a
is changing. patient’s oxyemia status.
TABLE 16-5 Characteristics of the four, basic acid-base states

Condition Problem Causes Treatment
Kidney failure, diabetic ketoacidosis, ingestion of toxic
Loss of substances such as antifreeze, aspirin overdose
Metabolic bicarbonate
Diarrhea Sodium bicarbonate
acidosis Increased fixed
Sepsis
acids
Lactic acidosis
Chloride-responsive alkalosis (urine chloride <20 mEq/L)
Vomiting
NG suction
Thiazides and loop diuretics (after discontinuation)
Post hypercapnia
Cystic fibrosis
Chloride-resistant alkalosis (urine chloride >20 mEq/L)
Hypertension
Adrenal adenoma or cancer
Primary hyperaldosteronism Hydrochloric acid
Potassium Use of diuretics in hypertension Potassium
Metabolic depletion, Cushing syndrome replacement
Alkalosis diuretics, high Mineralocortocoids or glucocorticoids Ammonium chloride
bicarbonate Renal hypertension Acetazolamide
Severe potassium depletion (Diamox)
Current use of thiazides and loop diuretics, reduced magnesium
Other causes:
Alkali administration
Antacids
NaHCO3 therapy renal failure
Metabolism of lactic or keto acids
IV penicillin
Massive blood transfusion
Hypercalcemia
Drug depression of respiratory center (by opiates, sedatives,
and/or anesthetics)
CNS trauma
Infarct, hemorrhage or tumor
Increase ventilation
Respiratory Ventilation Hypoventilation of obesity (Pickwickian syndrome)
Intubation
acidosis deficit C-spinal cord trauma/lesions at or above C4 level
Reduced sedation
High central neural blockade
Tetanus
Poliomyelitis
Cardiac arrest with cerebral hypoxia
Anxiety, pain, fever, sepsis, shock Sedation
Pulmonary emboli Pain relief
Respiratory
Hyperventilation Relaxation
alkalosis
techniques
Increased ventilation
Source: Adapted from Shoulders-Odom B. Using an algorithm to interpret arterial blood gases. Dimensions in Critical Care Nursing. January/February
2000;19,1:36–41.
Hypoxemia The more problematic oxyemia is hypox-

Age-Specific Competency emia, which means a low PaO2. In general, this is
understood to mean a PaO2 of less than 80 mm Hg
Infant Hyperoxyemia when a patient is breathing room air (FIO2 0.21).
Be sure that the PaO2 of infants is not too high. Hypoxemia is problematic because it has the greater
Infants are at increased risk for retinopathy of risk of causing harm to the patient and because,
prematurity (ROP), oxygen toxicity, and broncho- depending on its cause, it may be very difficult to
pulmonary dysplasia (BPD). overcome.
• PaO2 values between 60 and 80 mm Hg repre-

sent mild hypoxemia.
Hyperoxyemia The prefix “hyper-” indicates high. • Those in the 40–60-mm-Hg range are moderate.
Therefore, hyperoxyemia is an abnormally high PaO2. • PaO2 values below 40 mm Hg represent severe
In general, high PaO2 is not a critical problem in hypoxemia.
short-term exposures. However, exposure to high
When treating patients for hypoxia by administering
oxygen concentrations can lead to complications,
supplemental oxygen and monitoring the effects of the
including oxygen toxicity and ARDS, so avoid
treatment by ABGs and/pulse oximetry, note in the
clinically unnecessary exposure to significant eleva-
patient record that seemingly “good” or “normal”
tions of FIO2.
oxygenation values are “assisted” by the supplemental
oxygen.
In cases involving blunt force chest trauma, do
Best Practice serial chest X-rays (CXR) and closely monitor oxygen-
ation and CO2 elimination status. Oxygenation status
Factors That Affect PaCO2 should be monitored both by continuous pulse
oximetry and by periodic blood gas analysis to corre-
Some patient-associated variables, such as pain, late the oxygenation findings with the FIO2 and PEEP
emotional stress, fear, agitation, or crying, may levels.
result in hyperventilation or tachypnea. These
states can result in abnormal PaCO2 findings. To
Carbia. Carbia is the root form for words that refer to
prevent misinterpretation, note the presence of
conditions affecting or affected by carbon dioxide
these conditions on the blood gas request and
levels in the blood or gases in the lung. Many sources
report forms.
use the root form “capnea” instead of “carbia.”
CASE STUDY 16-9

J. J. is a 58-year-old post–open-heart patient. His maintained for a few hours at elevated oxygen levels,
postextubation blood gases on a 40% Venturi mask but this patient’s PaO2 level is probably too high for
revealed the following results: that application. Unless there is another indication
pH 7.43 for maintaining a high PaO2, a 28% or 32% Venturi
would probably provide a more appropriate PaO2.
PaCO2 36
PaO2 210 Questions
HCO3 22 1. On the basis of the assumption of a linear PaO2
O2 Sat 99% response to increased FIO2, which Venturi mask
The patient’s acid-base status was normal, with (28% or 32%) would bring this patient’s PaO2
only mild hyperventilation, perhaps from the pain of closer to 150 mm Hg?
the arterial puncture. 2. For at least the immediate postoperative period,
The oxygen status reveals a hyperoxyemia, since open-heart patients require close monitoring of
the PaO2 is greater than the normal 80–120 range. ventilation and ABGs. What conditions make
It is not unusual for open-heart patients to be this an important factor in their care?

R. M. is a 58-year-old Hispanic male with a E. W. is a 33-year-old asthmatic. She was brought
smoking history of 80 pack-years. He is in the to the emergency room in respiratory distress.
doctor’s office for a routine visit. He has a barrel She had pronounced wheezing in all lung fields
chest and is slightly tachypneic. His resting, throughout the respiratory cycle at a rate of 30
room air arterial blood gases reveal the following: bpm. She was placed on 2 Lpm oxygen by nasal
pH 7.36 cannula. Blood gas analysis revealed:
PaCO2 67 mm Hg pH 7.57
PaO2 65 mm Hg PaCO2 23 mm Hg
HCO3 35 mmol/dL PaO2 105 mm Hg
O2 Sat 93% HCO3 23 mmol/dL
The patient has a significant hypercarbia, but O2 Sat 99%
it has been compensated for by a rise in HCO3.
The patient has a significant hypocarbia,
Since HCO3 is slow to change, the hypercarbia
driven by her struggle to breathe with the bron-
must have been present for some time (i.e., it is
chospasm. At this point, a low PaCO2 is a good
chronic). The patient also has borderline hypox-
sign; it indicates that she has not tired to the
emia that he tolerates fairly well. Given the
point of failure. A rise in PaCO2 to or above
history, the patient probably has emphysema or
normal before treatment may indicate impending
chronic obstructive pulmonary disease (COPD),
respiratory failure.
although other testing is required to clearly
define the nature of his chronic lung disease. Questions
Questions 1. The ability to drive the PaCO2 below normal
indicates what physiologically?
1. What can Mr. M. expect to happen if he
should contract the flu or pneumonia during 2. What indicator means that this is an acute
the fall or winter? How would his blood gas condition? Why?
values change?
2. As Mr. M. continues to age, his pulmonary
function values will decline through the normal Hypocarbia The prefix “hypo-“ indicates low. Hypocar-
aging process. Given his smoking history and bias, or hypcapneas, are blood gas variances with low
current condition, what steps are appropriate to PaCO2. They can be caused by a number of conditions
reduce his risk of respiratory system failure? and can be positive signs in some clinical settings and
disturbing in others. Their correlation with the clinical
scenario is a key factor in determining causality and
diagnosis.
Hypercarbia An elevated PaCO2 is termed hypercarbia, or
hypercapnea. It generally indicates diminished alveolar
ventilation or an increase in carbon dioxide production. Best Practice
In any case, the patient is unable to adequately remove
the carbon dioxide produced by the body. SPCO2 Accuracy
Sometimes blood gas results do not seem to
Best Practice make sense. One example is a patient who
presents with an extremely low to nonexistent
PaCO2. The question is, “Why doesn’t this patient
Monitoring Oxygenation Status have a PaCO2? Was he drinking methyl alcohol?”
It is easy to see how PaO2 is reacting to PEEP Organic compounds sometimes bind carbon
and how FIO2 changes by keeping a trend line dioxide so that you cannot measure PaCO2.
graph that plots PEEP, FIO2, and PaO2 on the A patient who does not have a measurable
y-axis and time on the x-axis. If the patient is PaO2 or who has an extremely low PaO2 could be
improving, PaO2 should rise or remain constant metabolizing oxygen at a very rapid rate. Patients
relative to the PEEP and FIO2 lines. If the patient with hyperleukocytosis may have very rapid
is not improving or is getting worse, the gaps utilization of oxygen stores. Such issues must be
between the PEEP and FIO2 lines widen. raised in puzzling cases.
Analysis Techniques assessing electrical conduction through a blood

specimen, the Sanz electrode assesses the concentration
Analysis of the blood gases and acid-base balance is of of hydrogen ions (H), which is the defining characteristic
great importance in modern medicine. The techniques of pH.
used to obtain blood gas values range from invasive The Severinghaus PCO2 electrode builds on the
and complex electrochemical analysis to simple simpler Sanz electrode. The introduction of carbon
noninvasive spectrophotometric devices. The accuracy dioxide into an aqueous bicarbonate solution causes
and utility vary with the patient and with the environ- changes in the pH:
mental and medical conditions.
CO2 H2O ↔ H2CO3 ↔ H HCO3
The PCO2 electrode actually measures changes in
ARTERIAL BLOOD GAS ANALYZERS
pH. However, the change in pH is directly related to
Blood gas analyzers use three key electrodes: the PCO2 in an isolated environment; the pH change
• The Clark (O2) electrode causes change in the electrical flow in the electrode.
• The Sanz (pH) electrode The electrical flow is calibrated to the corresponding
• The Severinghaus (CO2) electrode pH levels, allowing the analyzer to display the PaCO2
of the sample.
Many also incorporate co-oximetry and other param-
eters, such as hemoglobin (Hgb) levels, hematacrit
(crit), basic electrolytes, lactose, and glucose. The PULSE OXIMETERS
operational bases of the electrolyte and glucose Pulse oximetry provides a revolutionary and completely
electrodes are outside the scope of this chapter and are noninvasive method of measuring oxygen saturation:
not specifically discussed here. no need to puncture arteries or veins; no need to
The Clark (O2) electrode uses a half cell design with invade the body with tubes, needles, or catheters.
positive and negative electrodes. This device measures Instead, a small lightweight device is fitted over the
oxygen by assessing the varying electrical current patient’s finger, toe, or earlobe, or it is attached to the
generated by the reduction of oxygen. In a reduction forehead. This device is painless and, best of all,
reaction, a substance gains electrons. The higher the provides continuous information.
oxygen concentration is, the more rapid the reaction The principles of operation for pulse oximetry are
and the higher the electrical current will be. As current spectrophotometry and plethysmography.
increases, more electrons are attracted to the positive • Spectrophotometry is the measurement of light
pole of the Clark electrode. The Clark electrode is a intensity generated at a known wavelength and
miniaturized polarographic electrode (Figure 16-11) passed through a substance and the measure-
that is housed in a chamber that optimizes the condi- ment of the intensity of that light as it leaves the
tions for measuring oxygen. As the current flows, a solution. Because substances absorb or reflect
sensor measures the current and reads out the current different wavelengths of light, the analysis of the
flow as PO2 based on a factor determined during the difference between the light entering and leaving
calibration procedure using a known PO2. a substance allows determination of the sub-
The modern pH electrode uses pH-sensitive glass stance’s constituent materials. The solution in
and is commonly referred to as the Sanz electrode. By this instance is the arterial blood.
• Plethysmography is the study of changes in the
Blood shape or size of an organ. It is used to distin-
Water bath
guish static or unchanging factors from dynamic
or variable components in the system being
measured. In other words, plethysmography
Electrolyte measures pulsate waves, felt as the difference in
pressures noted when taking a pulse.
Silver anode
These two principles enable pulse oximeters to
measure different wavelengths of light in pulsate waves,
giving them the specific ability to focus on arterial, or

pulsate, blood (Figure 16-12). Figure 16-13 illustrates
Platinum cathode
the application of this principle.
Modern pulse oximeters use two wavelengths of
Membrane light: one in the red wave band and the other in the
FIGURE 16-11 Schematic of a Clark electrode. infrared portion of the spectrum. The two wavelengths
Pulse
Variable A. Blood
V. Blood
Muscle
Absorption
Constant
Light
B
o
n
e
FIGURE 16-12 The pulse oximeter probe can be placed on

Time
any finger, though the index finger is most common. Con-
sideration of circulation, skin pigmentation, and finger FIGURE 16-14 Light transmission across a tissue block:
or fingernail discoloration should go into the decision of The light or optical path remains relatively stable over
which finger to use. time, with the exception of the volume added during pul-
sate flow. With the relative inability of the bone, muscles,
and extracellular fluid to change their size, added length
to the optical path must be caused by the pulse pressure.
Pulse
pressure
This is a measure of functional saturation. Pulse
Vessel oximetry does not take into account the presence of

Optical dyshemoglobins. Dyshemoglobin is an abnormal type of
caliber
path
hemoglobin such as carboxyhemoglobin (COHb),
methemoglobin (MetHb), and sulfhemoglobin
Area of increased optical density (SulfHb). These dyshemoglobins interfere with the
binding of oxygen, greatly decreasing the oxygen-
FIGURE 16-13 Pulsatile versus nonpulsatile blood flow and
carrying capacity of hemoglobin and significantly
optical density: The tissue bed increases in density as the
lowering the CaO2. However, because the pulse oxim-
increased blood flow during pulsate flow expands the ves-
sel, resulting in an increased extravascular tissue density eter differentiates only between bound and unbound
due to the compression forces of the pulse pressure. Vessel hemoglobin, in the presence of dyshemoglobins, the
caliber (diameter) increases as internal pressure increases. pulse oximeter reading will be falsely high.
Pulse oximetry has technological and physiological
limitations. The technological limitations are as
of light are transmitted from a light-emitting diode follows:
(LED) through the body part (the artery) to a photo
• Motion artifact due to shivering, tapping the
detector. At the red wavelength of 660 nm, red light
sensor on a bed rail, or continuous moving or
passes through oxyhemoglobin (HbO2) and is
twitching of the probe site
absorbed by reduced hemoglobin, or deoxyhemoglo-
• Ambient light, such as bright sunlight, xenon
bin (RHb). At the infrared wavelength of 940 nm,
lamps, fluorescent, and infrared lights, masking
infrared light passes through reduced hemoglobin and
the spectrographic waves in the critical
is absorbed by oxyhemoglobin. Figure 16-14 demon-
wavelengths
strates the concept behind the use of pulsate wave
• Optical shunting, that is, light passing from the
forms to coordinate sampling in pulse oximetry. The
LED to the photodetector by passing around the
pulse oximeter reports samples obtained only during
body part rather than through it (For example,
the period of pulsate flow.
the LED probe may have slipped to a transverse
Pulse oximeters compare oxyhemoglobin and
position rather than being in an anterior-
reduced hemoglobin, using two wavelengths of light.
posterior alignment.)
The percentage of oxygen saturated with hemoglobin
• Vascular dyes, such as methylene blue or cardio-
can be determined by applying the following formula:
green, blocking light passage at critical near-
% HbO2 [HbO2/(R Hb HbO2)] 100 infrared wavelengths
TABLE 16-6 Physiological factors affecting inability to carry oxygen is largely dependent on its
pulse oximetry geometry. Dyshemoglobins have structural abnormali-
ties that alter the shape of the molecule, making the
Low Saturation Low Perfusion Dyshemoglobin bind/release ability more difficult or impossible. These
False high Cardiac arrest COHb geometric changes are caused by chemicals such as
readings at Hypothermia MetHb carbon monoxide (CO) or by genetic agents as in the
SaO2 below 80% case of sickle cell disease.
Inaccurate Peripheral SulfHb The fractional concentration of hemoglobin is
readings at shunting determined by comparing oxyhemoglobin with total
SaO2 below 65% hemoglobin, as shown in the following formula:
Vasoconstriction
Shock % HbO2 HbO2/(HbO2 RHb COHb
MetHb) 100
• Deeply pigmented skin blocking light passage Because an arterial blood sample must be
(The SPCO2 readings may be off because the obtained, this is an invasive procedure. Co-oximetry is
accuracy of the sensors declines as light passes usually performed in conjunction with arterial blood
through dark skin.) gas analysis. Most modern blood gas analyzers include
• Nail polish, such as black, blue, or green, or offer built-in co-oximetry modules that allow the
hindering the effectiveness of probes applied to use of a single sample. The newer co-oximeter may also
darkly colored nails be capable of measuring other hemoglobin characteris-
• Low perfusion tics such as Hb A1-C, a measure of average blood
glucose over time; this is a good indicator of the
Physiological limitations of pulse oximetry are stability of serum glucose in diabetic patients.
inaccuracies caused by very low saturations, low
perfusion states, and the presence of dyshemoglobins.
Table 16-6 summarizes these limitations.
The pulse oximeter does more than measure O2 END-TIDAL CO2 ANALYZERS
saturation. Because it measures only during pulsate Two types of end-tidal CO2-measuring devices are
flow, it also measures (or counts) pulse rate. Further, currently marketed. They are classified according to
because it detects pulse, it also detects perfusion the basis of their method of providing output data.
through the area being sampled (the pulse pressure • The capnometer provides digital readings of the
drives perfusion). percentage of end-tidal CO2 (sometimes con-
Be aware that the pulse indicated on a pulse verted to a partial pressure).
oximeter may not match the pulse rate shown on an • The capnograph provides a waveform displaying
ECG monitor. The ECG monitor counts electrical the percentage of CO2 per unit of time for each
activity in the heart, whereas the pulse oximeter counts breathing cycle. The capnograph produces this
pulsate waves. Some abnormal heart diseases cause waveform, or capnogram, either on a breath-by-
periods of pulseless electrical activity (PEA) and may breath basis or as a trend chart illustrating a
result in incorrect pulse rates, while the pulse oximeter sequence of CO2 production for a series of
reports actual pulse episodes. Variances in these two breaths.
rates should be noted in the patient’s record and
reported to the patient’s nurse. A third type of end-tidal CO2 monitor combines
the features of both the capnometer and the
capnograph.
CO-OXIMETERS End-tidal CO2 (ETCO2) analyzers are fundamentally
Co-oximetry, like pulse oximetry, uses the principle of of two kinds: mainstream and sidestream.
absorption of light by hemoglobin to analyze blood
• On a mainstream analyzer, the sensor is within
samples. However, co-oximetry utilizes four wave-
the main flow of gas.
lengths of light rather than two and therefore measures
• On a sidestream analyzer, a sample is extracted to
all common dyshemoglobins. The result is a measure
a sidestream sensor.
of fractional saturation, not the simpler functional
saturation yielded by pulse oximetry. We therefore can The principle of operation is basically the same for
determine the composition of the total hemoglobin by both types. Both mainstream and sidestream systems
hemoglobin subtype or species. have advantages and disadvantages. Fortunately, newer
Some dyshemoglobins are incapable of carrying or technology has reduced the problems with both
releasing oxygen. The hemoglobin molecule’s ability or designs.
Best Practice
Calculation of Oxygen Content
Neither PaO2 nor SaO2 provides complete infor- With these factors in place, the math is simple.
mation about the capacity of the blood to deliver Given a patient with Hg 15 g%, PaO2 95 mm Hg,
oxygen to the tissues, which, of course, is the key and SaO2 98%:
point. Hemoglobin levels and hemoglobin’s oxygen-
(a) O2 attached to Hb Hb (g%) 1.34 SaO2
carrying capacity must be included in determining
oxygen content. In addition, some oxygen is car- 15 g% 1.34 0.98
ried dissolved in the blood. Oxygen content is the 20.1 0.98
total of all oxygen carried in 100 milliliters (mL) of 19.70 vol%
blood, either bound to hemoglobin or dissolved.
(b) Oxygen dissolved PaO2 0.003
Hemoglobin levels are expressed in grams percent
(g%), that is, the grams of hemoglobin in 100 mL 0.29 vol%
of blood. Oxygen content is expressed in volume (c) Total oxygen content A B 19.99 vol%
percent (vol%), that is, the volume in milliliters of
Thus, for this patient scenario, each 100 mL
oxygen in 100 mL of blood. Research has indicated
of blood can carry 19.99 mL of oxygen to the tis-
that 1 g of hemoglobin can carry (or bind with)
sues. Remember, however, that this is only part
1.34 mL of oxygen if fully saturated. Some studies
of the answer. If the heart fails, or if circulation
have indicated this number could be as high as
is restricted, the oxygen content of the blood is of
1.39 mL O2/g Hgb, but we will use 1.34 mL O2/g
little use, no matter how great. No single compo-
Hgb. Finally, the Bunsen solubility coefficient for
nent of patient assessment or laboratory testing is
oxygen in blood is 0.003 mL O2/100 mL blood;
all-revealing.
that is, 0.003 mL of oxygen will dissolve in 100 mL
of blood.
Mainstream. As the name implies, a mainstream adapters can be bulky, awkward, and affected by water
end-tidal CO2 monitor places the CO2 sensor within the vapor rainout and other contaminants.
main flow of patient gases. This positioning has the
advantage of not requiring aspiration and transport of Sidestream. A sidestream system requires that a sample
a sample via tubing. But the mainline sensors and of patient gas be aspirated from the main flow and
transported to a sensor. This approach reduces the bulk
and awkwardness at the patient’s airway, but water or
Best Practice mucus often makes its way into the sampling tubing,
blocking the narrow sampling tube and disrupting the
Measurement Mismatches sampling process.
A rapid-response CO2 analyzer is the major
The pulse oximetry reading is high and the ABG
component of any end-tidal CO2 monitor. Rapid
says low. What is happening? When SPCO2 and
analysis may be performed using a variety of devices:
SaO2 do not match, think hemoglobin abnormality.
carbon dioxide–specific infrared cells, Raman scatter-
Examples of such abnormal conditions include:
ing, mass spectrometry, or photo-acoustic technology.
• COHb. The most commonly used technology is infrared
• Sickle cell disease. absorption. In this technique, infrared light is filtered to
• SulfHb. a specific frequency, and the resultant beam is split
• Thalesemia. using mirrors. Each beam of light is then passed
• MethHb. through one of two sampling chambers. One sample
• Cooley’s anemia. chamber is for reference, and the other contains the
• Cyanide poisoning. patient’s exhaled respiratory gas sample. Carbon
• Iron deficiency anemia. dioxide absorbs infrared light. The higher the partial
• Organophosphate poisoning. pressure of carbon dioxide is in the sample, the lower
• Antirejection drugs. will be the amount of infrared reaching the infrared
sensitive detector cell (or sensor). The infrared sensor
emits an electrical current that is proportional to the hypothermia, the TCO2 is substantially lower
amount of infrared light reaching it. than the PaO2.
The level of CO2 in the patient sample can be • If adequate perfusion exists (that is, a cardiac
determined by comparing the expiratory sample index of 2 Lpm/m2), the TCO2/PaO2 ratio is 70%,
sensor’s current with the reference sample current. This plus or minus 12%. As a result, the TCO2 is 70%
information is then displayed numerically, graphically, (12%) of the PaO2.
or both ways.
Although the end-tidal CO2 is measured as a Temperature
percentage of the total gas, some analyzers mathemati-
• If the skin temperature is too low, adequate
cally convert the percentage data into a partial pressure
peripheral perfusion is not present, and the
using an algorithm based on Dalton’s law (Chapter 3).
TCO2 is lower than the PaO2. If the skin tempera-
Alternatively, clinicians can do the conversion them-
ture is too high, the TCO2 is higher than the
selves by solving the equation for Dalton’s law. The
measured PaO2 (as temperature increases, the
ETCO2 of most patients closely approximates the PaCO2
diffusion coefficient increases and observed
with results within 1–2 mm Hg of each other. This
pressure increases).
similarity is due to the high rate of diffusion of CO2
across the alveolar capillary membrane. So the diffusion coefficient is directly related to patient
temperature and TCO2.
TRANSCUTANEOUS GAS ANALYSIS
Age Transcutaneous monitoring is used almost exclu-
The principle of operation of transcutaneous monitor-
sively in neonates and newborns. Their skin is much
ing (TC) is the same for both oxygen (TCO2) and
thinner than that of adults, decreasing the length of the
carbon dioxide (TCCO2). Modified Clark and Severing-
diffusion pathway. Under proper conditions, the
haus electrodes are incorporated into a sensor that is
correlation of TCO2 and PaO2 is excellent. TCO2 can
attached to the skin. The skin is heated to 44°–45°C,
actually equal PaO2 if the proper temperature is main-
to promote vasodilation of the capillary bed and
tained, adequate perfusion exists, and the infant is
increase perfusion to the area. The increased perfusion
younger than 2 weeks old. This positive correlation
raises the diffusion of oxygen and carbon dioxide.
decreases with age as the skin thickens.
The resulting TCO2 and TCCO2 measurements should
correlate with PaO2 and PaCO2, assuming optimal
Transcutaneous CO2 Sensing. Because carbon dioxide
conditions.
diffuses more rapidly and easily across the skin than
The most significant hazard of transcutaneous
does oxygen, TCCO2 generally is correlated with PaCO2
monitoring is burns caused by the sensor. The risk of
more reliably than TCO2 is with it. In addition, CO2 is
burns increases greatly during conditions of low
not consumed by surrounding tissue, thereby affecting
perfusion because the heat is not dissipated as well
the TCCO2 relationship to PaCO2. However, other
owing to the diminished blood flow in the area of
factors that affect TCO2 can also affect the TCCO2.
the sensor.
Skin Thickness Although CO2 crosses the skin more
Transcutaneous Oxygen Sensing. Various factors
easily than O2, skin thickness can still affect the TCCO2,
determine how well TCO2 correlates with PaO2.
though not to the degree it affects TCO2.
Skin Thickness Thicker skin yields a longer diffusion
pathway for oxygen. The correlation between blood gas Perfusion Status Inadequate blood flow in the region
values and TC values are not strong; the TCO2 is lower causes the TCCO2 to be lower than the PaO2.
than the actual PaO2.
Temperature Temperature affects the TCCO2 just as it
Oxygen Consumption Regional oxygen consumption does the TCO2. A lower temperature causes lower
in the area of the sensor site affects correlation. The
TCO2 is lower than the PaO2 as regional oxygen
consumption increases. Best Practice
Perfusion Status Adequate or even hyperperfusion Preventing Burns
must exist for an accurate correlation; this is the
To prevent burns, rotate the sensor site for the
rationale behind heating the skin.
transcutaneous probe every 2–4 hours and never
• In low-perfusion states, such as a decreased place it over a bony area.
cardiac output resulting from vasoconstriction or
perfusion and thus lower than actual TCCO2. Higher

temperatures increase the pressure, as higher tempera- Age-Specific Competency
tures do to all gases, including those dissolved in
liquids, resulting in an artificially heightened TCCO2. POC Units
POC manufacturers claim that point of care units
Age The direct impact of aging on TCCO2 is less evident need a smaller sample size than other analyzers,
than on TCO2, but the physiological changes associated reducing blood loss. Although the consideration
with aging, such as thickening skin and decreased of reduced blood loss is important in neonatal
perfusion, can affect the TCCO2, generally causing it to patients and small children, it is rarely relevant
read lower than actual. TCCO2 can be a valuable in the care of adolescents and adults. Even so,
monitor in pediatric patients who are on high- compared with modern benchtop analyzers, POC
frequency ventilation. units offer virtually no advantage in sample size
if the benchtop unit is being used optimally.
POINT OF CARE TESTING
Point of care (POC) units, such as i-STAT™, have many
potential advantages over the traditional benchtop All of these advantages come at a price, however.
analyzer found in pulmonary or clinical laboratories. The sample analysis packs can be expensive. Some POC
The term “point of care” refers to the fact that these analyzers have bulk calibration and electrode packs
units are small and simple to use; they can be used at that are used over several analyses, but they also have
the patient’s bedside, potentially speeding the avail- expiration periods of 3–14 days from instillation and
ability of results. The principle of operation of POC activation. If the number of procedures performed
units is no different, essentially, from that of benchtop during the calendar life of the pack is not within the
units. Variants of the Sanz, Clark, and Severinghaus expiration range, the cost per analysis goes even higher.
electrodes are in place, though miniaturized and The number and frequency of blood gas analysis must
self-contained. The key difference is the short-term be carefully evaluated to determine which unit is best
disposability of the electrodes and the reduced size of for a facility or even whether POC makes sense in the
the units. facility.
Although the design and operation of the various Various studies have alternately validated and
POC units vary, they generally eliminate the repeated questioned the accuracy of POC units compared with
use of a set of electrodes. Instead, they use a disposable analyzers. Many facilities have adopted POCs house-
cassette that contains both the electrodes and the wide. Others have integrated POC and benchtop units.
electrolyte reagent in a sampling chamber. The perfor- Still others have rejected POC units, opting instead for
mance of the electrodes is tested immediately before satellite laboratories that bring the benchtop analyzers
the analysis is done, and the electrodes are discarded closer to the bedside. The future of POC testing rests on
after the analysis. many factors, including pricing of supplies and units,
POC units have several advantages: the ongoing accuracy of the units, the size and nature
• Discarding the electrodes eliminates the need to of health care facilities, and the makeup of the clinical
plot the ongoing performance of the electrodes. staff.
Statistical analysis and charting of the electrodes’
performance status are unnecessary because the
same electrode is never used twice. Role of Hemoglobin and Its
• Calibration and quality control materials are
often part of the electrode pack, eliminating
Variants in ABG Analysis
the need for inventories of separate supplies. The hemoglobin (Hb) molecule is a complex structure
In some cases, electronic calibrations eliminate with many variables. Its ability to combine with many
the need for calibration materials entirely. different substances is at once valuable and hazardous.
• Sampling-to-report time is reduced. Closely related to the myoglobin found in cardiac
• Sample transport requirements are eliminated. muscle, hemoglobin consists of two distinct parts:
• The number of “bad” samples due to delay is heme—a cluster-like arrangement of molecules—and
reduced. globulin—a polypeptide chain—form the functional
• Depending on the institution’s staffing and hemoglobin molecule (Figure 16-15).
policies, staff spend more “on location” when Adult hemoglobin (HbA) has a molecular weight
they do not have to transport the sample to of 64,500, and each red cell (erythrocyte) carries about
another location. 280 million Hb molecules. The body produces between
Spotlight
On
New and Emerging Techniques
Several new technologies that are being discussed in strategies for their use will emerge. As technology
research journals and at professional meetings may improves and methods are developed to reduce
prove to be clinically valuable in the near future. clot formation and motion artifact, the use of these
Ultrasound is being used in a wide variety of sensors should become more widespread. The abil-
ever-growing applications in medicine. Recently, an ity to obtain real-time, in vivo data on blood gases
ultrasound device for measuring blood sugar nonin- and acid-base balance will make these improved
vasively has been tested very successfully in a small optic sensors valuable additions to critical care
group of individuals. The ability to refine the use of technology.
ultrasound will make it an attractive technology for The use of newer applications of light absorp-
investigation for future noninvasive measurement of tion, frequencies, wavelengths, and better filters
more substances, including ABGs. and sensors will refine the accuracy and specificity
The potential of indwelling sensors will con- of light absorption technology, allowing for expanded
tinue to attract research efforts, and improved use and greater accuracy.
2 million and 10 million red blood cells in the bone the O2 and CO2 cannot dock properly, and the ability
marrow each day. Each erythrocyte has a life of approx- of the hemoglobin to carry those molecules is reduced.
imately 120 days. Normal hemoglobin levels of adults Think of the molecule of Hb as a lock; only certain
are 13.5–18.0 g/dL for males and 12.0–16.0 g/dL for keys allow the lock to function, and no other lock
females. One gram of hemoglobin can carry 1.34 g of works. If the shape of the key changes, the lock does
oxygen. not open, or if the lock itself changes shape, the key
The shape of the Hb molecule plays an important does not fit. If the heme molecule and its four iron
role in its ability to attract, carry, and release oxygen molecules, which are normally bound to oxygen, are
and carbon dioxide. Even slight alterations of this reconfigured by replacement of the oxygen with carbon
shape can prevent O2 and CO2 from binding with the monoxide, sulfur, or a methyl group, instead of
molecule. If the receptor sites are not properly aligned, oxyhemoglobin (HbO2), the species of hemoglobin
Heme group
Iron
β Chain
α Chain
Red blood cell

β Chain α Chain
Helical shape of the

polypeptide molecule
FIGURE 16-15 Hemoglobin molecule.

changes; it could be carboxyhemoglobin (HbCO), about 12 2 mEq/L. To determine the anion

sulfhemoglobin (HbS),* or methhemoglobin (HbM). gap (AG), subtract the sum of the anions from the
Each of these has different physical and chemical sum of the cations. For convenience sake, when
properties than oxyhemoglobin, and each has performing anion gap calculations, ignore the ions
decreased ability to attract, transport, and release with very low values (Ca2, Mg2, K, PO42); they
oxygen and carbon dioxide. This is an example of how have little effect on the AG. Thus the formula for
the geometry of a compound can affect both its anion gap (AG) is:
function and its limitations.
AG Na – (Cl HCO3)
Normally, small quantities of these Hb species are
in the blood. Methhemoglobin* levels of 1–2% are
typical (Hbmet). Sulfhemoglobin (HbS) levels of 1% Significance of the Anion Gap. The anion gap
are normal, and, in persons living and working in rural accounts for unmeasured anions such as ketones,
areas with low levels of environmental hydrocarbon sulfates, anionic proteins (proteins without an electri-
pollutants, levels of less than 1–2% are normal. cal charge), and lactic acid. The calculation indicates
Carboxyhemoglobin (HbCO) levels of 5–10% in city the effect of organic and volatile acids that are difficult
dwellers—especially smokers—are not uncommon. It to isolate and analyze. These effects can often explain
is believed that normal metabolic processes may result otherwise puzzling results in the acid-base portion of
in incomplete combustion of organic compounds, thus ABG analysis. Coexisting conditions, such as diabetes,
establishing a so-called normal level of CO in the body. malnutrition, or kidney disease, or conditions causing
HbSulf is far more common in blacks than in other increases in anaerobic metabolism cause most of the
racial groups and has been linked to sickle cell disease. alterations in the AG.
Interpretation of the Anion Gap. Interpretation of

anion gap data is tied to the overall acid-base status, for
Other Factors That Affect example, with metabolic acidosis:
ABG Results • High AG—This can result from alkali (HCO3)
Additional factors that affect the procurement or deficit secondary to increased unmeasured
accuracy of ABGs and that are causes of potential error anions (e.g., ketones).
are the anion gap, sampling errors, and problems with • Normal AG—Alkali deficit may occur secondary
the analysis itself. to direct loss of HCO3 and fluid (e.g., an
inability to form or reabsorb HCO3 or an excess
infusion of Cl).
ANION GAP • Decreased AG—This may be a sign of lab error of
Physiological factors include the anion gap (AG), the decreased unmeasured anions (e.g., hyperalbu-
difference between the anions (negatively charged minemia), or of increased unmeasured cations
electrolytes) and the cations (positively charged electro- (e.g., lithium overdose).
lytes) in the blood plasma. The cations are Na, K,
Ca2, and Mg2, and the anions are Cl, HCO3, and
PO42. Table 16-7 presents the normal values for serum
electrolytes. In normal subjects, the AG should be
Hemoglobin Variants
TABLE 16-7 Normal serum values In addition to carboxyhemoglobin, sulfhemo-
Cations (ⴙ) mEq/L Anions (–) mEq/L globin, and methhemoglobin, a normal variant
called fetal hemoglobin (HbF) exists in fetuses,
Na 135–145 Cl, 95–108
infants, and to a much lesser extent in adults
K 3.5–5.0 HCO3 22–26 (<2%). Fetal hemoglobin has different abilities
Ca2 3.5–4.0 PO42 1.7–2.6 than does HbO2 and a greater affinity for oxygen
than does HbA (adult hemoglobin), in order to
Mg2 1.3–2.1
enable the fetus to extract oxygen from the moth-
er’s blood. HbF concentration falls from 95% at
10 weeks gestation to about 50% at birth, and
*The abbreviation “HbS” is used to represent both sulfhemoglobin
and sickle cell disease. Be careful not to confuse the two. To avoid
it should be at 5% at 6 months of age, reaching
this issue in this chapter, the nonstandard abbreviation “HbSulf” adult levels soon after.
is used.
SAMPLING ERRORS
Errors in sampling technique can substantially affect Best Practice
the results of blood gas analysis. Consider the follow-
ing potential errors by sampling route or site. Heparin Type
Some types of heparin can affect specific values.
Arterial Puncture. Since the vast majority of arterial For example, sodium heparin is not best if your
blood gases are obtained by arterial puncture, consider sample will be used to measure sodium in an
the problems associated with that method first. electrolyte analysis. In these cases, use lithium
heparin.
Room Air Contamination The presence of room air
bubbles in a sample alters the values toward those of
room air. PaCO2 moves toward zero, and PO2 moves
toward 150. Since the level of PaCO2 affects the pH prevent blood clotting. If the solution is not adequately
through the hydration reaction, pH is shifted upward. removed before sampling, the resulting sample is
The impact of a bubble increases with the size of the diluted with the flushing solution. This dilution alters
bubble and with the duration of the presence of the all the results by moving gas values toward those of the
bubble in the sample. flushing solution. The pH is shifted owing to the
change in PaCO2, and any co-oximetry values from this
Venipuncture Inadvertent puncture of the venous sample are also affected.
circulation is a fairly common error. Clearly, upon
analysis, the blood gas values appear to be venous. Sampling from the Wrong Line Care must be taken to
Although venous pulse pressures are substantially avoid mistakenly withdrawing samples from venous,
lower than arterial pressures, some patients have high central venous, or intracardiac lines instead of arterial
enough venous pressures to cause syringe filling. Lack lines. The blood gas values normally range widely
of spontaneous filling of the syringe should be a signal among these sampling sources. All lines should be
that one of three conditions has occurred: color coded or identified with labels that indicate
• A venous sample was obtained. their purpose.
• There is a regional perfusion problem.
• The patient is extremely hypertensive. Capillary Sampling. In capillary sampling, the sam-
pling site is usually an earlobe or, in children and
Prolonged Puncture Prolonged and/or painful punc- infants, more commonly the heel. The chosen site
ture can result in patient hyperventilation, altering the is warmed with warm (not hot) wet gauze pads or
values significantly from their true resting state. Patients with a specially designed chemical heating pack for
sometimes breathe rapidly or deeply in anticipation of 10–15 minutes. This part of the procedure is critical
pain during a needle insertion. Other patients may because warming dilates the blood vessels in the area,
hold their breath as they anticipate the puncture and promotes perfusion, and thus arterializes the blood in
during the puncture procedure itself, resulting in a the area of the sampling site.
hypoventilation state. After warming, the sample site is cleaned with
Betadine and alcohol:
Residual Heparin Although most ABG kits use prehep-
arinized syringes, sometimes nonheparinized syringes • Make a stab incision on the fatty part of the heel
may be used. Liquid heparin poses a special concern. using a no. 11 scalpel blade, lancet, or other
Too much heparin remaining in the dead space of the appropriate instrument. The incision needs to be
sampling device can shift the sample’s values toward deep enough to produce a free flow of blood but
those of the heparin. Also, dilution of the sample can not so deep as to incise the muscle layer.
cause errors in hemoglobin and co-oximetry measure- • When active bleeding is accomplished, introduce
ments. Many institutions use preassembled and a capillary tube into the blood flow. At this
preheparinized ABG kits, which greatly reduce the point, blood should be drawn into the tube by
chance of heparin-related problems. capillary action.
• Seal the tube at both ends and ice it in prepara-
Arterial Lines. Arterial lines (or A-lines) are the other tion to be sent to the lab for analysis.
major source of blood gas samples. They come with • Wipe away the remaining blood at the sample
their own special types of potential sampling errors. site.
• Apply firm, but not tight, manual pressure to the
Inadequate Flushing of the Line Between samplings, site with a gauze pad until the bleeding stops in
arterial lines are flushed with a heparin solution to about 2–5 minutes.
• Document the puncture site, holding time, and the recommendations of the manufacturer, and the
success of the capillary stick on the lab request calibration schedule should be strictly enforced.
form and in the patient’s chart, along with the Personnel performing the analysis should be rigorously
patient’s oxygenation status, temperature, and trained in calibration and in verification rationales and
toleration of the procedure, including excessive techniques. Any question as to whether the ABG values
crying. obtained result from an instrument that is out of
calibration should lead to immediate reanalysis of the
Capillary sampling is largely confined to infants and
sample on a second analyzer.
small children, but it poses some significant problems
The issue of reporting the suspected out of calibra-
related to technique. The patient’s sample volume-to-
tion results along with the results of the second unit’s
surface area sets the diffusion rate across the collection
analysis is a matter of debate. One group says that both
device’s walls.
sets of data should be reported along with the per-
ceived out-of-calibration condition of the primary
Room Air Contamination The impact of room air
analyzer. Others contend that only the secondary
contamination on capillary samples is the same as it is
results need reporting, either with or without the
for arterial punctures.
out-of-calibration statement.
Of course, the primary analyzer should be exam-
Aggressive Squeezing Ideally, a capillary sample is
ined immediately to determine the cause of the
acquired with no squeezing of the site to prompt blood
out-of-calibration status and to resolve it as soon as
flow. Squeezing (milking) causes the forced introduc-
possible. Until the situation is resolved, the analyzer
tion of venous capillary blood into the sample. Milking
must be taken out of service and have a “Out of
shifts the values toward venous values, generally
Service” sign placed on it.
causing a lower PO2, a higher PaCO2, and a lower pH.
Out-of-Control Analyzer. As with results from an
Poor Site Preparation Inadequate heating of the site
uncalibrated analyzer, any results from an out-of-
results in a poorly arterialized sample, causing the
control analyzer are of questionable accuracy and
sample to reflect more venous values.
value. Reporting results from an out-of-control analyzer
also jeopardizes the laboratory’s accreditation.
ANALYSIS Out-of-control, in this context, means that the
The analysis itself can give rise to problems when analyzer gives an incorrect response to quality control
analyzing ABGs, from several potential sources. (QC) samples at a frequency beyond that predicted by
normal, random variation. In other words, the results
Out-of-Calibration Analyzer. The lab standard values of the analysis of quality control samples are outside
(the normal range of values) should conform to the accuracy range of the known quality control
national and regional norms. samples. The QC range is usually 1–2 standard devia-
tions (SD) from the known mean of the QC sample. A
• Critical values are those that fall outside the
2-SD QC range represents the range of values within
normal lab values. which one would expect to find 95% of all sample
• Panic values are analysis results that indicate a values or 95% of the population from which the
need for swift and decisive intervention by the sample was selected. A 1-SD range is equivalent to the
caregivers. results found in 68% of the population samples.
These values should be justifiable by reference to Inasmuch as the standard deviation range is
current literature and cross-analysis with peer and generally distributed equally on either side of the mean
reference labs. Membership in a reference group is data value, in the case of 2 SD, 47.5% of the data is
highly desirable for any lab. In addition, ongoing below the mean and 47.5% of the data is above the
recording and trending of calibration and quality mean. In nonbiological data, this distribution of
assurance results provide added safeguards and values, when viewed in terms of their frequency of
reference points for improved lab practices. occurrence, forms a bell-shaped or normal curve.
An out-of-calibration analyzer compromises all the Biological data often form a curve that is skewed or
results since the last calibration. Whether all those tipped slightly to the right. This type of curve, called a
results are accurate or, if not accurate, how they vary Gaussian curve, means that more data fall on the high
from correct results cannot be known. Performing side of the mean than on the left, or low, side of the
analysis using an out-of-calibration analyzer places curve. For QC purposes, assume a normal curve
laboratory accreditation at risk. Calibrations should be because the range of normal values used is very small
scheduled on the basis of the analyzer’s use pattern and and the population is very large.
Best Practice
Icing Samples
Icing a sample that will also be used for electro- • Make sure that the three-way valve is set to
lyte analysis yields inaccurate results for some of allow blood flow from the needle to the ABG
the electrolytes. When the sample will be used for syringe.
multiple types of analysis, the respiratory therapist • Have another syringe ready to place on the
walks a delicate line in deciding whether to ice it. free hub of the three-way stopcock as the
One solution is to split the sample: blood flow to the ABG syringe is halted by
turning the stopcock to the off position.
• Allow additional blood to enter the ABG syringe.
• Attach the other, needle-less, syringe on the
• Inject an appropriate amount of the ABG sample
empty hub and turn the stopcock so that
into the proper blood collection tube or tubes.
blood flows into the new syringe.
• Then ice the ABG sample but not the other
• When this is getting full again, turn the
tubes of blood.
stopcock off.
Another method, which requires another pair of • Remove both the needle and the new
hands, is to: syringe.
• Insert a three-way stopcock between the • Transfer the contents of the new syringe into
needle and hub of the ABG syringe before the correct venopuncture tube.
inserting the needle into the patient.
Improperly Handled Samples. Allowing a sample to wrist rhythmically from side to side for 1–2 minutes.
remain at room temperature for more than 15 minutes This action adequately mixes the sample.
allows metabolism within the sample to lower the PO2, Note: Rolling the sample syringe between the
raise the PaCO2, and lower the pH. The blood cells palms does not provide adequate mixing.
within the sample are still alive and are still metaboliz-
ing. Inside the sampling syringe, oxygen is still being
used to create energy, and carbon dioxide continues to Quality Control, Quality
be produced. As metabolism continues, the amount of
oxygen in the sample is decreasing, and the amount of
Assurance, and Performance
carbon dioxide in the sample is increasing in the Improvement
sample.
Anyone who is involved in health care, particularly in
These changes in key values are affected by the rate
direct patient care, needs to be aware of the need for a
of metabolism, which is a factor of the amount of metab-
well developed and defined system of quality control.
olism per unit of time and the temperature of the
Such systems include several components in which:
metabolic system. These two facts mean that we can
control the changes in PaO2 and PaCO2 by reducing the • Limits are set and defined (quality control, QC).
time from draw to analysis (decreasing the time effect) • Limits are measured and tested (quality assur-
or by reducing the temperature of the sample. Or we ance, QA).
can do both: Ice the sample, and then transport it • Remediation of errors is addressed (performance
quickly for analysis. improvement, PI).
Inadequately Mixed Sample. Poor mixing of the

sample before analysis can result in a nonhomoge- QUALITY CONTROL
neous sample. The separation of the formed elements A most important and, sadly, most misunderstood
and the plasma tends to alter the distribution of both issue surrounding blood gas analysis is quality control.
electrolytes and dissolved gases. This alteration can Too many therapists mistake quality control as a
cause unpredictable changes in the results for any mechanism to get them into trouble or to provide
measured ABG parameters. busywork when clinical analysis requirements are slow.
To prevent separation, always agitate the sample by Nothing could be further from the truth. Precise and
holding it upright (be absolutely sure that the transport accurate performance and recording of successful and
cap is on correctly and tightly), and then move the unsuccessful control samples are required to ensure
2-point calibration results 2-point calibration results
Instrument-reported QC values Instrument-reported QC values
Correct QC values Correct QC values
FIGURE 16-16 The ideal electrode performance documents FIGURE 16-17 Out-of-control electrode performance:
fully linear relationships between the electrical signal and Although the calibration points fall linearly, the quality
the displayed values. Not only the calibration points, but control points do not. This is the most problematic
the reported values for the quality control sample, fall electrode performance because the calibrations alone
linearly. indicate that the instrument is working properly. Only the
QC samples reveal the nonlinear (and thus nonpredict-
able) nature of the electrode’s readings.
accurate test results. The accurate control of sample
procurement and analysis helps to avoid problems and
trouble in the future and to protect the patient from Sometimes the cause of an out-of-range measure-
being treated on the basis of faulty information and ment is normal, random variation. Sometimes it is a
erroneous data. real machine problem. How does the operator tell the
The purpose of quality controls (QC) is to deter- difference and avoid unnecessary troubleshooting and
mine the measurement characteristics of the analyzer. maintenance? That question bothered Dr. James
Even though an instrument may be measuring properly Westgard, and in the late 1970s he applied statistics to
at the points tested during calibration, proper measure- the problem. What resulted were his so-called Westgard
ment performance at other points along the measure- rules.7 The so-called rules are based on 1, 2, and 3
ment continuum has to be confirmed. Figure 16-16 standard deviations and the percentage of probability
shows the hoped-for ideal performance of an electrode. associated with data falling within each range.
The response of the electrode to a given value in the Recall that a single standard deviation (1 SD) is
sample is linear, passing through the calibration points equivalent to approximately a 68%-confidence interval;
and the sample points in a predictable and linear that is, 68% of all potential values should fall within
fashion. However, Figure 16-17 illustrates what the that 1-SD range. Two standard deviations (2 SD) is a
response of the electrode could be: nonlinear and 95% confidence interval, meaning that 95% of all
unpredictable. Although the response passes through results should fall within the 2-SD range. Three stan-
the calibration points for the electrode, away from the dard deviations (3 SD) is a 99.7% confidence interval,
calibration points, the curve is far from linear. Notice meaning that 99.7% of all results should fall inside the
that the sample points are far different from the values 3 SD range. Beyond the 3rd SD are outliers, samples that
illustrated in Figure 16-16 because the response curve may really belong to another population rather than
is distorted. In the scenario presented in Figure 16-17, the one being studied.
running calibrations alone could lead the respiratory Now turn this notion around. In a 2-SD range, 5 of
therapist to mistakenly assume that the analyzer is 100 results could or should fall outside the range; these
measuring properly. results represent simple random variation within the
Quality controls (QCs) are predefined samples system. Although 5 of 100 is not a large number, it is
placed at other points along the expected response not all that unlikely that a single result will fall outside
curve; some are in the normal range, some are high, the range. However, a 3-SD range indicates that only 3
and some are low. Together, they check the perfor- of 1000 results is normally expected to fall outside the
mance across a clinically relevant range. If they are not range; this is a small enough expectation that a single
measured and reported properly by the analyzer, it value outside the range is truly suspect. That is how the
indicates a potential problem. Westgard rules approach QC values.
Suppose the respiratory therapist runs controls on The question, however, is whether those out-of-
the blood gas analyzer. The PaO2 value for the QC falls range QC values should be recorded and kept in the
outside the 2-SD range but is within the 3-SD range. Is database or be discarded. Many therapists choose to
this a real problem? The solution is to repeat the QC. If discard them, but discarding them creates problems in
the PaO2 falls within the 2-SD range on the repeat test, the long run. The first QC value that was out of range
a safe assumption is that this was just one of those 5 of should be retained in the database. The repeat value,
100 that fall outside the range. However, if the repeat is along with any repeat failures performed during the
also outside the 2-SD range, there must be a real troubleshooting, should not be retained because they
problem; the probability that two consecutive results are defined as not-normal variations. Why is discard-
would be part of the 5 of 100 is quite low. The repeat ing the data an issue, and what problem will discard-
result should be treated as a real problem, and trouble- ing it cause? Standard deviation is calculated on the
shooting and documentation should be done. basis of all values in the database. Figure 16-18
If the QC is outside the 3-SD range when the illustrates a Levy-Jennings plot (also known as a
control is run the first time, this is a problem because a Levy-Jennings chart or graph), in which analysis results
value outside the 3 SD is expected to occur only 3 are plotted in terms of their standard deviation
times out of 1000. The probability is that data which is distribution from the mean control values. Throwing
outside the 3 SD range represents samples that are out all out-of-range values means throwing out the
“outliers” and likely are from a different or variant “normal” 5% that fall outside the 2-SD range through
population. Troubleshooting and documentation normal variation and that are thus valid. The SD range
should be done. The instrument should be out of progressively shrinks, producing a QC target that the
service until the problem is resolved, and the measure- lab cannot hit.
ment is reliably falling within the 2-SD range.
51.9
d
51.3 +3 SD
a
b
50.7 +2 SD
50.1 +1 SD
49.5 MEAN
48.9 –1 SD
48.3 –2 SD
c
47.7 –3 SD
47.1
1
11
13
15
17
19
21
23
25
27
29
31
33
FIGURE 16-18 Levy-Jennings QC plot: Results of individual quality control runs are plotted
in a graphic display to make trends more apparent. Individual points are plotted against
the mean, 1 standard deviation (SD), ±2 SD, and ±SD. Note that points a, b, and c fall
beyond 2 SD from the mean and require repeat analyses. Because the repeat falls within
2 SD, no further action was carried out.
Numerous other Westgard rules help in determin- remains to detect systemic problems and to use them
ing whether a pattern of performance is likely to to improve the system. The idea is to:
represent normal variation or a system problem. If they
• Perform ongoing monitoring to ascertain the
were all applied to a single lab, getting any results
quality of the outcome.
reported successfully would be difficult. So a few
• Determine where improvements should be
should be selected that best protect the validity of the
made.
data from the individual blood gas lab. By all
• Then devise and carry out a plan to make the
means, all therapists must protect the validity and
improvements.
completeness of the QC database by properly retaining
or discarding the data. Additionally, a detailed, com- A key concept is that the QC/QA process must be
prehensive and contemporaneous QC/QA log should treated as a system, not as independent parts and
be rigorously maintained. A lab that consistently practices. The blood gas system is made up of more
documents fewer than 5% 2 SD violations is suspect than just the machine. The system also consists of the
because random variation should be an expected order processing, the therapists, the sample collection
outcome. and transport mechanisms, the sample-handling
procedures, and the result-reporting mechanism. The
system includes anything, including pre- and post-
QUALITY ASSURANCE analysis processes, that can affect the quality of the
Quality assurance and quality control are terms that are results (Figure 16-19). If a respiratory therapist
often used interchangeably. They are, however, very receives blood gas orders on the wrong patient,
different. Quality assurance (QA) has recently become the mistake has nothing to do with the blood gas
known as performance improvement (PI), but its focus machine, but it is a blood gas system problem. If the
Order Respiratory therapist

Order
transcription notification
Results
communicated Respiratory therapist
to physician interpretation
of order
Report placed
in chart Quality of
sample
collection
Transport/
electronic
delivery of
Sample
results
handling
Transcription/ Therapist
Analyzer
entry performance
performance
of results of analysis
FIGURE 16-19 Blood gas quality control components: Potential sources

of quality-control problems with blood gases range far beyond instru-
ment performance. These other sources are often classified as pre-
analytical and postanalytical. Potential issues are the appropriateness
and clarity of the order, misentry or misinterpretation of the order,
collection errors, errors in transcription of results, and errors in report
generation by computer systems.
computerized blood gas reporting system transposes (Who will guard the guardians?). In the case of ABG
numbers in results, that error is a blood gas system results, all the participants in the system must act as
problem. If the ABG results do not fit the patient’s guardians if patient care is to be enhanced, safe, and
clinical signs and symptoms picture, the reason may effective.
have to do with other ABG system failures unrelated
to the results.
Interpreting Blood Gas
PERFORMANCE IMPROVEMENT Analysis Results
Performance improvement (PI) monitors (tests and Before interpreting the results of an ABG analysis, the
processes to check the integrity of the system) should respiratory therapist, lab technician, and physician
be designed to cover all aspects of the system, should have all the information needed to understand
although not all at the same time. Trying to monitor the results. For example, they must know the patient’s:
everything all the time is a virtual guarantee of • Age.
failure. The monitors should be selective and change • Temperature.
periodically. Once or twice a year, a monitor should • Ventilator status.
compare blood gas machine output with actual • Diagnosis.
printed results at the patient unit. This practice • Respiratory rate.
checks the reporting system. Periodic monitoring • FIO2.
of turnaround times for blood gases helps in the • Tidal volume.
detection of problems in the ordering, handling,
or processing of orders. Table 16-8 indicates some
PI issues that have risen in the literature, along with METHODS AND RULES
their possible solutions. Of the many techniques for interpreting ABG results, the
Of course, monitoring technical performance system offered here is one of the many commonly used
should be a part of PI. For example, what is the rate of methods. Practicing this skill will make the respiratory
necessary repeated punctures? What is the rate of therapist an even better interpreter of blood gases.
patient complaints about punctures? The Clinical
Laboratory Improvement Act of 1988 (CLIA) requires ABG Interpretation Method Made Simple. First
the performance of proficiency testing (PT) throughout determine the acid-base status of the patient as indi-
the year to determine a lab’s proficiency at accurately cated by the results of the blood gas analysis. Then
running and reporting blood gases, and PT should be interpret the patient’s oxygenation and ventilation
included in any PI program. status. Recall that the ABG results indicated by the
Even though regulators and accrediting organi- blood gases must be correlated with the patient’s
zations act as guardians of proficiency, a sound PI clinical status and treatment regime.
program is just plain good for your patients and A simple yet accurate method of interpretation of
your organization. All the many parts of the ABG ABG findings is called the four-step acid-base analysis.6
system, other than the blood gas analyzer, may be a These four easy steps enable the respiratory therapist to
potential source of error. Juvenal, the Roman quickly master the art of blood gas interpretation.
satirist, wrote, “Quis custodiet ipsos custodes?” However, each step must be followed carefully and
taken in order.
1. List the three values responsible for acid-base
TABLE 16-8 Performance improvement
balance: pH, PaCO2, HCO3.
issues 2. Compare these with the normal values and
Issue Sample Indicator Remediation determine whether they are acid (A), base (B), or
ABG punctures Percentage failure Manikin practice normal (N). Write “A,” “B,” or “N” beside each
observed value:
punctures pH 7.50—B
PaCO2, 25—B
Air bubble Number of Reinstruct
HCO3 24—N
contaminated practice
3. Circle any letters that are the same, usually pH
samples
and either PaCO2 or HCO3.
Report speed Number of Electronic pH 7.50—B
complaints, mean reports, time and PaCO2, 25—B
response time motion study HCO3 24—N
Best Practice
Things to Know Before ABG Interpretation
Things the RT must know: Things the RT should know:
• FIO2 • Hgb/Hct
• Patient’s temp (There is some controversy • Drugs given
on this point.) • Fraction type specific Hgb
• Ventilator status • Chief complaint
• PEEP • Diagnosis
• Patient’s age • Respiratory rate
• Comorbidity • VT or MV
• Intake and Output (fluid balance)
4. Determine whether the uncircled value has TABLE 16-9 Blood gas prediction formulas
moved in the opposite direction of the circled
ones. If it has, compensation is occurring; if it has Respiratory-Driven pH Changes
not, compensation is absent. Acute acidosis/alkalosis
In addition, the RT might wish to know whether pH change 0.008 units/1 mm Hg PaCO2 change
the changes are acute (sudden) or chronic (old) Chronic acidosis
changes. The following formula will help in making pH change 0.003 units/1 mm Hg PaCO2 change
that determination.
Chronic alkalosis
Acute: pH and 1 factor change (e.g., pH and PaCO2
or HCO3 or AG) pH change 0.0017 units/1 mm Hg PaCO2 change
Chronic: More than pH 1 factor changes (e.g., Metabolically Driven PaCO2 Changes
pH and PaCO2 and HCO3 change and/or AG) Metabolic acidosis
PaCO2 1.54 (HCO3) 8 (2)
PREDICTING AND ESTIMATING CHANGES Metabolic alkalosis
IN BLOOD GAS VALUES PaCO2 0.7 (HCO3) 20 (1.5)
The ability to predict what blood gas levels should be If the PaCO2 predicted is greater than the observed,
under given conditions is helpful in the interpretation there is a superimposed respiratory alkalosis.
of ABG results. Tables 16-9 to 16-11 present prediction
If the PaCO2 predicted is less than the observed, there
formulas that enable the respiratory therapist to
is a superimposed respiratory acidosis.
determine the expected values for many variables under
a number of conditions.
TABLE 16-10 Respiratory-driven pH
New and Emerging Technologies or PaCO2 changes
Although the understanding of blood gas physiology To predict pH or PaCO2 change:
does not change radically in short periods of time,
Assume pH 7.40, PaCO2 40 mm Hg
fine-tuning regularly occurs. The technologies certainly
change, as does the understanding of how to measure For each acute 10 mm Hg rise of PaCO2, pH will
associated physiologic variables. For example: decrease by 0.05 unit.
For each acute 10 mm Hg fall of PaCO2, pH will
• An improved understanding of how to reduce
increase by 0.1 unit.
interference in pulse oximetry sampling has led
to pulse oximeters that dampen the effects of
artificial environmental light and movement to remove interfering patterns, filtering data, and
artifact. These devices have proved to be much ultrafast sampling techniques.
more accurate and reliable. • Research on the near infrared (NIR) wavelength
• Other improvements over the last 5–10 years are absorption by various hemoglobin species has
waveform stabilization through signal processing lead to improvements in and the expansion of
TABLE 16-11 Miscellaneous prediction • Measurement of tissue O2 (STO2) by transcutane-

formulas ous photospectometric methods has recently
become a reality.
pH Changes • Microtechnology, including nearly nanorobots
If PaCO2 > 40 mm Hg: (nanobots) and cameras have opened new vistas
(figuratively and in reality) for treatment and
(measured PaCO2 – 40)/100 diagnosis.
7.40 _________________________
2 • Enhanced data storage and display abilities
If PaCO2 < 40 mm Hg: through the microization of computers will
(40 – measured PaCO2) clearly allow faster, more accurate trend analysis
pH 7.40 ____________________ and response to changing physiology, drug
100
delivery, and improved disease and injury
HCO3ⴚ Changes survival rates.
• Advances in radiologic technology have already
To predict HCO3 from PaCO2 change:
changed the face of medicine. Medical imaging
HCO3 decreases 2 mmol/L per 10 mm Hg has allowed us to see into the deep spaces of the
decrease in PaCO2. body that were previously hidden from us.
HCO3 increases 1 mmol/L per 10 mm Hg
rise in PaCO2.
Age-Compensated PaO2 Summary
Arterial blood gas values are a key diagnostic tool in
PaO2 < 1 mm Hg per year of age over 60 from
many diseases and conditions. They allow the measure-
a base of 80 mm Hg
ment and analysis of acid-base balance. This technique
PaO2 80 (age – 60) involves the examination and determination of pH,
PaCO2, and HCO3. By examining the ratios of acid
(PaCO2) and base (HCO3) in relation to the pH,
respiratory therapists can, at least broadly, determine
the ability to accurately determine the fractional the source of acid-base disturbances. With knowledge
concentration of these species. of the anion gap, they can further define these altera-
• Pulse oximeters no longer are limited to using tions in acid-base homeostasis. Acid-base and blood
photospectometry to determine SPCO2. gas physiology are among respiratory care’s most
• Hemoglobin of several species (HbO2, MetHb, important knowledge bases. Very often the respiratory
SulfHb, COHb) can now be measured by therapists are the experts in this area, and their knowl-
mimicking the co-oximeter. edge is critical for the survival of the patient.
• Several types of ABG analyzers include co- ABGs can be measured directly by invasive sam-
oximetry and Hb determination. pling and direct analysis of blood and noninvasively
• Some ABG analyzers can provide information on and indirectly through the use of sophisticated devices
electrolytes, thanks to ongoing research on such as photospectrometers and pulse oximeters. Some
microsampling technology. of the methods and devices used, such as blood gas
• Blood glucose measurement by transcutaneous, analyzers, provide actual measured data; others, such as
photospectrometric methods is currently the capnograph, provide data that are more valuable
under study and will, if successful, be a when looking at trends over time. Remember that ABGs
welcome instrument for millions of diabetics are like a static picture, giving a look at the respiratory
worldwide. physiology at a single second in time. Trend data are
• Without doubt, patient care will be improved by: more like a video, enabling the RT to see how the
The ability to measure and quantify physi- physiology has acted over time. So the choice becomes
ologic variables, such as exhaled nitric oxide, the desirability of a static glimpse at the ABG values or
gastric, and esophageal pH, via minimally a dynamic presentation of real-time physiology under
invasive sensors. current conditions.
The use of ultrasound vascular location Arterial blood gas procurement, analysis, and
devices to minimize failed arterial and venous interpretation are skills that must be learned, prac-
punctures. ticed, and evaluated repeatedly over time. In addition
The use of pulse oximetry data to determine to maintaining current skill levels, the respiratory
perfusion index, differential perfusion, and pulse therapist must be aware that blood gas analysis
waveform analysis. technology, techniques, and procedures are constantly
being upgraded and improved. Such change only 6. Put the following steps in the proper order for
further emphasizes the need for continuous training in blood gas sampling by arterial puncture.
this area of respiratory therapist practice. An ongoing a. Assemble disposable blood gas kit according to
program of quality assurance, remediation, and review manufacturer’s specifications.
is a mandatory part of offering a blood gas service. b. Don gloves.
c. Inform the patient before the actual
puncture.
Study Questions d. Insert needle with the bevel up, at approxi-
REVIEW QUESTIONS mately a 45-degree angle.
e. Introduce yourself and explain the procedure to
1. Choose the correct acid-base status of this patient: the patient.
pH 7.32; PaCO2 36 mm Hg; PaO2 97 mm Hg; f. Transport sample to lab and analyze.
HCO3 17 mmol/dL; SaO2 98%. g. Wash hands.
a. respiratory acidosis h. Expel all air from sample.
b. mixed metabolic and respiratory i. Remove needle; cap syringe.
c. metabolic alkalosis j. Dispose of needle in appropriate biohazard
d. metabolic acidosis container.
2. Choose the condition indicated by the following k. Allow blood to fill to adequate sample size
ABG values: pH 7.52; PaCO2 28 mm Hg; PaO2 under arterial pressure.
97 mm Hg; HCO3 24 mmol/dL; SaO2 98%. l. Select the site for the puncture.
a. respiratory acidosis m. Establish collateral circulation, if possible, for
b. respiratory alkalosis site.
c. metabolic acidosis n. Obtain needed supplies, including ice if
d. metabolic alkalosis hospital policy.
e. mixed metabolic and respiratory alkalosis o. Watch for flash of blood in the hub of the
3. Choose the correct acid-base status of this patient: needle.
pH 7.32; PaCO2 36 mm Hg; PaO2 97 mm Hg; p. Swab puncture site with Betadine; wipe it clean
HCO3 17 mmol/dL; SaO2 98%. with alcohol.
a. respiratory acidosis q. Use smooth, consistent advancement of the
b. mixed metabolic and respiratory needle. If redirection is required, withdraw
c. metabolic alkalosis needle to just under the skin and advance it
d. metabolic acidosis again.
r. Dispose of all waste, remove gloves, and wash
4. Given the following information, calculate pre-
hands.
dicted blood gas values: pH 7.25; PaCO2 __ mm
s. Remove the needle, apply pressure for
Hg; PaO2 __ mm Hg; HCO3 17 mmol/dL; SaO2
3–5 minutes or until the bleeding stops.
98%. The patient is 69 years old and on room air.
t. Review chart for physician order and anticoagu-
a. PaCO2 50 mm Hg, PaO2 93 mm Hg
lant or bleeding disorder status.
b. PaCO2 65 mm Hg, PaO2 85 mm Hg
u. Mix the blood thoroughly.
c. PaCO2 70 mm Hg, PaO2 73 mm Hg
v. Label the sample.
d. PaCO2 30 mm Hg, PaO2 103 mm Hg
w. Localize the target artery using the fingers of the
5. What is the correct definition of each of the nondominant hand.
following terms? x. Place sample in ice if hospital policy.
a. oxygen saturation ____ a modifier of y. Assess puncture site. Ensure bleeding has
acid-base reactions stopped; check for distal pulse.
b. oxygen content ____ the proportion of z. Verify patient’s identity.
HbO2 to Hbtotal
7. Discuss the principles of operation for transcutane-
c. O2 combining ____ relationship
ous and gas-sampling techniques.
capacity between PaO2 and
SaO2 8. Identify the strengths and weaknesses of various
d. O2 dissociation ____ actual amount types of invasive and noninvasive analysis
curve of O2 present techniques.
e. pulse oximetry ____ ability of Hb to 9. Identify the indications and contraindications
carry O2 associated with various blood gas analysis and
f. buffer ____ light absorption monitoring techniques.
oxygen determination
10. What are the normal values for arterial blood gases, 7. The major energy-producing process in the body is
both measured and calculated at sea level? known as oxidative transphosphorylation or:
PaCO2 PaO2 HCO3 SaO2 AG a. respiration
pH mm Hg mm Hg mmol/dL % mmol/L b. ventilation
c. cyclic AMP
a. 7.35–7.50 25–32 80–105 8–15 88–96 22–34
d. TCA cycle
b. 7.35–7.45 35–45 95–100 22–26 96–99 12–14
c. 7.45–7.55 40–50 106–115 18–32 85–92 10–15 8. Regarding “normal values,” which of the following
d. 7.38–7.42 38–35 89–94 14–28 85–95 13–18 statements is correct?
a. Normal values are universal for each physi-
ological and biochemical value analyzed.
MULTIPLE-CHOICE QUESTIONS b. Normal values tend to be specific to each major
demographic, ethnic, or racial group.
1. Low hemoglobin levels has what effect on SPCO2
c. Most normal values are biased toward white
readings?
males of European ancestry.
a. SPCO2 reads higher than actual.
d. Normal values are not variable within a culture.
b. SPCO2 readings are not affected.
c. SPCO2 reads the same as SaO2 readings. 9. The anion gap (AG):
d. SPCO2 reads lower than actual. a. is the difference between the anions and the
other chemicals in the body.
2. Which of the following does not adversely affect
b. accounts for the effects of unmeasured organic
SPCO2 data?
acids on the acid-base balance.
a. decreased peripheral perfusion
c. roughly approximates the PaCO2 less the pH
b. Black Pearl nail polish
and is used to estimate HCO3.
c. increased methemoglobin level
d. determines the electrolyte difference between
d. increased pulse pressure
fluid intake and output.
3. Which of the following represents a 1-SD range of
10. The term “6.3” in the Henderson-Hasselbalch
normal blood gas values?
equation represents:
a. pH 7.42–7.45; PaCO2 35–37 mm Hg; PaO2
a. the slope of the line comparing PaCO2 with PaO2.
105–110 mm Hg
b. the relationship between gas saturation and
b. pH 7.38–7.42; PaCO2 38–42 mm Hg; PaO2
partial pressure.
95–98 mm Hg
c. the dissociation constant for human blood
c. pH 7.35–7.45; PaCO2 35–45 mm Hg; PaO2
plasma.
105–110 mm Hg
d. the intercept of the pH (x-axis) and PaCO2
d. pH 7.42–7.45; PaCO2 35–37 mm Hg; PaO2
(y-axis) on the O2 dissociation curve.
105–110 mm Hg
11. Is the available information in Review
4. A quality control tool that plots sample results as a
Question 5 sufficient to perform blood gas
function of standard deviation is the:
prediction equations?
a. Levy-Jennings plot.
a. Yes
b. Westgard rules.
b. No
c. May-Optely figure.
c. No, the FIO2 is needed
d. Thomas–Quigley chart.
d. Yes, but not necessary
5. Correction of respiratory acidosis is ________ than
that of metabolic acidosis because _________.
a. slower … the lungs have a larger surface area CRITICAL-THINKING QUESTIONS
than the kidneys
b. faster … we can change pH by holding our 1. What are the possible consequences of borderline
breath hypoxemia due to the shape of the oxyhemoglobin
c. faster … it is easier to get rid of CO2 than HCO3 curve?
d. slower … the urine is more acidic than expired air 2. Alterations of the anion gap (AG) can have pro-
6. In “normal” individuals, the ratio of HCO3 to found effects on the patient’s acid-base balance, yet
CO2 is: these alterations can be difficult to resolve. What
a. 20:1. are some diseases that cause these alterations, and
b. 1.5 mmol/L. why are effective solutions so difficult to initiate?
c. 0.80. 3. The use of noninvasive technologies has, without
d. 18 g/dL. doubt, enhanced our ability to monitor and care
for our patients. However, these gains have some 4. You B, Pesin R, Duvivier C, Dang Vu V, Grilliat JP.
drawbacks. What are some of the real and potential Expiratory capnography in asthma: evaluation of
problems with noninvasive monitoring? various shape indices. Eur Respir J. 1994;7:318–323.
4. What is the significance of the Latin phrase 5. Yaron M, Padyk P, Hutsinpiller M, Cairns CB.
“Quis custodiet ipsos custodes?” in relation to Utility of the expiratory capnogram in the assess-
QA/QI systems? ment of bronchospasm. Ann Emerg Med.
1996;28:403–407.
6. Tasota FJ, Wesmiller SW. Balancing act. Nursing 98.
References 1998;28:35–41.
7. Westgard JO, Lott JA. Critical reviews in clinical
1. Brooks SW. Integrated Basic Science. 3rd ed. laboratory sciences, 1549–781X, V13, N4, 1981:
St. Louis, MO: Mosby; 1970. 283–330.
2. Wojciechowski WV. Respiratory Care Sciences:
An Integrated Approach. 3rd ed. Clifton Park, NY:
Delmar Cengage Learning; 2000. Suggested Reading
3. American Association for Respiratory Care. Davila F. A comparison of clinical and research oxygen-
Sampling for arterial blood gas analysis. Respir related physiologic equations. Intens Care World.
Care. 1992;37:913–917. 2000;15:182–188.
CHAPTER 17
Pulmonary Function Testing

Robert A. Whitman and Susan A. Holland
OBJECTIVES
• List the indications for spirometry and for postbronchodilator studies.
• Explain how to perform pre- and postbronchodilator spirometry and interpret the results.
• Explain the results of a cardiopulmonary stress test.
• List the indications for more testing after spirometry is done, specifically MVV, diffusing capacity, lung
volumes, lung compliance, airway resistance, single-breath nitrogen washout, and bronchoprovocation.
• List the indications for cardiopulmonary stress testing.
• Explain how to perform the following tests and interpret the results: lung volumes, diffusing capacity, single-
breath nitrogen washout, MVV, airway resistance, lung compliance, and a CO2 response curve.
• Check equipment for proper function and explain infection control measures in pulmonary function testing.
CHAPTER OUTLINE
Indications for Pulmonary Function Testing Interpretation
Lung Assessment Through PFT Other Specialized Tests
General Disease Patterns Spirometers
Normal or Predicted Values Volume Displacement Devices
Lung Volumes Flow-Sensing Devices
Spirometry Body Plethysmograph
Forced Vital Capacity Calibration
Peak Flow Quality Assurance
Additional Laboratory Assessment Infection Control
Determining Lung Capacities and Volumes Age-Related Considerations
Diffusing Capacity (Single-Breath Method)
455
KEY TERMS
airway conductance (Gaw) diffusing capacity pressure transducer
airway resistance (Raw) lung capacities restrictive lung disease
anaerobic threshold (AT) lung compliance shutter
body plethysmography lung volumes spirometry
bronchoprovocation maximum voluntary thermal pneumotachometer
calibration ventilation (MVV) ultrasonic pneumotachometer
differential pressure obstructive lung disease
pneumotachometer pneumotachometer
P
ulmonary function testing consists of a group It is also done to assess the effectiveness of medications
of tests designed to measure aspects of lung and treatments prescribed. Follow-up exercise testing
function. The most commonly performed can assess the effectiveness of a rehabilitation or
test is spirometry, frequently referred to as a exercise program.
forced vital capacity maneuver. Spirometry measures the The purposes of pulmonary function testing are
maximal flows that a patient can generate and is the summarized in Table 17-1.
most useful in determining whether airway obstruction
is present. Spirometry also measures how much
volume a patient can exhale; a reduced volume can LUNG ASSESSMENT THROUGH PFT
indicate the presence of restrictive lung disease. Spi- Several pulmonary function tests measure the follow-
rometry can be performed using portable equipment, ing aspects of lung function.
allowing for on-site occupational screening, patient
• The condition of the airways is assessed by
bedside testing, and even testing at health fairs and
measuring flows.
in shopping malls.
• Lung volumes are measured both directly (by
Other, more sophisticated tests allow for a
physical measuring) and indirectly (through
more specific diagnosis of the type of lung disease
mathematical calculation).
(obstructive, restrictive, or a combination) and for
• The resistance of the airways and the compliance of
further assessment of the severity of the disease. These
the lung and thorax are also measured.
tests require larger, more sophisticated, and more
expensive equipment, so they are usually performed
in a pulmonary function laboratory.
TABLE 17-1 Purposes of pulmonary
function testing
Indications for Pulmonary Screening
Function Testing General population
A pulmonary function test (PFT) is typically done to: Occupational risk
• Establish the presence or absence of lung disease Disability determination
and assess level of severity. High-risk groups
• Evaluate operative risks. Preoperative evaluation
• Perform surveillance for occupational or
Diagnosis
environmental exposure.
• Evaluate disability or impairment. Type of disease
Severity of disease
More specialized tests provide additional informa-
tion (obstructive, restrictive, or combined) about a lung Reversibility of disease
disease. The severity and reversibility of the impairment Follow-up
can be assessed as well. The effect of exercise on Progression of disease
breathing can be assessed using exercise testing.
Effectiveness of medications
Follow-up testing or monitoring is used to check
periodically on the progression of lung impairment. Effectiveness of rehabilitation
CHAPTER 17 ■ Pulmonary Function Testing 457
TABLE 17-2 Parameters assessed in quickly as normal. This limitation is shown in reduced
pulmonary function testing maximal effort flow measurements and is defined by
an increase in airway resistance. The conducting
Exhaled flows airways have become narrowed because of any one or a
Inhaled flows (with some equipment) combination of the following:
Airway resistance • Inflammation
Lung compliance • Accumulation of secretions
Gas distribution in the lungs • Bronchospasm (muscle spasms in the airways)
• Loss of the supporting tissue in the airways,
Exercise tolerance
causing them to partially collapse during
Diffusing capacity exhalation
Reversibility of lung disease
Examples of obstructive diseases are asthma,
Airway hyper-reactivity chronic bronchitis, bronchiectasis, and emphysema.
Response to increased CO2
Normal or Predicted Values

• The distribution of air in the lungs can be
The results of a subject’s tests are compared with the
assessed, as well as the rate at which oxygen
normal or predicted values for that subject. Of the
is able to diffuse from the lungs into the
several sets of predicted values, some are more
blood.
commonly used than others. All of these sets were
• The degree to which a medication reverses a lung
developed by testing many people who did not have
disease can be assessed by giving a subject a
lung disease. Regression analysis (prediction equa-
bronchodilator treatment after all other tests
tions) or nomograms were then developed for all
have been completed and then repeating some
parameters. These equations take into account the
of the tests.
age, height, and sex of the subject. Some sets of
• The subject’s response or sensitivity to increased
predicted values also include race or body surface
concentrations of CO2 can also be measured.
area as variables. Separate sets of predicted values
Table 17-2 lists the parameters assessed in have been developed for children, adolescents,
pulmonary function testing. and adults.
Computerized equipment has the predicted
value sets installed. The subject’s performance in
GENERAL DISEASE PATTERNS each test is automatically compared with what is
Lung diseases are classified as restrictive, obstructive, or predicted. When noncomputerized equipment is
a combination of the two patterns. used, predicted normal values can be determined by
manual calculation of predictive equations or the
Restrictive Lung Diseases. Restrictive lung diseases use of nomograms (the graphical plots of predictive
are characterized by an inability to inhale as much as equations).
normal. This condition is due to one of the following Normal or predicted values are described
problems or a combination of them: in terms of BTPS (body temperature and pressure
saturated). Measurements made by pulmonary
• The lung tissue itself is stiff (with scar tissue or
function equipment are actually taken at ATPS
fluid accumulation).
(atmospheric pressure and temperature saturated).
• The chest wall cannot expand normally (due to
According to Charles’s law (Chapter 3), the volume
chest wall or spinal abnormalities).
of a gas at room temperature is less than the volume
Both cause a decrease in compliance, which at body temperature; so a conversion to BTPS must
restricts the expansion of the lungs. The defining be made. Computerized equipment makes that
characteristic of restrictive lung disease is a reduced correction automatically, and results are reported in
total lung capacity (TLC). Examples of restrictive BTPS. When noncomputerized equipment is used,
lung disease are pneumoconiosis, pulmonary the adjustment must be made by multiplying the
fibrosis, pleural thickening, scoliosis, lordosis, and results by a factor that is determined by the room
kyphoscoliosis. air temperature and the barometric pressure. Tables
listing these correction factors are widely available
Obstructive Lung Diseases. Obstructive lung from equipment manufacturers and in books on
diseases are characterized by an inability to exhale as pulmonary function.
Lung Volumes
Lung volumes are the four segments into which the
amount of air moving into and out of the lungs is IRV
divided. Lung capacities are combinations of two IC
or more lung volumes. The respiratory therapist (RT) VC
must be aware of the distinction between volume and TLC
capacity to understand the significance of the results of VT
several pulmonary function tests.
Three of the lung volumes are measured directly ERV
using spirometry, and one can be measured indirectly. FRC
The four capacities are calculated from the measured RV Time RV
volumes or, if possible, directly. The RT should learn
the following definitions before continuing this
chapter. FIGURE 17-1 Lung volumes (left) and capacities (right).
• Tidal volume (VT), measured directly, is the

amount of air moved into and out of the lungs
in a normal (resting) breath. Tidal volume is Spirometry
important because several of the other volumes Spirometry is a test to assess pulmonary mechanics
and capacities are defined by reference to it. under dynamic conditions. Spirometry is the most
• Inspiratory reserve volume (IRV), measured common test performed in assessing lung function and
directly, is the maximum amount of air that is frequently performed at the bedside, in the physician’s
can be inhaled after a resting tidal inhalation. office, at health fairs, as well as in the laboratory.
• Expiratory reserve volume (ERV), measured Spirometry consists of a series of forced vital capacity
directly, is the maximum amount of air that maneuvers in which both volume and flow rates are
can be exhaled after a resting tidal exhalation. measured.
• Residual volume (RV) is the amount of air that
remains in the lungs after a maximal exhalation
(i.e., after ERV has been exhaled). It cannot be FORCED VITAL CAPACITY
measured directly, but tests have been developed The forced vital capacity (FVC) test measures the VC of
to measure residual volume indirectly. the subject and, with a VT measurement, allows the
• Inspiratory capacity (IC) is the maximum amount calculation of the IRV and the ERV. Because the test is
of air that can be inhaled after a resting tidal done with the subject exhaling as hard as possible from
exhalation. This is the sum of the tidal volume TLC (full) to RV (empty), flows during various portions
and the inspiratory reserve volume (VT ⫹ IRV). and at specific times during the FVC can also be
It can be measured directly by spirometry. measured. Indications, contraindications, hazards,
• Functional residual capacity (FRC) is the amount procedure, and so on are discussed in the American
of air that remains in the lungs after a resting Association for Respiratory Care (AARC) clinical
tidal exhalation. This is the sum of the expiratory practice guideline for spirometry.1
reserve volume and the residual volume
(ERV ⫹ RV).
• Vital capacity (VC) is the maximum amount of CASE STUDY 17-1
air that can be forcibly exhaled after an inhala-
tion. This capacity is the sum of the inspiratory
reserve volume, the tidal volume, and the S. B., a 52-year-old male with COPD, completed
expiratory reserve volume (IRV ⫹ VT ⫹ ERV). pulmonary function tests for lung volumes.
It can be measured directly by spirometry. Question
• Total lung capacity (TLC) is the maximum
amount of air that the lungs can hold. This Complete the results that have not been
capacity is the sum of all the volumes calculated.
(IRV ⫹ VT ⫹ ERV ⫹ RV, or IC ⫹ FRC).
VT 0.63 L FRC 1.86 L RV 1.76 L
Figure 17-1 shows these lung volumes in terms of a VC L IC 2.54 L ERV L
volume-time spirometry tracing and two bar graphs.
TLC L IRV L
Normal lung volumes and capacities are shown in
Table 6-4.
6
Best Practice
FVC Test 5
FEV3
FEV2
The subject should not perform a glottic closure
(closing the glottis, as is done before a cough) 4 FEV1
Volume (liters)
during the inspiratory hold. To avoid glottic
closure, instruct the subject to continue to try FEV0.5
to inhale more air during the 2-second hold. 3
• Coaching is very important in this test

because maximal effort must be obtained. 2
The subject should be encouraged to blow
hard until the recommended 6 seconds have
passed or until the equipment has not 1
sensed any flow for 1 second.
• There should be no coughing during the 0
1 2 3
forceful exhalation. If the subject cannot
Time (seconds)
refrain from coughing at the end of the
forced exhalation, the results can be reported FIGURE 17-2 A volume-time curve for timed volumes.
with the coughing noted on the report.
• The position of the subject (seated or
standing) should be the same for all FVC
maneuvers. Usually subjects are seated. • If the equipment also measures inhalation, the
subject should then be instructed to inhale as
quickly as possible up to TLC (full). Most comput-
erized equipment has these criteria built in so that
poor test performance is not accepted as valid.
Patient Maneuver. The patient maneuver for the FVC
test is as follows: Graphics. The results of the patient’s forced vital
capacity (FVC) maneuver can be displayed graphically
• The subject generally wears noseclips for the FVC
in two ways.
test to ensure that all exhaled air is captured. The
One shows the FVC with time on the horizontal
best way to make sure that the clips are tight
and volume on the vertical side of the graph. Depend-
enough to prevent any airflow through the nose
ing on the equipment used, the time may be recorded
is to ask the subject to try to sniff air through the
from left to right or from right to left, and changes in
nose with the mouth closed. If airflow occurs,
volume may be recorded with exhalation going from
tighter noseclips are needed.
top to bottom or from bottom to top. This graph is
• Have the subject place the teeth and lips tightly
called a volume-time curve. Seven measurements can
around the mouthpiece. If the subject wears
be made from a volume-time curve (Figures 17-2
dentures, they should be removed, and the
and 17-3):
subject should be instructed to place the gums
and lips tightly around the mouthpiece. • FVC (forced vital capacity)—the maximum
• Instruct the subject to relax and breathe amount of air that can be forcefully exhaled after
normally to establish normal tidal volume. a maximal inhalation. This indicates the volume
• At the end of a tidal exhalation, tell the subject available for ventilation, which is decreased in
to inhale as much air as possible and then restrictive disease and in advanced cases of
immediately exhale as forcefully and for as long obstructive disease.
as possible. The exhalation should continue for • FEVt [timed (forced) exhaled volume]—the
at least 6 seconds, unless there is an obvious amount of air exhaled in the first half second
plateau with no flow occurring for 1 second. If (FEV0.5), first 1 second (FEV1), or first 3 seconds
the equipment used measures only exhalation, (FEV3) of a forced vital capacity maneuver. The
the test is completed at this time, and the FEV1 is the most commonly reported value.
subject can take his or her mouth off the The FEV1 is decreased in both obstructive and
mouthpiece. restrictive lung disease.
6 12
FEF200–1200 FEF25–75% FEF75–85%
10
5 · PEFR
FEF25% or Vmax75
85% of VC 8
4
Volume (liters)
75% of VC ·
6 FEF50% or Vmax50
3
4
·
Expiration
FEF75% or Vmax25
2
2
Flow (Lps)
25% of VC
1200 mL
1 0
1 2 3 4 5 6
Volume (liters)
Inspiration
200 mL
-2 FVC
0
1 2 3
Time (seconds)
-4
FIGURE 17-3 Volume-time curves for average flows.
-6
FIF25%
• FEVt% (ratio of the FEVt to the FVC as a FIF75%
-8 PIFR
percentage)—FEV1 is usually written as FIF50%
FEV1/FVC. This value is decreased in obstructive
-10
lung disease and is normal or increased in
restrictive disease. FIGURE 17-4 Flow-volume loop for flows and volumes.
• FEF200–1200 (forced expiratory flow from 200 to
1200 mL)—the average flow produced in the
forced vital capacity after the first 200 mL has
been exhaled until 1200 mL has been exhaled. following measurements can be shown on a flow-
This measurement assesses the large airways. volume curve or loop:
• FEF25–75% (forced expiratory flow from 25% to
• FEF25%, 50%, 75% (forced expiratory flow at 25%,
75% of the FVC, sometimes called the midflow)—
50%, and 75% of the FVC)—instantaneous
the average flow generated in the middle 50% of
flows, not average flows like the FEF25–75%. They
the FVC. This measurement assesses the small
are the flows generated by the subject at the exact
airways.
instants when 25%, 50%, and 75% of the FVC
• FEV75–85% (forced expiratory flow from 75% to
have been exhaled. This flow can be shown
85% of the FVC)—the expiratory flow rate at the
on both a curve (the expiration portion of
end of exhalation, after 75–85% of the volume
Figure 17-4) and a loop.
(FVC) has been expired.
• PIFR or PIF (peak inspiratory flow rate or peak
• PEFR or PEF (peak expiratory flow rate or peak
inspiratory flow)—the highest inspiratory flow
expiratory flow during the FVC)—the highest flow
generated during the FVC maneuver. This can be
rate generated during a forced vital capacity
shown only on a flow-volume loop. It is the
maneuver. It generally occurs at or near the
lowest point on the inspiratory curve.
beginning of the FVC maneuver and is sometimes
used to assess patient effort in the FVC maneuver.
Reporting Results. The American Thoracic Society
The other graphic for the FVC is the flow-volume
(ATS) has made recommendations about performing
curve or loop (Figure 17-4). This shows the FVC maneuver,
spirometry to ensure that the results reported are valid
with volume on the horizontal axis and flow on the
(i.e., that any abnormalities reported are real, not the
vertical axis. The flow-volume curve shows exhalation
result of poor performance).2 The ATS recommends that:
only; the flow-volume loop shows both exhalation and
inhalation. Both the curve and the loop show FVC and • At least three acceptable maneuvers be saved.
PEFR (the highest point on the curve or loop). In • Among these three, the largest FVC must not
addition to the preceding seven measurements, the vary more than 0.150 L from the second largest
TABLE 17-3 Withholding medications

CASE STUDY 17-2 before pulmonary function testing
The following are the FVC and FEV1 results from Withholding
one subject: Time Before
Medication Type Testing (hours)
Trial 1 Trial 2 Trial 3 Short-acting beta-adrenergics 4
FVC 1.20 L 1.26 L 1.27 L Anticholinergics 4

Long-acting beta-adrenergics 12
FEV1 0.92 L 0.98 L 0.94 L
Methylxanthines 12
Slow-release methylxanthines 24
Questions
Cromolyn sodium, necromodil 24
1. According to ATS standards, are the results sodium
of these three maneuvers acceptable?
Leukotriene inhibitors 24
2. What should be reported as the largest FVC?
3. What should be reported as the largest FEV1?
4. According to the ATS standards, which trial bronchodilator is usually given, unless another medica-
should be reported as the best? tion is specified.
5. According to the ATS, from which trial • If the medication is administered by a small-
should all other measurements be made? volume nebulizer, the subject should be
instructed to take deep breaths with a 3-to
5-second breath-hold.
• If the medication is given by metered-dose
inhaler (MDI), the subject should wait for
FVC, and the largest FEV1 must not vary more
2 minutes between puffs.
than 0.150 L from the second largest.
• If a beta-adrenergic medication is administered,
• Of a series of at least three maneuvers, the
retesting should be done after a 10- to 15-minute
largest FVC and the largest FEV1 should be
wait.
reported.
• If an anticholinergic is administered, retesting
• The test in which the sum of the FVC and the
should be done after 45–60 minutes.
FEV1 is the largest is to be chosen as the best test,
and all reported flow rate measurements are to Blood pressure and pulse should be monitored during
be made from this test. and after the administration of the medication. The test
that is usually repeated after the bronchodilator is the
Pre- and Postbronchodilator Studies. A patient who FVC maneuver, although airway resistance (see Other
is already taking bronchodilating medications should Specialized Tests on page 469), lung volume determi-
stop using them before testing unless symptom control nation, and diffusing capacity (see Additional Laboratory
is not possible without them. Assessment on page 464) may also be done.
The amount of change in any parameter after
• Short-acting beta-adrenergic bronchodilators
bronchodilation is generally reported as the percentage
and anticholinergics should be stopped at least
change from the baseline value. A significant response
4 hours before testing.
to the bronchodilator, according to the ATS, is at least a
• Long-acting beta-adrenergic bronchodilators and
12% and 200-mL improvement in the FEV1 or FVC.
methylxanthines should be stopped 12 hours
The response is also considered to be significant if the
before testing.
airway resistance is reduced by 30–40%. The ATS states
• Slow-release methylxanthines, cromolyn
that if the response is less than 12%, a bronchodilator
sodium, and necromodil sodium should be
can still be prescribed if it results in improved symp-
discontinued 24 hours before testing.
toms or exercise tolerance. A follow-up study is recom-
• Leukotriene inhibitors should be stopped
mended in these cases because the response of some
24 hours before testing.
subjects can improve over time. Contraindications,
Table 17-3 summarizes the withholding time schedules hazards, assessment of outcome, monitoring, and other
for these medications. topics are covered in the AARC clinical practice guide-
After all testing has been completed, the broncho- line for assessing the response to bronchodilator
dilator is administered. A fast-acting beta-adrenergic therapy at the point of care.3
Interpretation of Results. Interpretation follows a few TABLE 17-4 Abnormal spirometry values in
simple rules: restrictive and obstructive lung diseases
• If the measurement of a parameter is between Restrictive Obstructive
80% and 120% of the predicted value, it is
FVC ⬍ 80% predicted Normal or ⬍ 80%
considered to be normal.
predicted
• In general, any result value that is less than 80%
of the normal value is considered decreased and FEV1 Normal or ⬍ 80% ⬍ 80% predicted
therefore abnormal. predicted
• The TLC is also considered to be abnormal if it is FEV1% ⱖ predicted ⬍ predicted
over 120% of the predicted value.
• One exception to these general rules is the
FEV1%, for which any reduction from the • If the FVC is normal (ⱖ 80% of the predicted
normal percentage is abnormal. value) and the FEV1 is normal (equal to or
The pattern of abnormalities allows the interpreter greater than predicted), the test is normal.
to distinguish between obstructive disease, restrictive • If the FVC is normal and the FEV1 is less than
disease, and a combination of the two. 80% of its predicted value, obstructive disease is
Obstructive disease develops progressively, and the indicated. Postbronchodilator studies can reveal
number of abnormal values slowly increases. Before the reversibility of the disease.
obstructive disease can be diagnosed, the FEF25–75% is • If the FVC is decreased and the FEV1% is at or
decreased (i.e., the small airways are narrowed). Then above the predicted value, restrictive disease is
the medium-sized airways become narrowed, resulting suggested. Further testing should be performed
in a decreased FEV1. This narrowing, in turn, results in to confirm that the TLC is less than 80% of the
a decrease in the FEV1%. As air trapping develops, as predicted value.
evidenced by an increase in TLC (⬎120%), the FVC • If the FVC is decreased and the FEV1% is below
decreases below 80% of predicted. Further tests, such as its predicted value, obstructive disease is indi-
lung volumes and diffusing capacity, are indicated to cated. Again, postbronchodilator studies reveal
assess the severity of the disease. Postbronchodilator the degree of reversibility of the disease.
retesting is indicated to assess the reversibility of the The method described is summarized in the flowchart
disease. in Figure 17-5.
With restrictive disease, the FVC is decreased. The The shape of a flow-volume loop can provide
FEV1 is normal at first, and then it decreases. (In valuable information for interpretation (Figure 17-6).
severe cases, the predicted FEV1 is greater than the When a subject has obstructive disease, the expiratory
subject’s actual FVC.) Although both FVC and FEV1 curve has a concave, or dishlike, shape because the
may be decreased, the FEV1% remains within normal flows that the subject can produce are limited by the
limits or increases relative to normal individuals. decreased diameter of the medium-sized and small
Because the presence of restrictive lung disease is airways. If a normal flow-volume loop is available for
defined by a decrease in TLC, lung volume tests are comparison, the restrictive one is a miniature of the
indicated. Also, a diffusing capacity test is indicated normal one because the TLC is reduced.
to assess the effect of the restrictive disease on the The flow-volume loop is particularly useful in
ability of oxygen to diffuse from the lungs to the diagnosing upper airway obstructions.
blood. This are decreased in disease caused by lung
tissue abnormalities and normal in disease caused by • A fixed obstruction causes flat expiratory and flat
chest wall abnormalities. inspiratory curves because the obstruction limits
Combined disease states show characteristics of both flow on both inhalation and exhalation.
patterns.
See Table 17-4 for a summary of these patterns.
Interpretation of results should be approached FVC
methodically to avoid confusion and errors. To interpret
FVC test results, three parameters need to be examined: N <80% predicted
the FVC, the FEV1, and the FEV1/FVC (FEV1%).

FEV1 FEV1%
• The measured FVC and FEV1 are abnormal or
decreased if they are less than 80% of the N <80% predicted ≥predicted <predicted
predicted value. NORMAL OBSTRUCTIVE RESTRICTIVE OBSTRUCTIVE
• The FEV1% is considered abnormal if it is less
than the predicted value. FIGURE 17-5 A flowchart for interpretation of spirometry.
Intrathoracic Extrathoracic
Fixed Variable Variable
Small Large Large Large
Restrictive Airway Airway Airway Airway
Normal Disorder Obstruction Obstruction Obstruction Obstruction
Flow
Volume
FIGURE 17-6 The shape of flow-volume loops for restrictive and obstructive lung disease
and upper airway obstruction.
• A variable extrathoracic obstruction (airway The positive intrathoracic pressures generated on

exposed to atmospheric pressures) causes a flat exhalation cause the obstruction to narrow,
inspiratory curve and a normal expiratory while the negative intrathoracic pressures
curve. The negative intrathoracic pressures generated on inspiration cause the obstructed
(less than atmospheric) generated on area to widen.
inspiration cause the obstruction to narrow,
while the positive pressures generated on
exhalation cause the obstructed area to PEAK FLOW
widen. Small portable devices, called peak flowmeters, are used
• A variable intrathoracic obstruction (airway to monitor peak flow for subjects who have asthma or
exposed to intrathoracic pressures) causes a flat hyper-reactive airways. They can be used in clinics,
expiratory curve and a normal inspiratory curve. hospitals, or the home.
CASE STUDY 17-3

P. J. is a 52-year-old black male. He is 65 inches tall and weighs 222 pounds. The following are his
spirometry results, pre- and postbronchodilator (BD):
Percentage Percentage
Predicted Pre-BD Predicted Post-BD Predicted
FVC 3.59 L 2.34 L 65 2.62 73
FEV1 2.94 L 0.88 L 30 0.90 31
FEV1/FVC 82% 38% 46 34% 41
FEF25–75% 189 Lpm 16 Lpm 8 15 Lpm 8
PEFR 462 Lpm 152 Lpm 33 170 Lpm 37
Questions
1. What is your interpretation of the prebronchodilator results?
2. Is P. J. response to bronchodilator significant? (Hint: Calculate the percentage change.)
3. Why is the postbronchodilator FEV1/FVC less than the prebronchodilator FEV1/FVC?
To detect effort-induced bronchospasm, first zero, or difference indicates the amount of early airway
set, the peak flowmeter. Then the subject inhales closure (preventing further exhalation) that has
maximally, places teeth and lips around the mouth- occurred in the FVC.
piece, and exhales as forcefully as possible. This
performance should be repeated three times, with all Functional Residual Capacity (FRC) and Residual
results recorded. Volume (RV). Three tests can be used to determine FRC
When a peak flowmeter is used to monitor an and RV: the nitrogen washout method, the helium
asthmatic, take readings each morning and evening for dilution method, and body plethysmography.
a few weeks. The subject’s personal best is then deter-
mined. The personal best helps in determining when Nitrogen Washout (Open Circuit) Method The concen-
subjects’ airway obstruction is worsening so that they tration of nitrogen in the lungs is approximately
can seek further medical attention before severe 75–80%. The theory behind the nitrogen washout test
obstruction occurs. is that if all or most of the nitrogen is removed from
the lung and the volume of the nitrogen exhaled is
measured, the FRC can be determined.
• Place noseclips on the subject’s nose.

Additional Laboratory • The subject places lips tightly around the
Assessment mouthpiece, breathes normally, and then is
given time to relax.
If the spirometry results of a subject are normal, no
• At the end of exhalation, the subject is switched
further testing is needed. If the results are abnormal,
to 100% oxygen.
a physician may order further tests to confirm the
presence of restrictive lung disease or to assess the The computerized system measures the volume
severity of either restrictive or obstructive lung disease. exhaled in each breath and has an in-line nitrogen
The equipment used to perform these further tests analyzer to determine the volume of nitrogen exhaled
is not portable; therefore, they must be done in a with each breath. Continue the test until the concen-
pulmonary function laboratory. tration of nitrogen in the exhaled gas is reduced to
The tests done in a pulmonary function laboratory approximately 1%. For normal subjects, this concen-
can assess several aspects of lung function. tration should be reached within 3–7 minutes.
• Lung volumes and capacities can be measured Subjects who have obstructive disease take longer
and calculated. because of the uneven distribution of gas in their
• Diffusing capacity, airway resistance, lung lungs. Subjects with restrictive disease complete the
compliance, and the evenness of the distribution test in the normal 3–7 minutes. See Figure 17-7 for an
of air in the lungs can be assessed. illustration of this test, along with the equation for
• Specialized testing regimens (bronchoprovoca- determining results.
tion) can be performed to determine the pres-
• The FRC can then be calculated, thereby
ence or absence of airway hyper-reactivity and enabling the calculation of RV and TLC as well.
exercise-induced asthma. • The ERV, already known from the SVC test,
• The ventilatory response of the subject to can be subtracted from the FRC, measured by
increasing CO2 concentrations can be evaluated. the nitrogen washout, to calculate the RV
(FRC ⫺ ERV ⫽ RV).
DETERMINING LUNG CAPACITIES AND VOLUMES • The TLC is calculated by adding the VC
(measured in the SVC) to the calculated
Spirometry can be used to measure the three lung RV (VC ⫹ RV ⫽ TLC).
volumes and two lung capacities: VT, IRV, ERV, IC,
and VC (which account for all usable lung volume). The calculated results are for atmospheric conditions
Procedures for determining slow vital capacity, (ATPS), so a correction factor for BTPS must be applied
functional residual capacity, and residual volume are before reporting results if this has not already been
discussed here. done by the computerized equipment.
Slow Vital Capacity (SVC or VC). The patient performs Helium Dilution (Closed Circuit) Method The theory
the same maneuver as for forced vital capacity (FVC), behind the helium dilution test is that if a known
except that exhalation is slow rather than forceful. concentration of an inert gas is rebreathed by a subject
From this maneuver, VC, VT, IRV, IC, and ERV until its concentration is the same on inhalation as it is
are measured. If the VC is larger than the FVC, the on exhalation, the change in the concentration of the
COLLECTED EXHALED GAS VOLUME

GAS VOLUME AND N2 CONCENTRATION AND N2 CONCENTRATION AFTER
IN LUNGS BEFORE NITROGEN NITROGEN WASHOUT WITH
WASHOUT WITH OXYGEN 100% OXYGEN
28 Liters
7% Nitrogen
C1 V1
Exhaled
CAlvN2 = 0.75
Gas
VFRC = Unknown
C2 V2
CExhN2 = 0.07
C2 V2 (VExh) (CExhN2)
V 1= or VFRC = VExh = 28 liters
C1 CAlvN2
(0.07)(28 liters)
VFRC =
0.75
C = Concentration of gas (N2)
V = Volume of exhaled gas VFRC = 2.61 liters
FIGURE 17-7 Equipment set-up and graphics for the nitrogen washout test.
• The patient continues normal breathing until

Best Practice equilibrium is reached (i.e., the concentration of
helium exhaled is the same as the concentration
Nitrogen Washout Method of helium in the reservoir). The equilibration
time is usually about 7 minutes in normal
1. A sudden increase in the nitrogen
subjects. Subjects with obstructive disease take
concentration indicates a leak in the system.
longer.
Terminate the test at that time.
• The final concentration of helium in the reser-
2. If the nitrogen concentration does not go voir is then measured after thorough mixing.
down to 1%, the subject may have a
punctured eardrum, which allows room air The FRC is then calculated, leading to the calculation
to enter the airways through the eustachian of RV and TLC in the same way they are calculated
tube. when nitrogen washout is used. See Figure 17-8 for the
equipment used and the process of equilibration.
3. Retesting should be done after a 10-minute
wait to allow nitrogen to build up to normal
Body Plethysmography Body plethysmography measures
levels in the lungs.
changes in volume and pressure in the thorax. The
patient sits in an airtight booth and breathes through a
inert gas is due to dilution of the gas by the subject’s

FRC.
• With noseclips in place, the subject first breathes
Best Practice
normally through an open circuit.
• At end-exhalation, the patient is switched into a Helium Dilution Method
spirometer or reservoir containing a known 1. Helium concentration readings should
volume of air with a known concentration of decrease by less than 0.02% in 30 seconds
helium (usually 10–15%). or until 10 minutes have passed.
• An in-line CO2 absorber on the exhalation side 2. A sudden decrease in helium concentration
keeps the CO2 from building up in the reservoir, indicates a leak in the system; the test
and oxygen is added to keep the FIO2 at or should be terminated.
above 21%.
TESTS FOR PULMONARY VOLUMES AND VENTILATION Differential

pressure
pneumotachometer
SPIROMETER SYSTEM BEFORE HELIUM DILUTION
9.7% He Shutter
C1V1
VAdded He
VS = CIHe = 0.097
CIHe
VS = 5.15 liters + - Mouth pressure
VS = 0.5 liters
measurement
0.097 system (transducer)
VS = 5.15 liters
+ - Cabinet volume
measurement
SUBJECT/SPIROMETER SYSTEM AFTER HELIUM DILUTION system (transducer
6.0% He or pneumotachometer)
C2V2 Airtight booth
CFHe = 0.06
VS + FRC = Unknown
FIGURE 17-9 Components of the body plethysmograph

system.
C 1 V1 (VS)(CIHe) VFRC = VS + FRC – VS

= V2 or = VS + FRC
C2 CFHe VFRC = 8.33 liters – 5.15 liters
(0.097) (5.15 liters) = V VFRC = 3.18 liters
S + FRC • The subject then puts hands over the cheeks to
0.60
prevent their expansion when panting against
8.33 liters = VS + FRC
the closed shutter.
FIGURE 17-8 Equipment set-up and procedure for the • Instruct the subject to pant (in small pants)
helium dilution test. through the mouthpiece one or two times per
minute.
• At end-exhalation, close the shutter, and tell the
subject to try to pant against the closed shutter.
mouthpiece that is open to room air. In-line are a
• The shutter is then opened, and the test is complete.
pneumotachometer (a flow sensor), a pressure
manometer, and a shutter that cuts off airflow. The It is recommended that the test be repeated three
booth contains a flow sensor or pressure transducer times. The AARC clinical practice guideline for body
(depending on the methodology used). See Figure 17-9 plethysmography covers contraindications, hazards,
for the arrangement of these components. and equipment requirements.4
Although several tests can be done with this device, The volume of thoracic gas (VTG) is determined
only two tests require an airtight booth: airway resis- using the principle of Boyle’s law, where V1 is the
tance and volume of thoracic gas. The volume of air in volume of thoracic gas (VTG), V2 is the change in alveolar
the thoracic cavity at FRC is determined on the basis of volume, P1 is atmospheric pressure, and P2 is the change
Boyle’s law (P1 ⫻ V1 ⫽ P2 ⫻ V2, when temperature is in alveolar pressure. An SVC test in the same session of
constant). testing is required to calculate all lung volumes.
An oscilloscope is used to show pressure and
• The subject pants against the closed shutter, and
volume changes during panting, with volume on the
mouth pressures and changes in the volume of
horizontal axis and pressure on the vertical axis. The
air in the booth (displaced by the expansion of
oscilloscope display allows the test giver to be sure that
the thorax) are measured.
the pants are small enough to produce measurable
• The subject, with noseclips tightly in place and
loops (see Figure 17-10).
sitting in the booth with the door closed,
breathes normally through the mouthpiece. The
temperature in the booth rises because of the DIFFUSING CAPACITY (SINGLE-BREATH METHOD)
subject’s body heat, so it takes several minutes Of the several tests available to assess lung diffusing
for equilibration to be reached. Equilibration is capacity (the rate at which oxygen diffuses from the
indicated by the end-tidal level remaining stable alveoli to the capillaries), the single-breath method is
on the computer screen. the most common. Because oxygen is already in the
Angle of the 90˚ Closed

Tracing shutter
ΔP Mouth pressure change
30˚
ΔV
0˚
Cabinet volume change
ΔPA ΔVA
PAtm VTG
STORAGE OSCILLOSCOPE PLETHYSMOGRAPH

DISPLAY CABINET
FIGURE 17-10 Oscilloscope display for body plethysmography.
lungs and in the blood, measuring how much diffuses • Instruct the subject to exhale down to RV
from the lung into the blood in one breath is impossible and then inhale up to TLC as quickly as
because the partial pressure of oxygen in the capillary possible. The gas inhaled is a special mixture
blood cannot be determined. Therefore, another gas containing 0.3% CO, 10% He, 21% O2, and
(carbon monoxide, CO) is used in a very low concen- balance N2.
tration. Carbon monoxide has diffusing characteristics • The subject holds his or her breath at TLC for
similar to those of oxygen and is carried in the blood approximately 10 seconds and then exhales as
in the same way as oxygen, and because CO is almost quickly as possible.
completely taken up by the hemoglobin, no back
During the exhalation, the first 750–1000 mL is
pressure exists in the capillary blood and is assumed to
discarded because it is deadspace volume where no
be zero. The amount of CO that diffuses from the lung
diffusion takes place. If the subject’s VC is less than
into the blood (DLCO) gives a direct indication of the
2.0 L, the washout volume may be reduced to 500 mL.
rate at which O2 diffuses from the lung into the blood.
Then a small volume of exhaled gas is collected,
The relationship between the diffusion of carbon
usually 500 mL, and the sample is analyzed for
monoxide and oxygen can be expressed as:
He (or Ne) and CO concentrations.
DLO2 ⫽ DLCO ⫻ 1.23. Computerized equipment makes all calculations.
The first step is to make the dilution correction to
The change in CO concentration between inhala-
get the initial alveolar CO concentration using
tion and exhalation is not all due to diffusion out
the changes in He or Ne concentration. The
of the lungs. Some of the change is due to dilution by
second step is to calculate alveolar volume. Then
the gases that are still in the lungs when the test starts.
the DLCO is calculated. Results are reported at
Therefore, a known concentration of an inert gas
STPD as milliliters of carbon monoxide per minute
(called a tag gas), such as helium (He) or neon (Ne),
per millimeter of mercury (mm Hg is the partial
is added to the gas mixture inhaled by the subject.
pressure gradient across the alveolar-capillary
Because this gas does not diffuse or combine with
membrane). The normal value is around 25 mL
anything in the lung, the change in its concentration
CO/min/mm Hg.
gives a dilution factor. This dilution factor can be used
Factors other than abnormalities in the alveolar-
to calculate the amount of CO that is actually diffused
capillary membrane can cause abnormal results in this
out of the lung.
test: reduced lung volume, anemia, the presence of
• With noseclips in place, the subject makes a tight carboxyhemoglobin in the blood, and altitude.5
lip seal around the mouthpiece and breathes Correction factors are available to account for these
normally. conditions.
Abnormal values typical of obstructive lung disease

Best Practice are the same as in the interpretation of FVC results.
Postbronchodilator studies and DLCO results help to
Diffusing Capacity: further classify the obstructive disease.
Reversibility is demonstrated by a 12% and a
Single-Breath Method 200-mL or greater increase in FVC or FEV1 postbron-
1. The subject should be instructed not to chodilation. In general, asthma responds the most
smoke for 24 hours before testing. dramatically, sometimes returning abnormal values to
2. The test should be repeated only after a the normal range. Chronic bronchitis improves to a
4-minute wait. lesser degree, and the increase may or may not be
3. The inspiratory volume should be at least significant. Emphysema does not improve postbron-
90% of the previously measured VC or FVC. chodilation because no bronchospasm is involved in
this disease. In some cases, however, both emphysema
4. Two or more tests should be averaged and
and chronic bronchitis are present.
should be within 10% of each other.
The DLCO is decreased in emphysema because of
5. If the subject has a decreased hemoglobin the destruction of alveolar air space. Usually, the DLCO
(Hb) or an elevated carboxyhemoglobin is normal in asthma and chronic bronchitis, although
(COHb), less CO diffuses out of the alveoli it may become reduced in the presence of significant
than if the subject had normal levels. ventilation/perfusion mismatching.
Hemoglobin carries almost all the O2 and CO In restrictive disease, spirometry results show a
that enters the blood from the alveoli. If the decrease in all lung volumes and capacities. The FEV1
hemoglobin is less than normal, less CO than is normal or decreased, but the FEV1% is normal or
normal is able to diffuse into the blood. If increased. Lung volumes reveal a decrease in TLC. There
the COHb is abnormally high, some of the is no response to bronchodilators because no broncho-
hemoglobin already carries CO, so less CO spasm is involved in any of the restrictive lung diseases.
diffuses out of the alveoli into the blood. The DLCO helps in identifying the cause of the
Therefore, corrections should be made in the restrictive lung disease. Diseases caused by chest wall
results to compensate for abnormal Hb and abnormalities (kyphosis, scoliosis, neuromuscular
COHb. Both corrected and uncorrected diseases) have a normal DLCO when adjusted for
values should be reported. reduced lung volume. Parenchymal diseases (fibrosis,
pneumoconiosis, some connective tissue disorders)
have a decreased DLCO.
Table 17-5 summarizes the abnormal laboratory
INTERPRETATION values associated with obstructive and restrictive
diseases. Figure 17-11 shows a flowchart that can be
Several sets of predicted values are available. Comput-
used to interpret a combination of spirometry, lung
erized equipment units have these values installed, and
volume, and DLCO tests. The tests are examined in the
some manufacturers offer a choice of sets to install. In
following order:
general, results are normal if they are between 80%
and 120% of the predicted value for the subject. The 1. FVC (spirometry): FVC, FEV1, FEV1%
predicted values for each measurement are determined 2. Lung volumes: TLC, RV, VC
by the subject’s gender, height, and age. 3. DLCO
TABLE 17-5 Abnormal laboratory values in restrictive and obstructive and lung diseases
Restrictive Obstructive
FVC ⬍ 80% predicted Normal or < 80% predicted
FEV1 Normal or ⬍ 80% predicted ⬍ 80% predicted
FEV1% ⱖ predicted ⬍ predicted
VC ⬍ 80% predicted Normal or ⬍ 80% predicted
TLC ⬍ 80% predicted Normal or ⬎ 80% predicted
RV ⬍ 80% predicted Normal or ⬍ 80% predicted
Postbronchodilation Not significant Significant or not significant
DLCO Normal or < 80% predicted Normal or ⬍ 80% predicted
FVC
N <80% predicted
FEV1 FEV1%
N <80% predicted N <% predicted
NORMAL OBSTRUCTIVE RESTRICTIVE OBSTRUCTIVE

Lung volumes Lung volumes Lung volumes
DLCO DLCO DLCO
Change p BD Change p BD
OBSTRUCTIVE
• Lung volumes: normal, progressing to increased RV and decreased

VC, and then to increased TLC
• DLCO: normal—asthma, chronic bronchitis (unless there is
significant V/Q mismatching)
decreased—emphysema
• pBD (Postbronchodilator) change: significant—asthma, some chronic bronchitis
not significant—emphysema and some
chronic bronchitis
RESTRICTIVE
• Lung volumes: decreased TLC and all other volumes and capacities
• DLCO: normal—chest wall diseases
decreased—parenchymal diseases
FIGURE 17-11 Interpretation of pulmonary function tests.
OTHER SPECIALIZED TESTS Airway Resistance. The airway resistance (Raw) test can
The following tests are used to measure very specific be performed only with body plethysmography.
aspects of lung function and to assess the effect of lung • Place noseclips on the subject and instructed the
disease or other diseases on the subject’s activity level. subject to place the hands on the cheeks to
stabilize them.
Maximum Voluntary Ventilation. The maximum
voluntary ventilation (MVV) is the maximum
amount of air a subject can move into and out of the Best Practice
lungs in 1 minute, measured in liters per minute
(L/min). The patient is instructed to breath deeply and
rapidly for a 12-second interval at an ideal respiratory Maximum Voluntary
rate of 90 breaths per minute. The volume moved in Ventilation
the 12-second interval is then extrapolated for a period 1. To have the patient perform at personal best,
of 1 minute. This test is extremely effort dependent, so give the instruction to pretend that a large
much coaching and encouragement are required. The bag has to be blown up as much as possible.
results are then compared with normal values based
2. This test should be done at least twice; the
on gender, height, and age. This test is particularly
largest MVV should be reported.
valuable for subjects with very mild neuromuscular
disease. These individuals may be able to perform 3. Subjects with airway hyper-reactivity may
spirometry well and achieve normal values. With the achieve lower than expected results owing to
sustained effort required for this test, the subject may bronchospasm induced by hyperventilation.
tire as the test proceeds. The test is also useful as an 4. Results are acceptable if the volume moved
indicator of exercise tolerance in subjects with lung is 35 times the FEV1.
disease.
CASE STUDY 17-4

J. T. is a 39-year-old Caucasian female. She is 62 inches tall and weighs 237 pounds. She is a nonsmoker
who works as a department store salesclerk. Her test results are as follows:
Spirometry
Percentage Percentage Percentage

Predicted Pre-BD Predicted Post-BD Predicted Change
FVC 3.12 L 2.65 L 85 2.89 L 93 9
FEV1 2.65 L 2.03 L 78 2.36 L 89 16
FEV1% 86 77 — 82 — 6
FEF25–75% 186 Lpm 100 Lpm 54 145 Lpm 78 45
Lung Volumes
Predicted Actual Percentage Predicted

VC 3.12 L 2.64 L 85
TLC 4.66 L 4.40 L 94
RV 1.49 L 1.76 L 118
Single-Breath Diffusion
Predicted Actual Percentage Predicted
DLCO 20.9 21.6 103
Questions
1. How would you interpret the spirometry, lung volumes, and DLCO values?
2. Is there a significant response to bronchodilation?
• Seal the door to the plethysmograph. An airway resistance test reports two other
• The subject breathes normally through the parameters:
mouthpiece.
• The subject then pants through the mouthpiece, • Airway conductance (Gaw)—a measure of the
and pressure changes at the mouth and the flow ease with which air passes through the conduct-
through the mouthpiece are measured. ing airways of the pulmonary system—and
• Close the shutter. specific airway conductance (SGaw)
• The subject continues to try to pant against the • Airway resistance (Gaw ⴝ 1/Raw)—the difficulty
closed shutter. with which air passes through the airways.
Airway resistance is calculated by dividing the Airway conductance is the inverse, or the reciprocal,
pressure change at the mouth by the flow measured at of airway resistance. The specific airway conductance
the mouth, using the following formula: (SGaw) is calculated by dividing the airway conduc-
change in pressure ΔP tance by the VTG at which the closed-shutter panting
Raw⫽ _________________ ⫽ ___ was performed. If airway resistance (Raw) is above
flow at the mouth V
mouth normal, the airway conductance (Gaw) is below
Normal values range from 0.6 to 2.4 cm H2O/L/sec. normal.
Specific airway resistance (SRaw) is also calculated by Obstructive diseases such as asthma, chronic
dividing the airway resistance by the VTG, determined bronchitis, emphysema, bronchiectasis, and airway
during the closed-shutter panting (SRaw ⫽ Raw/VTG). hyper-reactivity increase airway resistance (Raw).
Lung Compliance. To test lung compliance (a measure vital capacity when the small airways start to close
of the distensibility of the lung): during a slow exhalation. Closing capacity (CC) is the
volume of air remaining in the lungs when the small
• Insert a catheter with a balloon near its end into
airways start to close (CV ⫹ RV). Results are often
the esophagus. The catheter is attached to a
reported as a ratio between these two results: CV/CC.
pressure transducer to get intrathoracic pressure
readings. • The subject first exhales maximally and then
• With noseclips in place, the subject inhales maximally inhales 100% O2.
maximally to TLC and then holds the breath • Then the subject immediately exhales very
with an open glottis. slowly. As the subject exhales, an in-line nitrogen
• The patient then exhales slowly and, at periodic analyzer monitors the exhaled nitrogen concen-
intervals, holds the breath. tration, and a flow sensor measures volume.
• Record the pressure and volume measurements. • The results are recorded on a graph, with the
nitrogen concentration on the vertical axis and
The pressures required to achieve a change in volume
volume on the horizontal axis. As shown in
are used to calculate static compliance (compliance
Figure 17-12, the tracing is divided into four
measured without airflow):
phases.
ΔV/ΔP ⫽ CL
Phase I is the exhalation of deadspace gas.
Compliance is measured in liters or milliliters per Phase II is a mixture of deadspace gas and
centimeter H2O. Normal lung compliance is 0.2 L/cm alveolar gas.
H2O.
Phase III is all alveolar gas.
Restrictive diseases that affect the lung parenchyma
(e.g., pulmonary fibrosis) reduce lung compliance. Phase IV is the closing volume (CV).
Emphysema typically results in an increase in lung The start of phase IV is when the small airways start to
compliance. close. The distribution of ventilation in the subject’s
lungs is assessed by the slope of phase III, reported as
Single-Breath Nitrogen Gas Distribution Test the change in nitrogen (ΔN2). Subjects with an uneven
(Closing Volume, Single-Breath Nitrogen Washout). distribution of ventilation have a steep phase III, and,
This test is used to assess the distribution of ventilation in severe cases, it may be difficult to determine the
in the subject’s lungs, as well as the closing volume. onset of phase IV. A steep phase III is characteristic of
Closing volume (CV) is the volume remaining in the moderate to severe obstructive lung diseases.
TLC
VC RV
30
IV
% N2
20
III
I
CV
Segment for ΔN2/L
10
30% VC
II CC
0
1.0 2.0 3.0 4.0 5.0 6.0
VE (Lpm)
FIGURE 17-12 Phases of the nitrogen washout gas distribution test.
Cardiopulmonary Stress Testing. In cardiopulmonary output (CO). This increase is accomplished first by an
stress testing (CPX test), subjects go through a series increase in stroke volume (SV, the volume of blood
of increasing exercise levels. During the exercise, the pumped with each ventricular contraction), and then
responses of the pulmonary system, such as minute by an increase in heart rate (HR). The CO can be
volume, CO2 production, and O2 consumption, are increased as much as 6 times the resting CO in a
assessed. The responses of the cardiovascular system, normal fit subject. Figure 17-14 illustrates these cardiac
such as blood pressure, stroke volume, cardiac responses to an increasing exercise workload.
output, and cardiac rate and rhythm, are also If the workload is steadily increased, as it usually
assessed. is in stress testing, oxygen consumption continues to
rise until the maximum oxygen consumption level
Normal Exercise Physiology Exercise increases the (VO2max) is reached. The production of CO2 (VCO2)
metabolic need of the tissues for oxygen. Both the also continues to rise until the body cannot continue
pulmonary system and the cardiovascular system must to metabolize aerobically. When the body switches over
meet this increased demand. Diseases in either of these to anaerobic metabolism, the rate of production of
systems can result in exercise limitation. CO2 increases dramatically owing to the increase in lactic
The pulmonary system increases the amount of acid production, which is buffered by serum bicarbon-
oxygen available at the alveolar-capillary membrane by ate. This point is called the anaerobic threshold (AT).
increasing minute volume (V E). This increase in Figure 17-15 illustrates the determination of the
alveolar ventilation is accomplished mostly by increas- anaerobic threshold.
ing tidal volume and, in more strenuous exercise, by Arterial blood gas measurements during exercise
increasing the respiratory rate (RR) as well. The minute show that the PaO2 remains stable throughout
volume can be increased in a normal fit subject as incremental exercise. The PaCO2 falls slightly until the
much as 20 times the resting minute volume. anaerobic threshold (AT) is reached, and then decreases
Figure 17-13 illustrates these changes as the exercise more rapidly, probably because of the chemoreceptor
workload is increased. response to the increased lactic acid produced in
The cardiovascular system increases the rate of anaerobic metabolism. Figure 17-16 shows these
oxygen delivery to the tissues by increasing the cardiac changes.
3.0 50 RR (bpm) Anaerobic 100

threshold
45 90
2.5
40 80
35 VT 70
2.0
VE (Lpm)
30 Start of 60
exercise
VT (L)
1.5 25 50
20 RR 40
1.0 VE
15 30
10 20
.5
5 10
0
Rest Maximum Work
Work Rate
FIGURE 17-13 Response of the pulmonary system to increasing exercise workloads.
HR
200 HR (bpm)
180 Anaerobic
threshold
160 16
CO 14
140
120 12
Start of
160 exercise
100 10
CO (Lpm)
140 SV
120 80 8
SV (mL/beat)
100
60 6
80
60 40 4
40
20 2
20
0
Rest Maximum Work
Work Rate
FIGURE 17-14 Response of the heart to increasing exercise workloads.
35 35
·
VCO2
30 30
·
25 VO2 25
VCO2 (mL/min/kg)
VO2 (mL/min/kg)
20 Anaerobic 20
threshold
15 Start of 15
exercise
10 10
5 5
0 0
Rest Maximum Work
Work Rate
FIGURE 17-15 Oxygen consumption and carbon dioxide production in increasing exercise
workload.
110
100
Gas Tension (mm Hg) PaO 2
90
50
40
PaCO2
30
Moderate Severe
Rest exercise exercise
0
1.0 2.0 3.0 4.0
Oxygen Consumption (Lpm)
FIGURE 17-16 Changes in arterial blood gases in response to increasing exercise

workloads.
Indications Cardiopulmonary stress testing is indicated During the test, a number of parameters are
for: monitored.
• Evaluating unexplained dyspnea upon exertion • A pneumotachometer (an electronic device used
to determine whether the cause is a problem in to measure flow) is used to measure minute
the pulmonary or cardiovascular system. volume, respiratory rate, and tidal volume.
• Monitoring the effect of previously diagnosed • A pulse oximeter is used to monitor oxygen
pulmonary, cardiovascular, or neuromuscular saturation (SPO2).
disease on exercise tolerance. • Oxygen and carbon dioxide analyzers are used
• Determining the magnitude of hypoxemia for to monitor exhaled oxygen and carbon dioxide
oxygen prescription. concentrations, respectively. Arterial blood gases
• Evaluating fitness or the patient’s progress in a should be performed before exercise to establish
rehabilitation program. the correlation between the SaO2 and the SPO2
and may be repeated during and after testing.
Contraindications There are a number of absolute • In addition, an electrocardiogram (ECG) is run
and relative contraindications to cardiopulmonary continuously to monitor heart rate and rhythm.
stress testing, mainly severe or potentially life- • Blood pressure is taken periodically.
threatening cardiovascular conditions. For a more
The following are some of the data collected and
detailed discussion of contraindications and hazards,
calculated during and after the test:
see the AARC clinical practice guideline for exercise
testing.6 • V⭈ O (maximum oxygen consumption) is
2max
expressed as liters per minute (L/min) or in units
Testing Procedure The exercise used can be steady called metabolic equivalents of energy expenditure
state (the same workload throughout the test) or (METs). One MET is the subject’s V⭈ O2 at rest,
incremental (increased workload at fixed intervals which is normally 3.5 mL/kg/min.
throughout the test). Incremental exercise is the more • V⭈ max (maximum minute volume) is usually
common. Either a treadmill or a cycle ergometer compared with the MVV acquired in another
(exercise bicycle) can be used. The patient continues test and is expressed as V⭈ max/MVV.
to exercise until he or she is unable to continue. • HRmax (maximal heart rate)
TABLE 17-6 Patterns of abnormalities at maximal exercise level in cardiopulmonary

stress testing
Pulmonary Disease* Cardiovascular Disease* Deconditioned*
V⭈ O2max ↓ ↓ ↓
⭈ ↑ ↓ ↓
V Emax
SpO2 Often ↓ N N
AT Not achieved ⭈
Achieved at low V O2
⭈
Achieved at low V O2
HRmax ↓ ↑ ↑
ECG rhythm N Dysrhythmias N
*↓, less than predicted; ↑, greater than predicted; N, normal.
• PaO2 and/or SPO2 (arterial partial pressure of Follow-up testing is also indicated to check for changes
oxygen and/or Hb saturation with O2 measured in the hyper-reactivity or its severity. The AARC clinical
by pulse oximeter) practice guideline for bronchial provocation covers
• ECG (heart rate and rhythm) contraindications, hazards, and limitations.7
• AT (anaerobic threshold) is the workload at The most common inhaled agents used for
which the subject changes from aerobic metabo- bronchoprovocation are methacholine (a cholinergic
lism to anaerobic metabolism. This is indicated agent) and histamine. Hyperventilation using cold air
by a sharp increase in CO2 production (V⭈ CO2). or room air may also be used. For suspected exercise-
induced bronchospasm (EIB), testing is done after
Interpretation Abnormal results can be due to three exercise.
causes: pulmonary disease, cardiovascular disease, and Before any bronchoprovocation test, all bronchodi-
deconditioning or unfitness. Table 17-6 summarizes lators should be withheld.
the results associated with each of these causes.
• Beta-adrenergics and anticholinergics should be
• Subjects with pulmonary disease are ventilation withheld for 8 hours.
limited in exercise. They may not achieve the • Sustained-action theophylline, cromolyn
anaerobic threshold, and their maximal minute sodium, necromodil sodium, and leukotriene
volume (V⭈ Emax) is greater than 70% of their MVV. inhibitors should be withheld for 48 hours.
The ECG is normal, and their maximal heart rate • Caffeine, smoke, and smoking should be
is less than 85% of the predicted rate. avoided for 6 hours before testing.
• Subjects with cardiovascular disease are circulation • Inhaled or oral steroids may be continued.
limited in exercise. Their heart rate is greater Table 17-7 summarizes the schedule for withholding
than 85% of the predicted rate, and the ECG medications.
may show dysrhythmias, or S-T segment
changes, or both. Their anaerobic threshold is
reached sooner than predicted, and their maxi-
mal minute volume is typically less than 50% of TABLE 17-7 Prebronchoprovocation
their MVV. withholding schedule for
• A deconditioned subject has the same abnormal bronchodilating agents
results as a subject with mild cardiovascular
Agent Hold Time (hours)
disease.
Beta-adrenergics 8
Bronchoprovocation. The purpose of a broncho- Anticholinergics 8
provocation test is to detect the presence of airway Sustained-action theophylline 48
hyper-reactivity. It is indicated: Cromolyn sodium 48
• When a subject has the symptoms of broncho- Necromodil sodium 48
spasm but normal pulmonary function tests. Leukotriene inhibitors 48
• When there is occupational risk.
Caffeine 6
• As a baseline study before occupational
exposure. Smoke and smoking 6
Methacholine and Histamine Procedure. The proce- • Severe bronchospasm may require the adminis-
dure is as follows: tration of a bronchodilator, with documentation
of reversal done with spirometry.
• Prebronchoprovocation spirometry is done. The
FEV1 should be ⬎ 60–70% of the predicted
CO2 Response Curve. The purpose of this test is to
value.
evaluate the subject’s response to increased levels of
• The subject is given nebulized normal saline,
CO2 while PaO2 is maintained within normal limits.
and the spirometry is repeated. If there is a 10%
The results are reported in liters per minute per
reduction in the FEV1, the test is positive for
millimeter mercury (L/min/mm Hg).
airway hyper-reactivity. No further testing should
Two methods can be used. One uses an open
be done. Continue if the reduction is equal to or
circuit and the other, a closed circuit.
greater than 10%.
• At fixed intervals, increasing doses of methacho- • In the open-circuit method, the subject breathes
line or histamine are given by nebulizer. A varying percentages of CO2 (usually 1–7%).
number of protocols for the dosing are widely For each percentage, the end-tidal CO2 (PetCO2),
available. Spirometry is done at 30–90 seconds the minute volume (V⭈ E), and the O2 saturation
after each dose, and the test procedure and (SPO2) are monitored and recorded.
results must meet the current ATS acceptability • In the closed-circuit method, a gas mixture
guidelines. A 20% decrease in FEV1 is considered containing 7% CO2 is placed in a reservoir.
a positive test for airway hyper-reactivity, and at The subject rebreathes from this reservoir. An
that time the testing is stopped. The dose after in-line analyzer measures PetCO2, a pneumota-
which this decrease occurs is the PD20 (the chometer measures V⭈ E, and a pulse oximeter
provocation dose resulting in a 20% or greater monitors SPO2. The FIO2 is maintained at 0.21
decrease in FEV1). by adding O2, as an oxygen analyzer indicates
• A bronchodilator is administered to reverse the the need. The subject continues to rebreathe
bronchospasm. The reversal is documented by a from the reservoir until the PetCO2 is higher
return to prebronchoprovocation values. than 9%, or for 4 minutes, whichever
occurs first.
Hyperventilation Procedure. The procedure is as
The results are recorded on a graph, plotting
follows:
minute volume on the vertical axis and PetCO2 on the
• Prebronchoprovocation spirometry is per- horizontal axis. The response to increased concentra-
formed. The FEV1 should be either ⬎80% tions of CO2 is linear, as shown in Figure 17-17. The
of the predicted value or ⬎80% of the highest normal increase in V⭈ E is 3 L/min/mm Hg, with a range
previous value for that subject to continue the of 1–6 L/min/mm Hg. Some subjects with obstructive
testing. disease have a reduced response to increases in CO2
• The subject hyperventilates either room air concentrations; others do not.
or cold air (21–22°C or 69.8–71.6°F ) for
4–6 minutes.
• Spirometry is then performed at fixed intervals
of up to 20 minutes. Again, the results must
be reproducible (per ATS acceptability guide-
lines). If the FEV1 is reduced by 20% in that
time, the test is positive for airway hyper-
reactivity.
VE (Lpm)
30
Exercise Challenge. The procedure is as follows:
• On a treadmill or ergometer, the subject exer- 20
cises to 60–80% of the predicted heart rate for
6–8 minutes. The ECG and blood pressure are 10

monitored during the exercise period.
• After exercise, spirometry is done 1–2 minutes
40 45 50 55 60
postexercise and then every 5 minutes. In a
positive test, the FEV1 decreases by 10–20% PCO2 mm Hg
(usually in 5–10 minutes) and then returns to FIGURE 17-17 Normal response to the inhalation of
baseline (usually in 20–40 minutes). increasing partial pressure of carbon dioxide.
Spirometers Voltage
Piston
outputs
There are two types of spirometer: volume displace-
ment and flow-sensing.
VOLUME DISPLACEMENT DEVICES
Gas flow
Volume displacement devices measure volumes directly
through changes in volume inside the device. The Potentiometer
volume displacement is recorded on graph paper;
either a pen is moving over the paper at a set speed, or
Dry rolling seal
the paper moves under the pen at a set speed. Flows
and volumes can be measured from the volume-time FIGURE 17-19 A rolling dry seal spirometer.
curve. There are three types of volume displacement
devices: water seal spirometers, rolling dry seal
spirometers, and bellows spirometers.
Pen
Water Seal Spirometers. In these devices, water Bellows Graph
provides a leakproof seal to record changes in volume
in the bell. A pen attached to the bell records changes Gas
in volume on a recorder that is moving at a set speed, flow
producing a volume-time curve. This type of spirometer
FIGURE 17-20 A bellows spirometer.
is shown in Figure 17-18.
Rolling Dry Seal Spirometers. In these devices, a

flexible dry seal provides an airtight seal around a Bellows Spirometers. As the subject exhales into the
piston. A potentiometer senses the movement of the opening of the bellows, the added gases are recorded
piston and electronically records the movement of by a pen, which records the change in volume either on
the piston as the subject exhales into it. The electronic graph paper moving at a set speed or by moving at a set
signals received are converted to a flow-volume loop speed across stationary graph paper. A volume-time
and to numerical measurements of flow and volume. curve is recorded, from which measurements are made.
Figure 17-19 illustrates this type of device. Figure 17-20 shows a bellows spirometer.
Recording FLOW-SENSING DEVICES

System Flow-sensing devices measure flows electronically and
then convert the measurements to volumes. Flow-
Spirometer
sensing devices are also called pneumotachometers,
Bell
which are electronic devices that measure flows. For
volume measurements, the computer converts the flow
measurements over time to volume measurements.
Flow-sensing devices have largely replaced volume-
Water Seal displacement devices in modern computerized pulmo-
nary function equipment. It is beyond the scope of this
chapter to discuss each of the several types of pneumo-
tachometer in detail.
Thermometer CO2 • Differential pressure pneumotachometers
Absorber (Figure 17-21) measure flow by the change in
pressure that occurs as gases pass through a
resistive device with a known resistance.
• Thermal pneumotachometers (Figure 17-22)
Subject Breathing measure flow through the change in temperature

Connection of a heated element as the gases pass over it.
• The ultrasonic pneumotachometer
Gas Inlet
(Figure 17-23) uses the disturbance of
(O2, HeO2)
ultrasonic waves as the gases pass through
FIGURE 17-18 A water seal spirometer. them to measure flow.
Flow Resistive
Element
Body Plethysmograph
Heated Flow Although it is used to perform spirometry, MVV, and
Sensor other tests, the body plethysmograph was developed
to make two measurements: VTG and Raw (discussed
earlier in the pages 466 and 469). There are five basic
components in a body plethysmograph (Figure 17-9).
Flow Flow
P1 P2 • A booth that can be sealed airtight is needed
• A differential pressure pneumotachometer to
measure flows
• A pressure transducer to measure pressure
changes at the mouth
P1 > P2 • A shutter to stop airflow at the mouth
• Either a pressure transducer in the plethysmo-
graph or a pneumotachometer in the wall of the
P1 P2 booth to measure changes in pressure or in the
Differential pressure volume of air in the booth that occur as a result
DC analog
transducer of the subject’s expanding the thorax in an
output signal
attempt to pant against the closed shutter.
FIGURE 17-21 A differential pressure pneumotachometer. Calibration

Calibration is the testing and adjusting of equipment
to make measurements more accurate. Calibration is
Heated
element
usually done using a special calibrated 3-L syringe
made for this purpose. The manufacturer prescribes the
procedure and frequency of calibration. Computerized
spirometers self-adjust after the calibration test using a
correction factor.
Calibration should be performed at least once on
any day the equipment is used. If the equipment is
moved, it should be calibrated at each site. If a large
number of tests are being performed, calibration

should be done every 4 hours.
Check volume displacement devices daily for leaks
Electrical before the calibration is performed. Leaks can be
output signal detected by applying a weight or constant pressure
FIGURE 17-22 A thermal pneumotachometer. against the spirometer when it is full. If no change
in volume is recorded over a period of time, there is
no leak.
Body plethysmographs have automatic calibration
systems. Follow the manufacturer’s calibration
Receiving crystal procedure.
Quality Assurance
Quality assurance is the periodic testing of equipment
for accuracy beyond the regular calibration of the
equipment. Volume measurements are checked daily in

the calibration procedure. In addition, on a quarterly
basis:
Sending crystal
• Volume devices should be checked with a wide
variety of volumes.
• Flow-sensing devices should be checked with a
FIGURE 17-23 A ultrasonic pneumotachometer. wide variety of flows.
• Flow-measuring accuracy should also be checked No matter what the age of the subjects, the criteria
quarterly. This check is not needed with flow-sensing for judging whether they can be tested are:
devices because, if the unit is measuring volumes
• Whether they can understand the instructions.
accurately, the flow measurements are accurate.
• Whether they are able to perform the required
• Volume displacement devices should be checked
maneuvers.
with accurate flow-generating devices over a
range of flows.
• Check the recorder of volume displacement
devices. The recorder is started, and volume Summary
changes are introduced at fixed intervals that are In pulmonary function testing, spirometry or forced
timed with a stopwatch. The tracing is then vital capacity measurements are used to find out
checked to ensure that the recorder matches the whether the subject’s lung function is normal or
actual time interval. abnormal. Abnormal findings indicate a need for
The American Thoracic Society has defined accept- further testing to assess the type and degree of lung
able degrees of error in spirometers. In general, for impairment. Such tests include lung volumes, diffusing
diagnostic spirometers, accuracy must be within ⫾3% capacity, postbronchodilator spirometry, maximum
or ⫾50 mL, whichever is larger.2 voluntary ventilation, airway resistance, lung compli-
Quality assurance can also be interpreted to mean ance, the nitrogen washout gas distribution test, and
that all tests are performed correctly by the subject and the CO2 response curve. Specialized test regimens, such
that the results reported are valid. This type of quality as cardiopulmonary stress testing and bronchoprovoca-
assurance requires technologists who are well trained tion, help assess the severity of lung disorders.
not only in giving the subject instructions but also in Equipment should be calibrated on a regular
judging whether the subject has followed them. The basis according to manufacturers’ recommendations.
technologist must also be well versed in the recom- Spirometers should have quality assurance assessments
mendations for reporting results. quarterly to ensure their accuracy. Infection control is
easy to achieve by the use of disposable mouthpieces
and noseclips and the sterilization of nondisposable
items after each use. Handwashing is, of course, impor-
Infection Control tant after handling equipment and between subjects.
There is very little risk of cross-contamination among
subjects or to technologists if certain commonsense
precautions are taken. Transmission among subjects Study Questions
can be prevented by:
REVIEW QUESTIONS
• The use of disposable mouthpieces and noseclips.
1. What are the indications for spirometry?
• The cleaning of nondisposable noseclips
between uses. 2. When are postbronchodilator studies indicated?
• The disinfection or sterilization of nondispos- 3. How would you instruct a subject to do a forced
able mouthpieces. vital capacity maneuver?
• Good handwashing techniques between patients 4. How are spirometry results interpreted?
and after handling contaminated equipment.
5. In the results of cardiopulmonary stress tests, what
• Following the manufacturer’s recommended
are the patterns of abnormal values for cardiovas-
method and frequency for cleaning other parts
cular disease, pulmonary disorders, and decondi-
of the equipment.
tioned subjects?
6. What are the indications for the following addi-
tional tests after spirometry: postbronchodilator
Age-Related Considerations MVV, diffusing capacity, lung volumes, compliance,
airway resistance, single-breath nitrogen washout,
The tests discussed in this chapter can be performed for
and bronchoprovocation?
adults, young children, and adolescents. For young
children and for adolescents, there are different 7. What are the indications for cardiopulmonary
regression equations and nomograms, and these stress testing?
should be used to arrive at an accurate assessment. 8. How are the following tests performed: lung
(Pulmonary function testing performed on infants volumes, diffusing capacity, single-breath nitrogen
requires special equipment and special techniques, washout, MVV, airway resistance, compliance, and
which are beyond the scope of this chapter.) the CO2 response curve?
9. What are typical results of the following tests in 7. In a single-breath nitrogen gas distribution test, the
obstructive and restrictive diseases: lung volumes, subject inhales a full vital capacity of 100% oxygen
diffusing capacity, single-breath nitrogen washout, and is to maintain a breath-hold for:
MVV, airway resistance, compliance, and the CO2 a. 0 seconds.
response curve? b. 4–8 seconds.
10. How are spirometers calibrated and how often? c. 5–10 seconds.
d. 9–11 seconds.
11. What quality-assurance tests should be performed
quarterly on spirometers? 8. When exhaled gas in a diffusing capacity test is being
collected, the first 750 mL is discarded because:
12. How is infection control achieved in using pulmo-
a. the subject is not exhaling as fast as possible at
nary function equipment?
that time.
b. these gases occupied alveolar deadspace.
c. that volume was not involved in gas exchange.
MULTIPLE-CHOICE QUESTIONS d. that volume is mostly helium.
1. The amount of air a subject can forcefully exhale 9. In an airway resistance test, the subject first pants
after a maximal inhalation is the: with the shutter open, and then with the shutter
a. ERV. closed. The closed-shutter panting segment is used
b. FRC. to determine:
c. FVC. a. airway resistance.
d. RV. b. compliance.
2. The amount of air remaining in the lungs after a c. FRC.
maximal exhalation is the: d. VTG.
a. ERV. 10. Which of the following is the formula for calculat-
b. FRC. ing lung compliance?
c. VC. a. ΔP/V
d. RV. b. V/ΔP
3. If a subject can still inhale air through the nose c. ΔV/ΔP
with the noseclip on while performing an FVC d. ΔP/ΔV
maneuver, the measured volumes will: 11. On the graph produced in a single-breath nitrogen
a. be less than actual. gas distribution (or closing volume) test, phase III
b. be more than actual. is analyzing:
c. be measured correctly. a. deadspace gas.
d. not be measurable. b. a mixture of alveolar and deadspace gas.
4. The ATS recommends which of the following c. alveolar gas.
criteria for choosing the best FVC maneuver? d. closing volume.
a. the one with the largest FVC 12. In incremental exercise (the workload is increased
b. the one with the largest FEV1 at specific intervals), the shift to anaerobic metabo-
c. the one with the highest peak flow lism is indicated by:
d. the one with the largest sum of the FVC and a. a marked reduction in O2 consumption.
the FEV1 b. a marked increase in minute volume.
5. A sudden increase in the nitrogen concentration c. a marked increase in CO2 production.
of exhaled air during a nitrogen washout test d. a marked drop in PaO2.
indicates: 13. Which of the following is a cholinergic agent used
a. air trapping. in bronchoprovocation testing?
b. therapist error. a. acetylcholine
c. a leak in the system. b. histamine
d. patient fatigue. c. methacholine
6. The results of a nitrogen washout, a helium d. atrovent
dilution, and a body plethysmograph are the same 14. Which of the following is considered to be a
in subjects with: positive methacholine challenge test result?
a. emphysema. a. a 10% reduction in FEV1
b. pulmonary fibrosis. b. a 20% reduction in FEV1
c. chronic bronchitis. c. a 20% reduction in FEF25–75%
d. cystic fibrosis. d. a 20% reduction in FEV1%
15. If pulmonary function equipment is being moved bronchodilator therapy at point of care. Respir Care.
to several different sites in one day, the equipment 1995;40:1300–1307.
should be calibrated: 4. American Association for Respiratory Care. AARC
a. before testing is started. clinical practice guideline: Body plethysmography:
b. every 4 hours. 2001 revision & update. Respir Care. 2001;46:
c. after arrival at each site. 506–513.
d. daily. 5. American Association for Respiratory Care. AARC
clinical practice guideline: Single-breath carbon
CRITICAL-THINKING QUESTIONS monoxide diffusing capacity, 1999 update. Respir
Care. 1999;44:91–97.
1. Maximal subject effort in a forced vital capacity 6. American Association for Respiratory Care. AARC
(FVC) maneuver is necessary for the results to be clinical practice guideline: Exercise testing for
valid. How can a therapist tell whether the subject evaluation of hypoxemia and/or desaturation:
has made a maximal effort? 2001 revision & update. Respir Care. 2001;46:
2. If a subject who has obstructive lung disease has a 514–522.
larger slow vital capacity than forced vital capacity, 7. American Association for Respiratory Care. AARC
can the test results be valid? clinical practice guideline: Methacholine challenge
3. A subject with obstructive lung disease has been testing: 2001 revision & update. Respir Care.
in a pulmonary rehabilitation program for several 2001;46:523–530.
months. Should pulmonary function tests or
cardiopulmonary stress testing be used to assess Suggested Readings
the subject’s progress? Explain your answer.
American Association for Respiratory Care. AARC
4. A subject who has moderate obstructive lung
clinical practice guideline: Static lung volumes: 2001
disease is doing the nitrogen washout test to
revision & update. Respir Care. 2001;46:531–539.
determine FRC. The subject has been doing the
Chang DW. Respiratory Care Calculations. 2nd ed.
washout for 12 minutes, and the exhaled nitrogen
Clifton Park, NY: Delmar Cengage Learning; 1999.
concentration is still 9%. There is no evidence of a
Des Jardins T. Cardiopulmonary Anatomy and Physiology.
leak in the system. Should the test be continued or
5th ed. Clifton Park, NY: Delmar Cengage
terminated? Explain your answer.
Learning; 2007.
Madama, VC. Pulmonary Function Testing and Cardiopul-
monary Stress Testing. 2nd ed. Clifton Park, NY:
References Delmar Cengage Learning; 1998.
1. American Association for Respiratory Care. AARC Ruppel GL. Manual of Pulmonary Function Testing.
clinical practice guideline: Spirometry, 1996 9th ed. St. Louis: Mosby; 2009.
update. Respir Care. 1996;41:629–636. Wanger J. Pulmonary Function Testing. Philadelphia:
2. American Thoracic Society/European Respiratory Williams & Wilkins; 1996.
Society Task Force. Standardization of spirometry. White GC. Equipment Theory for Respiratory Care. 4th ed.
Eur Respir J. 2005;26:319–338. Clifton Park, NY: Delmar Cengage Learning; 2005.
3. American Association for Respiratory Care. AARC Wilkins RL, Dexter JR, Heuer A. Clinical Assessment in
clinical practice guideline: Assessing response to Respiratory Care. 6th ed. St. Louis: Mosby; 2010.
CHAPTER 18
Polysomnography and Other Tests

for Sleep Disorders
Robert A. Whitman
OBJECTIVES
• List the four stages of sleep and describe the cycling of sleep stages that characterizes normal sleep
architecture.
• Discuss the EEG, EOG, and EMG criteria used to identify each sleep stage.
• Identify the cardiovascular and respiratory changes associated with each stage of sleep.
• Identify and discuss the four most common sleep disorders.
• Describe the electrode configuration used to monitor EEG activity during sleep.
• Describe the various technologies available to monitor breathing during sleep to include monitoring of
airflow, respiratory effort, and arterial oxygen saturation.
• Discuss the technical and procedural aspects of performing polysomnography.
• Identify the scoring criteria for staging sleep, quantifying respiratory events, and quantifying limb
movements.
• Explain the concept of CPAP and bilevel PAP therapy and describe the general protocols for titrating each.
• List the two tests used to assess daytime sleepiness and explain the rational for their use.
CHAPTER OUTLINE
Normal Sleep The Polysomnogram
Sleep Types and Stages EEG, EOG, and EMG
Sleep Architecture Respiratory Airflow and Effort
Cardiovascular and Respiratory Changes Arterial Oxygen Saturation
Sleep Disorders Electrocardiogram
Insomnia The Polysomnographic Recording
Sleep Disordered Breathing Sensitivity
Narcolepsy Frequency Filters
Restless Legs Syndrome Calibration
(continues)
482
CHAPTER 18 ■ Polysomnography and Other Tests for Sleep Disorders 483
(continued)
Recording and Monitoring During the Night Nasal Continuous Positive Pressure Therapy
Patient Calibration CPAP Titration
Recording Procedures CPAP Titration Protocol
Staging Sleep Bilevel Positive Airway Pressure
Identifying Arousals Split-Night Polysomnography
Quantifying Respiratory Events Autotitrating CPAP
Quantifying Leg Movements Measuring Daytime Sleepiness
KEY TERMS
apnea hypnagogic polysomnography (PSG)
apnea/hypopnea index (AHI) hypnogogic rapid eye movement (REM)
artifact hypopnea REM latency
autotitrating CPAP inductance plethysmography respiratory disturbance
bilevel positive airway pressure low-frequency filter index (RDI)
cataplexy mixed apnea restless legs syndrome (RLS)
central apnea nonrapid eye movement scoring
central sleep apnea (NREM) sleep apnea
continuous positive airway obstructive apnea sleep architecture
pressure (CPAP) obstructive sleep apnea (OSA) sleep deprivation
electroencephalogram (EEG) obstructive sleep disordered sleep disordered breathing
electromyogram (EMG) breathing (OSDB) (SDB)
electrooculogram (EOG) patient calibration sleep fragmentation
epoch periodic limb movements sleep histogram
excessive daytime in sleep (PLMS) sleep latency
sleepiness (EDS) polygraph sleep paralysis
high-frequency filter polysomnogram slow-wave sleep
P
olysomnography is the primary diagnostic and to the most common sleep disorders, as well as to
tool used by sleep specialists to characterize provide a basic review of polysomnography application
abnormal physiological patterns associated and interpretation and the related tests.
with sleep disorders. Frequently referred to as
a sleep study, polysomnography (PSG) is the monitor-
ing and recording of physiological patterns during Normal Sleep
sleep; it is used in the clinical setting for the diagnosis Researchers began to study patients with sleep com-
of sleep disorders. plaints in the 1960s. Their work subsequently evolved
Sleep disorders and the technology used to diag- into an organized methodology for the study of sleep
nose them are specialized and complex. To become called polysomnography. In an effort to standardize
fully proficient, respiratory technologists need on-the- sleep staging, in 1968 Rechtshaffen and Kales devel-
job training, usually teamed with an experienced oped a manual for scoring normal adult sleep (com-
therapist, as well as extensive education in data collec- monly referred to as the R&K manual).1 The rules
tion and interpretation. (Contact the Association of described in the manual have been used to characterize
Polysomnographic Technologists and the Association sleep patterns in adults for nearly 40 years. The scoring
of Sleep Technologists for credentialing requirements.) rules were based on normal values from young adults
The purpose of this chapter is to introduce respira- and did not accurately cover sleep criteria for children
tory technologists to the characteristics of normal sleep and older adults. Adjustments have been since made to
the rules to cover these patient populations in clinical

practice.
In March 2007, the American Academy of Sleep
Medicine (AASM) introduced a new manual for
scoring sleep that incorporated recommended guide-
Alpha Theta
lines for scoring sleep and other parameters com-
8–13 cps Delta 4–7 cps
monly monitored during polysomnography.2 These
guidelines are based on current scientific evidence and <4 cps
expertise in the advancing field of sleep medicine.
Because the R&K sleep stage scoring rules have been
used for many years and permeate the scientific
literature, the therapist must be able to make the
appropriate mental adjustments when reading prior
literature. In this chapter, the rules for scoring sleep are
based on the new AASM scoring guidelines. Significant
differences between the current rules and the R&K Spindle
rules are noted. 12–16 cps (beta)
Distinct patterns of brain activity are associated K-complex
with wakefulness and sleep. The characteristic patterns >0.5 cps
observed during normal sleep can be divided into
FIGURE 18-1 Examples of common waveforms found on
distinct stages, and the typical distribution of these
the electroencephalogram (EEG) that are the basis for
stages throughout the night is termed “sleep architec- sleep staging: The values below each waveform represent
ture.” In addition, characteristic cardiovascular and the range of frequencies in cycles per second (cps) that
respiratory changes are associated with sleep. define each type.
SLEEP TYPES AND STAGES

stages of NREM sleep are labeled N1, N2, and N3, with
Sleep is typically divided into two distinct types:
N designating REM sleep.
nonrapid eye movement (NREM) and rapid eye
movement (REM). As the names suggest, REM sleep is • During resting wakefulness in the adult with eyes
characterized by the occurrence of phasic rapid eye closed, the EEG is characterized by a dominant
movements, which are absent in NREM sleep. Both rhythm in the frequency range of 8 to 13 Hz, or
respiratory and cardiac rhythms are regular during alpha activity.
NREM sleep but fluctuate significantly during REM • With the transition to sleep, the rhythm changes
sleep. to a mixed low-amplitude frequency (4- to 7-Hz
NREM sleep is divided into three stages based on theta activity), termed Stage N1 sleep, the first
combined elements of: stage encountered, and is generally short in
duration. Sharp vertex waves (sharply contoured
• Electroencephalogram (EEG) patterns.
waves with duration ⬍0.5 seconds) may be seen.
• Eye movements, or the electrooculogram
The EOG shows slow, rolling eye movements.
(EOG).
• Stage N2 sleep is characterized by the same
• Muscle activity from electromyogram (EMG)
low-voltage, mixed-frequency activity seen in
recordings, typically, the chin muscles
Stage 1; in this stage, however, sleep spindles or
(submental EMG).
K-complexes or both appear. Eye movements are
Electroencephalographic activity is generally generally absent.
described by the frequency of the measured activity in • Stage N3 is defined by the presence of delta
cycles per second (cps). Frequencies are designated waves comprising at least 20% of the record and
alpha, beta, delta, and theta (Figure 18-1). In addition often is referred to as slow-wave sleep, or delta
to these signals, sleep spindles and K-complexes are sleep. Eye movements are absent. Slow-wave
also used to define sleep stages. Sleep spindles are sleep is the deepest sleep; in this stage, arousing
waxing and waning bursts of 11- to 16-Hz (beta) an individual is much more difficult than in
activity lasting 0.5 or more seconds. K-complexes are the other stages of sleep. In the R&K manual,
characterized by a well-delineated negative sharp wave slow-wave sleep comprised Stages 3 and 4 sleep,
immediately followed by a positive component with a in which Stage 4 sleep was defined as slow-wave
duration equal to or greater than 0.5 seconds. The activity accounting for 50% or more of the time.
• In Stage REM sleep, the EEG pattern is similar to occurs. The time between the initial sleep onset and the
Stage N1 sleep: a relatively low-voltage, mixed- first REM period is the REM latency. These two
frequency pattern. Unique to REM sleep, how- latencies are typically used to describe abnormal
ever, are phasic periods of rapid eye movements. alterations in sleep architecture.
Alpha activity may also be seen. Also characteris- The microstructure of sleep changes significantly
tic of REM sleep is a low level of muscle tone over the human lifespan (Figure 18-3). In general,
compared with other sleep stages, seen as these changes are:
decreased amplitude of the chin EMG. In the
• An increase in sleep latency with age.
REM stage of sleep, most dreaming occurs, and
• The percentage of Stage N1 increases with age.
the loss of muscle tone protects against acting
• The percentage of Stage N3 decreases with age.
out the dreams.
• The percentage of REM sleep decreases with age
in adults.
SLEEP ARCHITECTURE Slow-wave sleep shows the greatest decrease over the
lifespan, making up 40% of the total sleep time in early
The distinct cycling of sleep stages throughout the childhood and decreasing steadily until old age. There
night is referred to as the sleep architecture. The is also a significant and steady increase in wake after
cycle begins with NREM sleep, progressing from sleep onset (WASO) over the lifespan.
Stage N1 through Stages N2 and N3 and followed by
a REM sleep period. The duration of this cycle is
approximately 90 minutes. The time from sleep CARDIOVASCULAR AND RESPIRATORY CHANGES
onset to the end of the first REM period is the first
In normal individuals, measurable changes occur in
sleep cycle. The second and subsequent sleep cycles
both respiratory and cardiovascular variables with
are the sleep periods between the end of a preceding
sleep. Respiratory changes are as follows:
REM period and the end of the next REM period,
including the intervening NREM sleep, which is • During NREM sleep and when compared with
usually devoid of Stage N1 sleep. An individual wakefulness, minute ventilation falls by approxi-
typically has four to six sleep cycles during a normal mately 0.5–1.5 L/min, primarily owing to a
night’s sleep. reduction in tidal volume.
Brief awakenings generally occur during the night, • Respiratory rate typically increases.
although the individual is usually unaware of them • Both tidal volume and respiratory rate become
unless they are of sufficient duration. Figure 18-2 stable and rhythmic in slow-wave sleep.
shows the typical normal progression of sleep stages, • During REM sleep, the respiratory pattern varies,
known as a sleep histogram, or hypnogram. with most of the variation occurring during
The time it takes for a sleep stage to first occur is phasic REM when bursts of actual rapid eye
termed the “latency” for that stage. Of interest are the movements are seen.
sleep onset latency and the latency to the first REM • Upper airway resistance increases during sleep as
period. The sleep onset latency, or sleep latency, is the a result of hypotonia of the upper airway muscles
time it takes from going to bed until Stage N1 sleep that normally dilate the airway. During NREM
sleep, there is hypotonia of the intercostal
muscles with essentially normal function of the
diaphragm.
Awake
• In contrast, REM sleep is characterized by atonia
REM of the intercostal muscles and hypotonia of the
Stage 1 diaphragm. The reduced respiratory muscle
activity with sleep results in a decreased func-
Stage 2
tional residual capacity.
Stage 3 Cardiovascular changes during sleep can
Stage 4 be observed as changes in blood pressure and

0 1 2 3 4 5 6 7 8 heart rate.
Hours of Sleep
• Blood pressure falls by 5–14% during NREM
sleep and fluctuates during REM sleep.
= REM sleep • Heart rate decreases during NREM sleep and
FIGURE 18-2 Hypnogram depicting the normal progression remains stable. However, heart rate can be quite
of sleep stages through the night for a normal adult: The variable in REM sleep and periods of bradycardia
solid bars represent the occurrence of REM sleep. may be seen.
Image not available due to copyright restrictions
Sleep Disorders other factors. It is estimated that chronic insomnia

affects 9–12% of the population. The causes of insom-
When sleep is not of sufficient duration (sleep depri- nia are many and range from psychological to medical,
vation) or when sleep is disturbed by frequent arousals and in some cases the condition is of a primary
(sleep fragmentation), an individual usually com- etiology.
plains of excessive daytime sleepiness (EDS), or Insomnia is defined as difficulty initiating or
hypersomnolence. Most normal individuals experience maintaining sleep. It can take the form of difficulty
occasional EDS; chronic EDS, however, may indicate a initiating sleep after going to bed, difficulty going back
pathologic abnormality. A complaint of EDS must be to sleep after an awakening, waking up frequently
taken seriously because the condition can markedly during the night, or waking up early in the morning
affect psychosocial function, school performance, and and being unable to go back to sleep for the rest of the
work performance, and it can endanger the individual’s night. Many of the more than 84 known sleep disor-
and the public’s safety. ders have insomnia as a symptom; in fact, insomnia is
There are over 84 known sleep disorders. The four as much a symptom as it is a diagnosis. Patients with
most frequently encountered ones are insomnia, sleep insomnia frequently report EDS.
disordered breathing, narcolepsy, and restless legs
syndrome. For a more in-depth discussion of known
sleep disorders, see the International Classification of
Sleep Disorders.3 SLEEP DISORDERED BREATHING
Sleep disordered breathing (SDB), or sleep apnea
or hyponea syndrome, is by far the most common
INSOMNIA diagnosis in patients presenting to a sleep disorders
Insomnia is the most prevalent sleep-related com- clinic. Sleep disordered breathing is categorized as
plaint. Insomnia can be situational, lasting a few days either central or obstructive, depending on the physi-
to weeks, or chronic, lasting more than a month. ological mechanism involved. Central sleep apnea
Almost everyone occasionally suffers from short-term results from a transient failure of the central respiratory
insomnia resulting from stress, jet lag, diet, or many system to activate inspiratory effort.
Obstructive sleep apnea (OSA) is a continued • Patients with OSA have 2 to 3 times greater odds
effort to breathe against an occluded airway (apnea) or of having systemic hypertension.
partially occluded airway (hypopnea). This obstruction • The incidence of pulmonary hypertension is also
can include: increased, likely the result of the acute cyclic
hemodynamic changes associated with the
• Soft tissue occlusion of the airway, as might be
repeated obstructive events.
caused by an extremely elongated soft palate,
• There is a strong association of OSA with
large tonsils and adenoids, an edematous uvula,
myocardial infarction.
and occasionally macroglossia (large tongue).
• OSA has been shown to be an independent risk
• Craniofacial abnormalities that result in the
factor for atrial fibrillation.
narrowing of the oropharyngeal space.
• There is growing evidence for the involvement
• Nasal pharyngeal abnormalities, such as a
of OSA and sleep loss in general in the develop-
deviated nasal septum, large or swollen turbi-
ment of glucose intolerance and insulin
nates, or allergic nasal polyps, which increase
resistance.
upper airway resistance, leading to more negative
airway pressures and promoting the collapse of
the airway.
NARCOLEPSY
OSA is by far the most common form of sleep
Narcolepsy is a disorder of the central nervous system of
apnea. The collapse of the upper airway leads to an
unknown origin (i.e., idiopathic), characterized
increase in respiratory effort, which in turn leads to an
primarily by severe EDS. Secondary symptoms, which
arousal or an awakening. This cycle of apnea followed
may or may not be present, are cataplexy, sleep paraly-
by arousal or awakening can occur hundreds of times
sis, and hypnagogic hallucinations.
each night, resulting in sleep fragmentation and
presenting as EDS. • Cataplexy is a sudden loss of muscle tone,
In addition to EDS, sleep apnea has other physi- typically triggered by emotion, such as happi-
ological consequences. With OSA, the repeated ness, excitement, or anger. The loss of muscle
obstruction of the airway and associated large negative tone may be extensive, causing the individual to
intrathoracic pressures lead to predictable hemody- fall down, or it may be very subtle and indiscern-
namic changes. Additional effects may be seen in ible, merely causing an eyelid to droop. Many
patients who have significant hypoxemia (Table 18-1). experts feel that cataplexy must be present for a
• Many of these hemodynamic effects are magni- diagnosis of narcolepsy.
fied when chronic lung disease is also present. • Sleep paralysis is total-body paralysis, with the
• OSA has been linked to increased risk for exception of respiration and eye movements. It
cardiovascular disease, arrhythmias, and stroke. can last from seconds to minutes and can
initially be very frightening to the individual.
• Hypnagogic (occurring during the transition
TABLE 18-1 Potential cardiovascular from wakefulness to sleep) hallucinations are
effects of obstructive sleep disordered characterized as extremely vivid, often frighten-
breathing ing dreams that may be associated with sleep
Systemic hypertension
paralysis. Hallucinations may also occur upon
awakening (hypnogogic).
Pulmonary hypertension
Ventricular hypertrophy The sleep of patients with narcolepsy is typically
fragmented. A classic finding with this disorder is the
Serious arrhythmias
early occurrence of REM sleep—frequently within
Sinus bradycardia minutes—after sleep onset.
Asystoles Narcolepsy usually begins to appear in adoles-
Second-degree antrioventricular block cence or early adulthood, although the initial onset
can occur in early childhood or later in adult life. A
Runs of ventricular tachycardia
period of progressive onset is usually followed by a
Myocardial infarction fairly stable course with rarely any remission in
Aggravation of existing cardiac problems symptoms. There is a known genetic basis for narco-
Stroke lepsy, and the risk for narcolepsy is much higher for
children of narcoleptics and first-degree relatives
Increased release of atrial natriuretic peptide
than for individuals without a family history of
Death narcolepsy.
RESTLESS LEGS SYNDROME TABLE 18-2 Parameters typically recorded

Restless legs syndrome (RLS) is a neurological on a standard polysomnogram
disorder that is characterized by four specific
Channel* Parameter
complaints.
1 EEG (central lead)
• An urge to move, usually a result of uncomfort-
2 EEG (occipital lead)
able sensations in the legs, described as creeping,
burning, itching, pulling, or tugging. 3 EOG (right eye)
• The most uncomfortable symptoms when the 4 EOG (left eye)
individual is at rest, only partially relieved by 5 EMG (chin)
moving the affected extremity.
6 EMG (right leg)
• The worse symptoms in the evening and early
part of the night than during the day. 7 EMG (left leg)
• Relief from the discomfort by moving, particu- 8 ECG
larly walking. 9 Airflow
A feature frequently associated with RLS is 10 Thoracic effort
periodic limb movements in sleep (PLMS). Periodic 11 Abdominal effort
limb movements are stereotypical, repetitive move- 12 Arterial oxygen saturation
ments that occur most frequently during the first half
of the night. They are usually found during NREM *Additional channels may include snoring, position, and CPAP pressure, as
well as back-up EEG channels.
sleep and are uncommon in REM sleep. Most patients
with RLS exhibit PLMS, but patients with no RLS
symptoms can also have PLMS. Although periodic limb using identifiable skull landmarks (Figure 18-4). The
movements in sleep may occur at any age, the fre- electrodes are labeled according to:
quency increases dramatically in the elderly.
• Their location: for example, F for frontal, C for
central, and O for occipital.
The Polysomnogram • The side of the scalp. Even numbers designate
the right side, and odd numbers designate the
Polysomnography involves the use of equipment and left side. Numbers are larger farther from the
techniques to produce a recording of sleep data, called midline.
the polysomnogram. The type of equipment used to
collect physiological data varies considerably. However, So C4 would designate the central electrode on the
certain approaches to collecting and processing data right side farther from the midline.
are common to all types of equipment: The electrodes are then referenced to a second
electrode, either at the left mastoid process (designated
• EEG, EOG, and EMG M1) or at the right mastoid process (designated M2),
• Respiratory airflow and effort but always on the opposite side. [This positioning
• Arterial oxygen saturation
• Electrocardiogram
Table 18-2 shows those parameters typically measured C4 C3
with a standard polysomnogram. (Refer to The AASM (EEG) (EEG)
Manual for the Scoring of Sleep and Associated Events for
O2 O1
additional information.) A clinical practice guideline
(CPG) published by the American Association for (EEG)

ROC LOC (EEG)
Respiratory Care outlines the generally accepted (EOG)
A2 (EOG) A1
standards of practice for polysomnography.4 (EEG) EMG1 (EEG)
EMG3 EMG2
EEG, EOG, AND EMG
FIGURE 18-4 Standard placement of EEG, EOG, and EMG
EEG. The AASM guidelines recommend the monitoring
leads used in sleep studies: EEG electrodes are desig-
of at least three EEG channels for staging sleep. EEG is nated and placed according to the international 10–20
monitored by placing electrodes on the scalp according system. Note the placement of one eye electrode slightly
to the international 10–20 system of electrode place- above and one slightly below the horizontal center of
ment.5 In this neurodiagnostic procedure, electrodes the eyes. ROC ⫽ right outer canthus; LOC ⫽ left outer
are placed at equally spaced locations on the scalp, canthus.
creates a reference point—like longitude and latitude— expiration (body temperature) and produce a change
and completes an electrical circuit to allow measurement in voltage proportional to temperature change. These
of electrical potential across the distance (C4⫺M1).] types of devices do not provide a quantitative assess-
Thus, C4 would be reference to M1 (designated C4⫺M1). ment of airflow but are preferred because of their small
The recommended derivations for scoring sleep are size for patient comfort and their simplicity of opera-
F4⫺M1, C4⫺M1, and O2⫺M1. Backup electrodes are tion. These types of sensors are best at detecting the
usually applied with derivations of F3⫺M2, C3⫺M2, absence of airflow (apnea).
and O1⫺M2. The frontal electrode is preferred for More recently, nasal pressure monitoring has been
detecting sleep-wave activity, and the occipital electrode used to monitor airflow. The system used to measure
is best for detecting awake alpha activity. nasal pressure consists of a nasal cannula connected to
a pressure transducer. Nasal pressure is positive during
EOG Rapid eye movements characterize REM sleep, expiration and negative during inspiration. Nasal
and slow eye movements generally accompany the pressure is directly proportional to airflow and thus is
transition from wakefulness to sleep as well as the more sensitive to changes in airflow than thermistors
transition back to Stage 1 during sleep. An electropo- or thermocouples. The AASM recommends nasal
tential exists from the front to the back of the eye; the pressure monitoring for detecting hypopneas.
front is positive with respect to the back. Eyeball Although several techniques are available to
movement produces spatial changes in this potential. monitor respiratory effort, the two most frequently
The EOG electrodes are therefore typically applied to used methods are piezoelectric transducers and induc-
the outer canthus of each eye, one slightly above and tance plethysmography. Piezoelectric technology, a fairly
one slightly below the horizontal plane (Figure 18-4). recent addition, uses crystals that produce an electrical
The two eye electrodes are typically referenced to the current when squeezed. These crystals are attached to
same reference electrode (either M1 or M2). With this bands that go around the patient’s chest and abdomen.
configuration, both vertical and horizontal movements When the band is stretched, the crystals are squeezed,
of the eyes are detected and appear opposite in polarity producing a small current that is amplified by the
(out of phase) on the recording. This arrangement polygraph. The amount of current produced is directly
facilitates the differentiation of real eye movements related to the circumference changes of the thorax and
from artifact because any EEG interference appears as abdomen.
in-phase potentials. Inductance plethysmography uses a transducer
composed of an insulated wire sewn in sinusoid shape
EMG. The chin EMG facilitates detection of REM sleep onto an elastic band. One band is placed around the
and helps distinguish the waking state from REM sleep. thorax and one around the abdomen. Changes in lung
Typically three electrodes are placed: One electrode is volume produce changes in the cross-sectional areas of
placed in the midline 1 cm above the inferior edge of the rib cage and abdomen, which translate into changes
the mandible. The other two are placed 2 cm below the in the diameter of the bands. Changing the diameter
inferior edge of the mandible and 2 cm to the right and of the bands directly affects their self-inductance
left of the midline. Either of the inferior electrodes is properties, providing an output proportional to effort.
referenced to the midline electrode. The third electrode This type of technology can quantify airflow at the
serves as a backup in case one fails during the study mouth by summing the rib cage and abdominal signals
(Figure 18-4). using a unique calibration protocol. Inductance
transducers are configured to deliver either calibrated
or uncalibrated signals.
RESPIRATORY AIRFLOW AND EFFORT The AASM guidelines recommend using either
Because sleep disordered breathing is a frequently esophageal manometry or inductance phethysmogra-
diagnosed disorder in the sleep laboratory, a vital part phy for monitoring effort. Esophageal manometry
of standard polysomnography is monitoring the (esophageal pressure monitoring) involves inserting a
breathing pattern, which is accomplished by measuring balloon-tipped catheter into the esophagus. The
airflow and respiratory effort. Pneumotachometers catheter is connected to a pressure transducer. Pressure
provide a quantitative measure of airflow, but they are changes in the esophagus reflect intrathoracic pressure
bulky and must be attached to a mask. They are not changes, which represents effort. Esophageal manom-
comfortable for the patient and can interfere with sleep etry is considered the gold standard for measuring
quality. So, historically, airflow has been monitored effort. However, most patients do not tolerate the
using temperature-detecting sensors, either thermistors or technique well due to its invasive nature of this form
thermocouples. These sensors detect the temperature of monitoring. The AASM recommends inductance
difference between inspiration (room temperature) and plethysmography as the standard technique for monitoring
• Oximeters are unable to distinguish between

Spotlight hemoglobin bound with oxygen and hemoglo-
On bin bound with carbon monoxide. As a result,
the reading for oxygen saturation in patients
Airflow Monitoring with elevated carboxyhemoglobin levels, such as
Since the 1970s, when polysomnography began smokers, can be artificially high.
to be used in the clinical detection of sleep • Impaired systemic circulation may give false
apnea, thermistors and thermocouples were the readings.
primary sensors for monitoring airflow. Because • Pigmented skin may affect the oximeter reading.
these types of sensors monitor the temperature Newer technology has greatly reduced this
changes between inspiration and expiration, they problem.
provide only a qualitative indicator of airflow. It • There is a delay between the time blood passes
was later realized that these types of airflow through the lung and the time it reaches the
sensors were poor at detecting hypopneas oximeter probe, which is usually placed on the
(reduced airflow). In the late 1990s and early ear or finger. This delay results in a change in
2000s, devices designed to measure nasal saturation 6–30 seconds after the decrease in
pressure changes during inspiration and expira- ventilation is seen on the polysomnogram
tion were developed. They began to replace recording.
thermistors and thermocouples as the primary Pulse oximetry has become the standard for
airflow-measuring device in many sleep laborato- monitoring oxygenation in all types of patients in
ries. These devices gave a more quantitative many situations. It is well suited for monitoring
measure of airflow and were able to detect saturation during sleep, specifically for detecting
reductions in airflow similar to that provided by a arterial oxygen desaturation associated with apneas
pneumotachometer. However, for large reductions and hypopneas in sleep disordered breathing.
in airflow, the pressure change was difficult to
detect, and many hypopneas were classified as
apneas. As a result, in 2007, the AASM recom- ELECTROCARDIOGRAM
mended both thermal detectors and nasal airflow A single-channel electrocardiogram (ECG) is typically
transducers in the detection of respiratory included with polysomnography to monitor heart rate
conditions: thermistor/thermocouples for detect- and rhythm. Typically, either ECG electrodes or
ing apneas and nasal pressure devices for standard cup electrodes (used for EEG, EOG, and
detecting hypopneas. EMG) are employed, with one electrode placed below
the right clavicle and a second electrode placed on the
left side at about the level of the seventh rib.
effort as piezo belts are not felt to give a satisfactory
refection of respiratory effort.
The Polysomnographic Recording
The individual physiological signals must be amplified
ARTERIAL OXYGEN SATURATION and conditioned for display. Amplification and condi-
The measurement of arterial oxygen saturation is vital tioning are typically accomplished with a multichannel
to determining the severity of obstructive sleep disor- recording system, referred to as a polygraph, config-
dered breathing or the presence of alveolar hypoventi- ured to meet the requirements for sleep studies. The
lation. Oximeters (or more accurately pulse oximeters) number of channels of information that can be pro-
measure the relative absorbance of two wavelengths of cessed varies and is usually dictated by the sleep labora-
light: infrared and near infrared. This measurement tory requirements. Regardless of the specific type of
allows the determination of total hemoglobin and instrumentation used, to produce a quality recording,
oxygenated hemoglobin that is read out as a percentage technologists must understand several important
saturation of arterial blood, commonly designated as capabilities of sleep recording equipment.
SPO2. Pulse oximetry is the oximeter’s ability to analyze
the difference between light absorbed by the tissues
and light absorbed by blood that is pulsing through the SENSITIVITY
vascular bed with each heartbeat. The pulsing value Sensitivity is the ratio of signal voltage to the amount of
represents oxygen saturation. To ensure accuracy, deflection observed on the recording device. A standard
anyone using pulse oximetry to monitor oxygenation sensitivity for bioelectrical signals (EEG, EOG, EMG) is
must be aware of the following issues: 7 ␮V/mm; that is, every 7 ␮V of bioelectrical activity
causes the displayed signal to move vertically 1 mm. setting of 7 ␮V/mm should produce a display signal
Sensitivity is equal to input voltage (microvolts) with an amplitude of 7 mm. The display amplitude
divided by the output deflection on the display (mil- should be plus or minus 5% of the expected amplitude.
limeters). Because input activity can vary considerably, Make sure that extreme filter settings are not set.
a number of increasing sensitivity settings are available Use high-frequency filters of 70 Hz or low-frequency
to obtain the best display. As the microvolts per filters of 1 Hz or less. At the end of the study, a calibra-
millimeter sensitivity values decrease, signal amplification check is performed at the final sensitivity and filter
tion increases. Thus, 1 μV/mm is highly sensitive, settings used during the study.
whereas 50 μV/mm represents a very low sensitivity.
A sensitivity of mill volts per centimeter of display
deflection can record stronger electrical potentials, such Recording and Monitoring
as those recorded on the electrocardiogram (ECG).
During the Night
After completion of the patient hookup, the patient
FREQUENCY FILTERS should make preparations for bed, including such
Frequency filters eliminate or attenuate artifact, that is, rituals as brushing teeth and using the restroom. When
activity from the bioelectrical signal that interferes with the patient is in bed and comfortable, all electrodes
or distorts the desired signal. Three types of filters are and other monitoring devices should be plugged into
typically employed. the polygraph interface box, commonly called a jack
• A low-frequency filter minimizes unwanted box. Inform the patient at this time that the patient:
low-frequency artifact such as swaying of the • Should feel free to change position at any time
EEG caused by respiration, perspiration, and during the night.
motion. A typical setting is 0.3 Hz. • Will be monitored throughout the recording
• High-frequency filters filter out any high- period.
frequency artifact. A setting of 35–70 Hz is • Should use the intercom or other communica-
generally used. The specific filter setting chosen tion system (and should be instructed on how
reduces the activity at that particular frequency to use it).
by 20%. As the signal frequencies increase (as • Should call whenever he or she needs to use the
with high-frequency filters) or decrease (as with restroom or has any other problem or request.
low-frequency filters), the signal is attenuated. • Should let the sleep technologist disconnect
• The third type of filter is a 60-Hz notch filter, electrodes if he or she needs to get up.
which sharply attenuates frequencies between 58
and 62 Hz. This filter reduces the 60-Hz activity Also at this time, perform any other required proce-
from AC electrical interference. Activity outside dures: blood pressure and temperature measurements,
the 58–62 Hz range is barely affected. Sixty-hertz presale questionnaire, and so on.
filters should not be routinely used. In most
cases, 60-Hz artifact can be eliminated through PATIENT CALIBRATION
proper electrode application and good amplifier
operation. An exception is when recording in an The next step is patient calibration, or biological
electrically active environment, such as an calibration, which:
intensive care unit. • Identifies any problems with the recording
system.
• Allows repair before the test begins.
CALIBRATION • Provides qualitative signals that can be used later
Calibration checks the accuracy of a recording device. A to facilitate accurate analysis of the record.
calibration check should be performed both before and
after the PSG recording. Typically, a device has a Patient calibration is performed immediately before
calibration button with a known voltage, such as 50 ␮V. lights-out. Ask the patient to lie quietly face up and
When this known signal is used, the effect of the instru- listen for instructions, which vary depending on the
mentation on the bioelectrical signal can be evaluated. types of biological signals being recorded. For a
Pushing the calibration button introduces a positive standard PSG, the instructions typically consist of the
signal and causes an upward deflection; releasing the following:
button causes a downward deflection. Thus the polarity • “With your eyes open, look straight ahead.”
of the signal is checked. In addition, introducing a Have the patient maintain this state for
known calibration signal of 50 ␮V/mm with a sensitivity 30 seconds without moving.
• “Please close your eyes and lie very still.” Have

the patient hold this position for 30 seconds. Age-Specific Competency
This procedure allows a baseline reading of
alpha activity when the patient is awake and Although the general procedures for perform-
relaxed with eyes closed, as may occur during the ing polysomnography for children are similar to
recording. The technologist must verify that the those for adults, children present with a wide
patient’s eyes are closed during this period. range of physical, developmental, and behav-
• “Open your eyes and, without moving your ioral challenges that must be considered dur-
head, look to the right, look to the left, look up, ing polysomnography. In addition, a child may
look down, relax.” This step ensures that the be easily frightened by the unfamiliarity of the
EOG signals are deflecting appropriately (out of sleep laboratory and the attachment of numerous
phase). It also characterizes the pattern of slow, monitoring devices. Thus, personnel performing
rolling eye movements that typically occur the study should be:
during the transition from wakefulness through
• Skilled in dealing with the specific needs of
Stage 1 sleep.
infants, children, and adolescents.
• “Holding your head still, blink your eyes slowly
five times.” This step allows recognition of blink • Demonstrate knowledge of childhood behavior.
artifact, to differentiate wakefulness from REM • Be able to deal with the emotional responses
sleep. likely to be encountered.
• “Grit your teeth, and then relax.” This step • Understand the differences in procedural
should produce an increase in the EMG activity protocol between children and adults, such
and should note muscle artifact in both the EOG as timing of the study and techniques for
and EMG signals. placement and securing of monitoring
• “Inhale and hold your breath . . . . Now exhale devices.
and breathe normally.” This step allows you to
• Be certified in pediatric cardiopulmonary
calibrate respiratory channels.
resuscitation.
• “Flex your right ankle, relax. Now flex your left
ankle, relax.” This step calibrates the anterior
tibialis EMG channels.
During each of these calibration procedures, record the
type of activity performed. checks. For example, a half-hour check sheet may be
Throughout the process of patient hook-up and used to record various physiological parameters
calibration, the patient should not be allowed to fall observed, such as stage of sleep, heart rate, arterial
asleep. Keeping a hypersomnolent patient awake may oxygen saturation, the presence of respiratory events,
be difficult, and, on occasion, patient calibration may arrhythmias, arousals, and so on.
be impossible because of the patient’s inability to In addition, the technologist should note on the
maintain wakefulness. recording whenever:
After patient calibration, ask the patient to get
• The recording is altered in any way, for example,
comfortable and then turn out the lights.
changes made in sensitivity, filter settings, and
electrode configuration.
RECORDING PROCEDURES • Any patient activity is required to accurately
analyze the data—for example, coughing,
The sleep therapist’s responsibility is to ensure that a
moving, position changes, talking while asleep.
quality polysomnographic recording is obtained.
• Anything else happens that may affect the
Constant vigilance is also needed to identify and
evaluation of the data, such as external noises, a
correct problems with the recording equipment and
therapist entering the room to make repairs, or
electrodes, to document any observations that would
any other necessary intervention.
affect later analysis and interpretation of the data, and
to recognize any patient safety issues such as life- At the conclusion of the recording period, awaken
threatening arrhythmias or unsafe activities. The the patient. Be sure to caution the patient before
therapist accomplishes all this by monitoring the PSG turning on the lights. Perform a post-test patient
recording and using other monitoring equipment such calibration at this time along, with any post-test
as video and sound equipment to observe the patient. measurements such as blood pressure. A posttest
Sleep laboratories typically use some form of questionnaire assessing the patient’s perceived quality
standardized documentation to record routine interval of sleep and alertness, as well as any experiences the
stage that consumes the greatest portion of the

Best Practice epoch is recorded.
• Scoring Stage N1 requires a clear, discernible
Technologist Responsibilities slowing of the EEG tracings and an evident onset
of theta activity for more than 50% of the epoch.
Because polysomnography is a diagnostic test,
Slow rolling eye movements may or may not be
the technologist is responsible for ensuring
present but, if present, aids in the scoring of N1.
the quality of information and for document-
• Score Stage N2 sleep if one or both of the
ing all observations that may be important in
following wave activities occur during the first
the interpretation of the results. Generally, each
half of the epoch or the last half of the preceding
technologist monitors no more than two patients
epoch:
at a time. Monitoring more than two patients
• One or more K complexes unassociated with
increases the chance of missing important ob-
arousals
servations or of failing to keep a complete record
• One or more sleep spindles
during the study. Monitoring should be limited to
• Score Stage N3 sleep when 20% or more of an
only one patient per technologist in situations in
epoch consists of slow-wave activity.
which frequent intervention is anticipated, such
• Score Stage R sleep when the EEG is a low-
as with very ill patients, mentally disadvantaged
amplitude, mixed-frequency with low chin EMG
patients, and small children.
tone, and rapid eye movements are present
Becoming proficient at staging normal sleep takes
patient had that may have interfered with sleep, is time and practice, and accurately staging abnormal
commonly completed. Highly recommended is the sleep takes even longer. Consult the AASM’s scoring
therapist’s summary of the nighttime activity, including manual for a more in-depth description of the scoring
any unusual occurrences, recording difficulties, or other rules.
factors that may affect the interpretation of the results
such as the use of a fan, open window, or elevation of IDENTIFYING AROUSALS
the head of the bed.
A typical PSG record consists of 14 or more Many sleep disorders involve frequent, brief arousals
channels of data collected over 6–8 hours. The process that result in excessive daytime sleepiness. Arousals
of scoring reduces the recorded PSG data to a mean- occur frequently in patients with sleep disordered
ingful summary or, put another way, assigns values and breathing, periodic limb movement disorder, and
meaning to a series of physiological waveforms. These many other sleep disorders. Assessing the frequency of
values, used in combination with other observations of arousals is important in establishing the cause of EDS.
unusual events, are used to interpret the study. Thus, Arousal can occur in all stages of sleep.
scoring: An arousal can be defined as any clearly visible
abrupt shift of EEG frequency, including alpha, theta,
• Identifies the stages of sleep. and/or frequencies greater than 16 Hz (that are not
• Quantifies respiratory events. spindles) that last as least 3 seconds. There must be at
• Quantifies leg movements. least 10 seconds of stable sleep preceding the change.
• Identifies any other abnormalities noted in the To score an arousal in REM sleep, there must be a
record. concurrent increase in submental (chin) EMG lasting at
• Establishes other indices of sleep quality such as least one second. Arousals are summed and reported as
the degree of sleep fragmentation, which can an arousal index (number of arousals per hour of
explain symptoms of daytime sleepiness. sleep).
STAGING SLEEP
QUANTIFYING RESPIRATORY EVENTS
Identifying the stages of sleep, or staging sleep, is based
To establish a diagnosis of sleep disordered breathing,
on the criteria initially described by Rechtschaffen and
an abnormal respiratory pattern has to be demon-
Kales and subsequently revised by the AASM. Sleep is
strated. The respiratory disturbance index (RDI),
broken down into consecutive 30-second periods
commonly called the apnea/hypopnea index (AHI),
called epochs to facilitate scoring. Each epoch is staged
is the universal method used to establish a diagnosis of
independently based on the following general rules:
sleep disordered breathing. Respiratory events are
• If criteria exists that meets the definition for generally categorized as either a hypopnea or an apnea
more than one stage is present in an epoch, the on the basis of specific criteria.
The rules for scoring sleep stages and respiratory • Central apneas greater than 20 seconds that
events for children may vary significantly from those are not related to a sigh or to movement should
for adults. Infants younger than 6 months have be scored.
continuous developmental aspects with respect • Central apneas less than 20 seconds should be
to their central nervous system. Scoring of sleep scored if the duration is at least two standard
and wakefulness is based on both behavioral and breaths and a decrease in saturation of 3% or
polysomnographic characteristics. In general, the greater.
sleep of infants younger than 2 months is classified
• An obstructive apnea is scored when the apnea
as either quiet sleep, active sleep, or indeterminate
lasts at least two standard breaths and there is
sleep. Behavioral observations are necessary in
a drop in baseline flow of greater than 90%.
differentiating between wakefulness and sleep. The
scoring of sleep in infants and children at 2 months • Score respiratory hypopneas when there is a
of age and older is based on adult scoring rules with 50% or greater decrease in nasal or oral airflow
some modifications that account for the develop- amplitude and the duration is equal to or
mental aspects of the infant. greater than 2 breaths.
The scoring of sleep-related respiratory events Measurement of end-tidal PCO2 may be helpful
is also affected because children differ from adults in assessing hypoventilation. If measured, record
both physiologically and in the way sleep-related the peak end-tidal P CO2 and the duration of the
upper airway obstruction is manifested. Healthy end-tidal P CO2 that is greater than 50 mm Hg,
children rarely have obstructive respiratory events expressed as a percentage of total sleep time.
during sleep, so all obstructive apneas, regard-
Source: American Thoracic Society. Standards and indications for
less of length, are regarded as significant. During cardiopulmonary sleep studies in children. Am J Respir Crit Care Med.
scoring: 1996;153:866–878.
Hypopneas are defined as a reduction in airflow recognizable respiratory effort begins to appear
for at least 10 seconds. As mentioned earlier, the AASM during the latter part of the event (Figure 18-5).
rules require the use of nasal pressure monitoring to Mixed apneas must last a minimum of 10 seconds
establish the presence of a hypopnea. The nasal to be scored. Many laboratories consider this
pressure signal amplitude must drop by 30% or more type of event to be obstructive and do not report
of baseline and be associated with a 4% or greater it as a separate type.
decrease in saturation.
Figures 18-6 and 18-7 illustrate the characteristics
An apnea is the absence of airflow for a minimum
of central and obstructive apneas and obstructive
of 10 seconds and is scored when the thermal airflow
hypopneas, as would be observed on a standard
sensor signal has decreased 90% or more of the
polysomnogram.
baseline value that existed prior to the event. Apneas
are designated as either a central apnea, obstructive
apnea, or mixed apnea (Figure 18-5).
• The apnea is scored as central apnea if no effort
Airflow
is detectable in either the chest or abdominal

effort signal. Chest
• The apnea is scored as an obstructive apnea
when there is a paradoxical pattern between the Abdomen
chest and abdominal signals; that is, the signals Central Obstructive Mixed
are out of phase and frequently show increasing
FIGURE 18-5 The three types of respiratory apnea found
amplitude (increasing effort) as the event on a polysomnogram in patients with sleep disordered
continues. breathing: Flat lines represent absence of airflow or
• In addition, events classified as mixed apneas absence of respiratory effort or both. Vertical dashed
are routinely reported. These events start lines show that the chest and abdomen are moving in a
off looking like a central apnea; however, paradoxical manner.
C3A2
EEG Arousal
O1A2
FLO2
Central Apnea
THRM
THOR
ABDM
96 98 96 96 94 96 94
91 89 86 92 91 88 91 89
83 86 83 85 84 83 87 87 85 SAO2
Desaturation
FIGURE 18-6 Example of a central apnea: Airflow is absent in both the nasal pressure (FLO2)
and thermo sensor (THRM). In addition, there is the absence of effort in the thoracic
(THOR) and abdominal effort (ABDM) signals, indicating the absence of a neural drive to
breath. An associated decrease in saturation is delayed due to the transit time from the
lungs to the finger sensor. Central apneas may or may not be associated with an arousal, as
indicated in the EEG signal (C3–A2).
C3M2
Arousal
O1M2
SNOR
Obstructive
Hypopnea FLOW
Obstructive Apnea
THRM
THOR
ABDM
96 94 93 94 95 94 94 97 99 98 98 98 97 97 95 93 97 98 98 97 97 96 96
90
Desaturation SpO2
FIGURE 18-7 Example of an obstructive apnea and obstructive hypopnea from a polysomno-
gram: With an obstructive apnea (right side of figure), airflow is absent in both the nasal
pressure and thermo sensor signals, but a continued effort to breathe, as indicated by the
progressively increasing amplitude in the thoracic (THOR) and abdomen (ABDM) sensor
signals with a typically paradoxical motion of the two effort sensors. An obstructive hypop-
nea (left side of figure) looks similar to an obstructive apnea except that there is evidence
of airflow in the thermo sensor and nasal pressure sensor. Obstructive events are typically
terminated with an arousal as evident in the EEG signal (C3–M2). An associated decrease in
saturation is delayed due to the transit time from the lungs to the finger sensor.
Once the scoring of respiratory events is complete, each other) are considered one movement. Movements
the total number of each type of event is divided by the may occur simultaneously in both legs or appear in
total hours of sleep to obtain a frequency index. For one leg only. Frequently, movements switch from one
example, if 140 obstructive apneas were scored during leg to the other or occur in both legs but out of phase;
a study that took a total sleep time of 7.0 hours, the this type of movement is referred to as alternating leg
obstructive apnea index would be 20 events per hour muscle activation (ALMA).
of sleep. To be used in the assessment of periodic limb
When all events are summed and divided by the movements in sleep (PLMS), a movement must occur as
total sleep time, the respiratory disturbance index part of a series of rhythmic jerks with intermovement
(RDI), or apnea/hypopnea index (AHI), is obtained. intervals of 5–90 seconds. There must be a series of at
The RDI is used to define the severity of the disorder. least four movements. PLMS are generally scored as
being either associated with or not associated with an
• A respiratory disturbance index over 5 per hour
arousal or an awakening. An overall PLMS index
is considered abnormal.
(number of movements per hour of sleep) is typically
• An apnea index of 5 to 15 per hour is considered
reported, and an index of greater than 5 per hour of
mild.
sleep is considered pathologic.
• An index of 15–30 is considered moderate.
• An index greater than 30 is considered severe.6
QUANTIFYING LEG MOVEMENTS

Leg movements or leg jerks are recorded using bioelec-
trical electrodes placed over the anterior tibialis muscle CASE STUDY 18-1
of both legs. A leg jerk or movement is identified when
a burst of leg EMG activity lasts 0.5–10 seconds and has J. G., a 43-year-old male with a complaint of
an increase in amplitude of at least 8 ␮V in EMG excessive daytime sleepiness, was referred to the
voltage above the resting EMG level. Movements sleep disorders center for evaluation. His history
occurring synchronously (within less than 5 seconds of and physical examination showed a morbidly
obese male with disruptive snoring, a large neck,
a large soft palate, and systemic hypertension. A
nocturnal polysomnogram was performed with
the following results:
Best Practice Sleep latency 20 minutes
REM latency 294 minutes
Reporting Data Slow-wave sleep 2%
There is generally a uniform approach to prepar- Sleep efficiency 88%
ing a final report. RDI 38/h
• Data are usually presented in either a Mean arterial oxygen 94%
tabulated or a narrative form or in a combi- saturation
nation of the two formats. At minimum, Percentage time with 8.5%
presented data should show the time in bed, saturation less than 85%
total sleep time, and the time spent in the
various sleep stages. Arousal index 52/h
• Other data—such as respiratory events (RDI, PLMS index 2/h
type and number of events, saturation
levels), cardiovascular events (occurrence of Questions
arrhythmias), and limb movements—are 1. On the basis of these data, what primary
included when relevant. The extent of data sleep disorder is present? Can the severity
included in the report may vary considerably be classified?
among sleep laboratories. 2. Do the data suggest the presence of a
• Finally, the sleep disorders clinician renders second sleep disorder?
a narrative conclusion, relating the findings 3. Is there significant sleep disturbance? On
from the polysomnogram to a final diagnosis. what data is the decision based?
Nasal Continuous Positive individuals and depends on structural and functional

abnormalities, positional effects, sleep stage, weight,
Pressure Therapy and behavioral factors such as alcohol consumption.
Obstructive sleep disordered breathing is by far the As a result, the level of positive pressure required to
most common sleep disorder encountered in the sleep eliminate upper airway obstruction also varies among
disorders laboratory. Although a number of interven- individuals. The therapeutic or effective CPAP pressure
tions exist to treat this disorder—such as weight loss, is determined through titration.
positional training, oral appliance, and surgical Typically, CPAP titration is performed with full
intervention—the most effective and accepted form of polysomnography (PSG) on a second night after the
therapy is continuous positive airway pressure patient’s initial diagnostic evaluation. Performing full
(CPAP). With this form of therapy, first described in PSG along with CPAP titration allows an objective
1981, a positive pressure, established in the patient’s assessment of the most effective pressure for eliminat-
airway, acts as a pneumatic splint to prevent the airway ing all evidence of upper airway obstruction and for
from collapsing. verifying the effect on sleep quality. Of equal impor-
A blower that establishes airflow is attached via a tance is the presence of an experienced sleep technolo-
length of wide-bore tubing to the patient’s airway. gist, who can influence how well a patient responds to
Interfaces such as masks or nasal prongs are used. A CPAP therapy.
positive pressure is generated through changes in • Sleeping with a mask over the nose and the
airflow and resistance within the system (Figure 18-8). pressure sensation encountered during CPAP can
Most CPAP systems can deliver pressures from 2 to lead to significant anxiety. An experienced
20 cm H2O. Pressure is controlled either by adjusting technologist can explain CPAP, decrease anxiety,
the speed of the blower fan or by a valve in the blower and increase cooperation.
housing that controls the amount of flow delivered to • An experienced technologist is required to
the patient’s airway. determine the best type of airway interface and
An important requirement of a CPAP system is to ensure an appropriate fit, both very important
venting to allow exhaled gas to be flushed from the in the patient’s acceptance of CPAP.
patient interface, thus preventing rebreathing. Venting is • The technologist manually titrates pressure
typically accomplished by establishing a vent hole in the upward when evidence of obstruction persists
patient interface that provides a leak of at least 10–15 and validates that all evidence of flow limitation
Lpm at low CPAP pressures. This amount is sufficient to is absent at the optimal pressure.
flush the system of all exhaled carbon dioxide. • Technologist intervention may be required
during titration to correct leaks, add humidifica-
CPAP TITRATION tion if needed, and address any concerns or side
Obstructive sleep disordered breathing is a complex effects the patient may experience.
disorder. The nature of the obstruction varies among
These topics are discussed in more detail in the
following sections.
C
D Patient Education. Explaining CPAP, how it works,
E A and its possible side effects—all before beginning the
treatment—goes a long way in getting the patient to
accept this form of therapy. Some patients want to
touch or examine the equipment. The videos provided
by equipment manufacturers are an excellent medium

B for educating the patient about obstructive sleep
disordered breathing and CPAP therapy. The technolo-
gist should also be available to answer the patient’s
questions.
FIGURE 18-8 A nasal CPAP system and the mechanism by
which airway obstruction is prevented: (A) Entrainment Choosing the Airway Interface. Once the patient
of room air through a filter. (B) Blower unit capable of becomes knowledgeable about CPAP, the next step is to
delivering a high airflow that enables a constant positive determine the most suitable airway interface. Three
pressure output during respiration. (C) Wide-bore tubing. general types of interface are available (Figure 18-9):
(D) Nasal mask. (E) Vent allowing washout of deadspace
in the mask to prevent rebreathing. ⫹ ⫽ positive pressure • A nasal mask that encircles and seals around the
in airway produced by nasal CPAP. patient’s nose.
specifically for a given mask, and interchanging

A B C headgear is not recommended.
Once an appropriate interface has been deter-
mined, have a practice session before starting the
polysomnogram. In the practice session, the patient
wears the CPAP mask and experiences both low and
high pressures. This session can improve tolerance
during the study.
CPAP TITRATION PROTOCOL
There is no universally agreed-on method for how
CPAP titration should proceed. As a general rule, the
initial CPAP pressure is set low and is titrated incre-
mentally to higher pressures until the optimal pressure
is determined. There are several reasons for this
FIGURE 18-9 Three common styles of CPAP mask: (A) Nasal approach. First, starting at low pressures enhances
mask. (B) Nasal pillows or prongs. (C) Full face mask. patient tolerance and allows the subject to achieve
sleep. Second, low pressures may be enough to be
therapeutic in some patients. Third, higher pressures
are generally associated with mask leaks and patient
• Nasal prongs or bellows that form a seal at the
discomfort, and so they are to be avoided unless
opening to the nacres.
required therapeutically.
• An oral-nasal mask (full-face mask) that encir-
CPAP is typically initiated with a low pressure of
cles both the nose and the mouth.
4 cm H2O and increased in steps (at a minimum of
The nasal mask and nasal prongs are the most 1 cm H2O). CPAP pressure is usually increased rapidly
frequently used. Which one is selected as the inter- when obstructive events are frequent and at a slower
face usually depends on patient preference; however, rate when respiratory events become less frequent.
the use of one type over the other may be based on CPAP pressure is increased until:
its ability to provide a seal and thus effective therapy.
• Either evidence of obstruction has been
In some circumstances, a patient may be intolerant of
eliminated.
the nasal mask or nasal prongs, or the mask or nasal
• Or a maximum pressure of 20 cm H2O is
prongs may not provide an adequate seal. Or the
reached.
patient may have a problem keeping the mouth
• Or the patient is unable to tolerate the pressure.
closed while asleep, leading to an inadequate positive
pharyngeal pressure or significant sleep disruption. This protocol results in optimal treatment at the lowest
In many cases, a chinstrap, available from some possible pressure.
CPAP equipment manufacturers, may help keep the The elimination of apneas and hypopneas may
mouth closed. However, a chinstrap may not be not represent optimal treatment. Elevated upper
effective, and, in some cases, an oral-nasal mask airway resistance may still be present and result in
should be considered. Full-face masks are less frequent arousals from sleep. Inspiratory flow limita-
likely to be accepted because they may induce tion is best detected by the measurement of pleural
claustrophobia. pressure using an esophageal balloon or a nasal
Other considerations in choosing the type of pressure transducer, which provides better detection of
interface are risk of aspiration if the patient should flow characteristics than a thermistor. When flow
vomit and the theoretical concern of limited ability to limitation is detected, pressure increases of 1–2 cm
breathe if the machine should fail. Safety valves should above that needed to eliminate apneas and hypopneas
be present in the circuit close to the patient in the are generally sufficient to eliminate all obstruction and
event of machine failure to allow the patient to breathe resulting arousals. The technologist must monitor the
fresh air. effects of CPAP in REM sleep and, if possible, in the
Both masks and prongs are available in different supine position because higher CPAP pressures are
sizes to accommodate variations in facial contours, typically required to resolve upper airway obstruction
thereby reducing leaks. Nasal masks are also available in these situations.
in a variety of shapes; trying several shapes gives
patients some freedom about choice and comfort. All Dealing with Side Effects. CPAP is generally well
varieties of interface are attached to the face by head- tolerated, but it has some side effects or conditions that
gear that fits over the head. Headgear is designed may lead to arousals and reduce CPAP tolerance or
TABLE 18-3 Common side effects

associated with CPAP use and Best Practice
possible remedies
Ensuring CPAP Compliance
Side Effect Possible Remedies Good therapeutic effectiveness on the CPAP titra-
Mask-related: tion night does not guarantee that the patient
Pain or abrasion on Loosen mask headgear will be compliant with CPAP use at home. Fac-
bridge of nose if too tight tors that may lead to reduced use or to nonuse
(noncompliance) are generally related to its side
Switch to nasal prongs
effects. Early follow-up can help identify and
Leaks around mask Check for proper mask size resolve problems that patients may have with
Switch to nasal prongs CPAP. Follow-up at regular intervals thereafter is
Oral air leaks (mouth Chinstrap helpful in ensuring continuing compliance.
drops open) Full-face mask
CPAP-related:
Nasal dryness/ Saline spray/gel
irritation Adding humidification to the airflow may help
Humidification
and is now the standard of practice with CPAP.
Chinstrap if air is escaping • Some patients may feel claustrophobic on their
from mouth first encounter with CPAP. Progressive desensiti-
Nasal congestion Antihistamine zation and using nasal prongs rather than a
Nasal steroids mask may help.
• A few patients simply refuse CPAP.
Full-face mask
Difficulty exhaling Use ramp function
Use bilevel PAP to lower
BILEVEL POSITIVE AIRWAY PRESSURE
expiratory pressure Bilevel positive airway pressure (bilevel PAP) is a
variation of CPAP that allows inspiratory and expira-
Claustrophobia Switch to nasal prongs
tory pressures to be adjusted independently. During the
Bilevel PAP respiratory cycle, a critical level of pressure is needed to
Behavioral desensitization maintain a patent airway. With complete or nearly
training complete airway occlusion, the expiratory pressure
Air swallowing Bilevel PAP to lower required to prevent the collapse of the airway is the
expiratory pressure same as the inspiratory pressure required to prevent
anemic events. Bilevel PAP takes advantage of the fact
Raise head of bed
that if positive pressure is applied to inspiration, thus
eliminating the anemic obstruction, then less pressure
effectiveness (Table 18-3).The technologist must is required to maintain the airway during exhalation.
address side effects during CPAP titration because they Thus, with bilevel PAP, the inspiratory positive airway
may affect how the patient receives the long-term pressure (IPAP) is similar to the pressure titrated with
therapy. Most side effects are related either to the standard CPAP. However, expiratory positive airway
patient interface (e.g., mask, nasal prongs) or to the pressure (EPAP) is typically 4–6 cm H2O lower than
sensation of high pressure or high airflow. IPAP. A bilevel device cycles between the preset IPAP
and EPAP pressures by monitoring changes in respira-
• Poor mask fit can lead to air leaks around the
tory flow.
mask; those occurring around the eyes are the
The titration of bilevel PAP is more complex than
most disruptive.
that of conventional CPAP because it involves estab-
• Frequently, the patient relaxes the lower jaw,
lishing two separate pressures. IPAP and EPAP pres-
producing an oral leak. This leak not only may
sures are independently adjusted and thus generally
produce arousals but also frequently reduces the
require more time to establish therapeutic levels. A
effectiveness of CPAP. A chinstrap designed to
typical protocol for the titration of bilevel PAP is to:
hold the lower jaw closed may help.
• A full-face mask may also help but is generally • Begin with an IPAP of 8 cm H2O and an EPAP of
less preferred by the patient. 4 cm H2O.
• Pressure-related side effects include difficulty • If obstructive apneas persist, EPAP is increased to
exhaling, nasal congestion, and nasal dryness. equal IPAP.
• If obstructive apneas still continue, then increase 3 hours to ensure adequate PSG documentation that
IPAP and EPAP together until apneas are elimi- CPAP eliminates or nearly eliminates the respiratory
nated. EPAP is left at the pressure that eliminated events during REM and NREM sleep, including REM
apneas while IPAP is increased incrementally sleep with the patient in the supine position.
until all evidence of obstruction has been
eliminated (e.g., snoring, desaturation, arousals).
AUTOTITRATING CPAP
Variations in the protocol can be found between
The level of CPAP pressure required to eliminate upper
laboratories.
airway obstructions in sleep-disordered breathing
Bilevel PAP devices are frequently used in noninva-
varies with conditions. The optimal pressure may vary
sive nasal ventilation of patients with respiratory
during the night with respect to position changes and
failure, especially patients with neuromuscular or chest
sleep stage. It may also vary from night to night
wall disease. These patients may be sent to the sleep
because of alcohol consumption, sedative medication,
disorders laboratory for a PSG and to establish ventila-
and previous sleep deprivation. The hypothesis that
tory parameters using bilevel PAP. Bilevel PAP is also
changing CPAP according to the patient’s need at any
used in patients who have difficulty tolerating CPAP,
given time could improve CPAP compliance has
especially at higher CPAP pressures (i.e., greater than
resulted in the development of autotitrating CPAP
15 cm H2O). These patients tolerate lower expiratory
devices that automatically adjust pressure according to
pressures better.
the patient’s requirements. Autotitrating CPAP
machines continuously adjust the positive pressure
SPLIT-NIGHT POLYSOMNOGRAPHY level depending on the presence of flow limitation.
These machines use flow, pressure, sound, or vibra-
A full night of recording is generally needed to estab-
tion—or a combination of those variables—to estab-
lish and assess the degree of obstructive sleep disor-
lish whether flow limitation is present. They increase or
dered breathing. For patients with severe obstruction,
decrease pressure in predetermined increments to
however, a diagnosis may be feasible after only a few
maintain the lowest effective pressure. Autotitrating
hours of monitoring. In such cases, CPAP titration
CPAP has been advocated for use in CPAP titration
could be performed on the same night to detect and
studies, both attended and unattended, and as a
assess the disorder. Condensing the assessment and
standard mode of therapy for patients.
titration segments in this way is referred to as a split-
night polysomnogram. The trend toward using split-night
studies reflects an effort to reduce costs and to decrease
waiting time for a sleep disorder assessment, which Measuring Daytime Sleepiness
may be weeks or months. Daytime somnolence or sleepiness is a hallmark
However, making a split-night study the routine symptom of many sleep disorders. Assessing the degree
has its disadvantages. First, apneas may occur only of sleepiness may be useful in diagnosing certain sleep
during REM sleep or only when the patient is supine. disorders and in monitoring the effects of treatment.
REM sleep is the most plentiful during the second half Two tests are currently in use to objectively assess
of the night, and sufficient supine sleep, especially in sleepiness: the multiple sleep latency test (MSLT) and
conjunction with REM sleep, may not occur during the the maintenance of wakefulness test (MWT). The MSLT
first half of the night. Therefore, the severity of the was the first such test to be described and remains the
disorder may not be adequately assessed during the most commonly used test. The AASM practice param-
first half of the study. Second, confining CPAP titration eter for the clinical use of the MSLT and MWT describes
to just half of the night may not allow sufficient time to the protocols for both tests.8
titrate to the optimal pressure, especially in patients The multiple sleep latency test consists of a series of
with severe obstructive sleep disordered breathing. This four or five nap opportunities given at 2-hour intervals
problem is compounded when bilevel PAP is used throughout the day. The test is usually preceded by a
because it requires a more complex titration protocol. nocturnal PSG to provide accurate documentation of
The AASM recommends that an AHI of at least the preceding night’s sleep, which influences the
40 events per hour be documented during a minimum accurate interpretation of MSLT results. The first nap is
of 2 hours of diagnostic PSG before considering a performed 1.5–3 hours after the nocturnal PSG ends.
split-night study.7 Split-night studies may sometimes be During the monitoring of the naps, sleep onset is
considered at an AHI of 20–40 events per hour, based determined, and sleep stages are identified. The
on clinical judgment (e.g., if there are also repetitive standard montage includes a C3 or C4 EEG lead, right
long obstructions and major destructions). CPAP and left EOG leads, and a chin EMG. A second occipital
titration should be carried out for a minimum of lead is frequently monitored to help in distinguishing
wakefulness from sleep. Additional channels Summary

include ECG and airflow if snoring was noted in the
nocturnal PSG. Normal sleep consists of alternating periods of rapid
The MSLT must be performed in an environment eye movement and nonrapid eye movement sleep.
conducive to sleep. The sleeping area should be quiet Sleep patterns and stages can be observed by using
and dark. Intermittent noises should be avoided. EEG, EOG, and EMG and by monitoring breathing and
Maintaining quiet may necessitate being away from arterial oxygen saturation. The resulting data can be
elevators, toilets, outside traffic, and heavily used interpreted to detect the presence of sleep disorders,
hallways. Any audible noises that could interfere with including sleep-disordered breathing, narcolepsy, and
sleep onset must be documented to facilitate accurate periodic limb movements in sleep.
interpretation. The polysomnogram is used to report sleep data.
In addition, specific patient preparation routines The therapist sets filters and sensitivities for the equip-
need to be followed. ment used and prepares the patient for the testing,
including patient or biological calibration to ensure
• The patient should change into street clothes accurate data collection and minimal artifact. The
sometime before preparing for the first nap. therapist also monitors the test in progress. The data
• Keep the patient awake except during the actual collected are scored or interpreted to determine
nap time. Keeping the patient awake requires the whether any sleep disorders are present.
attendance of laboratory staff throughout the day. Effective forms of therapy for sleep-disordered
• Patients who smoke should stop smoking breathing include continuous positive airway pressure,
30 minutes before nap time. in which positive pressure established in the patient’s
• Fifteen minutes before nap time, the patient airway acts as a pneumatic splint to keep the airway
should prepare for bed. This preparation open. CPAP may be applied with a mask or other
includes using the restroom, removing shoes, device, depending on the patient’s needs and tolerance.
and loosening restricting clothing. The amount of pressure must be titrated to produce
• The patient should be in bed and relaxed 5 maximum therapeutic results while maintaining
minutes before nap time. At this time, perform a patient comfort. Bilevel positive airway pressure allows
biological calibration similar to one done during inspiratory and expiratory pressure levels to be adjusted
the nocturnal PSG. independently, and autotitrating CPAP devices
• Immediately before lights-out, ask the subject to automatically adjusts pressure according to patient
get into a comfortable position, and given a requirements.
short set of instructions that encourage falling
asleep, such as, “Close your eyes, lie still, and let
yourself fall asleep.” (Repeat the same set of
instructions before each nap.) Study Questions
There are also specific criteria for terminating the nap. REVIEW QUESTIONS
1. Identify the four stages of sleep, and discuss the
• Terminate the nap if, after 20 minutes, the
relative percentages of each stage and the pattern of
patient has not fallen asleep.
occurrence through the night.
• If the patient falls asleep within 20 minutes,
continue the nap for 15 minutes after the first 2. Define excessive daytime sleepiness, and identify
epoch of sleep to assess any occurrence of REM three common sleep disorders for which this is a
sleep, which is useful in establishing a diagnosis prominent symptom.
of narcolepsy. Sleep latency is calculated from 3. Identify the physiological parameters typically
data gathered from combined nap periods. measured on a standard polysomnogram, and
discuss available technologies for monitoring each
The maintenance of wakefulness test is similar to the of them.
MSLT in that a series of five nap opportunities is given
4. Define and discuss the importance of sensitivity,
at 2-hour intervals and a mean sleep latency is
frequency filters, and impedance checking when
reported. In contrast to the MSLT, however, the patient
performing a polysomnogram.
remains upright in a dimly lit room and is instructed to
try to stay awake for 40 minutes. The test is terminated 5. Discuss the importance of performing a patient
if sleep is noted or after 40 minutes if the patient calibration before starting a polysomnogram.
remains awake. This test is used less frequently than the 6. Identify four common side effects of CPAP
MSLT and no clear standards exist for interpreting the therapy, and discuss methods to reduce or
results. eliminate each.
MULTIPLE-CHOICE QUESTIONS and sleep spindles is characteristic of which stage

of sleep?
1. An EEG frequency ranging between 4 cps and 8 cps
a. REM
is classified as:
b. Stage N1
a. delta rhythm.
c. Stage N2
b. theta rhythm.
d. Stage N3
c. alpha rhythm.
d. beta rhythm.
2. A patient experiences 78 impaired respiratory
events throughout the night. She has a total sleep 1. What approach might be taken to convince a
time of 312 minutes during a recording period of patient to try CPAP therapy on the CPAP titration
400 minutes. This patient’s respiratory disturbance night after he has refused to wear the nasal mask
index is: because of feelings of claustrophobia?
a. 10 per hour. 2. During monitoring of a standard nocturnal
b. 15 per hour. polysomnogram, the onset of a cardiac arrhythmia
c. 25 per hour. is observed and identified as ventricular tachycar-
d. 40 per hour. dia. What action should be taken?
3. An epoch is an interval of time used when staging
sleep, and in polysomnography it has a standard
duration of: References
a. 15 seconds. 1. Rechtschaffen, A., and Kales, A., eds. A Manual of
b. 20 seconds. Standardized Terminology, Techniques and Scoring
c. 30 seconds. System for Sleep Stages in Human Subjects. Washington,
d. 60 seconds. DC: U.S. Government Printing Office; 1968.
4. Which of the following MSLT results is the 2. Iber C, Ancoli-Israel S, Cheeson A, Quan SF. The
most consistent with a diagnosis of AASM Manual for the Scoring of Sleep and Associated
narcolepsy? Events: Rule, Terminology and Technical Specifications.
a. a mean sleep latency of 15 minutes and no Westchester, IL: American Academy of Sleep
sleep onset REM periods Medicine; 2007.
b. a mean sleep latency of 2.5 minutes and no 3. American Academy of Sleep Medicine. International
sleep onset REM periods Classification of Sleep Disorders, 2nd ed: Diagnostic
c. a mean sleep latency of 8 minutes and a sleep and Coding Manual. Westchester, IL: American
onset REM period in the first nap Academy of Sleep Medicine; 2005.
d. a mean sleep latency of 4.5 minutes and 4. American Association for Respiratory Care.
sleep onset REM periods in naps 1, 3, Cardiopulmonary Diagnostic CPG Focus Group
and 4 and the Association of Polysomnographic Tech-
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5. Which of the following controls on the polygraph
polysomnography. Respir Care. 1995;40:1336–1343.
can be used to reduce electrical supply line interfer-
5. Harner PF, Sannit T. A Review of the International
ence in the EEG channels?
Ten-Twenty System of Electrode Placement. Quincy,
a. sensitivity
MA: Grass Instrument Co; 1974.
b. high-frequency filter
6. The report of the American Academy of Sleep
c. low-frequency filter
Medicine Task Force. Sleep-related breathing
d. 60-Hz notch filter
disorders in adults: recommendations for syn-
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and is accompanied by continuous paradoxical 7. Kushida CA, Littner MR, Morgenthaler T, et al.
motion between the thoracic and abdominal effort Practice parameters for the indications for poly-
channels is defined as: somnography and related procedures: An update
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c. a mixed apnea. Academy of Sleep Medicine. Practice parameters for
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7. A relatively low-voltage, mixed-frequency EEG the maintenance of wakefulness test. Sleep.
pattern with variable occurrences of K-complexes 2005;28:113–121.
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1992;9:21–31. Terminology, Techniques and Scoring System for Sleep
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Lee-Chiong TL. Sleep: A Comprehensive Handbook.
Hoboken, NJ: Wiley; 2005.
CHAPTER 19
Cardiac and Hemodynamic Monitoring

Barbara Ludwig and L. Micky Mathews
OBJECTIVES
• Describe the timing of electrical and mechanical events of the cardiac cycle.
• Identify the lead placement for the 12-lead ECG.
• Identify the steps involved in analyzing an ECG strip.
• Correctly identify various abnormal ECG patterns from a selection of examples.
• Identify and choose lethal arrhythmias from a sample of ECG tracings.
• Given a sample ECG tracing, calculate the heart rate.
• Identify the signs, symptoms, and causes of cardiac dysfunctions.
• List the factors that affect preload, afterload, and contractility, and discuss the impact of preload, afterload,
and contractility on cardiac output.
• Given the appropriate data, calculate various hemodynamic variables.
• Discuss the significance of monitoring mixed venous oxygenation to evaluate hemodynamic status.
• Describe the thermodilution method of measuring cardiac output, and identify the thermodilution curve
associated with poor injection technique and with normal, high, and low cardiac output.
CHAPTER OUTLINE
The Cardiac Cycle T-Wave
Cardiac Leads U-Wave
Standard 12-Lead ECG Q-T Interval
Alternative Leads Determination of Heart Rate
Continuous ECG Monitoring Six-Second Technique (Universal Technique)
Special Diagnostic Monitoring Regular Rhythm Rate Calculation Technique
The ECG: Waveforms and Intervals Steps in Dysrhythmia Recognition
P-Wave Causes of Cardiac Dysrhythmias
P-R Interval and Segment Disorders of Automaticity
QRS Complex Disorders of Conductivity
S-T Segment Combined Disorders of Automaticity
and Conductivity
(continues)
504
CHAPTER 19 ■ Cardiac and Hemodynamic Monitoring 505
(continued)
Types of Cardiac Dysrhythmia Monitoring Oxygenation

Sinus Dysrhythmias Monitoring Cardiac Output/Cardiac Index
Atrial Dysrhythmias Monitoring Central Venous Pressure
Junctional Dysrhythmias Monitoring Pulmonary Artery Pressure
Disturbances of Atrioventricular Conduction Monitoring Pulmonary Capillary
Ventricular Dysrhythmias Wedge Pressure
Pulseless Electrical Activity Monitoring Arterial Pressure
Description Systemic Vascular Resistance
Clinical Significance Pulmonary Vascular Resistance
Ventricular Stroke Work Index
Hemodynamic Evaluation
Evaluation
KEY TERMS
action potential diastasis P-R segment
afterload diastole P-wave
AV dissociation myocardial scintigraphy QRS complex
bicycle ergometer overwedging refractory period
cardiac cycle pericarditis repolarization
cardiac output (CO) preload S-T segment
cardiac tamponade pulmonary vascular systemic vascular resistance
catheter whip resistance (PVR) (SVR)
compensatory pause pulsus alternans systole
contractility pulsus bisferiens T-wave
damped pressure curve pulsus paradoxus T-wave inversion
depolarization pulsus parvus
T
his chapter presents an explanation of basic relaxation, rapid ventricular filling, reduced ventricular
cardiac function, the normal ECG waveform, filling and diastasis, and atrial systole.
the basics of electrocardiography, the analysis
• During the isovolumetric relaxation period, the
of the ECG tracing, and the collection and
myocardial cells are relaxed; all four of the
interpretation of hemodynamic data. Common cardiac
cardiac valves are closed. Venous blood returning
abnormalities, both electrical and functional, are
to the atria causes the pressure in the atria to
discussed. The effects of altered cardiac function, blood
increase.
flow, and pressure in the cardiovascular system are
• After the atrial pressure exceeds ventricular
illustrated, and the concepts of shock are detailed. The
pressure, the atrioventricular valves open,
reader is advised to review the discussion in Chapter 6
allowing for rapid ventricular filling. During this
of the structure and function of the circulatory system.
period, venous blood returns to the atria quickly
but passively, filling the ventricles. As the
ventricles begin to fill with blood, the pressure
The Cardiac Cycle within the ventricles rises and becomes equal
The cardiac cycle (one complete heartbeat) consists of with that of the atria.
two phases: a period of relaxation called diastole • As the pressure equalizes, the rate at which
followed by a period of contraction called systole. The blood flows from the atria into the ventricles
diastolic phase has four components: isovolumetric begins to slow (reduced filling) and eventually
comes to a virtual standstill (diastasis). At this balance of ions (potassium, sodium, chloride, and
point, the atria contract in response to an calcium).
electrical impulse generated by the sinoatrial
• Depolarization (a change in transmembrane
(SA) node.
potential from negative toward positive) is
• The contraction of the atrial muscle cells
referred to as the fundamental electrical event of
(systole) increases pressure in the atria and
the heart because it stimulates the cardiac cells to
propels the remaining atrial blood into the
contract. Depolarization spreads from cell to
ventricles. This propulsion is referred to as the
cell, producing a wave of electrical current
atrial kick. After the atrial kick, pressure within
that spreads (is propagated) throughout the
the atria drops, and the atrioventricular valves
myocardium.
close, thereby ending diastole.
• Repolarization (a change in transmembrane
Systole occurs in response to electrical activation of potential from positive toward negative) occurs
the ventricular myocardial cells. The systolic phase of after depolarization is complete. With repolar-
the cardiac cycle has three components: isovolumetric ization, the cardiac cells return to their resting
contraction, rapid ejection, and reduced ejection. potential (i.e., negative inside, positive outside).1
• Once the ventricular myocardium has received a One electrical cycle of depolarization and repolar-
nerve impulse, the muscles contract; however, ization within a single cell is an action potential, and
the semilunar valves remain closed initially. it is the stimulus that initiates the contractile process.
Because there is no change in the ventricular An action potential is generated (initiated) by a change
volume at this point, this component is referred in cardiac cell membrane permeability to specific ions
to as isovolumetric (iso- means “same”) contrac- (sodium and calcium). This change allows a sudden
tion. Contraction of the ventricular myocardial influx of positively charged ions into the cell, thus
cells increases the pressure in the ventricles. causing depolarization. Every time an action potential
When the intraventricular pressure becomes is generated, it stimulates adjacent cells to depolarize
greater than the pressure in the aorta and pulmo- until the entire heart has been depolarized.1,2
nary artery, the semilunar valves are pushed There are three basic types of cardiac cells in the
open. atria and ventricles: pacemaker cells, conducting cells,
• With the opening of the semilunar valves, blood and myocardial cells.
is rapidly ejected into the great vessels.
• The pacemaker cells are the electrical generators of
• The rapid ejection period is followed by the
the heart. These cells spontaneously discharge an
reduced ejection period. Although the ventricular
action potential at a “preset” rate. The primary
muscle cells remain contracted during the
pacemaker of the heart is the SA node, which
reduced ejection period, the flow of blood out of
generates action potentials at a rate of 60–100
the ventricles begins to slow as the volume of
times per minute. This rate can vary considerably
blood in the ventricles diminishes.
depending on the activity of the autonomic
Secondary to the reduction in blood flowing out of the nervous system and the demands of the body for
ventricles, pressure in the ventricles and the great more blood flow.1,2
vessels begins to drop. When the electrical stimulus is • Each time the SA node fires an action potential,
no longer present, the ventricular muscle fibers relax. it propagates depolarization throughout the
During relaxation, pressure in the ventricles drops so heart via the conducting cells. These cells, found
dramatically that the pressure in the aorta and pulmo- in both the atria and the ventricles, carry the
nary artery is greater than that in the ventricles; the electrical current quickly from the pacemaker
difference in pressure pushes the semilunar valves cells to the myocardial cells.
closed. Once the aorta and pulmonary valves are • As the electrical impulse spreads to the myocar-
closed, isovolumetric relaxation begins, and the cardiac dial cells, muscle contraction occurs. The
cycle repeats.1 contraction is secondary to a process called
The events of the cardiac cycle involve a series of excitation-contraction coupling, which is the
complex electrical, chemical, and physical events in response of the muscle fibers to the excitation
the cardiac cells. When cardiac cells are at rest, they are signal with rapid depolarization followed by a
electrically polarized; specifically, the inside of the cell mechanical response, in this case cardiac con-
is negatively charged, and the outside of the cell is traction. The myocardial cells contain the
positively charged. (This difference in charge from contractile proteins actin and myosin, which are
inside to outside is called the transmembrane potential.) necessary for the heart to contract. When the
The resting cell remains polarized owing to the action myocardial cells are depolarized, calcium is
of a membrane pump that maintains the proper released into the cell. The calcium allows the
coupling of actin and myosin for contraction. STANDARD 12-LEAD ECG

After depolarization is complete, the cardiac cells The three bipolar leads are the original leads selected by
repolarize, returning to their resting polarity, Einthoven to record the electrical impulses of the heart
calcium is no longer available, the bond between in the frontal plane. (Willem Einthoven was a Dutch
actin and myosin molecules is broken, and the physician who received the Nobel Prize for physiology
cell relaxes.1,2 and medicine in 1924 for the invention of the electro-
The normal cardiac cycle begins with the stimulus cardiograph.) Electrodes are applied to the body limbs:
originating from the SA node. The electrical impulse is the right arm (RA), left arm (LA), and left leg (LL), as
conducted through the atrial muscle cells to the atrio- shown in Figure 19-1. The right leg (RL) electrode is the
ventricular (AV) node. The transmission of the electrical ground (G), or neutral, electrode. The RA electrode is
impulse is momentarily delayed at this point to allow always the electrically negative pole. The LA electrode is
the atria to contract, ejecting the last bit of blood into electrically positive in lead I and negative in lead III.
the ventricles. From the AV node, the electrical impulse The LL is always the electrically positive pole.1,3,4
is conducted through the bundle of His to the ventricles • Lead I: Left arm positive (⫹) and right arm
via the left and right bundle branches. From the bundle negative (⫺)
branches the impulse is then carried through the • Lead II: Left leg positive (⫹) and right arm
Purkinje fibers to the ventricular muscle.1,2 negative (⫺)
The electrocardiogram (ECG) records the electrical • Lead III: Left leg positive (⫹) and left arm
impulse as it moves through the conducting system of negative (⫺)
the heart by means of electrodes placed on the body.
The relationship among the three leads is expressed
The waveforms inscribed on the ECG reflect the waves
mathematically by Einthoven’s equation:
of depolarization and repolarization.
electrical potential of lead II ⫽ electrical potential
• As the wave of depolarization spreads through of lead I ⫹ electrical potential of lead III
the atria, the ECG records a positive deflection
called the P-wave. The limb electrodes have standard color designations to
• After the atrial depolarization, the wave of help the practitioner attach the correct ECG machine
depolarization is delayed at the AV node. This AV leads to the patient’s surface limb electrodes:1,3,4
nodal delay is recorded as a straight line called • Right arm (RA) is white.
the P-R segment. • Left arm (LA) is black.
• Depolarization of the ventricles is also recorded • Right leg (RL or G) is green.
as a positive deflection, called the QRS complex. • Left leg (LL) is red.
• Because the atria repolarize during ventricular
Unipolar leads are divided into different types:
depolarization, atrial repolarization is not seen
limb leads, precordial (V) leads, and intraesophageal
on the ECG.
leads. Of these three types, only the intraesophageal
• For a short time following ventricular depolar-
leads are not included in the 12-lead ECG. Unipolar
ization, the ventricular muscle cells are refractory
limb leads resemble bipolar frontal leads in several
to further stimulation. This refractory period,
ways. They measure the patient’s cardiac activity in the
called the S-T segment, is seen as a straight line
frontal plane, and they have the same electrically
on the ECG.
positive pole. The unipolar limb leads differ from
• Following the refractory period, the ventricles
bipolar leads in that, instead of a negative electrode, the
repolarize; the cardiac cell has recovered its
unipolar leads have a so-called indifferent electrode.1,3,4
normal resting membrane potential. On the
The indifferent electrode is the average of the other
ECG, ventricular repolarization is seen as
two augmented leads acting as the negative electrode
another positive deflection, called the T-wave.
(RA, LA, LL). Therefore, when the electrodes are placed
One complete cardiac cycle is represented by the on the extremities (RA, LA, LL), the ECG deflections
P-wave, QRS complex, and T-wave.1,2 represent the difference in potential between the
selected limb lead and the average potential of the
remaining two unipolar limb leads.
Cardiac Leads The unipolar limb leads are termed aVR, aVL, and aVF.
The standard 12-lead ECG comprises bipolar and • The a before VR, VL, and VF indicates that wave-
unipolar leads that record the electrical activity of the forms are amplified (1.5 times). The amplifica-
heart from 12 different views. Leads are placed on the tion is necessary to see ECG deflections.
patient’s chest and limb skin surface. Each lead acts as • The V identifies that it is a unipolar lead.
an “eye” that looks at the heart from a unique • The letters R (right), L (left), and F (left leg) refer to
perspective. the limb lead that acts as the positive electrode.1,3,4
Lead I
Right Arm Left Arm

(−) (+)
Negative Positive
I
Lead II Lead III
Right Arm Left Arm

(−) (−)
Negative Negative
II III
Left Leg Left Leg

(+) (+)
Positive Positive
The Einthoven Triangle
R L
(−) (+)
(−) (−)
I
II III
(+) (+)
F
FIGURE 19-1 The six frontal plane leads consist of three bipolar leads (I, II, III) and three unipolar
leads (aVR, aVL, aVF). The electrode placements for the frontal leads are the right arm (RA), left arm
(LA), and the left leg (LL), with the ground, or right leg, designated as G. The electrode polarity
(⫹ or ⫺) is identified for each lead electrode placement site.
• V3: Fifth intercostal space midway between V2

and V4
• V4: Fifth intercostal space, midclavicular line
• V5: Fifth intercostal space, anterior axillary line
• V6: Fifth intercostal space, midaxillary line
Bedside monitors can be used to obtain a 12-lead
ECG. Software available on bedside monitors allows
clinicians to intermittently obtain a 12-lead printout
V1 V2 V3 using the monitor leads.1,3,4
V4V5 V6
ALTERNATIVE LEADS
Any lead may be placed on any part of the body to
obtain an ECG tracing. These alternative leads are
RA
RA L
LA standardized and used in clinical electrocardiography.
MCL System. An alternative bipolar lead system is the

MCL (modified chest left arm) system, which is frequently
used for continuous monitoring in intensive care units.
A common lead of this system is MCL1, which is a
RL
R L LL
LL modification of the precordial lead V1. The positive
electrode (exploring electrode) is placed at the V1
position (fourth intercostal space, to the right of the
sternum). The left arm is the electrically negative pole,
and the ground, or neutral, electrode is in the RA
FIGURE 19-2 Six standard precordial leads: The V before position (Figure 19-3).
the lead number identifies it as a unipolar lead. The primary use of this lead in continuous ECG
monitoring is to detect bundle branch conduction
abnormalities. MCL6 is also commonly used to identify
Six unipolar precordial, or chest, leads (V1–V6) are
bundle branch conduction abnormalities (Figure 19-4).
placed on specific areas of the anterior chest wall
The Lewis lead is a special bipolar chest lead that
(Figure 19-2). These leads measure the heart’s electrical
amplifies atrial waves and makes it easier to identify
activity in the horizontal plane. The common chest
the presence and possible physiological mechanism of
positions of precordial leads are as follows:
atrial dysrhythmias (Figure 19-5). The other precordial
• V1: Fourth intercostal space, right sternal border chest leads could also be used for monitoring and
• V2: Fourth intercostal space, left sternal border diagnostic purposes.1,3,4
RA or RL serves Negative electrode

as ground near left shoulder
G –
Positive electrode +
in V1 position
FIGURE 19-3 The MCL1 lead helps in the differential diagnosis of a bundle branch block.
RA or RL serves Negative electrode

as ground near left shoulder
G –
+ Positive electrode
in V6 position
FIGURE 19-4 The MCL6 lead helps in the differential diagnosis of a bundle branch block.
Negative electrode
near right shoulder
–
Positive electrode + Left leg serves
in V1 position G as ground
FIGURE 19-5 The Lewis lead allows better visualization of P-waves and aids in the
diagnosis of atrial dysrhythmias.
Esophageal and Intra-Atrial Leads. Esophageal leads, electrode at the tip is threaded through the nasal
or E-leads, are used for diagnosis, not for continuous catheter and advanced into the esophagus. The number
monitoring. Since the esophagus is behind the left after the E represents the distance of that electrode in
atrium and in close proximity to the heart, E-leads can centimeters from the nares.6,7
be used to reveal atrial activity more clearly than the Similar information can be obtained with an
standard leads.5 They are also helpful in evaluating the intra-atrial lead, which is inserted directly into the right
function of the conducting system and in revealing atrium by way of a peripheral vein. The lead permits
mechanisms of dysrhythmias. A nasal catheter is bundle of His electrical studies, which provide defini-
introduced into the patient’s nares. A wire with the tive information for diagnosing cardiac dysrhythmias.7
limbs (RA, LA, LL) may be identified as the positive

electrode and negative electrode. The electrode posi-
tions determine the lead monitored—lead I, II, or III.
MCL1 may also be continuously monitored using the
three-lead system. The positive electrode is placed in
the V1 position, and the negative electrode is placed
under the left clavicle (LA). The ground is usually
positioned on the RL, LL, or RA. Placing the positive
electrode in the appropriate precordial chest position
V2R V1R
can also monitor other modified chest leads (MCL2⫺6).
V6R
V3R A five-electrode monitoring system uses four limb
V5R
V4R electrodes (RA, LA, RL, LL) in the traditional locations.
The fifth electrode may be placed in the desired
MCL1⫺6 position. This five-electrode system permits
monitoring of one or more of all 12 leads at the
patient’s bedside.1,4
Special Diagnostic Monitoring
Holter monitoring is a type of continuous monitoring
used to diagnose the occasional dysrhythmia. The
FIGURE 19-6 Alternative precordial lead placement: The Holter monitor is a portable ECG monitor with a
ECG leads are placed on the right side of the chest in the memory. The patient wears the monitor for 24–48
same location as the left-sided leads; for example, V2R is
hours. Since these patients’ dysrhythmia occurs infre-
the same as V1.
quently, it is more likely to occur within this extended
time period than in a short office visit. The Holter
equipment records two or three channels of the ECG
Other Unipolar Precordial Lead Systems. Unipolar onto a cassette tape or flash card for analysis by the
precordial leads can be positioned in different locations cardiologist after the 48-hour period. The leads are
on the anterior and posterior chest. usually modified chest leads that resemble V1 and
V5 because they are more sensitive at detecting atrial
• They can be continued to the vertebral border on
dysrhythmias and bundle branch blocks. The patient’s
the left posterior chest and, if so, are designated
chest is wrapped in an elastic bandage to keep the leads
V1–V9.
in place. Patients are instructed to keep a diary and
• They may be placed on the right side of the
write down the precise times they experience symp-
chest. The placement mirrors the left-sided
toms. The diary is then compared with the downloaded
electrode placement, and the leads are
ECG recordings to determine whether a dysrhythmia
designated V1R–V9R.
occurred at the time that the patient felt symptoms.6
• They can also be placed on the right side of the
For patients whose dysrhythmias occur too infre-
chest at one intercostal space higher than the
quently for the Holter monitor to record them, a
traditional placement on the left chest and
transtelephonic event monitor may be necessary. Patients
designated 3V3R–3V6R or 3V9R.
wear the unit and activate it only when they experience
symptoms, such as palpitations or dizziness. The unit
The positions of the special leads allow examination of records the ECG for 3–5 minutes and stores it in
the electrical activity of the posterior wall of the heart memory. The patient then attaches the unit to a
or of the right ventricle (Figure 19-6).1,4 modem and transmits the ECG information for
evaluation. This diagnostic technique allows monitor-
ing for months, making the dysrhythmia diagnosed
Continuous ECG Monitoring accurate.6
Continuous bedside ECG monitoring is often per- The cardiac stress test, or exercise tolerance test, is a
formed. Up to 12 leads can be monitored continuously diagnostic procedure that allows assessment of the
from the patient’s bedside. individual’s cardiovascular response to exercise. This
A three-lead monitoring system uses one electrode noninvasive procedure is used as the initial screening
designated as positive (⫹), a second designated as test for the detection of coronary artery disease. An
negative (⫺), and a third as a ground. Any two of the ECG monitor and a noninvasive blood pressure cuff
Best Practice
Double Product
Double product is a calculated monitoring
parameter that is used to determine the patient’s
cardiovascular response to exercise. Equal to the
product of the patient’s exercise blood pressure
multiplied by the exercise heart rate, it is a good
measure of myocardial oxygen consumption. If
the patient’s myocardial oxygen needs exceed
myocardial oxygen consumption, the patient will
show signs of myocardial ischemia, such as chest
pain, and ECG changes. Two such ECG changes
are T-wave inversion (a symmetrical, sharply
pointed T-wave that has negative amplitude in
leads that are typically positive) and depressed
ST segment (discussed later in this chapter). If
the patient manifests any of these symptoms, the
cardiac stress test must be terminated, and the

patient must be closely monitored for continuing
or worsening symptoms.
Exercise BP ⫻ Exercise Heart Rate
⫽ Double Product
FIGURE 19-7 A stress test is performed to test cardiac
function.
are attached to the patient, who then ambulates on a

treadmill (a bicycle ergometer may also be used) at patient with radioactive imaging agents during the
gradually increasing speeds and angles of incline stress test permits visualization of areas of poor
(Figure 19-7). If a bicycle ergometer is used, the coronary circulation. If no defects are observed, the
resistance is gradually increased. According to the patient does not have to go through cardiac catheter-
American College of Cardiology/American Heart ization, which is more invasive and associated with
Association (ACC/AHA), it is an absolute indication to more complications.8,9
stop an exercise stress test when the patient:8,9
• Is unable to continue.
• Experiences moderate to severe angina. The ECG: Waveforms
• Reaches the maximum exercise heart rate and Intervals
{predicted maximum HR ⫽ [210 ⫺ (patient’s
age ⫻ 0.65)]}. The ECG produces a printout that shows the electrical
• Is manifesting cardiac symptoms such as ST events in all the leads (Figure 19-8). The ECG wave-
segment elevation, poor tissue perfusion, or forms represent the electrical activity of the cardiac
sustained ventricular tachycardia. chambers during systole and diastole. The intervals
between waveforms are time measures that indicate the
A cardiac stress test is by no means infallible. amount of time in fractions of a second that the heart
The results can be false positive or false negative. A requires to depolarize and repolarize the atria and
positive test result indicates coronary artery disease ventricles (Figure 19-9 and Table 19-1).1
(CAD), but this finding must be closely examined in
light of the individual’s risk factors, such as age,
family history of CAD, smoking history, diabetes, P-WAVE
hyperlipidemia, or hypertension. A positive stress test The P-wave is the first waveform seen on the ECG and
in an otherwise healthy young individual with represents atrial depolarization. Normally, the atrial
minimal risk factors may lead the physician to tissue does not initiate the electrical impulse. The
recommend a myocardial scintigraphy study in P-wave reflects atrial depolarization after the SA node
conjunction with the exercise stress test. Injecting the impulse reaches the atria.1,10
I aVR V1 V4
II aVL V2 V5
III aVF V3 V6
FIGURE 19-8 The 12-lead ECG consists of three standard leads and three augmented leads that view the
heart in the frontal plane, and six precordial chest leads that view the heart in the horizontal plane.
3 seconds
P
T
S
Q
Time (ms)
FIGURE 19-9 ECG waveforms.
P-R INTERVAL AND SEGMENT (Figure 19-10), lasting from the end of the P-wave to
The P-R interval (P-RI) and the P-R segment are time the beginning of the Q-wave. Any changes in the P-R
measures. The P-R interval lasts from the beginning segment alter the P-RI. Because the P-RI is easier to
of the P-wave to the beginning of the Q-wave. The calculate, it is the more commonly used of the two
P-R segment is a component of the P-R interval time measures (Table 19-2). Although the P-RI is
TABLE 19-1 ECG Waveforms

Waveform
Characteristic P-Wave QRS Complex T-Wave U-Wave
Shape Symmetrical, gently Sharp and narrow; Variably shaped; Symmetrical and
rounded consists of ⱖ1 waves usually asymmetrical round
representing ventricular and slightly rounded
electrical activity
(Q-, R-, and S-waves)
Amplitude 0.5–2.5 mm Deflection height from ⬍5 mm Usually flat;
baseline—positive or ⬍2 mm
negative—varies from
2 to 15 mm
Duration ⬍0.11 s ⬍0.12 s 0.10–0.25 s Not known
Direction Positive in lead II; Variable, depending on In lead II, positive; in In lead II, positive;
variable in other leads lead and patient’s other leads, variable in other leads,
electrical axis; net direction parallels the
amplitude may be preceding T-wave
positive, negative, or
equally positive and
negative
Miscellaneous Normal P-wave Normal QRS indicates Abnormal T-wave Abnormal U-wave
information indicates normal origin ventricular activation indicates abnormal information seen in
of electrical impulse with occurred through the ventricular repolarization hypokalemia,
normal depolarization of normal conduction (premature ventricular hyperthyroidism, left
right and left atria pathway contraction, bundle ventricular hyper-
branch block, electrolyte trophy, certain
disturbance, medication, cardiac drugs; not
myocardial infarction) observed in most
ECGs
stimulation, by severe heart disease and the effects of

the disease process on conductivity, and by medica-
tions affecting the autonomic nervous system.1,10
QRS COMPLEX
The QRS complex represents ventricular depolariza-
tion. It is the waveform from the beginning of the
P-R Interval
Q-wave to the end of the S-wave. The time from Q to S
is referred to as the QRS time or QRS duration. The

complex consists of one or more of the following: a
positive deflection called the R-wave and two negative
deflections called the Q-wave and the S-wave. Each
Time (ms)
wave represents a different aspect of ventricular depo-
FIGURE 19-10 The P-R interval (bar between vertical lines)
larization (Figure 19-9).1,10
and the P-R segment (portion of wave between diagonal
lines).
Q-Wave. The Q-wave is the first negative deflection in
the QRS complex that is not preceded by an R-wave.
predominately used as an indicator of electrical The Q-wave deflection represents ventricular septal
conduction through the AV junction, remember that depolarization.
P-RI normally changes with heart rate. The primary
causes of P-RI abnormalities are slowed or blocked R-Wave. The R-wave is the first positive deflection in
conduction caused by parasympathetic nervous system the QRS complex. If the QRS complex has additional
TABLE 19-2 ECG timing and intervals

Characteristic P-R Segment P-R Interval R-R Interval S-T Segment Q-T Interval
Significance Detects changes in Same as Detects changes Deviation indicates Deviation reflects
AV nodal conduction; P-R segment; in heart rate and abnormal ventricu- changes in time
short line seen in lengthens in rhythm regularity; lar repolarization; required for ven-
junctional dysrhyth- bradycardia short interval seen elevation indicates tricular repolariza-
mias and sinus or in tachydysryth- acute myocardial tion; prolonged Q-T
atrial tachycardia; mias; long intervals infarction; depres- interval more com-
long line seen in seen in bradydys- sion indicates myo- mon than short-
first-, second-, and rhythmias; variable cardial ischemia ened one: caused
third-degree heart intervals seen with by some cardiac
blocks premature beats, drugs, hypokalemia
some heart blocks, and calcemia, and
atrial fibrillation or acute myocardial
flutter infarction; patient
is susceptible to
lethal dysrhythmias
How Time from end of Time from start Measured by Time from end of Time from the
calculated P-wave to start of of P-wave to number of large S-wave to begin- beginning of the
QRS complex start of QRS or small squares ning of T-wave; QRS complex to
complex from beginning of normal allowed the end of the
one QRS complex baseline deviation: T-wave
to end of next QRS 2 mm above,
complex 0.5 mm below
Normal duration 0.05–0.08 s 0.12–0.20 s Consistent with ≤ 0.20 s Heart rate
rate 60–100 pbm dependent; less
than half of
preceding R-R
interval
Miscellaneous Less practical than Varies with Variation indicates Duration is heart Trend changes
Information P-RI heart rates rhythm irregularity rate dependent more important
than absolute
values
positive deflections, the second positive wave is called baseline on the ECG tracing. It represents the early part
R⬘ (R prime), and the third positive wave is called R⬙ of ventricular repolarization, the time from the end of
(R double prime). The R-wave deflection represents an S-wave to the beginning of the T-wave. During the
early ventricular depolarization. S-T segment, the ventricles are absolutely refractory to
additional electrical stimulation. The area on the ECG
S-Wave. The S-wave is the first negative deflection after tracing where the QRS complex ends and the S-T
an R-wave. If the QRS complex has more than one segment begins is called the junction, or J point. The S-T
negative deflection after the R-wave, then the second segment extends to the point at which the T-wave
negative deflection is called S⬘ (S prime), the third is begins (Figure 19-11).1,3,10
called S⬙ (S double prime), and so on. The S-wave
deflection represents late ventricular depolarization. T-WAVE
The T-wave (Figure 19-9) represents ventricular repolar-
QS-Wave. A QS-wave is a wave in the QRS complex ization. The T-wave always occurs after a QRS complex,
with a single negative deflection and no positive even though it may be difficult to see because of low
deflection (i.e., no R-wave). 3,10 amplitude.1,11
S-T SEGMENT U-WAVE

The S-T segment is usually observed as an isoelectric The U-wave is not observed in most ECG tracings. It is
(straight) line or as a sloping shape relative to the thought to represent the final stage of Purkinje fiber
repolarization. It is a small deflection after the T-wave in therapist should understand. Measured from the
a direction that usually parallels that of the T-wave.1,11 beginning of the QRS complex to the end of the
T-wave, the Q-T interval represents ventricular depolar-
Q-T INTERVAL ization and repolarization. Normally it varies with
The Q-T interval (Figure 19-12) is not normally used gender, age, and heart rate. The term QT(c) is the Q-T
in ECG analysis, but it is something the respiratory interval that has been “corrected” or adjusted for the
patient’s heart rate.3,4 For a heart rate of 70 bpm, the
QT(c) is ⱕ0.40 s. It is calculated by Bazett’s Formula:12
QT
QT(c) ⫽ ________________
RRR (in seconds)
For every 10 bpm increase above 70, subtract 0.02 s,
T and for every 10 bpm decrease below 70, add 0.02 s.
For example:
S QT ⱕ 0.38 @ 80 bpm
QT ⱕ 0.42 @ 60 bpm
Determination of Heart Rate

Time (ms) Two of the various techniques that can be used to
FIGURE 19-11 The S-T segment. determine the patient’s heart rate using the ECG tracing
are discussed here.
Timing is measured by the grid on the ECG paper.
Time markers (1 second, 3 seconds, 6 seconds) appear
on some ECG paper. If they do not, just remember that
there are 30 large squares in 6 seconds, 15 large squares
in 3 seconds, and 300 large squares in 1 minute
(Figure 19-13).
SIX-SECOND TECHNIQUE (UNIVERSAL

TECHNIQUE)
If the patient has an irregular rhythm, use a sampling

procedure to determine heart rate (the most common
is to count the heart rate for 6 seconds). To use this
technique, count the number of R-waves (which is the
Time (ms) same as the number of QRS complexes) in a 6-second
FIGURE 19-12 The Q-T interval. sample of the ECG strip and then multiply that num-
ber by 10. The result is a close estimation of the actual
3 second marks
1 sec
2 sec
3 sec
4 sec
5 sec
6 sec
Each 1-second interval is composed of 5 large boxes or 25 small boxes

FIGURE 19-13 ECG intervals.
heart rate (beats per minute). (Also count the number Step 2: Analyze the heart rate.
of P-waves if the P-wave rate is needed to help with • Is the rate normal? The rate eliminates a large
dysrhythmia interpretation.) Using a 3-second sample group of dysrhythmias from the possibilities.
of R-waves and then multiplying by 20 is possible, but Tachycardia eliminates bradycardias and AV
the resulting heart rate estimation is less accurate. blocks. Bradycardia eliminates atrial tachycardia,
sinus tachycardia, and ventricular tachycardia.
REGULAR RHYTHM RATE CALCULATION
Step 3: Analyze the ventricular rhythm.
TECHNIQUE
• Is the R-R interval regular or irregular?
When the patient has a regular rhythm, use the follow-
• Is there a pattern to the irregularity, or does it
ing heart rate calculation technique: Count the number
occur unpredictably?
of large squares between two QRS complexes and
• If the rhythm is irregular, eliminate the problems
divide the count into 300. The quotient is the
that would show a regular rhythm, such as sinus
heart rate.
bradycardia and tachycardia.
If the QRS complexes do not fall exactly on the
large square lines, an alternative method is to count the Step 4: Analyze the P-waves.
number of small squares between two QRS complexes • Are P-waves present?
and divide that number into 1500 (there are 1500 • Do all the P-waves look the same?
small squares in 1 minute of ECG paper). The quotient • Is the P-wave upright or inverted in lead II?
is the heart rate.1 • Is the P-P interval regular or irregular? Are F- or
f-waves present? (See Atrial Dysrhythmias on
page 520.)
Steps in Dysrhythmia
Step 5: Analyze the PQRST relationship to determine
Recognition whether a heart block or ectopic beats are present.
When interpreting an ECG, the keys to accuracy are • Is there one P-wave for each QRS complex?
consistency and thoroughness. The key to interpreting • How long is the P-RI?
an ECG is similar to that for performing any clinical • If the relationship of the P-wave to the QRS
procedure: Follow the same steps every time when complex is abnormal, does the abnormal pattern
analyzing each ECG. Using a systematic approach repeat in a constant time interval, or does the
ensures that nothing is overlooked. Although no one interval vary?
set sequence is standard, analyzing the QRS com-
plexes must always come first because it identifies Step 6: Identify the site of the dysrhythmia.
life-threatening cardiac dysrhythmias that require • Is the dysrhythmia supraventricular or ventricu-
emergency treatment. The following suggested lar in origin?
sequence for interpreting an ECG enables the inter- • Are the P-waves upright in lead II (sinus), or are
preter to eliminate possibilities at each step. Through they inverted (junctional)?
this process, the reader can identify whatever dys- • Is the QRS complex of normal duration (supra-
rhythmia appears. ventricular)?
• If the QRS complex is wide, is it really a ventricu-
Step 1: Analyze the QRS complexes. lar beat, or is a conduction delay in the ventricle
• Are there recognizable or normal QRS com- causing the prolonged QRS duration?
plexes? If not, consider ventricular fibrillation,
asystole, or ventricular tachycardia—all pulseless Step 7: Now the dysrhythmia should be identifiable.1
rhythms.
• In the presence of normal QRS complexes, does Causes of Cardiac Dysrhythmias
the patient have a pulse? If not, consider pulse- There are many causes of cardiac dysrhythmias (abnor-
less electrical activity—a cardiac emergency. mal cardiac rhythms): coronary artery disease, electro-
• After determining that the patient does not have lyte imbalance, congestive heart failure, drug toxicity,
a life-threatening dysrhythmia, identify the and many more. But all these clinical problems cause
shape and duration of each QRS complex. Do just three abnormalities in cardiac electrophysiology:
all the QRS complexes look the same? If not, abnormal automaticity, abnormal conductivity, or a
identify normal and abnormal QRS durations. combination of the two.1
With a normal QRS duration, the rhythm is
supraventricular; a wide QRS indicates a ven- DISORDERS OF AUTOMATICITY
tricular rhythm or a conduction disturbance in The heart rate is determined by the inherent rate of
the ventricle.5 self-depolarization by specific cardiac cells (automaticity).
The SA node, AV junction, and ventricular conducting spontaneous depolarization and a conduction distur-
system have their own intrinsic levels of spontaneous bance exist together. These problems may be present in
depolarization that determine their pacemaker rates. a variety of clinical situations. For example, ventricular
The working cells of the myocardium do not normally tachycardia or sinus bradycardia might be combined
possess the property of automaticity but can become with first-degree heart block. Or premature atrial
more excitable in disease states such as coronary artery contraction may coexist with a ventricular bundle
disease and congestive heart failure. Clinical situations branch block. These problems may be transient or
that disturb the inherent excitability of the pacemaker permanent, and they may range from fairly benign
tissue or the myocardial tissue of the atria and ven- to lethal.1
tricles can cause the heart rate to speed up, slow down,
or be irregular. A few examples of dysrhythmias that
may be caused by a disturbance of automaticity are Types of Cardiac Dysrhythmia
sinus bradycardia, premature ventricular contractions, Of the many categories of dysrhythmia, in this chapter
and ventricular tachycardia.1 dysrhythmias are categorized as sinus, atrial, junc-
tional, AV block, and ventricular. The dysrhythmias
discussed are those included in the Advanced Cardiac
DISORDERS OF CONDUCTIVITY
Life Support Course offered by the American Heart
Conductivity is determined by many variables, such as Association. They are common cardiac dysrhythmias
electrolyte balance, stimulus intensity, and repolariza- seen in critically ill patients and may require mainte-
tion disparity. If conduction is accelerated or slowed, nance or emergency treatment.
then the wave or segment duration is shortened or It is paramount during the analysis of a dysrhyth-
prolonged. For example, if conduction is slowed through mia that you keep in mind the best monitor of how the
the AV junction, as one would see in a heart block, then patient is handling the dysrhythmia is clinical observa-
the P-R interval is prolonged (more than 0.20 second). tion of the patient. You are first and foremost treating
Another common cause of a conductivity problem the patient NOT the monitor.
is the phenomenon known as reentry, which occurs
when there are unequal refractory periods in the heart.
This situation might occur with a premature (early)
SINUS DYSRHYTHMIAS
beat such as a premature atrial contraction. The P-wave In sinus dysrhythmias, the electrical impulses originate
occurs too early in the cardiac cycle, and part of the in the sinus node. The electrical current follows the
conducting system is still refractory to electrical stimu- normal electrical path through the atria, the AV junc-
lation. Consequently, the depolarization wave travels tion, and the ventricles. The ECG has normal waves in
only through the part of the conducting system that the normal sequence. The basic abnormality is the
has recovered. This abnormal depolarization pathway heart rate or the regularity of the waveforms. Table 19-3
takes longer than the normal one. When the previously lists the causes of sinus tachycardia and sinus bradycar-
unresponsive part of the heart muscle has recovered, it dia, and Table 19-4 lists their physiological mecha-
depolarizes and creates a new depolarization wave that nisms and their ECG characteristics.
restimulates the heart. Essentially, the premature atrial
complex has set up a circular wave of self-depolarization, Sinus Tachycardia. Sinus tachycardia is a common
and the resulting dysrhythmia is a very fast, self- dysrhythmia in both healthy and critically ill individu-
perpetuating tachycardia. This dysrhythmia is called als. It has the same characteristics as a normal sinus
paroxysmal supraventricular tachycardia (PSVT). rhythm except for the heart rate.
Other examples of conduction disturbance are
first-degree heart block and second-degree type I heart Description Sinus tachycardia occurs when the baseline
block. In both of these dysrhythmias, conduction is rate sinus node discharge is greater than 100. As the
slowed through the AV junction. This conduction most common dysrhythmia in critically ill patients, it is
problem is reflected by a prolonged P-R interval. In the result of a physiological need for greater cardiac
some cases, the conduction can be so delayed that the output (CO), the amount of blood ejected by the left
depolarization wave does not propagate through the ventricle each minute. Because the causes are so diverse,
AV junction to the ventricle.1 the physician must identify the underlying cause before
attempting to control the dysrhythmia. Figure 19-14
shows the ECG of a patient with sinus tachycardia.
COMBINED DISORDERS OF AUTOMATICITY
AND CONDUCTIVITY Clinical Significance Sinus tachycardia is the most
A combined disorder involving both automaticity common dysrhythmia in the critically ill. Because it can
and conductivity occurs when an abnormal rate of be the result of any of myriad clinical problems, the
TABLE 19-3 Causes of sinus dysrhythmias

Causative Category Sinus Tachycardia Sinus Bradycardia
Autonomic nervous Sympathetic nervous system stimulation: Parasympathetic nervous system stimula-
system exercise, emotion, fever, pain, hypoxemia, tion: carotid massage, vomiting, suctioning,
acidosis, hypercarbia, stimulants (coffee, increased intracranial pressure
tea, nicotine, chocolate)
Drugs or drug toxicity CNS stimulants: norepinephrine, epineph- Beta-adrenergic blockade, calcium chan-
rine, isoproterenol, dopamine, cocaine, nel blockade, organophosphate poisoning,
amphetamines, methamphetamines; adenosine, cholinergic drug toxicity
parasympathetic stimulants: anticholinergic
drugs, tricyclic antidepressants
Diseases or conditions Acute myocardial infarction, congestive heart Well-conditioned athlete, sick sinus syn-
failure, acute pulmonary embolism, pulmo- drome, inferior wall, myocardial infarction
nary edema, shock, hyperthyroidism, sepsis
TABLE 19-4 Sinus dysrhythmia: physiological mechanisms and ECG characteristics

Sinus Tachycardia Sinus Bradycardia
Physiological mechanism Increased automaticity of the SA node Decreased automaticity of the SA node
Rate 100–150 bpm (may go up to 180 bpm) 40–60 bpm (may be lower)
Ventricular rhythm Regular Regular
P-wave Regular sinus P-waves; P-wave rate is same Same as sinus tachycardia
as QRS rate; P-wave upright in lead II
PQRST relationship Normal sequence: one P-wave for each Normal sequence
QRS complex
QRS complex Usually normal ≥0.12 s if bundle branch Same as sinus tachycardia
block or anomalous ventricular conduction
pathway is present
Waveform intervals P-RI and Q-T interval may be shorter than P-RI and Q-T interval may be longer than
normal normal © Delmar/Cengage Learning
FIGURE 19-14 Sinus tachycardia: The rhythm is regular, and the rate is
approximately 136 bpm. The P-wave is visible, and all the P-waves look
the same.
best approach is to treat the underlying mechanism. • In the elderly or individuals with underlying
For example: cardiovascular disease, the reduced ventricular
filling time associated with tachycardia may
• If fever is the cause, the treatment may be the
significantly reduce cardiac output. These
administration of an antipyretic.
patients may require additional treatment to
• If the cause is a bacterial pneumonia with
stabilize their cardiovascular function.1
hypoxemia, then antimicrobial and oxygen
therapy may be sufficient to decrease the Sinus Bradycardia. Sinus bradycardia may occur in
heart rate. normal individuals with a healthy heart, such as
• If the sinus tachycardia is associated with heart well-conditioned athletes. Sinus bradycardia has the
failure, then improving heart function by admin- same characteristics as a normal sinus rhythm except
istering cardiac drugs may decrease the heart rate. for the slower-than-normal heart rate.
ATRIAL DYSRHYTHMIAS
Atrial dysrhythmias originate not from the sinus node,
but from the atrial tissue or atrial conducting struc-
tures. Consequently, the P-wave (atrial depolarization)
may have a different shape, duration, and direction
FIGURE 19-15 Sinus bradycardia: The rhythm is regular, than on a normal ECG. The P-wave alterations depend
but the rate is only about 33 bpm. The P-wave is visible, on the ectopic (abnormal) beat’s origin in the atria
and all the P-waves look the same. and on the ECG lead in which you are viewing the
waveforms.
• If the ectopic beat arises from atrial tissue close
to the sinus node, the P-wave is similar to the
Description Sinus bradycardia occurs when the baseline
P-wave of a sinus rhythm.
rate of sinus node discharge is less than 60 bpm. Found
• If the ectopic beat arises from tissue close to the
in many situations, this dysrhythmia is most common
AV junction, the P-wave may be negative (below
in individuals with underlying heart disease. Many
baseline) because the electrical stimulus depolar-
cardiac drugs may also cause sinus bradycardia. Mild
izing the atria is traveling in an opposite direc-
sinus bradycardia is well tolerated, but for severe drops
tion from normal.
in heart rate (⬍50 bpm), medical treatment is necessary.
Figure 19-15 shows the ECG of a patient with sinus A disturbance in automaticity, conductivity, or a
bradycardia. combination of the two may cause atrial dysrhythmias
(Table 19-5). Table 19-6 describes the physiological
Clinical Significance The individual with sinus mechanisms and ECG characteristics of atrial
bradycardia is not usually symptomatic until the heart dysrhythmias.1,13
rate falls below 50 bpm. With the increasing numbers
of people doing regular physical workouts, the inci- Premature Atrial Contraction. Premature atrial
dences of otherwise healthy persons having bradycar- complexes or contractions (PACs) are also known as
dia has risen. When manifesting symptoms, the person atrial premature contractions (APCs).
usually complains of dizziness, faintness, and light-
headedness. These symptoms appear because of Description An early atrial beat is caused by an
decreased cardiac output and reduced perfusion of ectopic pacemaker in the atria. The ectopic atrial
the brain. pacemaker spontaneously depolarizes before the
For the individual who has suffered an acute next sinus node discharge and causes a premature
myocardial infarction, a mild sinus bradycardia has P-wave. The early P-wave, called a P⬘ (P prime), is
some positive benefits. The slower heart rate different in morphology from the sinus-generated
decreases the work of the heart and thereby lessens P-wave. Usually, the P⬘-wave is conducted and is
the oxygen requirements of the heart muscle. If the followed by a normal or an abnormal QRS complex.
heart rate is too slow, however, cardiac output If the P⬘ wave is too premature, the AV junction
decreases, reducing coronary blood flow and coro- or the bundle branches may still be refractory from
nary perfusion of the heart muscle. When the heart the previous depolarization wave and does not
muscle is not adequately perfused, it becomes propagate the impulse. Consequently, the PAC
oxygen deprived (ischemic), and systolic function is not conducted to the ventricle. Figure 19-16
deteriorates. shows the ECG of a patient with premature atrial
Another complication of sinus bradycardia is contractions.
the increased incidence of ventricular escape beats.
These premature beats help support the cardiac Clinical Significance In the normal person, premature
output by adding to the heart rate. However, they atrial contractions are usually benign and not signifi-
also increase the risk of precipitating serious ven- cant. In individuals with underlying heart disease,
tricular dysrhythmias, such as ventricular tachycar- PACs indicate increased automaticity of the atrial
dia, ventricular fibrillation, or ventricular asystole. tissue or a conduction disturbance. The sudden
The ventricular premature beats are not specifically appearance of frequent PACs warns of greater cardiac
treated because they help support the patient’s irritability and may indicate worsening of cardiac
cardiac output. The basic direction of treatment is to function. When symptomatic, the individual usually
increase the rate of the sinus node. This increase in complains of dizziness, faintness, and lightheaded-
rate may suppress the patient’s premature ventricu- ness. These symptoms appear because of decreased
lar contractions.1,11 cardiac output and reduced perfusion of the brain.1
TABLE 19-5 Causes of atrial dysrhythmias

Premature Atrial Paroxysmal Nonparoxysmal
Causative Contraction Atrial Atrial Atrial
Category (PAC) Tachycardia Tachycardia Atrial Flutter Fibrillation
Autonomic Increased Same as PAC Increased Normal individu- Normal individuals
nervous system sympathetic sympathetic als, secondary secondary to
tone, increased tone, increased to excessive excessive
catecholamines, catecholamines stimulants stimulants
emotion, infec- (coffee, tea, (coffee, tea,
tion, hypoxemia, nicotine, nicotine,
stimulants (coffee, chocolate) or chocolate), or
tea, nicotine, emotional emotional
chocolate) distress distress
Drugs or drug Sympathomimetic Same as PAC Digitalis toxicity Digitalis toxicity Digitalis toxicity
toxicity drugs, digitalis (rare) (rare)
toxicity
Diseases or Occurs in people Occurs in people Heart diseases: Small incidence Small incidence
conditions with apparently with apparently coronary artery in people with in people with
healthy heart; healthy heart; disease or cor apparently apparently healthy
heart diseases: heart diseases: pulmonale healthy heart; heart; heart
myocardial coronary artery heart diseases: diseases; mitral
ischemia, acute disease, rheumatic heart valve disease,
myocardial rheumatic heart disease, hyper- congestive heart
infarction, early disease, acute tensive heart failure, coronary
congestive heart myocardial disease, coronary artery disease,
failure, mitral infarction artery disease, myocardial
valve disease congestive infarction,
heart failure, hypertensive heart
thyrotoxicosis disease
FIGURE 19-16 Premature atrial contractions: The sinus rhythm has three prema-
ture atrial contractions (beats 2, 6, and 9). These early beats have a positive
P-wave before each early QRS. These premature P-waves differ in appearance
from the normal sinus P-waves. The rhythm strip is irregular, and the total rate
is 70 bpm, with an underlying sinus rate of 68 bpm.
Atrial Tachycardia. Atrial tachycardia applies to approximately in the same proportion (11–12%). If
dysrhythmias that originate in the left or right atria this dysrhythmia becomes a chronic problem in
and have identifiable, uniform P-waves preceding the children, the mechanism is usually secondary to
QRS. This definition excludes atrial flutter, atrial automaticity.14
fibrillation, and multifocal atrial tachycardia. Atrial
tachycardia accounts for about 15% of cases of Best Practice
supraventricular tachycardias in adults and up to 23%
in children. It may be secondary to reentry (paroxys- Leads for PAC
mal) or to abnormal automaticity (nonparoxysmal).
The reentry, or paroxysmal, form is a much more The best leads for assessing PACs are II, aVF,
common mechanism of atrial tachycardia in adults. and V1 because the P-wave is more prominent in
However, in children, reentry and automaticity occur these leads.
TABLE 19-6 Atrial dysrhythmia: physiological mechanisms and ECG characteristics

Premature Atrial Paroxysmal Atrial Nonparoxysmal
Contraction (PAC) Tachycardia Atrial Tachycardia Atrial Flutter Atrial Fibrillation
Physiological Increased Rapid reentry Increased Increased Increased
mechanism automaticity circuit in the atria automaticity of automaticity of automaticity of
of an ectopic ectopic atrial ectopic atrial ectopic atrial
arterial pacemaker pacemaker pacemaker or rapid pacemaker or
or reentry circuit reentry circuit in multiple rapid
in the atria the atria reentry circuit in
the atria
Rate Adds to patient’s 160–240 bpm 160–240 bpm Atrial rate Atrial rate
baseline rate 240–400 bpm; 360–700 bpm;
ventricular rate may ventricular rate
be half or one third slower
of atrial rate
Ventricular Irregular, secondary Regular Regular, with Usually regular, Irregular
rhythm to early beat constant AV or irregular with
conduction, or variable conduction
grossly irregular ratio
with variable AV
conduction block
(digitalis toxicity)
P-wave Early P-wave arises Not visible in PSVT, Ectopic P-waves P-waves (called P-waves called
from atrial tissue; but may be seen at have different F-waves) with F-waves; atrial rate
morphology lower atrial rates appearance from saw-toothed not determinable;
different from sinus P-waves appearance baseline may look
sinus P-waves wavy or flatline
PQRST Normal relation- Varies with origin of Usually normal, Conduction ratio One-half to
relationship ship, usually; in dysrhythmia (atria except physiologi- usually constant one-third of
nonconducted or AV junction) cal AV block may but may vary F-waves are
PACS, early P-wave exist at atrial rates randomly
occurs during ⬎ 200 bpm; in conducted;
refractory period; digitalis toxicity, ventricular
noncompensatory AV block may exist, stimulation
pause present with more P-waves controlled by
than QRS physiological
complexes AV block
QRS Normal duration Usually normal; Same as Same as Same as
complex unless early-wave ⱖ0.12 s if bundle paroxysmal atrial paroxysmal atrial paroxysmal atrial
occurs when branch or anoma- tachycardia tachycardia tachycardia
ventricle is variable lous ventricular
refractory; then the conduction
QRS ⱖ0.12 s pathway is present
Waveform R-R interval P-RI not deter- Normal P-RI and P-RI usually equal R-R interval
intervals irregular minable in PSVT R-R intervals, but may vary; R-R varies widely,
because P-wave not except prolonged interval usually except in atrial fib
seen; Q-T may be P-RI and/or regular, except with superimposed
short irregular R-R interval variable R-R third degree AV
in physiological intervals with block
AV block or varying AV block
secondary to
digitalis toxicity
(A) (B)
FIGURE 19-17 (A) Paroxysmal atrial tachycardia (supraventricular tachycardia): The rhythm is regular, with 1:1 conduction.
The rate is approximately 188 bpm. (B) Paroxysmal supraventricular tachycardia: The rhythm is regular, and the P-wave
is not seen. The rate is approximately 188 bpm.
Description Atrial tachycardia occurs when there are at quickly develop myocardial ischemia and have a
least three successive ectopic atrial complexes. The catastrophic deterioration in ventricular function. This
atrial heart rate is very fast, and, in the paroxysmal is a life-threatening emergency that requires immediate
form, the relationship is usually 1:1 between the treatment.1
ectopic atrial beat and a ventricular response.
Atrial tachycardia is thought to be the result of one Atrial Flutter. Atrial flutter (Tables 19-5 and 19-6) is a
of two mechanisms: enhanced automaticity of an area supraventricular dysrhythmia that is sometimes difficult
of the atrial tissue (nonparoxysmal atrial tachycardia) to distinguish from paroxysmal atrial tachycardia. A
or, more commonly, a reentry conduction disturbance helpful clue is that the atrial flutter waves are continu-
that is started by a PAC occurring when part of the ous on the ECG, whereas the P-waves of atrial tachycar-
heart is still refractory (paroxysmal atrial tachycardia). dia are separated by a short isoelectric line (compare
Figure 19-17 identifies important clinical differences Figures 19-17 and 19-18).
between the two types of paroxysmal atrial tachycardia.
By convention, when there is a single wave between the Description Atrial flutter (Table 19-6) is a tachycardia
QRS complexes and no visible P’-wave, the atrial in which the atrial rate is very rapid: between 240 and
dysrhythmia is simply called a supraventricular tachycardia. 400 bpm (average, 300 bpm). The electrophysiological
If the onset is sudden, the dysrhythmia may be called mechanism of atrial flutter is the presence of an ectopic
paroxysmal supraventricular tachycardia.1 focus in the atria, with a rapid atrial rate that is main-
tained by either enhanced automaticity or reentry. The
Clinical Significance The tolerance to atrial tachycardia atrial wave, known as the F-wave, is characteristically
depends on the heart rate and the presence of underly- described as having a saw-toothed or picket fence
ing heart disease. A common symptom of atrial appearance. A classic feature of atrial flutter dysrhyth-
tachycardia is palpitations. Other symptoms are the mia is a 2:1 conduction ratio: very regular F-waves have
result of a rapid decrease in cardiac output and cerebral a rate of 300 per minute with a ventricular rate of
blood flow: dizziness, fainting, sweating, pallor, and 150 bpm. The ventricular rate is commonly one half or
dyspnea. less of the atrial rate; the conduction ratio is usually
In the elderly or individuals with underlying constant but it may vary.
cardiovascular disease, the rapid heart rate reduces Atrial flutter occurs rarely in people with a normal
ventricular filling, and the reduced ventricular filling heart and infrequently in people with heart disease. It
may significantly reduce cardiac output. The reduction is more often seen in patients with diseases involving
in cardiac output also decreases coronary blood flow the right heart such as tetralogy of Fallot, cor pulmo-
(an estimated drop of 25%) and coronary perfusion of nale caused by severe lung disease, or pulmonary
the myocardium. Consequently, individuals with embolism. Frequently, atrial fibrillation may develop
coronary artery disease or congestive heart failure may during atrial flutter, and the patient may fluctuate
FIGURE 19-18 Atrial flutter: This rhythm is regular, but there is a 4:1 conduction ratio
(four F-waves for each QRS complex). The flutter rate is approximately 273 bpm, and the
ventricular rate is approximately 68.
FIGURE 19-19 Atrial fibrillation: The rhythm is regular, with no recognizable P-waves. The f-wave
rate is not determinable, but the ventricular rate is approximately 110 bpm. This dysrhythmia is
called uncontrolled because the ventricular rate is greater than 100 bpm.
between the two rhythms. The term used to describe Consequently, the ventricular rate is rapid and very
this phenomenon is flutter-fibrillation.14 irregular. The electrophysiological mechanism that
sustains atrial fibrillation is enhanced automaticity, or
Clinical Significance The problems associated with a reentry phenomenon, or a combination of the two.
atrial flutter are similar to those of atrial tachycardia. The atrial waves in atrial fibrillation (Figure 19-19)
Patient tolerance depends on the heart rate and on the are known as the f-wave. They are characteristically
presence of underlying heart disease. The usual symp- described as coarse or fine waves located between
toms are palpitations, dyspnea, and breathlessness, normal-appearing but very irregular supraventricular
which are characteristic of all tachycardias. An addi- QRS complexes. Sometimes the net electrical ampli-
tional problem with atrial flutter is the loss of effective tude of the 400⫹ atrial depolarization waves (f-waves)
atrial contraction during atrial systole. Therefore, this is so small that the sections between the QRS com-
atrial dysrhythmia may decrease cardiac output by as plexes are flat, or isoelectric. Fine atrial fibrillation has
much as 25% because of impaired ventricular filling, deflections of less than 1 mm; coarse atrial fibrillation
and it may increase the severity of symptoms.1,14 has deflections of more than 1 mm. This deflection is
equivalent to one small square on the ECG paper.
Atrial Fibrillation. Atrial fibrillation has the most rapid
atrial rate of all the atrial dysrhythmias. A hazard of Clinical Significance The problems associated with
atrial fibrillation is the formation of blood clots in the atrial fibrillation are more serious than with atrial
atrium because of stagnant blood in the atrial chamber flutter. Usually atrial flutter has a regular ventricular
secondary to absent atrial muscle contraction during rate, and the ventricular rate is usually lower than in
atrial systolic time. Heparin is indicated for patients patients with uncontrolled atrial fibrillation. Patients
with chronic atrial fibrillation to prevent clot formation with atrial fibrillation have no atrial systole, but they
and to lessen the risk of stroke or pulmonary embo- also have an irregular cardiac rhythm and a rapid
lism. The most important single factor encouraging the cardiac rate. Because ventricular filling time varies with
onset of atrial fibrillation in high-risk clinical problems the irregular tachycardic pattern, the blood pressure
is the advancing age of the patient. Most people with changes from one beat to the next, creating hemody-
atrial fibrillation have structural heart disease such as a namic instability. A simple clinical test can detect this
valve disease, coronary artery disease, hypertension, problem. If you listened to the apical pulse of a patient
cardiomyopathy, and myocarditis. with atrial fibrillation and also feel the patient’s
The dysrhythmia can be short-lived or chronic. peripheral pulse at the same time, many times the
apical pulse is higher. This clinical sign, called a pulse
• In the short-lived type, the rhythm either
deficit, occurs because stroke volume varies from beat to
converts spontaneously or responds to
beat. Some cardiac contractions may have so little
cardioversion.
stroke volume that the pulse wave heard at the cardiac
• In chronic atrial fibrillation, the rhythm is
apex is imperceptible at the peripheral pulse points.14
refractory to cardioversion, and therapy is
directed to improving cardiac function. 14
Description Atrial fibrillation (Tables 19-5 and 19-6) JUNCTIONAL DYSRHYTHMIAS

arises from multiple ectopic areas in the atria and Junctional dysrhythmias (Tables 19-7 and 19-8) are the
causes a chaotic “twitching” of atrial tissue. The atrial result of automaticity abnormalities in pacemaker cells
rate can range from 360 to 700 depolarization stimuli of the junctional tissue, or of conduction abnormalities
per minute. The AV junction is bombarded with this in the AV junction, or of both. The AV node and the
outpouring of stimuli from twitching atrial tissue, and bundle of His make up the AV junction. The AV
its depolarization timing in turn becomes chaotic. junction’s primary role is to act as a conduction
CASE STUDY 19-1

This is the first admission for D, G., a 49-year-old Questions
white male, who was admitted for a cardiac cath- 1. Discuss the patient’s rhythm strip, and relate
eterization. His chief complaint was that of a the strip to his symptoms.
4-month history of angina. At approximately 0800,
2. What are possible causes for this patient’s
he was taken to the cardiac lab, where the catheter-
dysrhythmia?
ization was performed. After the procedure was
finished, Mr. G. complained of shortness of breath
and lightheadedness. This was his ECG tracing:
TABLE 19-7 Causes of junctional dysrhythmias

Nonparoxysmal Junctional
Tachycardia Paroxysmal
Premature Accelerated Junctional
Causative Junctional Junctional Junctional Junctional Tachycardia
Category Contraction Escape Rhythm Rhythm Tachycardia (same as PSVT)
Autonomic Sympathetic Excessive vagal Not a cause Not a cause Increased
nervous system nervous system depression of the sympathetic
stimulation; SA node tone; increased
stimulants catecholamines,
(coffee, tea, emotion, infec-
nicotine, tion, hypoxemia,
chocolate) stimulants (coffee,
tea, chocolate)
Drugs or drug Digitalis toxicity Digitalis toxicity Digitalis toxicity Digitalis toxicity Sympathomimetic
toxicity drugs, digitalis
toxicity
Diseases or Normal finding, or Inferior wall Inferior wall MI, Same as Occurs in persons
conditions congestive heart myocardial acute rheumatic accelerated with apparently
failure (CHF), infarction (MI), fever, CHF, junctional healthy heart or
myocardial CHF, valvular heart valvular heart rhythm heart disease
ischemia, coronary disease, AV node disease, AV node (CAD, rheumatic
artery disease ischemia ischemia heart disease,
(CAD), valvular acute MI)
heart disease,
hypokalemia
“bottleneck” so that the atria have sufficient time to SA node fails to initiate an electrical stimulus because
adequately fill the ventricles with blood during atrial of either disease, drugs, or increased parasympathetic
systole. The speed of AV nodal conduction is slowed or tone, the AV junction may initiate the stimulus and
enhanced by changes in autonomic control. assume the pacemaker role. The pacemaker cells of the
A secondary but important role of the AV junction AV junction have an inherent excitability; therefore, if
is to act as the back-up pacemaker for the heart. If the not suppressed by the normal functioning of the SA
TABLE 19-8 Junctional dysrhythmia: physiological mechanisms and ECG characteristics

Nonparoxysmal Junctional
Tachycardia Paroxysmal
Premature Accelerated Junctional
Junctional Junctional Junctional Junctional Tachycardia
Contraction Escape Rhythm Rhythm Tachycardia (PSVT)
Physiological Increased automa- Decreased auto- Increased Same as acceler- Reentry circuit
mechanism ticity of AV junction maticity of the SA automaticity on ated junctional in the AV junction
or reentry circuit node or decreased the AV junction rhythm or increased
involving the AV conductivity of the automaticity of
junction SA node impulse AV junction
Rate Adds to patient’s 40–60 bpm (may 60–100 bpm 100–150 bpm 160–240 bpm
baseline rate be lower) (may vary)
Ventricular Irregular, secondary Regular Regular Regular Regular
rhythm to early beat
P-wave Early P-wave arises May be absent or Same as junctional Same as junctional Usually absent,
from junctional present; differs escape rhythm escape rhythm especially at the
tissue; if present, from sinus P in faster rates
the P-wave is size, shape, and
inverted direction and is
inverted in lead II
PQRST Early P-wave may Early P-wave may Same as junctional Same as junctional If P-waves are not
relationship be before, during, be before, during, escape rhythm; if escape rhythm seen, it is called
or after, the QRS; or after, the QRS; P-wave is visible PSVT; cannot be
if P-wave occurs if P-wave occurs it may have no differentiated from
simultaneously simultaneously electrical relation paroxysmal atrial
with QRS, P-wave with QRS, P-wave to the QRS; this is tachycardia
is not visible is not visible AV dissociation
QRS complex Normal duration Normal duration Same as junctional Same as junctional Same as junctional
unless early unless preexist- escape rhythm escape rhythm escape rhythm
P-wave occurs ing bundle branch
when ventricle is block is present
variable refractory;
then the QRS ⱖ
0.125 second
Waveform If P-wave is before If P-wave is before Same as junctional Same as junctional Same as junctional
intervals QRS, PR-I is QRS, PR-I is escape rhythm escape rhythm escape rhythm
ⱕ0.12 second ⱕ0.12 second
R-R intervals equal R-R intervals equal
node, the cells self-depolarize at a rate of 40–60 times arising from the AV junction. Like all premature beats,
per minute. they occur in normal hearts but occur less commonly
Junctional dysrhythmias caused by automaticity or than premature atrial or ventricular contractions. The
reentry disturbances are: electrophysiologic mechanism of premature junctional
contractions is either increased automaticity or reentry.1
• Premature junctional contraction.
• Junctional escape.
Description An ectopic stimulus in the AV junction is
• Nonparoxysmal junctional tachycardia.
the primary cause of an early junctional beat. The
• Paroxysmal supraventricular tachycardia.
ectopic junctional pacemaker spontaneously depolar-
izes before the next discharge of the sinus node and
Premature Junctional Contraction. Premature junctional causes an early beat. Because the pacemaker stimulus
contractions (PJCs) (Figure 19-20) are premature beats occurs out of the normal sequence in the conduction
FIGURE 19-20 Premature junctional contraction: There are three premature junctional contractions
(beats 7, 11, and 13). The P-wave is visible and inverted before each premature beat. Each QRS com-
plex is ⬍0.12 second, and each premature beat has an abnormally short P-RI. The rhythm is irregular,
and the rate is 68 bpm.
network, the atrial depolarization is backward, or Since PJCs can occur in individuals with underly-
retrograde. In lead II, this retrograde conduction creates ing heart disease, their presence indicates a situation of
an inverted or negative P-wave. Conversely, the QRS increased automaticity of the junctional tissue or a
complex remains normal because the conduction conduction disturbance. The sudden appearance
direction is unchanged in the ventricles. of frequent PJCs suggests cardiac irritability and a
The location of the ectopic pacemaker in the AV worsening of cardiac function, requiring immediate
junction determines the placement of the P-wave in the treatment.1
ECG tracing. These are the possible variations of
P-wave placement in the patient’s ECG: Junctional Escape Rhythm. Junctional escape rhythm
• If the ectopic stimulus arises from an area close is the pacing of the heart by the AV junction. If the AV
to the atrial tissue, it depolarizes the atria before junction supports the heart rate for under 3 consecu-
the ventricles, and the inverted P-wave occurs tive beats, then those beats are junctional escape
before the QRS complex. Because the stimulus beats, not junctional escape rhythm. Physiologically,
originated from an area close to the atria, the the AV junction is a secondary or default pacemaker
P-RI is abnormally fast (⬍0.12 second). and does not normally pace the heart, a persistent
• If the ectopic stimulus comes from the middle of junctional escape rhythm is too slow for long-term
the AV node, then the atria are depolarized at the support.1
same time as the ventricles, and the inverted
P-wave is hidden in the QRS complex—not visible. Description Two situations allow the AV junction to
• If the ectopic stimulus arises from a site in the take over as the cardiac pacemaker.
AV node that is closest to the ventricular tissue, • First, if the baseline discharge rate of the sinus
then the ventricles are depolarized first, and the node falls below the normal discharge rate of the
P-wave appears after the QRS complex.1 AV junction, then the AV junction has escaped
from the inhibitory control of the SA node and
Clinical Significance In the normal person, premature has become the cardiac pacemaker (Figure 19-21).
junctional contractions are usually benign and not The normal stimulus discharge rate of the AV
clinically significant. Some nonbenign causes of junction is 40–60 bpm. If the SA node increases
persistent PJCs are: its rate of discharge to above that of the AV
• Digitalis toxicity. junction, the SA node again becomes the
• Increased automaticity of the AV junction. dominant pacemaker.
• Increased vagal tone on the SA node. • Second, if the impulse from the sinus node does
• Cardiac drugs. not reach the AV junction because of SA node
• Hypoxia. disease or a conduction abnormality, then the
• Heart disease. AV junction takes over as the pacemaker.1,14
FIGURE 19-21 Junctional escape rhythm: The rhythm is regular with a rate of 40 bpm, and there is an
inverted P-wave before each QRS complex. The QRS is ⬍0.12 second, and the P-RI is abnormally short.
FIGURE 19-22 Accelerated junctional rhythm: The rhythm is regular, with a rate of 83 bpm, and
an inverted P-wave precedes each QRS complex. The QRS complex is ⬍0.12 second, and the
P-RI is abnormally short.
Clinical Significance Individuals with junctional
escape rhythm have the same clinical manifestations
as those with sinus bradycardia. If the junctional
escape rhythm is persistent and if attempts to reestab-
lish the SA node as the pacemaker fail, then a perma-
nent pacemaker is inserted. Back-up pacemakers
such as the AV junction are not reliable, and there FIGURE 19-23 Nonparoxysmal junctional tachycardia: The
is a risk of AV node failure and deterioration into a rhythm is regular, and the rate is approximately 167 bpm.
very slow ventricular escape rhythm or ventricular P-waves are inverted and precede the QRS complexes.
asystole.1,14
Nonparoxysmal Junctional Tachycardia (Accelerated • Injury to the AV junction following a myocardial

Junctional Rhythm and Junctional Tachycardia). infarction.
The mechanism of nonparoxysmal junctional tachycardia
is increased automaticity. The ectopic focus in the AV Any patient with this dysrhythmia is at risk for develop-
junction takes over as the pacemaker because the rate ing a more lethal rhythm, and treatment is necessary.1
is faster than the SA node. The rhythm is regular, with A condition called AV dissociation occurs when
a rate that ranges from 60 to 150 beats/minute.1 the atria and ventricles beat independently. It appears
for two reasons:
Description Nonparoxysmal junctional tachycardia
includes two distinct cardiac dysrhythmias: • Either the sinus rhythm is slightly less than the
normal AV junctional rate. In this case, the rates of
• A junctional rhythm with a rate of 60–100 is both pacemakers are very close, and the P-wave
accelerated junctional rhythm. rate is slightly less than the ventricular rate.
• With a rate greater than 100, it is junctional • Or the AV junction has increased automaticity.
tachycardia. With enhanced automaticity, the AV junction’s
rate is higher than normal, and the AV junction
The rhythm is regular, and, as with PJCs, the innerva-
usurps pacemaker control from the sinus node.
tion of the ventricle is controlled by the ectopic
The atrial rate is also less than the ventricular
pacemaker in the AV junction, not by transmission
rate, but the ventricular rate is greater than the
from the SA node. Therefore, the P-wave does not have
usual AV pacemaker’s rate, ranging from 60 to
the normal relationship to the QRS.
240 beats/minute.1
Nonparoxysmal junctional tachycardia is classically
gradual in starting and stopping because it is due to
Clinical Significance The presence of nonparoxysmal
enhanced automaticity of the AV junction. It takes time
junctional tachycardia raises the red flag for digitalis
to develop this condition, and it takes time for treat-
toxicity. If digitalis is the likely cause, treatment must
ment to suppress the cause.1,14
be started before the patient develops a life-threatening
Both accelerated junctional rhythm and nonparox-
dysrhythmia. The clinical manifestations of rapid
ysmal junctional tachycardia (Figures 19-22 and 19-23)
nonparoxysmal junctional tachycardia are the same as
can develop with digitalis toxicity. Other causes are:
those for atrial tachycardia.1
• Drugs that increase automaticity
(sympathomimetics). Paroxsymal Supraventricular Tachycardia. Paroxsymal
• Hypoxemia. supraventricular tachycardia (PSVT) is a dysrhythmia
• Electrolyte disturbances. (Low potassium can arising as a result of an reentry circuit, or loop, within
worsen the effects of digitalis.). the AV node or between the AV node and an accessory
pathway located between the atria and the ventricles. (Tables 19-9 and 19-10). The primary method used
The rate is usually very fast, ranging from 160 to 240 to categorize the different types of AV block is by
beats/minute (rates may be lower or higher). P-waves degree:
are usually not visible. The rate is so high that the
• First-degree AV block
P-waves are hidden in the QRS complex or the P-waves
• Mobitz type I second-degree AV block
merge with the T-wave, showing T/P-waves separating
• Mobitz type II second-degree AV block
the QRS complexes.
• Third-degree AV block
The onset and termination of PSVT are sudden. A
common event precipitating the rhythm is a premature Other terms, complete and partial, separate these conduc-
atrial contraction, which occurs when part of the heart tion disturbances according to the extent of the block.
is still refractory. This creates a reentry pathway, allow-
ing a sudden rapid tachycardia. Table 19-8 identifies Partial AV Block. Partial AV block refers to the degree of
important clinical differences between the two types of conduction impairment through the AV junction. If
junctional tachycardia: nonparoxysmal and paroxysmal. some of the P-waves are conducted and activate the
By convention, a narrow-QRS tachycardia with no ventricular muscle, the block is partial.
distinct P-wave, is supraventricular tachycardia (SVT)
unless the onset is sudden, then the dysrhythmia is First-Degree AV Block. First-degree heart block is the
paroxysmal supraventricular tachycardia.1 least serious of the heart blocks (Figure 19-24). This
block is associated with digitalis toxicity and should be
Clinical Significance The clinical manifestations of monitored for progression to more serious AV blocks.
PSVT are the same as those with atrial tachycardia.
However, clinicians must be aware of an additional Description First-degree AV block is a disorder of
problem identified in patients with PSVT. When the slowed conduction in the AV junction, characterized by
rhythm suddenly terminates, the SA node does not a prolonged P-R interval (⬎0.20 second). The underly-
immediately pace, and patients’ experience dizziness or ing ventricular rate may be normal. The ECG has the
even lose consciousness during this asystolic period.1 normal P-QRS-T-wave sequence, and the appearance
and duration of the waves are normal.
DISTURBANCES OF ATRIOVENTRICULAR
CONDUCTION Clinical Significance First-degree AV block is not
Atrioventricular (AV) block is a conduction disturbance common in young healthy adults. As people age, the PR
occurring between the initiation of the sinus impulse interval lengthens beyond 0.20 to 0.24 seconds, even in
and the ventricular response to that impulse those without heart disease. This abnormal conduction
TABLE 19-9 Causes of AV block

Second-Degree (Partial)
Causative First-Degree Type I Second- Type II Second- Third-Degree
Category (Partial) Degree Degree (Complete)
Autonomic Increase in vagal Increase in vagal Not applicable Increase in vagal (parasym-
nervous system (parasympathetic) (parasympathetic) pathetic) tone of the AV
tone of the AV tone of the AV junction (transient
junction junction third-degree block)
Drugs or drug Digitalis toxicity Digitalis toxicity (e.g., Not applicable Drug toxicity (e.g., digitalis,
toxicity digitalis, beta-blocker, beta-blocker, calcium
calcium channel channel blocker)
blocker)
Diseases or Acute inferior Acute inferior MI; Acute anteroseptal Acute inferior MI; ischemia
conditions myocardial infarction ischemia of the AV MI (necrosis of of the AV junction; chronic
(MI), ischemia of junction; infection conduction network) degenerative aging changes
the AV junction causing rheumatic in the conduction network;
fever or myocarditis; infection causing rheumatic
electrolyte imbalance fever or myocarditis;
electrolyte imbalance
TABLE 19-10 AV block: physiological mechanisms and ECG characteristics

Second-Degree (Partial)
First-Degree Type I Second- Type II Second- Third-Degree
(Partial) Degree Degree (Complete)
Physiological Decreased conductivity Repetitive cycle of Defective conduction Absent conduction
mechanism of AV junction progressive decrease in through AV junction at the level of the AV
conductivity through or ventricular bundle node, bundle of His,
AV junction until branches, with regular or or ventricular bundle
conduction is unpredictable episodes branches; AV junctional
completely blocked of complete AV block pacemaker or ventricle
and absent conduction pacemaker controls
ventricular rate
Rate Does not affect rate of Ventricular rate is less Same as type I Rate controlled by
underlying rhythm than atrial rate; rate is pacemaker controlling
determined by the the ventricle rate: AV
underlying primary junction: 40–60 bpm;
rhythm ventricular pacemaker:
⬍40 bpm
Ventricular Does not affect Irregular; atrial rhythm Same as type I Usually regular
rhythm underlying rhythm is regular
P-wave Regular sinus P-waves; Regular sinus P-waves; Regular sinus P-waves; P-wave rate determined
P-wave rate same as P-wave rate greater P-wave rate greater by underlying atrial
QRS rate; P-wave than QRS rate; P-wave than QRS rate; P-wave rhythm
upright in lead II upright in lead II upright in lead II;
conduction ratio may be
variable or constant
PQRST Normal sequence: one Abnormal relationship; Same as type I No electrical relation-
relationship P-wave for each QRS nonconducted P-waves ship between atria and
complex present ventricles; each beat
independently
(AV dissociation)
QRS complex Usually normal; ⱖ0.12 Same as first-degree Usually abnormal Usually abnormal
second if bundle branch (ⱖ0.12 second) (ⱖ0.12 second): block
block or anomalous because AV block is is below bundle of His;
ventricular pathway is below bundle of His normal duration if block
present is in AV junction or the
bundle of His
Waveform P-RI is prolonged P-RI varies: progres- P-RI may be abnormal P-RI varies (AV disso-
intervals (⬎0.20 second) and sively lengthens until but is usually constant ciation); R-R intervals
does not vary P-wave is not conducted regular and P-P intervals
through AV junction; regular but do not have
R-R intervals irregular, electrical relationship
with interval decreasing
during cycles of
increasing P-RI
does not typically cause any clinical signs and symptoms, Mobitz Type I Second-Degree AV Block. This cat-
and it therefore does not require treatment.15 The egory of heart block, also called the Wenckebach
conventional wisdom is that any P-RI greater than phenomenon (Figure 19-25), is one of the less clinically
0.45 sec does not conduct the P-wave through the AV significant AV blocks. Most patients do not require
junction. However, in rare cases, the P-RI conducting definitive treatment, but in some cases they should be
the P-wave has been as long as 1 second.16 monitored for clinical deterioration.
Best Practice
Wenckebach Phenomenon
FIGURE 19-24 First-degree AV heart block with accompa- Here is a memory jogger to help identify the
nying sinus bradycardia: The rhythm is regular, and the Wenckebach phenomenon on an ECG.
rate is approximately 55 bpm. The P-RI is very prolonged.
• First, there are more P-waves than there are
QRS complexes with a varying R-to-R interval.
• Second, the P-RI varies.
Two variables, or “V’s,” put together, make the
letter “W”—for Wenckebach. So the rule is
“variable PR and variable RR is Wenckebach.”
FIGURE 19-25 Type I second-degree AV block (Wenckebach

phenomenon): The rhythm is irregular, and the rate is ap-
proximately 60 bpm. One nonconducted P-wave appears treatment. Most patients do not develop significant
between the third and fourth ventricular beats. The P-RI clinical problems with this dysrhythmia. In some
increases in duration before the nonconducted P-wave. patients, however, this partial AV block progresses to a
complete block. Therefore, high-risk patients must be
carefully monitored, and, if deterioration is detected,
Description This dysrhythmia represents a greater aggressive treatment should be given. Drug toxicity can
abnormality in AV conduction than first-degree heart also cause partial AV block, and medical treatment is
block. Type I second-degree AV block, or Wenckebach always necessary.
phenomenon, is characterized by the progressive
lengthening of AV conduction time for a series or group Mobitz Type II Second-Degree AV Block. This block,
of electrical stimuli until the AV node becomes totally also known simply as Type II AV block, is always serious
refractory and the last stimulus is blocked and does not and requires close monitoring and treatment
activate the ventricle. The ECG of a patient with (Figure 19-26). In particular, patients suffering from
Wenckebach phenomenon shows a group of P-QRS-T- an anterior wall myocardial infarction are at risk of
waves that are close to each other and are separated developing a life-threatening dysrhythmia.1,16
from the other groups by a pause. This configuration is
called grouped beating. Within each group, the P-RI for Description The presence of a Type II second-degree
each successive P-wave is longer than that of the AV block indicates that the patient has a serious
preceding one, and the R-R interval becomes progres- abnormality in the conduction network. Its appearance
sively shorter. This pattern continues until finally the indicates irreversible tissue necrosis. The conduction
last P-wave is not conducted. The pause between block typically occurs below the bundle of His, in the
groups represents a failure of AV conduction. During bundle branches, and involves a complete block of
this pause, the AV node recovers, and the process starts one bundle branch and intermittent block of the other
again. Marriott called this pattern “the footsteps of bundle branch.1 The ECG characteristics of Type II
Wenckebach.”16 second-degree AV block show a constant PRI with
episodes of AV conduction block and nonconducted
Clinical Significance Type I second-degree AV block P-waves. The AV block may show a repeating pattern or
occasionally occurs in people with a normal heart. be unpredictable. The QRS complex is usually wider
If present, it is usually transient or reverses with than normal (⬎0.12 second), indicating the bundle
FIGURE 19-26 Type II second-degree AV block: The rhythm is regular with a ventricular
rate of 34 bpm. There are three P-waves for each QRS complex with a constant P-R
interval of 0.14 second. The QRS is ⬍0.12 second; therefore the patient’s block is in
the AV junction.
branch block. More rarely, a normal QRS duration Clinical Significance In patients with 2:1 heart
(0.10 sec) may indicate that the block is at the level of block with wide QRS complexes and advanced
the bundle of His without an existing bundle branch heart block with wide QRS complexes, these rhythms
block.1,16 are more serious and can deteriorate into complete
heart block or asystole. If the heart rate is excessively
Clinical Significance Mobitz Type II second-degree AV slow, the signs and symptoms are the same as in
block does not appear in someone with a normal clinically significant sinus bradycardia. The insertion
heart. When present, it is usually a permanent or of a cardiac pacemaker is necessary.1
recurrent dysrhythmia. Most people with this conduc-
tion disturbance are not hemodynamically stable and Complete Heart Block or Third-Degree AV Block. In
are symptomatic. Many have just suffered an anterior complete AV block, there is a total absence of conduction
wall myocardial infarction, and they are manifesting between the atria and the ventricles. The conduction
signs and symptoms of circulatory insufficiency and defect could be anywhere from the AV junction
need emergency care. The insertion of a permanent through the bundle branches. The only block in this
pacemaker is an emergency procedure, not elective. category is third-degree AV block. If the block is located
These patients are at high risk for deterioration, which below the bundle of His, this rhythm requires aggres-
may take the form of complete heart block or a pulse- sive treatment because the patient is in danger of
less rhythm, such as asystole.1 deteriorating into asystole without warning.
Second-Degree 2:1 and Advanced Heart Block. Description Third-degree AV block exists when there is
These types of heart block are not the classic Type I or a complete lack of electrical communication between
Type II second-degree AV block. Patients with these the atria and the ventricles (Figure 19-27). Atria are
rhythms have defective conduction in the AV junction controlled by a supraventricular pacemaker and the
and/or the bundle branches, and the pattern reveals a ventricles are paced by the AV node or ventricular
P-to-QRS ratio of 2:1 or greater, with or without a pacemaker cells. In the absence of His-bundle record-
bundle branch block. ings, the location of the block may be identified by the
width of the QRS complex and the ventricular rate.
Description Closely associated with Type I AV block is a
• If the QRS complex is narrow, the block is
2:1 AV block with a normal QRS duration. The ECG
proximal to the bundle of His in the AV node,
shows:
and the underlying rate is consistent with a
• Two P-waves for each QRS. junctional pacemaker (40–60 bpm).
• Regular rhythm. • If the QRS complex is wide (⬎0.12 second), the
• Normal or prolonged P-RI. block is distal to the bundle of His, and the
underlying ventricular rate is slower (⬍40 bpm).
Two-to-one heart block and advanced heart block
This ventricular pattern is typically described as
with wide QRS complexes are associated with Type II
an idioventricular rhythm.1
AV block because the wide QRS indicates bundle
branch conduction defects. Any conduction ratio of 3:1 The ECG characteristics of third-degree AV heart
or greater is a high-grade, or advanced, heart block. The block are:
ECG characteristics show:
• Normal P-P intervals.
• A constant P-RI that may be normal or prolonged. • Normal R-R intervals.
• Regular or irregular rhythm, depending on • Variable PR intervals.
whether the conduction ratio remains constant.
The atrial rate is usually faster than the ventricular rate
• Either a normal QRS time duration, indicating
because of the difference in automaticity of the respec-
an AV node conduction delay, or a prolonged
tive pacemakers.
duration, indicating a bundle branch block.
FIGURE 19-27 Third-degree AV block: The rhythm is regular with a rate of approximately 34 bpm. The
R-R interval is constant, and the P-RI is variable. The QRS is 0.12 second, indicating a ventricular
pacemaker.
Complete heart block has a varying duration. In pulseless state. Patients with these dysrhythmias need
the presence of acute myocardial infarction, a conduc- advanced life-support measures to convert the cardiac
tion defect in the intraventricular conduction system rhythm into one that supports life.
indicates significant irreversible disease, and the patient
needs a permanent pacemaker.1 Premature Ventricular Contraction. Premature ven-
tricular contraction (PVC) is a common dysrhythmia
Clinical Significance The clinical presentation of a that is found in people with normal or abnormal
patient in third-degree AV block is the same as that hearts (Figure 19-28). The treatment varies according to
of a patient with any symptomatic bradycardia. These the clinical situation.
patients complain of dizziness and syncope. Their
blood pressure is low, secondary to reduced cardiac Description An early ventricular beat is caused by an
output. ectopic stimulus that arises in any part of the ventricu-
If the conduction defect is in the AV node, the lar myocardium. The ectopic ventricular pacemaker
heart block is reversible and responsive to treatment. If spontaneously discharges before the next expected
the conduction defect is in the ventricle, as evidenced sinus beat. The premature ventricular contraction does
by a wide QRS complex, the prognosis is more serious not stimulate the SA node because the AV node is
because permanent damage to the ventricular conduc- usually refractory to retrograde conduction; thus, the
tion network has occurred. All patients in a third- SA node timetable is not disturbed. Therefore, the
degree block should be treated because of the interval between the sinus beats before and after the
possibility of backup pacemaker failure, with the premature ventricular beat is two times the normal R-R
sudden development of asystole.1,16 interval. This compensatory pause is found for each
PVC.1
PVCs indicate increased ventricular automaticity or
VENTRICULAR DYSRHYTHMIAS reentry in the bundle of His–Purkinje network.
Ventricular dysrhythmias (Tables 19-11 and 19-12) are PVCs may be unifocal or multifocal and may have
the most serious of all cardiac dysrhythmias. None of a repeating pattern. That is, they may occur in couplets,
these dysrhythmias can sustain life. Ventricular escape salvos (a number of events in regular succession), or
or ventricular tachycardia may initially support life, but regular coupling intervals.
they cannot create a stable blood pressure that can
sustain life. Ventricular fibrillation and asystole are Clinical Significance In people with a normal heart,
always pulseless rhythms. Patients with ventricular premature supraventricular beats are more common
tachycardia may initially have a pulse and blood than premature ventricular contractions. If present in
pressure, but continuation of the rhythm usually results the normal heart, PVCs are usually benign. More
in cardiovascular instability and deterioration into a commonly, however, premature beats occur in people
TABLE 19-11 Causes of ventricular dysrhythmias

Idioventricular
Rhythm or Accelerated
Causative Ventricular Idioventricular Ventricular Ventricular Ventricular
Category Escape Rhythm Tachycardia Fibrillation Asystole
Autonomic Decreased automa- Increased Increased Increased Absent
nervous ticity of the higher automaticity of automaticity of automaticity of automaticity of
system pacemakers ectopic pacemaker ventricular ectopic ventricular ectopic pacemakers
in ventricular pacemaker in bundle pacemaker in bundle
bundle branches branches, Purkinje branches, Purkinje
network, or myocar- network, or myocar-
dium or reentry cir- dium or reentry cir-
cuit in the ventricle cuit in the ventricle
Drugs or ⬍40 bpm 40–100 bpm ⬎100 bpm 300–500 bpm with 0
drug toxicity no effective cardiac
output
Diseases or Usually regular Usually regular Usually regular Chaotic, totally Absent
conditions irregular
534
SECTION III
TABLE 19-12 Ventricular dysrhythmia: physiological mechanisms and ECG characteristics
Premature Idioventricular Accelerated
Ventricular Rhythm or Ventricular Idioventricular Ventricular Ventricular Ventricular
■
Contraction Escape Rhythm Tachycardia Fibrillation Asystole
Essential Diagnostics
Physiological Increased automaticity Decreased automaticity Increased Increased automa- Increased automaticity Absent
mechanism of ectopic ventricular of the higher pacemakers automaticity of ticity of ventricular of ventricular ectopic automaticity of
pacemaker or reentry ectopic pacemaker ectopic pacemaker pacemaker in bundle pacemakers
circuit in the ventricle in ventricular in bundle branches. branches. Purkinje
bundle branches Purkinje network, or network, or myocar-
myocardium or reentry dium or reentry circuit
circuit in the ventricle in the ventricle
Rate Adds to patient’s ⬍40 bpm 40–100 bpm ⬎100 bpm 300–500 bpm with 0
baseline rate no effective cardiac
output
Ventricular Irregular, very Usually regular Usually regular Usually regular Chaotic, totally Absent
rhythm early beat irregular
P-wave P-wave may be present May be present or absent; May be present or May be present or Absent P-waves may
if present, rate is different absent; if present, absent; if seen, be present or
from ventricular rate rate is different from the wave is usually absent
ventricular rate inverted
PQRST P-wave not related to If present, P-waves have P-waves are P-waves are None No relationship
relationship QRS complex and no set relationship to electrically electrically present
occurs with normal QRS; AV dissociation unrelated to QRS; unrelated to QRS;
sinus time; T-wave may be present AV dissociation AV dissociation is
opposite in polarity to is present present
QRS; compensatory
pause present
QRS complex ⱖ0.12 s increased ⱖ0.12 s ⱖ0.12 s ⱖ0.12 s Absent Absent
amplitude
Waveform P-RI not present; Q-T P-RI usually absent; R-R P-RI absent; R-R P-RI usually absent; No intervals present; No intervals
intervals interval prolonged; intervals may be equal or intervals may vary R-R intervals may be fine v-fib: amplitude present
R-R interval irregular vary equal or vary ⬍3 mm; coarse v-fib:
amplitude ⬎3 mm
FIGURE 19-28 Premature ventricular contraction—multifocal: The rhythm is irregular with a ventricular
rate of 70 bpm. The two premature ventricular contractions do not have the same direction and
amplitude. The premature beats have a duration of ⬎0.12 second, and the other sinus beats have a
normal QRS duration.
with heart disease. The sudden appearance of frequent sometimes the treatment is worse than the ailment.
PVCs suggests cardiac irritability and a worsening of Anti-arrhythmic therapy is used sparingly because these
cardiac function, which requires immediate evaluation. drugs have side effects that may be serious, especially in
Digitalis toxicity is a cause of many cardiac dysrhyth- elderly patients. Clinical drug studies have shown that
mias, and PVCs is one of them. anti-arrhythmics do not increase patient survival, and
A classification system for ranking the severity of some drugs may actually increase the risk of death.
the patient’s ventricular ectopy is a helpful clinical Therefore, these drugs are limited to patients at risk for
guide. sudden death.
• Currently, patients are not treated with an
anti-arrhythmic medication unless they are at Ventricular Escape Rhythm (Idioventricular Rhythm)
high risk of developing a life-threatening dys- and Accelerated Idioventricular Rhythm. These two
rhythmia. Examples of PVCs that place the rhythms are very separate despite their being grouped
patient at risk are runs of three or more PVCs in together.
a row, couplets of PVCs, and R on T PVCs. • Idioventricular rhythm (Figure 19-29) is a slow
• Less serious categories of PVC, such as multifocal escape pacemaker rhythm that is incompatible
PVCs or frequent PVCs, are considered in with life.
conjunction with the patient’s clinical condition • Accelerated idioventricular rhythm (Figure 19-30) is
before treatment decisions are made. also known as “slow ventricular tachycardia.”
• Usually, anti-arrhythmics treatment is given for
patients with a suspected myocardial infarction Description Idioventricular rhythm occurs when the SA
and for patients showing evidence of cardiac node and AV junction fail as cardiac pacemakers.
ischemia with accompanying ectopic ventricular Before its onset, there is a pause because of SA node
irritability. These PVCs place the patient at a failure. When the AV junction also fails to discharge,
high-risk of a lethal dysrhythmia. the tissue of the bundle of His–Purkinje network
Anti-arrhythmic agents are not given to all heart initiates the impulse and prevents asystole. If the
disease patients with ventricular ectopy because pacemaker failure persists, the ventricle acts as the
FIGURE 19-29 Idioventricular rhythm (ventricular escape): The rhythm is regular with a ventricular
rate of 40 bpm. Each ventricular complex is wide with a QRS duration of ⬎0.12 second and no
visible P-waves.
FIGURE 19-30 Accelerated idioventricular rhythm: The rhythm is regular
with a ventricular rate of 44 bpm. Each ventricular complex is wide with
a QRS duration of ⬎0.12 second and no visible P-waves.
pacemaker, and the established rhythm is ventricular Three scenarios exist for the patient in ventricular
escape or idioventricular rhythm with AV dissociation. tachycardia:
The rate is usually ⬍40 bpm. A rate that is greater than
• The dysrhythmia is sustained and does not
40 but less than 100 bpm is accelerated idioventricular
convert despite treatment.
rhythm.
• It is treated and converts into another rhythm.
• It spontaneously converts into another rhythm.
Clinical Significance People in ventricular escape are
symptomatic because of their very slow heart rate. They The newly established rhythm is either life-sustaining
manifest all the signs and symptoms of low tissue or incompatible with life. In the latter case, the patient
perfusion, such as low blood pressure, dizziness, and needs immediate cardiac life support.
fainting episodes. In more severe cases, they may
deteriorate into cardiogenic shock. These people need Clinical Significance The rate and duration of ventricu-
emergency care to elevate the heart rate and reestablish lar tachycardia and the individual’s own cardiac
a viable cardiac output. function primarily determine tolerance to this dys-
People with an accelerated idioventricular rhythm rhythmia. A person in ventricular tachycardia who has
are usually not symptomatic at the higher ventricular severe heart disease is probably not able to maintain
rates. This rhythm is usually transient and does not adequate heart function. Cardiac filling is severely
require treatment. hampered secondary to two major hemodynamic
alterations that occur with ventricular tachycardia. First,
Ventricular Tachycardia. Ventricular tachycardia is a the fast heart rate severely limits filling time. Second, in
rapid heart rate that constitutes a cardiac emergency the presence of AV dissociation, there is no synchro-
(Figure 19-31). If untreated, it rapidly deteriorates into nous, coordinated atrial systole to aid in filling the
ventricular fibrillation. ventricles. Therefore, ventricular tachycardia causes a
significant decrease in the amount of blood pumped
Description Either an increased automaticity of an out of the heart. The individual may be hypotensive or
ectopic area in the ventricle or a reentry disturbance in experience a severe drop in arterial blood pressure that
the bundle of His–Purkinje system causes ventricular it is incompatible with life.1,17
tachycardia. Like supraventricular tachycardia, ventricu-
lar tachycardia usually starts with a premature beat. If Ventricular Fibrillation Ventricular fibrillation is a cardiac
increased automaticity is the mechanism, the ectopic rhythm that does not provide circulation (Figure 19-32).
ventricular pacemaker spontaneously discharges before The rhythm requires immediate conversion into a
the next expected sinus beat. The ventricular ectopic viable rhythm, or the patient will not survive.
pacemaker discharges at a faster rate than the sinus
node and usurps that pacemaker’s function. If a reentry Description Ventricular fibrillation is an extremely
loop exists, the rhythm is self-sustaining, with a faster rapid, chaotic dysrhythmia, with unsynchronized
discharge rate than other pacemakers. Converting out twitching of the heart muscle. It is secondary to either
of the rhythm requires interruption of the reentry enhanced automaticity or a reentry conduction
loop.1,17 disturbance with multiple conduction pathways that
FIGURE 19-31 Ventricular tachycardia: The rhythm is

regular, with a ventricular rate of approximately 136 bpm. FIGURE 19-32 Ventricular fibrillation: The rhythm is
No P-waves are present. chaotic with no ventricular rate.
vary in size and direction. In ventricular fibrillation,

minute parts of the ventricular muscle are in various Best Practice
stages of depolarization and repolarization. Conse-
quently, the ventricular muscle does not depolarize as Use of an Automatic
a unit, and the muscle contraction is totally ineffective,
with a twitching heart muscle that is unable to fill up
Implantable Cardiac
with or eject blood. In effect, the heart is in a state of Defibrillator
cardiac arrest. This dysrhythmia is fatal if left A large randomized study (MADIT II) of patients
untreated. with a left ventricular ejection fraction of ⱕ30%
The two classifications of ventricular fibrillation— and a history of a heart attack compared the
coarse and fine—are distinguished from each other by effect of an automatic implantable cardiac defi-
wave amplitude. brillator (AICD) to the that of conventional medi-
• Coarse ventricular fibrillation exists when wave cal therapy. The study revealed that the AICD
amplitude is more than 3 mm (3 small squares). significantly reduced mortality. The reduction in
Coarse ventricular fibrillation is of a more recent sudden cardiac death was reduced by 68% in
onset than fine and is likely to respond to patients under 65 years, by 65% in patients
defibrillation. between 65 and 74 years, and by 68% in
• When the amplitude is less than 3 mm, the patients aged 75 years. New guidelines released
rhythm is classified as fine ventricular fibrillation. by the American College of Cardiology with the
Fine ventricular fibrillation is close to ventricular American Heart Association recommend the
asystole, and someone with this rhythm is likely AICD with a class I indication for many types
to need epinephrine and anti-arrhythmic of patients with preexisting heart problems who
medications in addition to defibrillation in order are high risk for sudden death. Additionally, the
to convert the rhythm.1 AICD is now used to treat patients with conges-
tive heart failure who need synchronization of the
Clinical Significance Ventricular fibrillation is a cardiac heart rhythm to improve cardiac function.
emergency that is incompatible with life. The patient This needs several safety warnings:
must be treated immediately. The recommended • don’t apply external defibrillation paddles
treatment is CPR, electrical shock (defibrillation), and over the AED or lead locations.
medications, if necessary. • do not defibrillate over medication patches
• Chest compressions and artificial ventilation • do defibrillate between automatic shocks
keep the individual alive until a life-sustaining or pacemaker initiated beats.
heart rhythm is reestablished. Source: Aronow WS. Treatment of ventricular arrhythmias in the
elderly. Geriatrics. 2007;63,8:20–28.
• The first definitive treatment is electrical shock.
Defibrillation immediately depolarizes the
entire heart in synchrony. This action stops the
heart’s chaotic electrical activity and allows the commonly known as flatline, although the baseline
opportunity for the normal cardiac pacemakers may not be completely isoelectric.
to resume control of the heart’s rate and
rhythm. Description Ventricular assystole exists when there is an
• If defibrillation fails to convert the patient to a absence of electrical activity and of contraction in the
viable rhythm, then medications are adminis- ventricles. If atrial electrical activity is still present and
tered to aid in rhythm conversion. the dysrhythmia has only P-waves on the ECG, it is
ventricular standstill. Death is imminent without
Ventricular Asystole. Ventricular asystole, or ventricular immediate intervention.
standstill, is a rhythm characterized by an absence of When asystole occurs outside the hospital, it has
electrical activity (Figure 19-33). This rhythm is likely developed from the deterioration of a ventricular
FIGURE 19-33 Ventricular asystole: There is no ventricular rhythm, and only P-waves are
present. The ventricular rate is 0, and the atrial rate is approximately 55 bpm.
fibrillation and indicates prolonged cardiac arrest. The There are different degrees of PEA. The most severe
prognosis is better when asystole occurs when the form occurs when the heart has no ventricular contrac-
person is in the hospital. Besides the obvious benefit of tion; it is totally motionless. A less severe form of PEA
rapid discovery and treatment by trained professionals, is the presence of ventricular contractions that are too
another explanation of improved survival is that weak to produce a pulse or blood pressure.
patients with specific causes of asystole respond well to Treatment is always attempted because the under-
resuscitation measures. If the mechanism is massive lying cause may be reversible. In addition to the
parasympathetic discharge resulting in excessive vagal standard treatment of cardiac arrest—CPR and drug
tone, or heart block, atropine administration sup- therapy—attempting to determine the cause of PEA
presses the vagus nerve and improves AV conduction so and reversing the problem are necessary to resuscitate
that a heart rate and rhythm may return. When asystole the patient.
develops because of severe heart disease, the possibility
of survival is poor.
CLINICAL SIGNIFICANCE
Clinical Significance Ventricular asystole is a cardiac
PEA is a cardiac emergency that is incompatible with
emergency that is incompatible with life. The patient
life. The patient must be treated immediately.
must be treated immediately.
Pulseless Electrical Activity Hemodynamic Evaluation

One can never interpret an ECG strip as pulseless The goal of hemodynamic monitoring is to ensure
electrical activity (PEA) unless a patient is attached to adequate delivery of oxygen to the tissues, primarily
the monitor and the patient’s pulse can be obtained at through the manipulation of cardiac output. Because it
the same time that the ECG is being observed. is the product of heart rate times stroke volume, cardiac
output can be altered by altering either of those two
DESCRIPTION factors.
Heart rate is primarily controlled by the central
Pulseless electrical activity (PEA) is not a dysrhythmia; it nervous system. Sympathetic stimulation increases
is a clinical condition that exists when there is no heart rate, and parasympathetic stimulation decreases
detectable pulse or blood pressure but there is a viable heart rate (Table 19-13). The parasympathetic nervous
rhythm on the ECG. The heart is showing electrical system predominantly keeps the heart rate within
activity, but there is no effective mechanical contrac- normal limits (60–100 bpm). In general, increases in
tion, and the patient has no cardiac output. The types heart rate raises cardiac output up to a point. When the
of cardiac dysrhythmias seen on the ECGs for patients heart rate becomes too rapid, however, diastolic filling
with PEA are: time is greatly reduced; thus, cardiac output may drop.
• Supraventricular rhythms. Decreases in heart rate usually do not significantly
• Wide QRS rhythms such as accelerated idioven- reduce cardiac output because slower heart rates allow
tricular rhythm or ventricular escape. for improved ventricular filling, thereby increasing
• Very slow bradycardia. stroke volume.
CASE STUDY 19-2

In the intensive care unit, the cardiac monitor alarm Questions
goes off and the monitor displays this rhythm: 1. Analyze the rhythm strip and discuss its clinical
implications.
2. What types of clinical information is needed?
TABLE 19-13 Factors that affect heart rate TABLE 19-15 Factors that affect afterload
Increase Heart Rate Decrease Heart Rate Factor Increase Decrease
Circulating catecholamines Vagal stimulation Blood volume Polycythemia Anemia
Sympathomimetic Long-term, high-intensity and viscosity
medications exercise Vascular Arterial Arterial
Parasympatholytic Sedatives resistance hypertension, hypotension,
medications pulmonary pulmonary
hypertension, hypotension,
Stress Myocardial infarction
vasoconstrictors vasodilators
Pain Intracranial tumors
Cross-sectional area Valvular stenosis
Fear Digitalis of vascular bed
Low blood volume
hypertrophy or myocardial scarring due to an infarc-

TABLE 19-14 Factors that affect preload tion), preload is reduced because of lower end-diastolic
Factor Influences on Factor volumes. At slower heart rates, the longer diastolic
filling time allows for greater end-diastolic volume and
Venous return Venomotor tone, pumping action
thus improves preload. Atrial contraction at the end of
of skeletal muscle, circulating
diastole contributes 25–30% of total ventricular filling.
blood volume
Therefore, the loss of atrial contraction decreases the
Ventricular Ventricular hypertrophy, end-diastolic volume and preload. In patients with
compliance myocardial scarring, ventricular decreased ventricular compliance (e.g., postmyocardial
enlargement infarction or ventricular hypertrophy), atrial contrac-
Duration of diastole Heart rate, premature tion is extremely important to maintain adequate
ectopic beats ventricular filling.
Atrial contraction Atrial fibrillation, atrial flutter Afterload is the force against which the ventricles
must work to pump blood; in other words, afterload is
the resistance to flow from the ventricle. As the resis-
tance increases (e.g., in hypertension or valvular
stenosis), stroke volume may decrease. On the other
Stroke volume is the net result of three factors: hand, as the resistance decreases (e.g., in sepsis or
preload, afterload, and contractility (see Chapter 6). exercise), stroke volume may increase. Afterload is
In general, the higher the preload is (i.e., the reflected in the arterial systolic pressure because blood
stretching of the ventricle before the next contraction), pressure equals cardiac output times vascular resistance
the stronger the subsequent contraction will be. (Table 19-15).
However, once the myocardial fibers are stretched Factors that tend to increase afterload are:
beyond a certain point, even though preload continues
• Hypertension.
to increase, the force of contraction deteriorates.
• Semilunar valve stenosis.
The amount of stretching is determined by the
• Polycythemia.
volume of blood in the ventricles at the end of diastole
• Vasoconstrictor medications.
and is reflected in ventricular end-diastolic pressure.
Changes in end-diastolic volume alter preload, such Factors that typically decrease afterload are:
that an increase in preload raises stroke volume.
• Hypotension.
End-diastolic volume is influenced by several factors,
• Anemia.
including venous return, ventricular compliance,
• Vasodilator medications.
duration of diastole, and atrial contraction
(Table 19-14). Contractility is the intrinsic vigor of contraction
Increases in venous return to the heart increase of the myocardial fibers; that is, it is the force generated
preload. Factors that increase venous return are by the shortening of the myocardial muscle fibers.
increased venomotor tone, pumping action of the Whenever contractility increases (positive inotropism) or
skeletal muscles, and greater circulating blood volume. decreases (negative inotropism), stroke volume and
When the ventricles are less compliant (e.g., ventricular therefore cardiac output also increase or decrease.
TABLE 19-16 Factors that affect of murmurs, and gallop rhythms aids in detecting the
contractility early onset of congestive heart failure.
Rate and rhythm are further evaluated by checking
Increase Decrease the upper and lower extremity pulses for rate, regularity,
Sympathetic stimulation Hypoxemia and pulse volume. Pulse volume is evaluated by
Circulating catecholamines Hypercapnia assessing the strength of each beat. Typically, shorter
cardiac cycles produce a weak pulse, whereas longer
Positive inotropic agents: Acidosis
cardiac cycles produce a stronger pulse. Premature
Epinephrine Myocardial ischemia beats are usually not felt because of reduced ventricular
Digitalis Myocardial infarction filling secondary to the shortened ventricular filling
Isoproterenol Negative inotropic agents: time, the lack of atrial contraction, and the distorted
ventricular contractility. These extrasystolic beats are
Dopamine Procainamide
often referred to as nonperfusing beats because the
Dobutamine Beta-blockers pressure generated by the contracting ventricles is not
Amrinone Calcium channel blockers enough to eject blood.
Milrinone Anesthetic agents Pulse volume changes with alterations in cardio-
vascular function. Patients with a hyperdynamic
circulation (e.g., fever, anemia, excited state, preg-
nancy) have increased pulse volume, whereas those
Many factors influence contractility (Table 19-16), with significant tachyarrhythmias or hypodynamic
including: circulation (e.g., left ventricular failure, hypovolemia)
• Sympathetic stimulation. will have decreased pulse volume.
• Metabolic abnormalities. Capillary refill is assessed by pressing the patient’s
• Heart rate. nailbed to squeeze blood from the underlying capillary
• Pharmacological agents. bed. If tissue perfusion is normal, color returns to the
nailbed within 2 seconds. In states of reduced tissue
perfusion (e.g., shock, heart failure), the return of color
EVALUATION takes longer than 2 seconds.
Evaluating the hemodynamic status of a patient can In circulatory failure, blood is shunted to the major
take the form of a brief noninvasive physical assess- organs; therefore, the skin becomes cool and pale. This
ment or of a more complex procedure involving change in color and temperature begins distally and
invasive catheters. If the patient’s condition is critical, a moves toward the trunk as the hemodynamic status
rapid assessment should be completed, focusing on the deteriorates. Cyanosis is possible, but it is not a reliable
parameters that provide evidence of tissue perfusion: indicator of tissue perfusion.
Level of consciousness is a sensitive indicator of
• Heart rate and rhythm. cerebral perfusion and therefore of hemodynamic
• Presence and quality of pulses. status. Early signs of underperfusion are the inability to
• Capillary refill. think or perform complex mental tasks, restlessness,
• Color of skin and mucus membranes. apprehension, uncooperativeness or irritability, and
• Skin temperature. loss of short-term memory.
• Level of consciousness. Urine output is another sensitive indicator of tissue
• Urine output. perfusion. Decreased urine output in adequately
• Neck veins. hydrated patients indicates hypoperfusion and may
Typically, in the presence of decreased tissue occur long before other signs of impaired perfusion.
perfusion, the heart rate increases. However, when Examining the neck veins, specifically the jugular
assessing a patient’s heart rate and rhythm, the respira- veins, provides information regarding the hemody-
tory therapist needs to evaluate more than just the rate namic status of the right heart. The neck veins are
and rhythm from the cardiac monitor. In addition to examined with the patient lying supine, with the
determining the number of beats per minute, listen to head elevated approximately 30°, and with the head
heart sounds to ensure that the valves open and close and neck relaxed. The external jugular vein is rela-
with the electrical events. If arrhythmias are present, tively easy to identify because it lies superficially and
ascertain the hemodynamic tolerance for this rhythm can be seen just above the superior border of the
disturbance. (For example, can the patient maintain midclavicle. Pressing gently on the superior border of
an adequate blood pressure with this rhythm?) the midclavicle allows the external jugular vein to fill
Auscultating for the quality of heart sounds, presence and makes it easy to identify. In the patient with
TABLE 19-17 Causes of elevated venous MONITORING OXYGENATION

pressure Oxygen delivery (DO2) is calculated by multiplying the
cardiac output (CO) by the oxygen content of arterial
Cardiac Causes Noncardiac Causes
blood (CAO2). The amount of oxygen delivered to
Right ventricular failure Superior vena cava tissues is regulated by the metabolic needs of each
secondary to left ventricu- obstruction, thoracic organ system. The normal response to increased oxygen
lar failure, right ventricular tumor, hematoma demand by the tissues is to increase oxygen supply by
infarction, cor pulmonale increasing cardiac output.
Tricuspid or pulmonic Increased blood volume Arterial oxygen content (CAO2) is the total amount
stenosis of oxygen carried in arterial blood, which is equal to
Pericardial effusion or Increase intrathoracic the oxygen bound to hemoglobin (Hb) plus the
tamponade pressure, positive oxygen dissolved in plasma. Normal values for
pressure mechanical CAO2 are 18–20 mL O2/dL blood. Normal values for
ventilation, Valsalva venous oxygen content (CVO2) are 14–16 mL/dL
maneuver, COPD, blood.
tension pneumothorax A gross indicator of tissue perfusion is the arterial-
venous oxygen content difference [D(a – v)O2], which
Restrictive cardiomyopathy Increased intra-abdominal
is normally 3–5.5 mL/dL blood. Typically, as cardiac
pressure, pregnancy,
output falls owing to poor ventricular function, the
obesity, ascites
D(a – v)O2 increases. This increase is secondary to a
Constrictive pericarditis large drop in CVO2 as the tissues extract more oxygen
Space-occupying lesions of from the hemoglobin molecule.
the right heart, right atrial One method of monitoring oxygenation is to
thrombus or tumor measure arterial oxygen saturation (SaO2). Normal
values for SaO2 are 9–100%. Arterial oxygen saturation
can be:
• Estimated on the basis of arterial oxygen tension
good right heart function, the vein quickly collapses (PaO2).
after compression is released. The internal jugular • Measured noninvasively via a pulse oximeter
vein is more difficult to identify because it lies deep (SPO2).
within the neck lateral to the carotid arteries. How- • Measured invasively via a light source in the
ever, internal jugular vein pulsation can be seen at arterial catheter.
the base of the neck just lateral to the head of the The SaO2 is the percentage of total hemoglobin that
sternocleidomastoid. Distention of the jugular veins combines with oxygen; that is, it is a measure of
indicates elevated venous pressure. High venous oxyhemoglobin plus carboxyl and methemoglobin.
pressure can be due to cardiac or noncardiac Therefore, pulse oximetry is not accurate in the pres-
abnormalities (Table 19-17). ence of dysfunctional hemoglobin or poor distal
If upon completion of the physical assessment, it perfusion (e.g., shock, vasoconstrictor agents).
has been determined that the tissues are not being Arterial oxygen saturation provides information
adequately perfused, further hemodynamic monitoring regarding the patient’s pulmonary function and
may be necessary. Important hemodynamic parameters oxygenation, but the venous oxygen saturation (SVO2)
that can be measured directly are: indicates whether oxygen supply is meeting oxygen
• Oxygenation. demand. Venous oxygen saturation reflects the amount
• Cardiac output/cardiac index. of oxygen consumed by the tissues. Normal SVO2 is
• Central venous pressure. 60–80%; however, SVO2 varies depending on the organ
• Pulmonary artery pressure. system it serves (e.g., the kidney and skin have a higher
• Pulmonary capillary wedge pressure. SVO2, owing to high flow, than the heart).
• Arterial pressure. Decreased cardiac output is the most common
cause of decreased SVO2; however, SVO2 can also
Important derived hemodynamic parameters are: decrease because of a lowered CaO2, decreased Hb, or
• Mean arterial pressure. increased oxygen consumption. Patient movement,
• Systemic vascular resistance. agitation, pain, shivering, seizure activity, or increased
• Pulmonary vascular resistance. body temperature all raise oxygen demand. Changes in
• Ventricular stroke work index. SVO2 usually precede hemodynamic changes and
therefore signal the need to reassess the patient’s status. • Posture. (CO measured in the supine position
Cardiac output should be measured to confirm the decreases by approximately 20% when the
presence of underperfusion. person stands up.).
• Body size. (Larger people have a greater CO.)
MONITORING CARDIAC OUTPUT/CARDIAC INDEX Cardiac Index. The effect of body size can be corrected
by calculating the cardiac index (CI). This index is
Cardiac Output. Cardiac output is the amount of
determined by dividing the cardiac output by the
blood ejected by the heart per unit of time; it is
patient’s body surface area (BSA), and it is expressed in
reported in liters per minute (Lpm). Reasons for
units of liters per minute per square meter (Lpm/m2).
cardiac output monitoring are:
The cardiac index provides a greater clinical value than
• Assessment of left ventricular function. cardiac output because it is a more precise indicator of
• Assessment of perfusion status. hemodynamic status and tissue perfusion.
• Evaluation of hemodynamic status. A normal cardiac index of 2.5–4.2 Lpm/m2
• Evaluation of response to medical therapy. indicates good cardiac function.
• Calculation of cardiac index, vascular resistance,
• An increase in CI is normally seen during exercise
and ventricular stroke work index.
or in patients with mild tachyarrhythmias.
Cardiac output monitoring is routinely measured at the • Reduced CI is seen in patients with an abnormal
bedside by means of a pulmonary artery catheter and heart rate, preload, or afterload; decreased
the thermodilution technique, which measures the contractility; and arrhythmias.
temperature change of blood after an injection of a • A cardiac index of 1.8–2.1 Lpm/m2 indicates
solution colder than body temperature. A specified moderate cardiac depression and impending
quantity of cold saline (iced or at room temperature) is deterioration.
injected rapidly into the proximal (right atrium) port • A cardiac index of 1.7 Lpm/m2 or less indicates
of a thermodilution pulmonary artery catheter. The severe cardiac depression with a poor prognosis.
temperature drop, measured at the distal tip of the
catheter, is plotted against time to produce a thermodi-
lution curve. The cardiac output is then calculated by MONITORING CENTRAL VENOUS PRESSURE
computer. Central venous pressure (CVP) monitoring provides
measurement of right atrial (RA) pressures, which are
• The normal curve should have a smooth rapid
reflective of changes in right ventricular (RV) function
upstroke with an even downslope.
and cardiovascular status. The purposes of CVP moni-
• In cases of high cardiac output, the area under
toring are to:
the curve is small.
• Low cardiac output produces a longer downslope • Assess blood volume status.
with a greater area under the curve. • Administer fluids.
• An uneven upslope indicates poor injection • Sample blood.
technique (i.e., perhaps the solution was not • Measure SVO2.
injected quickly and evenly). • Assess right ventricular preload.
The following protocol should be used to ensure The central venous catheter is typically inserted via
the accuracy of cardiac output measurements: the subclavian, internal jugular, or external jugular
vein, with the distal tip of the catheter positioned in
1. Repeat the procedure three times.
the superior vena cava just above the right atrium.
2. Wait 1.5–2 minutes between injections.
The graphic waveform recorded by the CVP
3. Calculate the average of all three measurements
catheter is the same as a right atrial pressure curve, with
(if all are within 10% of each other).
the classic a-wave, c-wave, and v-wave configuration.
4. Repeat the procedure a fourth time if one
measurement is greater than 10% of the • The a-wave is an increase in pressure due to
others. RA contraction.
• The c-wave, which is not always seen, is a brief
Normal cardiac output is 4.0–8.0 Lpm, but this
“bump-up” in pressure due to the tricuspid
value varies. Variables that affect cardiac output are:
valve’s closing.
• Metabolic rate and oxygen demand. • The v-wave is a gradual rise in pressure caused by
• Gender. (Females have lower CO than males.) the right atrium’s filling during ventricular systole.
• Age. (CO is highest in childhood and diminishes • The x-descent is the downward slope of the
with age.) a-wave, representing right atrial relaxation.
• The y-descent is the downward slope of the hemodynamic information regarding right and left
v-wave, representing right ventricular relaxation ventricular function. The pulmonary artery (PA)
and right atrial emptying. catheter is inserted via a peripheral vein (internal or
external jugular, subclavian, basilic, or femoral) and
The normal CVP is 0–7 mm Hg, with the a-wave
advanced through the heart into the pulmonary artery.
slightly higher than the v-wave. This is a mean value
A balloon at the distal tip of the catheter is inflated to
because systolic and diastolic pressures are not
allow the catheter to advance itself with the flow of
recorded. Since the CVP values vary with intrathoracic
blood. The PAP catheter allows the following hemody-
pressures, CVP measurements should be made at
namic parameters to be measured and assessed:
end-expiration to minimize the effect of respiratory
variations on pressures. • Pulmonary artery pressures (systolic, diastolic,
High CVP readings occur normally during sponta- mean)
neous expiration or during positive pressure inspira- • Right ventricular preload (via RA pressure)
tion. However, increased CVP may indicate: • Right ventricular afterload (via PA systolic
pressure)
• Increased right ventricular preload, which may
be due to fluid overload, a left-to-right shunt, or As the catheter is advanced from the right atrium
tricuspid valve regurgitation. to the pulmonary artery, a pressure waveform is
• Increased right ventricular afterload, which may generated. As the catheter tip enters the right atrium,
be due to chronic left ventricular failure, cor the pressure waveform looks like a CVP waveform
pulmonale, pulmonary embolism, COPD, (i.e., low pressure with a-wave, c-wave, and v-wave
hypoxemia, or positive pressure ventilation configuration). The normal right atrial mean pressure
(especially with PEEP). is 0–7 mm Hg.
• Decreased right ventricular contractility, which The catheter then advances through the tricuspid
may be due to cardiac tamponade (compres- valve into the right ventricle. The RV waveform displays
sion of the heart caused by a large volume of a steep upstroke to peak right ventricle systolic pressure
fluid in the pericardium), cardiomyopathy, (RVSP), followed by a sharp downstroke to the right
constrictive pericarditis (inflammation of the ventricular end-diastolic pressure (RVEDP). The normal
pericardium), right ventricular infarct, or right RVSP is 15–25 mm Hg, and the normal RVDP is
ventricular failure. 0–7 mm Hg. The RVEDP is roughly the same as the
• Other problems, such as tricuspid valve stenosis, right atrial mean pressure (in the absence of tricuspid
catheter tip migrated into the RV, patient posi- valve disease) and reflects right ventricular preload. In
tion change, transducer position change, or a the case of tricuspid stenosis, RVEDP is less than the
clot in the monitoring line. right atrial mean pressure because the valve obstructs
the blood flow and causes pressure to increase in the
Low CVP readings occur normally during sponta-
right atrium.
neous inspiration or positive pressure expiration.
From the right ventricle, the catheter is advanced
However, low CVP readings may indicate:
through the pulmonic valve into the pulmonary artery.
• Hypovolemia. The PA waveform displays a steep upstroke to peak
• Positional changes in patient or transducer. pulmonary artery systolic pressure (PASP) and is followed
by a sharp downstroke to pulmonary artery diastolic
Clinically, trends in CVP measurements are more
pressure (PADP). This downstroke is interrupted by the
important than absolute values. The CVP measure-
dicrotic notch, which is caused by the pulmonic valve’s
ments are most useful in monitoring blood volume,
closing. The normal PASP is 15–25 mm Hg; the normal
venous return, and right ventricular function. When a
PADP is 8–15 mm Hg; pulmonary artery mean pres-
change in CVP is noted, however, the respiratory
sure is 10–20 mm Hg.
therapist should assess additional hemodynamic
The catheter is advanced to the pulmonary capil-
parameters to determine the cause of that change. A
lary wedge position by slowly inflating the balloon
pulmonary artery pressure measurement may be
while observing the PAP waveform. The balloon
necessary to further evaluate the patient’s hemody-
catheter floats out toward the pulmonary capillaries
namic status because the CVP is not useful for monitor-
until the balloon becomes “wedged” in the smaller
ing left ventricular function.
vessel. At this point, the pressure waveform changes,
measuring the pressure distal to the tip of the catheter,
MONITORING PULMONARY ARTERY PRESSURE that is, the pulmonary capillary wedge pressure (PCWP).
Pulmonary artery pressure (PAP) monitoring utilizes a Since there are no valves between the pulmonary
flow-directed, balloon-tipped catheter to provide capillaries, pulmonary veins, and left atrium (LA), the
PCWP measures pressure changes in the left atrium and TABLE 19-18 Causes of a damped pressure
therefore the left ventricular preload. curve
The PCWP waveform displays low-amplitude
oscillations similar to the right atrial waveform, with Cause Remedy
the a-wave (atrial contraction)–v-wave (atrial filling) Fibrin at the catheter tip Gently aspirate, and then
configuration. The normal mean PCWP is 4–15 mm flush catheter.
Hg. The PCWP is equal to left ventricular end-diastolic Tip of catheter against Reposition catheter.
pressure (LVEDP) in the absence of mitral valve disease vessel wall
and reflects left ventricular preload.
Air bubbles in the tubing Gently aspirate, and then
The pulmonary artery diastolic pressure is typically
system flush catheter.
used as a reflection of left ventricular end-diastolic
pressure, instead of pulmonary capillary wedge pres- Kinks in catheter or tubing Reposition catheter or
sure, because the PADP and PCWP are nearly equal. tubing.
The pulmonary artery systolic pressure is roughly the
same as right ventricular systolic pressure in the
becomes rounded out, the upstroke of systole slows,
absence of pulmonary valve disease. Both pulmonary
and the dicrotic notch disappears. Damping of the
artery systolic and diastolic pressures decline during
pulmonary artery pressure curve can be due to several
spontaneous inspiration; therefore, pulmonary artery
factors, which can be easily checked and corrected
and pulmonary capillary wedge pressures should be
(Table 19-18).
measured at end-expiration. For continuous monitor-
ing purposes, the balloon should always be left
deflated, with the catheter tip in the pulmonary artery MONITORING PULMONARY CAPILLARY
as evidenced by the waveform. The balloon should be WEDGE PRESSURE
deflated passively by opening the valve; never aspirate Because the pulmonary artery diastolic pressure closely
the balloon. reflects changes in the left ventricular end-diastolic
Arrhythmias cause the pulmonary artery pressure pressure and the left ventricular preload, it can be
to vary. For example, in the presence of atrial fibrilla- continuously monitored instead of the pulmonary
tion, the pulmonary artery pressure varies with the capillary wedge pressure. In certain conditions, how-
heart rate. In other words, with slower ventricular ever, the PCWP must be measured directly. An increase
response, the ventricular filling time is longer in pulmonary vascular resistance increases PADP
(increased preload), causing an increase in both PASP measurements, while the PCWP measurements are
and PADP. Conversely, premature ventricular contrac- normal or low. Pulmonary vascular resistance can be
tions cause the pulmonary artery pressure to drop increased by:
owing to reduced stroke volume (secondary to reduced
• Pulmonary embolism.
ventricular filling). Therefore, pressure measurements
• Hypoxia.
should exclude ventricular ectopic beats.
• COPD.
Elevated pulmonary artery pressures are due to one
• Acute respiratory distress syndrome (ARDS).
of four factors:
In addition, in the presence of tachycardia, PADP may
• Increased pulmonary vascular resistance (e.g.,
be falsely elevated owing to the shortened diastolic
pulmonary disease, pulmonary hypertension,
filling period.
pulmonary embolus, hypoxemia, or acidosis).
An elevated pulmonary capillary wedge pressure
• Increased pulmonary venous pressure (e.g.,
indicates an increase in left ventricular preload and can
mitral valve stenosis or left ventricular failure).
be due to several factors: left ventricular failure, mitral
• Increased pulmonary blood flow (e.g., hypervol-
valve stenosis or regurgitation, cardiac tamponade,
emia, left-to-right shunt).
constrictive pericarditis, or volume overload. A PCWP
• Cardiac tamponade.
of 18–20 mm Hg usually produces mild pulmonary
Decreased pulmonary artery pressures are typically congestion and shortness of breath as fluid moves from
associated with hypovolemia owing to either vasodila- the capillaries into the alveoli. As the PCWP
tor therapy or dehydration. However, when the pulmo- approaches and exceeds 30 mm Hg, acute pulmonary
nary artery pressure is reduced, the therapist must edema is present.
ensure that it is not a damped pressure curve. The In a patient with normal cardiac function, a low
damped pressure curve both changes the shape of PCWP (less than 5 mm Hg) indicates hypovolemia. In
the waveform and decreases the pressure measure- a patient with compromised cardiac function, however,
ments. The waveform loses its sharp definition and hypovolemia may be present despite normal or high
PCWP measurements; therefore, cardiac output must higher than the level of the patient’s heart, the
be measured. If measuring cardiac output directly is pressure reading will be falsely low. Conversely,
not possible, calculate the D(a – v)O2. If the D(a – v)O2 if the transducer is lower than the patient’s heart,
is increased, the patient has poor cardiac function. the pressure reading will be falsely high because
Pulmonary capillary wedge pressure should be of the effects of gravity on the transducer-air
monitored every 2–4 hours or whenever a change in interface. Also, the patient should be in the
pulmonary artery pressure or SVO2 is noted, but the supine position, with the head elevated no more
catheter should never be left in the wedge position than 20 degrees. With the head elevated greater
because it can cause a pulmonary infarction. The than 20 degrees, measurements will be inaccurate,
balloon should be deflated within 15 seconds or a but that position is acceptable for monitoring
maximum of five breaths. Once the balloon is deflated, trends in pressure changes rather than absolute
the PA waveform should reappear immediately. numbers.
To ensure accurate PCWP measurements, verify • Second, a phenomenon known as catheter
that the catheter is positioned properly by observing whip (“fling”) artifact is the excessive movement
the pressure waveform. The pulmonary artery wave- of the catheter tip, as seen as a spike superim-
form flattens to a left atrial waveform with a pressure posed on the PA pressure waveform. Pressure
drop once the balloon is inflated. The pulmonary measurements are inaccurate because the artifact
capillary wedge pressure mean should be less than causes an overestimation of systolic pressure and
the pulmonary artery mean. A PCWP that is greater an underestimation of diastolic pressure. Cath-
than the PADP, an artifact known as overwedging, eter whip artifact can be due to the catheter tip’s
indicates a problem with catheter position and must being too close to the pulmonic valve. This
be corrected. Overwedging is caused by overinflation problem can be corrected by slightly advancing
or eccentric inflation of the balloon. Either may the catheter farther into the pulmonary artery.
produce artificially elevated, damped, and inaccurate This artifact can also be due to external noise
pressure readings. To correct this problem, deflate the (such as shivering or patient movement).
balloon, reposition the catheter, and reinflate the Keeping the patient still and comfortable usually
balloon. eliminates the problem. A hyperdynamic heart
Other common artifacts seen with PCWP monitoring (e.g., early sepsis or excessive catecholamines)
that can lead to abnormal pressure measurements are a can also cause catheter whip artifact. This cause
damped pressure curve and mixed PA-PCWP waveforms. is not easily corrected, so only trends in the
pressure measurements can be observed, not
• Damping of the pressure curve produces a
absolute numbers.
rounded-out appearance of the curve, with a lack
• Third, in certain types of cardiac dysfunction,
of clearly defined a-waves and v-waves. To correct
pulmonary capillary wedge pressure does not
this problem, deflate the balloon, aspirate, and
equal left atrial pressure or left ventricular
gently flush the distal port of the catheter. Never
end-diastolic pressure. In cases of decreased left
flush the distal port with the catheter in the
ventricular compliance (e.g., acute myocardial
wedge position.
infarction, aortic regurgitation, cardiac tampon-
• A mixed PA-PCWP waveform occurs because of
ade, or constrictive pericarditis), the PCWP is
incomplete wedging of the catheter tip. The
lower than the LVEDP. Typically, when the
waveform varies with respiration such that,
LVEDP is greater than 25 mm Hg, the pressure is
during inspiration, a PA curve is present, but,
not adequately reflected back to the pulmonary
during expiration, a PCWP curve is present.
capillary bed.
Slight advancement of the catheter usually
• Finally, the PCWP is greater than the LVEDP for
corrects the problem.
a number of reasons:
The respiratory therapist must be aware of • Whenever there is an obstruction between the
several clinical pitfalls to obtain accurate PA/PCWP pulmonary artery and the left ventricle, there is
measurements. increased resistance. This type of finding
• The first is body position relative to the pressure typically occurs with patients with pulmonary
transducer. For accurate pressure measurements, disease (e.g., acute respiratory distress syn-
the transducer-air interface must be level with drome, COPD, and pulmonary emboli).
the patient’s heart—that is, at the patient’s • PCWP can be greater than LVEDP secondary to
midaxillary line. Pressure measurements must be increased pulmonary artery pressure in
made with the transducer and patient in the patients receiving positive pressure ventilation
same position each time. If the transducer is or CPAP.
• Other causes are tachycardia (heart rate over TABLE 19-19 Determining zone placement
125 bpm), hypovolemia, hypoxemia, mitral
valve stenosis, pulmonary venous obstruction, Zone 1 or 2 Zone 3
and left atrial myxoma. PADP < PCWP PADP > PCWP
The position of the catheter tip in the pulmonary PCWP curve damped PCWP curve displays
artery relative to the lungs can have an impact on the with smooth contour clear a-, c-, and v-waves
accuracy of the PA-PCWP pressures. (The position of An increase in PEEP An increase in PEEP
the catheter tip may be identified by a lateral chest causes PCWP to increase causes PCWP to increase
X-ray.) to more than half the to less than half the PEEP
PEEP change change
• Pulmonary artery pressures increase progres-
sively toward the base of the lungs, such that at
the apexes (zone 1) the alveolar pressure (Palv) is
greater than the pulmonary artery systolic and
diastolic pressures (PA) and the pulmonary • The PCWP-waveform exhibits clear a-, c-, and
venous pressure (PV) (i.e., Palv ⬎ PA ⬎ PV). v-waves.
Therefore, in zone 1, the vessel is closed, and no • With a change in positive end-expiratory pres-
vessel is open to the left atrium. As a result, the sure (PEEP), the PCWP mean is less than half
catheter tip is sensing Palv, the PCWP waveform the change in PEEP.
is damped, and the pressure measurement is In addition, placement of the catheter in zone 3
equal Palv, not LA pressure. can be confirmed by the presence of the catheter tip
• As the catheter tip moves toward the middle of below the left atrium on the chest X-ray.
the lungs (zone 2), PA is greater than Palv, and Palv The catheter is in zone 1 or 2 if:
is greater than PV (i.e., PA ⬎ Palv ⬎ PV). As a
result, the vascular channel is open intermit- • The PA diastolic pressure is less than the PCWP.
tently. The vessel is open during systole because • The PCWP-waveform is damped with a smooth
PA systolic pressure is greater than Palv; therefore contour.
PCWP is accurately measuring LA pressure. • With a change in PEEP, the PCWP mean is
During diastole, the vessel is closed off because greater than half the change in PEEP.
PA diastolic pressure is less than Palv, and PCWP On a chest X-ray, the tip of the catheter is shown at or
is recording alveolar pressure, not LA pressure. above the left atrium.
Therefore, hemodynamic measurements are The PCWP tracing and therefore measurements
not accurate when the catheter tip is in zone 2 are affected by ventilation. During normal spontane-
of the lungs. ous breathing, the PCWP is minimally affected by
• With the catheter tip placed at the base of the changes in intrathoracic pressures. In general, during
lung (zone 3), PA systolic and diastolic pressures inspiration PCWP drops slightly, whereas during
are greater than PV, and PV is greater than Palv exhalation it increases slightly. As spontaneous
(i.e., PA ⬎ PV ⬎ Palv). The vessel remains open breathing becomes more labored, the PCWP and PAP
throughout the cardiac cycle, and the PCWP is become greatly affected. Inspiration causes a large
accurately measuring LA pressure. Therefore, for decrease in PCWP, and expiration causes a large
accurate PCWP measurements, the catheter tip increase in PCWP.
must be placed in zone 3. When the patient is Mechanical positive pressure ventilation (PPV) has
supine, the majority of the lung is zone 3. several physiological effects, and therefore it affects
However, zones 1 and 2 enlarge with positive PCWP and PA pressure measurements.
pressure ventilation, especially with PEEP or air
trapping (as in asthma or COPD), secondary to • During PPV, inspiration causes an increase in
the increases in alveolar pressure. A drop in PCWP secondary to increased alveolar, intratho-
arterial and venous pressure, as seen with racic, and intravascular pressures.
hypovolemia, hemorrhage, or diuresis, also • In addition, the increased alveolar and intratho-
enlarges zones 1 and 2. racic pressures decrease venous return, thereby
reducing cardiac output.
To perform a zone placement check, observe the • The sizes of zones 1 and 2 increase with PPV
PA and PCWP waveform (Table 19-19). The catheter is secondary to alveolar pressures increased to
in zone 3 if: greater than PA pressures.
• The PA diastolic pressure is greater than the • The cardiovascular effects of PPV are directly
mean PCWP. proportional to the increase in intrathoracic
pressures (i.e., level and mode of ventilation as downstroke is interrupted by the dicrotic notch, which
well as lung compliance). Patients with preexist- is caused by the aortic valve’s closing.
ing depressed cardiac function or hypovolemia The normal BPsys is 100–140 mm Hg and reflects
are highly susceptible to the pressure changes. left ventricular systolic pressure (in the absence of
Therefore, hemodynamic measurements should aortic stenosis). Arterial systolic pressure increases in
be made at end-expiration, when pressure the distal vessels, such that the BPsys in the femoral
changes are minimal. artery is 20–50 mm Hg greater than the BPsys in the
brachial artery.
The use of PEEP exaggerates the effects of PPV on
The normal BPdia is 60–80 mm Hg and indicates
PCWP measurements. In general:
the distal runoff of arterial blood and the elastic recoil
• With a PEEP of 0–10 cm H2O, the PCWP is of the arteries. Arterial diastolic pressure decreases
approximately equal to LA pressure and LVEDP. slightly or remains the same in the distal vessels.
However, with PEEP greater than 10 cm H2O, Arterial diastolic pressure is greatly affected by heart
there is an increased disparity between PCWP rate: a longer diastole (as occurs with bradycardia)
and left heart pressures. allows the BPdia to decline further, whereas faster heart
• The exaggeration of PCWP measurements with rates increase BPdia secondary to a shorter diastole. In
PEEP is most pronounced in lungs with increased addition, BPdia greatly affects coronary perfusion
compliance. However, the effects of PEEP are not pressure (CPP), because most of coronary blood flow
as significant in patients with decreased lung occurs during diastole. Therefore, heart rate also affects
compliance because the increased pressures are CPP. A CPP of less than 50 mm Hg indicates poor
not well transmitted to the pulmonary vasculature. myocardial perfusion and threatens cardiac perfor-
mance. Myocardial perfusion can be improved by
The use of PPV and PEEP almost always results in
increasing BPdia or decreasing PCWP, or both.
an overestimation of the actual PCWP. However, these
Normal mean arterial pressure (MAP) is 70–95 mm
measurements are still useful clinically to determine
Hg and reflects cardiac output (CO) and systemic
the patient’s hemodynamic status. Keeping the patient
vascular resistance (SVR). The MAP is the same in the
on PPV and PEEP while taking pressure measurements
distal vessels and represents the average arterial pres-
is preferable because doing so provides the clinician
sure throughout the cardiac cycle. Since the diastolic
with valuable information regarding the patient’s
period (approximately two-thirds of the cardiac cycle)
hemodynamic status during mechanical ventilation.
is longer than the systolic period, the MAP is calculated
by the following equation:
MONITORING ARTERIAL PRESSURE
BPsys ⫹ (2 BPdia)
Arterial pressure monitoring allows the constant MAP ⫽ _______________
3
monitoring of arterial blood pressure via an intra-
arterial catheter, which is indicated when the patient’s Pulse pressure, calculated by subtracting BPdia from
blood pressure is unstable. In addition, continuous BPsys, reflects changes in stroke volume and arterial
arterial monitoring is used to assess the patient’s compliance. Wide pulse pressures are associated with a
response to therapeutic interventions and for arterial large stroke volume (e.g., aortic valve regurgitation or
blood sampling. hypervolemia) or with an increase in ejection velocity
Note: Arterial lines are not indicated for medication due to medications (e.g., dobutamine, dopamine,
administration or fluid maintenance. isoproterenol). Narrow pulse pressures, on the other
The most common site for arterial catheter inser- hand, are associated with low stroke volume (e.g., heart
tion is the radial artery because this site provides good failure or shock) or an increase in ejection time (e.g.,
accessibility, good collateral circulation, low injury risk aortic valve stenosis).
at insertion, good patient comfort and mobility, and Increased arterial pressures are typically seen with
easy access to control or observe bleeding. Other sites specific diseases or disorders such as aortic valve
for arterial catheter insertion are the axillary, brachial, regurgitation, arteriosclerosis, and systemic hyperten-
femoral, and dorsalis pedis arteries. sion. Aortic valve regurgitation allows blood to leak
The arterial pressure waveform reflects the function back into the left ventricle during diastole, thereby
and pressure changes in the left ventricle and systemic increasing preload and consequently increasing stroke
vascular resistance. The pressure waveform generated volume. As a result, the BPsys rises while BPdia drops,
by the intra-arterial catheter closely resembles the and the pulse pressure increases. Medications that
pulmonary artery pressure waveform: a steep upstroke increase systemic vascular resistance (SVR), such as
to peak systolic pressure (BPsys), followed by a positive inotropic agents and vasopressors, also
sharp downstroke to diastolic pressure (BPdia). This increase arterial pressures.
Low arterial pressures are typically associated with A small rounded arterial pressure curve with a slow
arrhythmias (e.g., atrial fibrillation, premature ventricu- upstroke, no clear dicrotic notch, decreased BPsys, and
lar contractions) and decreased stroke volume. The decreased BPdia indicates pressure damping, which may
effect of atrial fibrillation on arterial pressure is highly be caused by:
variable, but, because of the loss of atrial kick, stroke
• Air bubbles in the pressure tubing or catheter.
volume is usually diminished in the presence of atrial
• A partial clot in the catheter.
fibrillation. Premature ventricular contractions also
• Inadequate pressure on the IV flush bag.
decrease stroke volume secondary to the lack of
• Loss of infusion solution.
diastolic filling, and therefore reduce arterial pressure.
• The catheter’s being lodged against the vessel wall.
Other disorders that decrease stroke volume are left
• Loose connections in the tubing.
ventricular failure, shock, cardiac tamponade, and left
ventricular outflow tract obstruction (e.g., aortic valve To correct for pressure damping, follow this
stenosis). procedure:
There are several variations to the arterial pressure
1. Aspirate the catheter and flush the system.
curve, each of which indicates a change in the patient’s
2. Make sure all connections are tight and the
hemodynamic status: pulsus alternans, pulsus bis-
tubing is not kinked.
feriens, pulsus paradoxus, and pulsus parvus.
3. Check for proper pressure on the IV flush bag and
• Pulsus alternans is a regular waveform pattern to ensure there is enough IV solution in the bag.
in which, on every other beat, the amplitude and 4. Recheck zeroing or calibration.
therefore the pressure are larger. This irregularity Catheter whip (fling) artifact is an erratic, or “noisy,”
occurs because of alternating ventricular contrac- pressure curve with sharp negative or positive waves.
tility associated with arrhythmias or left ventricu- This type of abnormality is usually associated with
lar failure. excessive movement of the catheter tip, excessive
• Pulsus bisferiens is an arterial pressure curve connecting tubing, rapid heart rates, or some combina-
that displays two systolic peaks. One peak may tion of those. To correct for this problem, limit patient
be higher than the other, or the two peaks may movement, reposition the catheter tip, or use a fre-
be equal. The first peak is due to early systolic quency filter. Some monitoring equipment comes with
rapid ejection, followed by a brief drop in a filter to eliminate this type of high-frequency artifact.
pressure. The second peak is due to forward
blood flow later in systole. This type of pressure
waveform is indicative of aortic valve regurgi- Spotlight
tation, hypertrophic cardiomyopathy, or On
hyperthyroidism.
• With pulsus paradoxus, BPsys falls by more The Pulse Oximeter
than 10 mm Hg during spontaneous inspiration There is a new use for a common monitoring tool:
despite a regular heart rate. This finding is most the pulse oximeter. In the February 1999 issue
commonly seen in patients with cardiac tam- of Chest, T. V. Hartert and colleagues identified a
ponade. Other causes of pulsus paradoxus use of pulse oximetry in critically ill patients with
include COPD, pulmonary embolus, hypovole- severe airway obstruction. They suggested that
mic shock, severe asthma, and constrictive the respiratory variation of the baseline pulse-
pericarditis. A reverse pulsus paradoxus, in which oximetry waveform, termed RWV (respiratory
the BPsys rises by more than 10 mm Hg, can waveform variation), is an indicator of severe
occur during positive pressure ventilation. airway obstruction. Monitoring the baseline pulse
Reverse pulsus paradoxus is usually caused by oximetry variation during breathing identifies the
hypovolemia. presence of pulsus paradoxus. It is already
• Pulsus parvus is a weak pulse seen on the known that pulsus paradoxus is positively
arterial pressure curve as a low BP with decreased correlated with severe air trapping in critically ill
pulse pressure. Pulsus parvus is indicative of asthmatic and COPD patients. Improvement in
decreased cardiac output caused by aortic valve the number of millimeter change from the
stenosis, left ventricular failure, or shock. baseline waveform can be used as a noninvasive
measure of clinical improvement.
Other variations of the arterial pressure curve may
Source: Hartert TV, Wheeler AP, Sheller JR. Use of pulse oximetry to
be due to mechanical abnormalities rather than recognize severity of airflow obstruction in obstructive airway disease:
physiological changes: damping, catheter whip (fling) correlation with pulsus paradoxus. Chest. 1999;115:475–481.
artifact, and inaccurate zeroing or calibration.
SYSTEMIC VASCULAR RESISTANCE TABLE 19-20 Causes of changes in systemic

Systemic vascular resistance (SVR) is the force that vascular resistance
the left ventricle must overcome to maintain systemic
Increase Decrease
blood flow. Hence, SVR is a measure of left ventricular
afterload. This important hemodynamic parameter Vasoconstriction Vasodilation
cannot be measured directly, but it can be derived from Decreased cardiac Vasodilator therapy
pressure measurements and cardiac output by the output Shock (anaphylactic,
following equation: Excessive catecholamine hyperdynamic
secretion sepsis, neurogenic)
MAP ⫺ CVPmean (mm Hg) ⫻ 80
SVR ⫽ ____________________________ Hypertension Other
CO Lpm
Hypothermia Anemia
Resistance to flow is the ratio of the mean pressure
Hypovolemia Aortic regurgitation
drop across the system to the flow through the system.
In the cardiovascular system, the pressure drop across Stress response Cirrhosis
the system is measured from the proximal end (i.e., the Vasopressors
aorta) to the distal end [i.e., the right atrial or central Decreased distensibility
venous pressure (CVP)] of the system, and flow is of vessels
cardiac output. The correction factor of 80 is used to
Aortic stenosis
convert millimeters of mercury to dynes per square
centimeter and liters per minute to cubic centimeters Atherosclerosis/
per second to yield units of dyne⭈s⭈cm⫺5. The normal arteriosclerosis
SVR is 900–1400 dyne⭈s⭈cm⫺5.
Under normal hemodynamic conditions, the
cardiovascular system rapidly adjusts SVR in response
to changes in body position, activity, or stress to dehydration, polycythemia, or significant temperature
maintain stroke volume and a narrow blood pressure changes), vessel radius is the primary determinant of
range. Therefore, in a normal heart, stroke volume SVR. Causes of changes in systemic vascular resistance
remains constant with fluctuations in SVR, and myo- are summarized in Table 19-20.
cardial oxygen consumption (VO2) is directly related to
SVR, such that an increase in SVR increases myocardial
VO2 and vice versa. However, in the presence of cardiac PULMONARY VASCULAR RESISTANCE
disease, as the left ventricule fails and cardiac output Pulmonary vascular resistance (PVR) is the force that
drops, stimulation of baroreceptors causes vasocon- the right ventricle must overcome to maintain pulmo-
striction, and SVR rises in an attempt to maintain nary blood flow; that is, PVR is a measure of right
blood pressure. The increased SVR increases afterload ventricular afterload. To calculate PVR, measure the
and further burdens the already failing heart, thereby mean pressure difference across the pulmonary capil-
decreasing stroke volume even more. In cases of lary bed and divide by the flow:
myocardial dysfunction, stroke volume is inversely
related to SVR, whereas myocardial oxygen consump- PAmean ⫺ PCWPmean (mm Hg) ⫻ 80
tion is directly related to SVR. That is, an increase in PVR ⫽ ________________________________
CO Lpm
SVR decrease stroke volume while increasing myocar-
dial VO2, and vice versa. With afterload-reducing The normal PVR is 20–120 dyne⭈s⭈cm⫺5. Under
medications, SVR is decreased, thereby improving normal conditions PVR is low; approximately one-sixth
stroke volume and decreasing myocardial VO2 without of SVR. When the right ventricle is faced with an
a significant drop in blood pressure. increase in afterload (PVR), it dilates as a compensatory
Regulation of SVR, according to Poiseuille’s law, is mechanism to maintain stroke volume (i.e., Frank-
a function of the length of the vessel, the viscosity of Starling mechanism). However, the thin-walled right
the blood, and the radius (R) of the vessel: ventricle is not able to withstand high afterload for very
long before it begins to fail. As the right ventricle
(8 ⫻ length) ⫻ viscosity begins to fail, its stroke volume falls while myocardial
SVR ⫽ ______________________ oxygen consumption increases.
␲ ⫺ R4
A change in PVR can be assessed by monitoring the
Because the length of the vessel does not change signifi- pulmonary artery pressure. Increased pulmonary artery
cantly once growth is complete and the viscosity of the systolic, diastolic, and mean pressures indicate
blood remains relatively constant (except in cases of increased PVR. When PVR increases, pulmonary artery
TABLE 19-21 Causes of increased grams per square meter per beat. The normal LVSWI
pulmonary vascular resistance is 40–70 g/m2/beat, and the normal RVSWI is
7–12 g/m2/beat.
Pulmonary arteriolar constriction Stroke volume (SV) is the volume of blood ejected
Sympathetic nervous system stimulation by the ventricles with each contraction. The stroke
Acidosis volume is simply the difference between the ventricular
volume at the end of diastolic filling and the ventricu-
Hypercarbia
lar volume at the end of systolic ejection. At the
Hypoxemia bedside, the stroke volume, in milliliters per beat, is
Drugs (epinephrine, norepinephrine) calculated by dividing cardiac output (Lpm) by heart
Obstruction of pulmonary vascular bed rate (bpm):
Pulmonary emboli
CO Lpm
Pulmonary stenosis SV ⫽ ________
HR bpm
Positive pressure ventilation/PEEP
The stroke index (SI), in units of milliliters per beat
Adult respiratory distress syndrome (ARDS) per square meter, is calculated to account for the effects
Alveolar septal destruction of body size on stroke volume. It is calculated by
Surgical lung resection dividing stroke volume (SV) by the patient’s body
Pulmonary edema surface area (BSA):
SV
SI ⫽ ____
BSA
pressures rises while the pulmonary capillary wedge
pressure remains normal. Therefore, in these types The normal stroke volume is 60–120 mL/beat, and
of patients, PCWP must be measured to determine the the normal stroke index is 30–60 mL/beat/m2. Factors
left ventricular end-diastolic pressure because the affecting stroke volume and stroke index are preload,
PCWP does not reflect changes in PVR. A drop in afterload, contractility, and muscular synchrony (as
pulmonary artery systolic, diastolic, and mean pres- previously discussed).
sures indicates a decrease in PVR. In the presence of a low or dropping cardiac
The regulation of PVR is primarily accomplished output, calculating RVSWI and LVSWI can help in
via vasoconstriction and vasodilation. An increase in identifying the cause. A fall in cardiac output can be
PVR can result from either pulmonary arteriolar due to low preload, excessive afterload, or diminished
constriction or obstruction of the pulmonary vascular ventricular contractility. Preload and afterload can be
bed. Factors that lead to an increase in PVR are listed in evaluated by monitoring pressures (CVP, PA, PCWP,
Table 19-21. and MAP) and vascular resistance. In the presence of
Decreases in PVR typically indicate hypovolemia stable preload and afterload with a decrease in cardiac
or pulmonary vasodilation due to medications output, altered contractility should be considered, and
(e.g., captopril, diltiazem, hydralizine, isoproterenol, LVSWI and RVSWI should be calculated.
nifedipine, nitroprusside, and nitrous oxide). Decreased LVSWI and RVSWI can occur secondary
to hypovolemia or myocardial ischemia or infarction
or with the use of certain pharmacological agents
VENTRICULAR STROKE WORK INDEX (e.g., verapamil and beta-blockers). Ventricular
Calculating the ventricular stroke work index provides contractility, and therefore LVSWI and RVSWI, can be
an indirect evaluation of contractility and therefore of increased with the use of positive inotropic agents
ventricular function. The right ventricular stroke (e.g., digoxin, dopamine, dobutamine, isoproterenol).
work index (RVSWI) and the left ventricular stroke Recall that an increase in contractility is associated
work index (LVSWI) are calculated separately using with an increase in myocardial oxygen consumption.
the calculated stroke index (SI) and pressure In the presence of compromised myocardial blood
measurements: flow (e.g., ischemia or infarction), this increase in
oxygen demand can be detrimental. Therefore,
LVSWI ⫽ SI ⫻ (MAP ⫺ PCWPmean mm Hg) ⫻ 0.0136 for these patients, administering medications that
RVSWI ⫽ SI ⫻ (PAmean ⫺ CVPmean mm Hg) ⫻ 0.0136 reduce contractility (e.g., beta-blockers) is often more
beneficial. In shock patients, inotropic agents should
The factor of 0.0136 is used to convert units of pressure be titrated to maintain an LVSWI greater than 55 g/
to units of work, that is, millimeters of mercury to m2/beat.
Summary c. one electrical cycle of depolarization and

repolarization.
Managing the critically ill patient in the clinical setting d. a wave of electrical current.
requires a complete assessment of the patient’s cardiac
2. Which electrode of the ones used in the Einthoven
status. Noninvasive assessment includes determining
triangle is considered the ground or neutral
the patient’s heart rate and rhythm and correlating them
electrode?
with the presence and quality of peripheral pulses. In
a. right leg
addition, a quick check of the patient’s capillary refill,
b. left leg
skin color and temperature, level of consciousness,
c. right arm
urine output, and neck veins determines whether
d. left arm
further invasive monitoring is necessary. With the use of
invasive catheters, important hemodynamic parameters 3. Which wave or time interval represents ventricular
can be measured directly: oxygenation, cardiac output, depolarization on an ECG?
central venous pressure, pulmonary artery pressure, a. P-wave
pulmonary capillary wedge pressure, and arterial b. QRS complex
pressure. With the information obtained from the c. T-wave
invasive catheters, additional parameters can be calcu- d. ST segment
lated (mean pressures, vascular resistance, and ventricu- 4. Which of the following dysrhythmias is considered
lar stroke work index), allowing for the optimal use of the most life threatening?
medications to maintain hemodynamic stability. a. sinus tachycardia
b. sinus brachycardia
c. atrial flutter
Study Questions d. ventricular fibrillation
REVIEW QUESTIONS 5. If an AV block results from digitalis toxicity, which
1. What is the normal time range for the P-R interval? AV block would you not see?
a. first-degree block
2. What is the landmark on the patient’s chest for the b. type I second-degree block
placement of lead V4? c. type II second-degree block
3. Name the seven steps in dysrhythmia recognition. d. third-degree block
4. Identify the following dysrhythmia: 6. Which type of AV block is also called the
Wenckebach phenomenon?
a. first-degree block
b. type I second-degree block
c. type II second-degree block
d. third-degree block
5. If the R-R interval is regular and each R-wave hits 7. Which type of ventricular dysrhythmia does
on the every second large square line, what is the not have any effective cardiac output associated
calculated rate? with it?
6. What is the most common symptom of atrial a. ventricular escape
tachycardia? b. accelerated idioventricular rhythm
7. What factors increase venous return and can result c. premature ventricular contraction
in an increase in preload to the heart? d. ventricular fibrillation
8. Using a cardiac output of 5 Lpm, a hemoglobin of 8. Which of the following categories of PVC is not
14.8 gm/dL, a PaO2 of 100, and an SaO2 of 98%, considered a serious condition?
calculate oxygen delivery. a. multifocal PVCs
b. couplets of PVCs
9. What is the most common cause of a decrease in SVO2?
c. three or more PVCs in a row
10. What substance is used to measure cardiac output d. R on T PVCs
using the thermodilution technique?
9. What is one unable to do with a central venous
pressure invasive line?
MULTIPLE-CHOICE QUESTIONS a. administer fluids
1. The action potential of a single cell is described as b. assess blood volume status
a. depolarization. c. sample blood
b. repolarization. d. measure SaO2
10. If a patient had a blood pressure of 160/100 mm 7. Prystowsky E, Pritchett E, Gallagher J. Origin of the
Hg, what is the estimated mean arterial pressure? atrial electrogram recorded from the esophagus.
a. 80 mm Hg Circulation, 1980;61,5:1017–1023.
b. 100 mm Hg 8. Fletcher G, Froelicher V, Hartley L, Haskell W,
c. 120 mm Hg Pollock M. Exercise standards. A statement for
d. 140 mm Hg health professionals from the American Heart
11. What are the ECG characteristics of Mobitz type I Association. Circulation. 1990;82,6:2286–2322.
second-degree AV block? 9. Akinpelu D, Gonazalez JM. Treadmill and pharma-
a. constant PR intervals, and constant QRS cologic stress testing. eMedicine Specialties,
intervals Cardiology and Cardiovascular Syndromes in
b. variable PR intervals, and variable QRS intervals Systemic Diseases; 2008.
c. variable PR intervals and constant QRS intervals 10. Wiederhold R. The 12-lead electrocardiogram. In:
d. constant PR intervals and variable QRS intervals Wiederhold, R. Electrocardiography, the Monitoring
and Diagnostic Leads. 2nd ed. Philadelphia: W.B.
12. What is the physiologic mechanism of paroxysmal
Saunders Co; 1999:103–116.
supraventricular tachycardia?
11. Catalano JT. Guide to ECG Analysis. 2nd ed. Phila-
a. increased automaticity
delphia: Lippincott Williams & Wilkins; 2002.
b. decreased conduction through the AV node
12. Goldenberg I, Moss AJ, Wojciech Z. QT Interval:
c. the initiation of a reentry pattern
how to measure it and what is “normal.” J Cardio-
d. decreased automaticity
vasc Electrophysiol. 2006;17:333–336.
13. In which of the following cardiac emergencies will 13. Bollinger B, Heidenreich J. Cardiac arrhythmias. In:
the patient’s ECG show a life-sustaining ECG Stone C, Humphries R, eds. CURRENT Diagnosis
pattern but the patient may have no pulse? and Treatment, Emergency Medicine. 6th ed. New
a. ventricular fibrillation York: McGraw-Hill; 2008:Chapter 33.
b. ventricular tachycardia 14. Kastor JA. Supraventricular tachyarrhythmias. In:
c. PEA Kastor JA, ed. Arrhythmias. Philadelphia: WB
d. asystole Saunders; 2000:39–276.
14. Which of the following dysrhythmias may have a 15. Kastor JA. Atrioventricular block. In: Kastor JA, ed.
rate of 42? Arrhythmias. Philadelphia: WB Saunders;
a. sinus bradycardia 2000:509–565.
b. junctional escape rhythm 16. Marriott HJ. ECG/PDQ. Baltimore: Williams &
c. third-degree heart block Wilkin; 1987.
d. a and b 17. Kastor JA. Ventricular arrhythmias. In: Arrhythmias.
e. a, b, and c Philadelphia: WB Saunders; 2000:277–308.
References Suggested Readings

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Care Anatomy and Physiology. St. Louis: Mosby- advanced technique for measuring continuous
Yearbook; 1998:267–281. cardiac output. DCCN-Dimens Crit Care Nurs.
3. Beachy W. The electrocardiogram and cardiac 1996;15:25–30.
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282–303. 1998;21:78–83.
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NJ: Prentice Hall; 2002:59–71. mias. In: Heger JW, Niemann JT, Roth RF, Criley JM,
5. Van Hare GF, Dubin AM. The normal electrocardio- eds. Cardiology. 4th ed. Baltimore, MD: Williams &
gram. In: Moss AJ, et al., eds. Moss and Adams’ Wilkins; 1998:33–80.
Heart Disease in Infants, Children and Adolescents. Ignatavicius D, Workman M. Medical-Surgical Nursing.
7th ed. Philadelphia: Lippincott Williams & 5th ed. St. Louis, MO: Elsevier Saunders; 2006:698–
Wilkins; 2007:253–268. 705, 708, 226–244.
6. Ibid.
Lippincott Manual of Nursing Practice. 7th ed. Philadel- Rieter MJ, Rieffel JA. Importance of beta blockade in
phia: Lippincott Williams & Wilkins; 2001:105–103, the therapy of serious ventricular arrhythmias. Am J
319–395. Cardiol. 1998;82:91–191.
Lodato R. Use of the pulmonary artery catheter. Semin Sarubbi B, Jucceschi VD, Andrea A, Liccardo B,
Respir Crit Care Med. 1999:20:29–42. Santangelo L, Iacono A. Atrial fibrillation: what
Porth C. Essentials of Pathophysiology Concepts of Altered are the effects of drug therapy on the effectiveness
Health States. 2nd ed. Philadelphia: Lippincott and complications of electrical cardioversion?
Williams & Wilkins; 2007:311–349. Can J Cardiol. 1998;14:1267–1273.
Ramsey J, Tisdale L. Use of ventricular stroke work index Thaler MS. The Only EKG Book You’ll Ever Need. 3rd ed.
and ventricular function curves in assessing myocar- Philadelphia: Lippincott Williams & Wilkins; 1999.
dial contractility. Crit Care Nurs. 1995;15:61–67.
SECTION IV
Essential Therapeutics
CHAPTER 20
Oxygen and Medical Gas Therapy

Jodi Green and Victoria Frain
OBJECTIVES
• Describe the physical characteristics of medical gases.
• Summarize the production and storage methods for medical gases.
• Categorize the responsibilities of the various agencies involved in the regulation of medical gases.
• Describe the characteristics of oxygen regulation devices.
• Describe the causes, assessment, and treatment of hypoxemia.
• Identify the goals, indications, and hazards of oxygen therapy.
• Differentiate between high- and low-flow oxygen delivery systems.
• Choose the proper method of oxygen delivery and treatment, given specific patient data.
• Describe the invasive and noninvasive methods of monitoring oxygen therapy.
• Identify the methods of operation for the various types of oxygen analyzers.
• Describe the therapeutic uses of gas mixtures.
CHAPTER OUTLINE
Physical Characteristics of Medical Gases Bulk Storage Systems
Oxygen Central Piping Systems
Air Connector Systems
Carbon Dioxide Oxygen Regulation Devices
Helium Therapeutic and Diagnostic Uses
Nitrous Oxide of Oxygen
Nitric Oxide Goals and Objectives of Oxygen Therapy
Production and Regulation of Medical Gases Causes of Hypoxemia
Production of Medically Safe Gases Assessment of Hypoxemia
Regulation of Medical Gas Safety Indications for Oxygen Therapy
Storage and Distribution of Medical Gases Hazards of Oxygen Therapy
Compressed Gas Cylinders Oxygen Delivery Systems
Liquid Oxygen Cylinders Oxygen Conserving Devices
(continues)
557
558 SECTION IV ■ Essential Therapeutics
(continued)
Hyperbaric Oxygen Therapy Therapeutic Use of Gas Mixtures

Monitoring Oxygen Therapy Carbon Dioxide and Oxygen (Carbogen)
Oxygen Therapy Protocols Helium and Oxygen (Heliox)
Analyzing Oxygen Concentrations Nitric Oxide Therapy
KEY TERMS
carbogen hyperbaric oxygen therapy plethysmography
fraction of inspired oxygen (HBO) polycythemia
(FIO2) hypercapnea shunt effect
fractional saturation hypoxemia specific gravity
functional saturation hypoxia spectrophotometry
heliox hypoxic drive transcutaneous monitoring
high-flow oxygen system low-flow oxygen system true shunt
O
xygen and medical gas therapy is the very TABLE 20-1 Fire risk for medical gases
foundation of respiratory care. Equipment
for oxygen administration ranges from the Support
simplest nasal catheter to the most sophis- Nonflammable Combustion Flammable
ticated mechanical ventilator. The respiratory therapist Carbon dioxide Oxygen Most anesthetic
(RT) must have a clear understanding of all aspects of gases
medical gases, from their production and regulation to Nitrogen Air
their proper administration and monitoring. The RT’s
Helium Nitrous oxide
skills must range from simple motor skills to complex
assessment of the effects of medical gases on the Oxygen–nitrogen
cardiopulmonary system and other body systems. Oxygen–carbon
Many institutions have adopted the use of proto- dioxide
cols, care plans, and practice guidelines for the admin-
Helium–oxygen
istration of medical gases. This development represents
a great advance for the respiratory care profession; Nitric oxide
however, caution must be taken. Protocols and
guidelines must never be used as cookbook recipes
for treatment. They actually increase the responsibility
of the respiratory therapist. The importance of OXYGEN
critical thinking and assessment skills cannot be
Oxygen (O2) is a colorless, odorless, tasteless,
overemphasized.
transparent gas. It constitutes 20.95% of the atmo-
sphere, exerting a partial pressure of 159 mm Hg at the
Physical Characteristics normal sea level barometric pressure of 760 mm Hg.
It is slightly heavier than air, having a density of
of Medical Gases 1.429 g/L and a specific gravity of 1.108, compared
Gases are categorized according to their fire risk. with the 1.29 g/L density and 1.0 specific gravity of air.
Although most institutions provide training in fire These physical characteristics of oxygen are at standard
safety to their employees, this training rarely includes temperature and pressure, dry (STPD), which is 0°C
the fire risks imposed by specific medical gases. (32°F) and 760 mm Hg without the presence of water
Table 20-1 groups the common medical gases accord- vapor. Specific gravity is a ratio of the density of one
ing to whether they are nonflammable (will not burn), substance to the density of a standard substance,
nonflammable but will support combustion, or flammable which, for gases, is air (see Chapter 3). The physical
(will readily burn, may be explosive). characteristics of oxygen are summarized in Table 20-2.
CHAPTER 20 ■ Oxygen and Medical Gas Therapy 559
TABLE 20-2 Characteristics of oxygen (O2)

Best Practice
General Colorless, odorless,
tasteless, transparent For safety reasons mixtures of oxygen and other
Fire risk Supports combustion gases meant for inhalation should never contain
Percentage of atmosphere 20.95% less than 20% oxygen. Common He/O2 mixtures
are 70% HeⲐ30% O2 and 80% He/20% O2.
Partial pressure 159 mm Hg
Density 1.429 g/L
Specific gravity 1.108 pulmonary disorders. The therapeutic use of carbogen
is limited (discussed later in the chapter).
Critical temperature –118.8°C
Critical pressure (at critical 50 atm HELIUM
temperature) Helium (He) is an odorless, tasteless, nonflammable
Solubility coefficient 0.0244 (mL/mL H2O) gas. At STPD, helium’s density is only 0.1785 g/L. It is
one of the lightest of all gases, second only to hydro-
gen. Helium is present only in minute quantities in the
TABLE 20-3 Composition of air atmospheric air.
Partial Because of its low density, a combination of
Fractional Pressure at helium and oxygen (Heliox) is used therapeutically as a
Concentration in Sea Level transport agent to carry oxygen distal to airway obstruc-
Gas Atmosphere (%) (mm Hg) tions. Therapeutic uses of heliox are discussed later in
the chapter.
Nitrogen (N2) 78.08 593.0
Oxygen (O2) 20.95 159.0 NITROUS OXIDE
Carbon dioxide 0.03 0.2 Nitrous oxide (N2O) is nonflammable but, like oxygen,
(CO2) supports combustion. It is a colorless gas and slightly
Argon (Ar) and 0.93 7.0 sweet in odor and taste.
trace gases Inhaled nitrous oxide must always be mixed with
at least 20% oxygen. It is used clinically as an anes-
thetic agent because of its depressant effect on the
AIR central nervous system. True anesthesia is achieved
Air is the naturally occurring atmospheric gas mixture only with dangerously high levels of N2O; therefore, it
composed of nitrogen, oxygen, carbon dioxide, argon, is almost always used in combination with other
and trace gases. The composition of atmospheric air is anesthetic gases.
summarized in Table 20-3. Air has a density of 1.29 g/L
(STPD) and a specific gravity of 1.0. NITRIC OXIDE
Compressed air has various medical applications. Nitric oxide (NO) is nonflammable, but it supports
It is used to power pneumatically driven medical combustion. It is a colorless, toxic gas. When combined
equipment and is commonly used as a source carrier with air, this gas is a strong irritant. If inhaled, it can
gas when oxygen is not indicated or is contraindicated. cause a strong chemical inflammation, pulmonary
edema, or death.
CARBON DIOXIDE Nitric oxide has been FDA approved for some
Carbon dioxide (CO2) is a colorless and odorless gas. It is disorders. In very low concentrations, it is found to
nonflammable and does not support combustion. dilate pulmonary blood vessels. Therapeutically, nitric
Carbon dioxide constitutes a miniscule percentage of our oxide has potential in the treatment of pulmonary
atmospheric air (0.03%), exerting a partial pressure of hypertension owing to its vasodilating properties. This
only 0.2 mm Hg. The specific gravity of CO2 (STPD) is use of NO is discussed later in the chapter.
1.53, making it 1.5 times as heavy as air. The solubility
coefficient of CO2 is 0.592, showing much more solubil- Production and Regulation
ity in water than oxygen (0.0244). On the basis of both
Henry’s and Graham’s laws (see Chapter 3), CO2 is
of Medical Gases
approximately 20 times more diffusible in water than O2. Gases that are used for medical purposes—for obvious
Most medical uses for carbon dioxide are for reasons—must meet much higher standards of produc-
laboratory purposes, such as diagnostics and equip- tion and stricter regulations than those produced for
ment calibration. A mixture of carbon dioxide and general industry. The U.S. Food and Drug Administration
oxygen (carbogen) is occasionally used for specific (FDA) requires an oxygen purity of at least 99.0%.
PRODUCTION OF MEDICALLY SAFE GASES

Oxygen is commercially produced for medical purposes
by two main methods: fractional distillation and
physical separation.
Fractional distillation is the most common and
cost-effective method of oxygen production.
Atmospheric air is first filtered, removing water, carbon
dioxide, and pollutants. The resulting air is then
compressed to high pressure, liquefying the mixture,
and cooled by rapid expansion. The mixture (oxygen,
nitrogen, and trace gases) is then heated slowly in a
distillation tower, causing gases to escape in the order
of their boiling points. Nitrogen escapes first, followed
by the various trace gases. Liquid oxygen remains. The
liquid oxygen is stored in cryogenic storage containers,
to be converted to gas for later use or for storage in
high-pressure cylinders. Fractional distillation produces
oxygen that is 99.5% pure, exceeding FDA standards.
The physical separation of oxygen is accomplished
by two methods, resulting in very different concentra-
tions of oxygen.
• The molecular sieve method of separation incor-
porates the use of inorganic mineral pellets that
absorb nitrogen and water vapor, allowing FIGURE 20-1 Oxygen concentrator.
oxygen to pass through. The resulting oxygen Courtesy of Philips Respironics
concentration is approximately 90% at flows of

1–2 Lpm. The oxygen concentration decreases
with an increase in flow rate.
Electric motor One-way valves
• The second method uses a permeable plastic
membrane, through which gases diffuse at
different rates. Oxygen and water vapor pass
through the membrane at a faster rate than
nitrogen. The result is humidified oxygen at an
approximate concentration of 40%. This concen-
tration remains constant, regardless of flow rate.
The physical separation of oxygen production is
used almost exclusively for oxygen concentrators in the Piston
home care setting. The effect of flow rate on oxygen
concentration must be fully understood by the respira-
tory therapist. Figure 20-1 shows a typical oxygen Connecting rod
concentrator used in the home. FIGURE 20-2 A functional diagram of a piston compressor.
Medical-grade air is produced by filtering and
compressing atmospheric air. The air must be dry and
free of oil and particulates. Drying is accomplished by
cooling to produce condensation. Freedom from oil
working pressure of 50 psig (pounds per square
and particulates is accomplished through the use of
inch gauge).
inlet filters and Teflon piston rings. Air compressors can
• Diaphragm compressors (Figure 20-3) cannot
be large enough to provide the compressed air source
generate large amounts of compressed air, so
for an entire institution or compact enough to provide
they should not be used as a power source for
medication nebulization at the bedside, whether in the
large medical equipment.
hospital or at home.
• Centrifugal compressors (Figure 20-4) can be small
There are three main types of air compressors.
enough to be incorporated into a mechanical
• Piston compressors (Figure 20-2) use a reducing ventilator or large enough to provide the com-
valve to reduce the high pressure down to a pressed air source to an entire hospital.
Electric motor One-way valves TABLE 20-4 Responsibilities of

governmental and nongovernmental
agencies in gas regulation
Agency Responsibilities
U.S. Department of Compressed gas cylinders:
Transportation (DOT) shipping, marking, filling,
labeling, purity levels
U.S. Food and Drug Identification tags,
Diaphragm Administration (FDA) precaution statements
Occupational Safety and Occupational safety
Connecting rod U.S. Health related to medical gases
FIGURE 20-3 A functional diagram of a diaphragm
Administration (OSHA)
compressor. Compressed Gas Compressed gas cylinders:
Association (CGA) handling, storage, piping,
fittings, markings
National Fire Protection Codes and safety
Association (NFPA) recommendations for
Check valves storage of flammable and
oxidizing gases
International Standards Technical standards for
Organization (ISO) manufacture terminology
and testing procedures
Impeller
American National Coordination of standards
Standards Institute (ANSI) for health devices
Z-79 Committee
REGULATION OF MEDICAL GAS SAFETY

on
at i
Various governmental and nongovernmental agencies

ot
R
regulate medical gas safety. The responsibilities of these
agencies include overseeing:
Shaft • The production of compressed gas cylinders and
FIGURE 20-4 A functional diagram of a centrifugal bulk systems.
compressor. • The inter- and intrastate transportation of gases.
• The handling, storage, and labeling of medical
gases.
• Gas safety, purity, precautions, education, and
occupational safety.
Other medical gases are produced in alternate ways:
Table 20-4 summarizes the responsibilities of the main
• Carbon dioxide is usually produced by heating agencies involved in the regulation of medical gases.
water-contacted limestone. The gas is liquefied
by cooling and compression. The resulting
carbon dioxide meets the FDA purity standards
Storage and Distribution
of 99.0%. of Medical Gases
• Helium is produced by the liquefaction of natural
Medical gases are stored in one of three types of storage
gas. Purity standards are at least 95.0%.
containers: compressed gas cylinders, liquid oxygen
• Nitrous oxide is produced by thermal decomposi-
cylinders, and bulk storage systems.
tion of ammonium nitrate.
• Nitric oxide is produced by the oxidation of
ammonia at high temperatures with the aid of a COMPRESSED GAS CYLINDERS
catalyst. When combined with air, the resulting Compressed cylinders are a convenient method for
nitrogen dioxide (NO2) is toxic. the storage and delivery of oxygen. Manufactured in
various sizes, the smaller cylinders are portable and

easy to transport. Compressed oxygen cylinders are a
high-pressure storage system that requires a reduction
in pressure down to a working pressure of 50 psig before
delivery to a patient.
Cylinder Construction. Oxygen cylinder construction

is strictly regulated by the U.S. Department of Trans-
portation (DOT). Medical gas cylinders are seamless,
spun into shape while the steel is still hot. DOT type
3A cylinders are manufactured from carbon steel, and
DOT type 3AA cylinders are manufactured from
heat-treated, high-strength steel. Type 3AL indicates
aluminum construction. Aluminum cylinders are
popular because they are lighter.
Hydrostatic Testing. The DOT requires hydrostatic (A)

testing of cylinders every 5 or 10 years. The test is a
measure of the cylinder’s elasticity. Cylinders are
pressurized to five-thirds of their service pressure.
Cylinder expansion, leakage, and wall stress are
measured. “EE” followed by a number indicates the
cylinder’s elastic expansion. A cylinder that has been
approved by the DOT for 10-year testing has a star
next to the test date. A plus sign () indicates that the
cylinder can be filled to 10% above its service pressure.
Cylinder Markings and Identification. Identification
and markings of medical gas cylinders appear as metal
stamps on their shoulder. Typically, the front of the
cylinder has the letters “DOT” or, for older cylinders,
“ICC” (Interstate Commerce Commission). On the
same line are the cylinder classification (3A, 3AA, or
3AL) and the service pressure. Below this line are the (B)
cylinder letter size (not present on all cylinders), the
serial number, the ownership mark, and the manufac- FIGURE 20-5 Markings on the front (A) and on the back
turer’s mark. (B) of an oxygen cylinder.
The rear of the cylinder contains hydrostatic test
information and may also include the cylinder’s elastic TABLE 20-5 Color coding for medical
expansion rating. The type of steel used and the gas cylinders
spinning process may be listed. Hydrostatic retest dates
are listed vertically, along with the inspector’s mark. Medical Gas United States International
The exact location of identification marks may vary. All Oxygen Green White
cylinders are also color coded and labeled to identify Air Yellow Black/white
their contents. Figure 20-5 shows the front and back
Carbon dioxide Gray Gray
cylinder markings.
Carbon dioxide– Gray/green Gray/white
Cylinder Color Coding and Sizes. The Compressed oxygen
Gas Association (CGA) has developed a system of color Helium Brown Brown
coding for medical gas cylinders. The color code used Helium–oxygen Brown/green Brown/white
in the United States differs slightly from the interna- Nitrogen Black Black
tional code. The FDA requires that cylinders also be
labeled to identify their contents. The label and the Nitrous oxide Blue Blue
color code must match, or the cylinder should not be Nitrogen–oxygen Black/green Pink
used. Table 20-5 compares the U.S. color-coding system Cyclopropane Orange Orange
with the international system. Ethylene Red Red
COMMON METRIC EQUIVALENTS (APPROX.)

1 Cubic Foot....7.48 gallons....28.3 liters
1 Gallon................3.785 liters........0.132 cubic feet
1 Liter.....................0.264 gallons....0.035 cubic feet
B/BB D/DD E M G H
Liters 370 940 1590 7570 12300 15800
Gals. 100 250 420 2000 3263 4180
CO2 C.F.
Wt.
13.37
1 lb., 8 oz.
33.2
3 lbs., 13 oz.
56.1
6 lbs., 7 oz.
267
30 lbs., 10 oz.
436
50 lbs., 0 oz.
558
64 lbs., 0 oz.
Liters 400 660 3000 5330 6000
CO2 Gals. 105 174 793 1408 1585
O2 C.F.
Wt.
14.1
1 lb., 3 oz.
23.3
2 lbs., 0 oz.
106
8 lbs., 15 oz.
188
15 lbs., 14 oz.
212
17 lbs., 14 oz.
Liters 378 871
C3H6 Gals.
C.F.
100
13.37
230
30.75
Wt. 1 lb., 7.25 oz. 3 lb, 5.5 oz.
Liters 300 500 2260 4000 6000
Gals. 79.2 132 597 1057 1585
He C.F. 10.6 17.6
0 lbs., 2.9 oz.
79.8
0 lbs., 13.2 oz.
141
1 lb., 7.5 oz.
213
1 lbs., 2.8 oz.
Wt. 0 lbs., 1.8 oz.
Liters 500 2260 4000 4500
He Gals. 132 597 1057 1189
O2 C.F.
Wt.
17.6 79.8 141 159
Liters 940 1590 7570 13800 15800

Gals. 249 420 2000 3657 4200
N2O C.F.
Wt.
33.2
3 lbs., 13 oz.
56.1
6 lbs., 7 oz.
267
30 lbs., 10 oz.
489
56 lbs., 0 oz.
558
64 lbs., 0 oz.
Liters 200 400 660 3450 5300 6900
O2 Gals.
C.F.
52.8
7
105
14.1
174
23.3
912
122
1400
187
1825
244
Wt. 9.4 oz. 1 lb., 3 oz. 1 lb.,15 oz. 10 lbs., 1 oz. 15 lbs., 8 oz. 20 lbs., 3 oz.
Liters 375 625 3275 5050 6550
Air Gals.
C.F.
99
13.2
165
22
865
116
1334
178
1730
232
Wt. 1 lb., 0 oz. 1 lb., 10 oz. 8 lbs., 11 oz. 13 lbs., 5 oz. 17 lbs., 6 oz.
Liters 610 6400
N2 Gals.
C.F.
161
21.5
1676
224
Wt. 1 lb., 9 oz. 16 lbs., 6 oz.
FIGURE 20-6 Gas cylinder sizes, factors, and conversions.
Medical gas cylinders are manufactured in various piping system, H cylinders are still used in older
sizes, designated by letters. institutions and in older areas of the hospital.
• Sizes AA–E are small cylinders, typically used for Figure 20-6 provides condensed information on
patient transport. Small cylinders have a unique gas cylinder sizes and includes cylinder factors and
valve and yoke connection. conversions.
• The larger cylinders, F–K, use a threaded valve
connection. Filling Methods for Medical Gas Cylinders. A cylin-
• The sizes most commonly used in the hospital der is filled according to its service pressure, which is
setting are E and H cylinders. E cylinders are usually 2000–2015 psi. A cylinder that has passed
used for patient transport and ambulation. hydrostatic testing, as signified by the plus sign (⫹),
Although most large institutions use a central can be filled to 10% above its service pressure. For

Storage Temperature Duration of Flow
Because of thermal expansion, cylinders stored For safety considerations, use 500 psig as a
in a very cold environment, such as outdoors, buffer when calculating how long a cylinder will
should be allowed to warm before cracking last. To do so, simply subtract 500 psig from the
and use. starting cylinder pressure.
example, if an approved cylinder’s service pressure is • The next step is to find the contents of the
2000 psi, it can be filled to a pressure of 2200 psi. cylinder in liters by multiplying the cylinder
factor by the existing gauge pressure.
Safety Factors for Medical Gas Cylinders. Gas • The duration of flow, in minutes, is then deter-
cylinders should always be transported in a stand and mined by dividing the contents by the existing
kept in place with a chain or other restraining device. gas flow (liters per minute).
Before it is attached to a regulator, a cylinder should be
cracked, that is, a small amount of gas is allowed to duration of flow (minutes)
escape to free the valve of any particulate matter. When gauge pressure cylinder factor
____________________________
cracking the cylinder and attaching the regulator, be flow (LPM)
sure the valve is facing away from you and from any
other persons in the area. For example, how long will an E cylinder last, if it has
Cylinders should not be stored in direct sunlight. 1000 psig pressure and a flow rate of 4 Lpm?
An increase in temperature results in an increase in 1000 psig 0.28 L/psig
pressure inside the cylinder. In very high temperatures, duration of flow _____________________
4 LPM
such as during a fire, the cylinder may explode. There-
fore, cylinders are equipped with high-pressure relief duration of flow 70 minutes, or 1.16 hours
valves. Of the several types of relief valves, all are
designed to vent gas from the cylinder in order to
prevent an excessive build-up of pressure. LIQUID OXYGEN CYLINDERS
Oxygen gas occupies a volume that is 861 times that of
Duration of Cylinder Gas Flow. The practitioner must liquid oxygen per cubic foot. Therefore, liquid oxygen
be able to estimate how long a cylinder will last for containers are much more practical when large
circumstances such as patient transport. The duration amounts of oxygen are needed or when oxygen is
of gas flow from a cylinder can be estimated if the running at a constant high-liter flow. Because maintain-
following factors are known: cylinder size, starting ing oxygen in its liquid state requires very low tempera-
pressure, and gas flow. tures, liquid oxygen is stored in cryogenic, insulated,
vacuumized thermal containers.
• First, the volume, in cubic feet, of a full cylinder Liquid containers are filled to a filling density rather
must be converted to liters. There are 28.3 L in than to a filling pressure. The filling density is the ratio
one cubic foot. For a full cylinder, the cylinder of the weight of liquid gas to the weight of water that
factor is derived by dividing the volume, in liters, the container could contain. The gauge pressure
by the pressure (psig). Cylinder factors are indicates only the pressure of the vapor above the
constant; they are calculated from full cylinder liquid. This pressure remains constant as long as liquid
volume and pressure. is remaining in the container. When all the liquid is
gone from the container, the gauge pressure begins to
cubic feet (full cylinder) 28.3
cylinder factor (L/psig) ____________________________ drop according to the volume of gas remaining. At this
pressure (full cylinder)
point, rapid falls in gauge pressure can occur. Although
244 ft3 28.3 L/ft3 a liquid container is a relatively low-pressure system
H cylinder _________________
2200 psig compared with a gas container, a small amount of
H cylinder factor 3.14 L/psig vapor above the liquid is constantly venting. Therefore,
the only accurate way to measure liquid contents is to
22 ft 28.3 L/ft
3
E cylinder ________________
3
weigh the container.
2200 psig Liquid oxygen systems are very popular in the
E cylinder factor 0.28 L/psig home care setting, especially when a continuous flow
FIGURE 20-7 Portable oxygen concentrator.

Courtesy of Philips Respironics
of oxygen is needed. The systems include floor and

portable models. Portable units often include a shoul-
der bag, which is an advantage for patients who are not Relief valve
Gaseous oxygen
confined to the home (Figure 20-7).
Control valve
BULK STORAGE SYSTEMS
A bulk oxygen storage system holds a minimum of Liquid oxygen
13,000 ft3 of oxygen gas. Bulk oxygen is stored in either Insulation
liquid or gaseous form. Liquid storage is more common Heat exchanger
and convenient as an oxygen source for facilities that
use large volumes of oxygen because they vastly reduce Regulator
the space requirements for bulk storage (1 ft3 liquid
oxygen 861 ft3 gaseous oxygen).
Keeping liquid oxygen from reverting to its gaseous
state requires storage below its critical temperature of
FIGURE 20-8 A bulk liquid oxygen storage and supply
–118.8°C. The construction of the storage container is system.
similar to that of a thermos insulated bottle, with inner
and outer steel shells separated by a vacuum space. This
construction enables liquid oxygen to be stored
Gas bulk oxygen systems are usually large cylinders
without the need for refrigeration. Figure 20-8 illus-
linked together in a manifold system. Manifold systems
trates a typical liquid bulk storage system.
have two banks of cylinders, a primary bank and a
Bulk liquid oxygen systems have several advantages
reserve bank.
over gas cylinders.
The National Fire Protection Association (NFPA)
• Liquid systems operate at much lower pressures, sets the safety standards for bulk oxygen systems. A key
approximately 250 psig, rather than the 2200 psig NFPA requirement is the presence of a reserve back-up
pressures of compressed gas cylinders. gas supply. This supply must be equal to the hospital’s
• The delivery pressures of bulk liquid systems are average daily gas use. Figure 20-9 illustrates the reserve
regulated centrally, eliminating the need for systems for three bulk storage systems.
pressure-reducing valves at individual outlets. In The distribution of medical gases takes place via
any event, all medical gas systems are reduced to central piping systems, connector systems, and oxygen
a working pressure of 50 psig at the final outlet. regulation devices.
Zone valves
3rd floor
A.
2nd floor
Station outlets
Main supply
shutoff Riser shutoff valve
B.
Valve
Station outlets
FIGURE 20-10 Zone valve placement in a central piping
system.
C.
FIGURE 20-9 Bulk oxygen supply systems. (A) Liquid
primary and liquid reserve. (B) Liquid primary and cylinder but also a connector system. Indexed safety systems
reserve. (C) Cylinder primary and cylinder reserve. make it virtually impossible to connect one gas source
to a system designed to deliver another. For example,
connecting an oxygen delivery system to a cylinder of
carbon dioxide is impossible.
CENTRAL PIPING SYSTEMS The American Standard Safety System (ASSS)
A central piping system delivers gas from the bulk storage provides standards for threaded systems. These are the
area, via seamless copper pipes, to its various points of high-pressure connections (>200 psig) between large
use. The piping system is tested for leaks by pressuriz- compressed gas cylinders (F–K) and their attachments.
ing it to 1.5 times its working pressure. This pressure is Figure 20-11 depicts typical ASSS connections.
maintained for 24 hours. To pass final inspection, the The Pin-Index Safety System (PISS) was designed for
system must remain leak free. the valve outlet of small cylinders (A–E). Small cylin-
The gas pressure is reduced to the normal working ders use a yoke connection. The two pins on the
pressure of 50 psig at the bulk storage location. Sensors connector must fit precisely into the pin index holes of
are placed at various locations in the piping system to the cylinder valve. There are six pinhole positions and a
continuously monitor pressure. Alarms are included to
alert personnel of pressure drops in the system caused
by leaks or gas depletion.
Zone valves are located at strategic points. These
permit the gas to be shut off to certain areas in the
event of a fire. Respiratory therapists must be able to
identify the locations of the zone valves. Of course, in
the event of a shutoff, all oxygen patients must be
provided with supplemental oxygen from cylinders.
Figure 20-10 illustrates the zone valve placement in a
central piping system.
CONNECTOR SYSTEMS
The Compressed Gas Association (CGA) developed not
only a system of color coding for medical gas cylinders, FIGURE 20-11 Two-thread ASSS connections.
OXYGEN REGULATION DEVICES

Gas contained in cylinders is under high pressure,
usually 2200 psi when the cylinder is full. Cylinder
valves and reducing valves are necessary to regulate gas
pressure and for the safe attachment of pneumatic
equipment. Specialized regulation devices are also
needed to control gas flow and oxygen concentration.
1 6 Cylinder Valves. There are two types of cylinder valves:

2 5
3 4 direct-acting cylinder valves and diaphragm cylinder
valves.
• The direct-acting cylinder valve (Figure 20-13) is a
needle valve that opens and closes the valve seat
directly. When the valve seat opens, gas flows
through the valve from the high-pressure interior
of the cylinder to the lower outside pressure.
• A diaphragm cylinder valve (Figure 20-14), as its
Oxygen Pins 2,5
Air Pins 1,5
name suggests, uses a diaphragm to open or
He/O2 (80% and under) Pins 2,4 close the valve seat. Gas pressure displaces the
CO2/O2 (7% or under) Pins 2,6
diaphragm, allowing the gas to flow from the
Nitrous oxide Pins 3,5
cylinder.
FIGURE 20-12 Six different pin index positions for medical

gases.
number of possible combinations. For example, the

pin index position for oxygen is 2–5. Only the yoke
connection pins for an oxygen delivery system precisely
correspond to the pin index holes of a small oxygen
Teflon
cylinder valve. Figure 20-12 illustrates six pin index washers
positions.
The Diameter-Index Safety System (DISS) also
prevents the interchange of medical gas connectors.
The DISS system, however, is designed specifically for
low-pressure connections, that is, when the pressure
has already been reduced to under 200 psi, usually to a
working pressure of 50 psi. DISS connections are “Gasloc”
seal
usually found at the station outlets of the central and cap
piping system and at the inlets of pneumatic equip-
ment such as flowmeters, humidifiers, nebulizers, and
Pressure
mechanical ventilators. DISS systems incorporate check
relief
valves to prevent gas loss when the system is not in use. valve
Quick-connect systems, a variation of the DISS
connection, are also designed for low-pressure connec-
tors. Each medical gas has a differently shaped connec- Nylon
seat
tion and fitting. Quick-connect systems are convenient,

and they provide easy and rapid connection and
disconnection of equipment. Unlike DISS connections,
the design of quick-connect systems varies among
manufacturers. The variation should not pose a
problem as long as the facility is standardized on a
specific system. FIGURE 20-13 A direct-acting cylinder valve.
Handle
Spring
Valve stem
High–
pressure Outlet
Diaphragm
Threads inlet
Pressure relief
Diaphragm
valve Nozzle
Gas Poppet valve
outlet FIGURE 20-15 A single-stage reducing valve.
Valve seat
Spring
Gas inlet
channel
High–
pressure Outlet
FIGURE 20-14 A diaphragm cylinder valve. inlet
Nozzle Poppet Diaphragm

Pressure relief devices are incorporated into Poppet valve closing spring
cylinder valves. These devices are designed to open if
FIGURE 20-16 A modified single-stage reducing valve.
either the pressure or the temperature rises beyond safe
limits; their opening prevents the cylinder from
rupturing.
usually 50 psi. Each stage of a multistage
Reducing Valves. All reducing valves have a flexible reducing valve operates independently of the
diaphragm that separates the opposing forces of spring others. Multistages allow for more precise pressure
tension and gas pressure. When these two opposing regulation and greater flow rates, such as those
forces are equal, the diaphragm is flat and the poppet required for operating mechanical ventilators.
valve is closed. Spring tension determines the outlet Each stage of a reducing valve incorporates a
pressure from the reducing valve. The spring tension pressure relief valve, or pop-off valve, for safety in the
may be fixed or adjustable, depending on the construc- event of excessive pressure build-up. The relief valve is
tion of the reducing valve. designed to vent the excess pressure, preventing the
• Single-stage reducing valves (Figure 20-15) reduce reducing valve from rupturing. The reducing valve inlet
the cylinder pressure to the working pressure in is indexed with either the ASSS or the PISS. The valve
one step. outlet is indexed with the DISS.
• Modified single-stage reducing valves (Figure 20-16)
provide greater flow rates by utilizing a poppet Regulators. A regulator is a combination of a reducing
closing spring in addition to the spring above valve and a flowmeter in a single unit. This unit not
the diaphragm. This closing spring allows the only reduces gas pressure but also regulates gas flow to
poppet valve to open and close much more the patient. Regulators are much more convenient than
rapidly. separate reducing valves and flowmeters. Only one
• A multistage reducing valve (Figure 20-17) consists high-pressure connection is required.
of two or more single-stage reducing valves in a
series. The pressure reduction is accomplished in Proportioners (Air-Oxygen Blenders). Air-oxygen
steps. The first stage reduces the pressure to blenders (Figure 20-18) are devices that mix air and
approximately 200 psi. The second stage reduces oxygen in precise proportions, resulting in very
this pressure to a normal working pressure, accurate and stable oxygen concentrations. Blenders
Spring
High–
pressure Outlet
inlet
Nozzle Diaphragm
Poppet valve
FIGURE 20-17 A multistage reducing valve (two stages).
50 psi air 50 psi oxygen

Coiled tube
Gear
mechanism
Pressure
Balance regulator
stage Outlet
Gas inlet
Mixture
control
FIGURE 20-19 A Bourdon gauge flowmeter.
Proportioning Most blenders are equipped with an alarm to

50 psi mixture
valve signal a pressure drop in either the air or the oxygen
FIGURE 20-18 A functional diagram of an air-oxygen supply line in the regulator.
blender. Note: The oxygen concentration from a blender
should always be verified by analysis.
Flowmeters. There are two major types of oxygen

require a 50-psi source of air and oxygen and provide a flowmeters: the Bourdon gauge flowmeter, and the
50-psi source of blended gas. Be aware that changes in Thorpe tube flowmeter.
gas densities can affect mixing ratios. The Bourdon gauge flowmeter (Figure 20-19) is a
Air and oxygen, occupying two separate chambers, fixed-orifice type of flowmeter that uses a Bourdon
enter the blender separately. A regulator is incorporated gauge and an adjustable reducing valve. As pressure
to ensure that the pressures of the two gases are equal. increases between the reducing valve outlet and the
Each gas passes through a proportioning valve. As the fixed orifice, the coiled copper tube in the Bourdon
control is adjusted to allow more of one gas, the valve gauge uncurls and begins to straighten out. Although
closes proportionally to the other gas. For example, if a the Bourdon gauge actually measures pressure, it is
higher concentration of oxygen is desired, dialing for calibrated to illustrate flow rather than pressure.
this higher concentration not only opens the valve An advantage to the Bourdon gauge is that it is not
for more oxygen but also closes the valve to air, gravity dependent; therefore, an accurate reading can
proportionally, allowing less air to exit. be obtained in any position. This flowmeter is very
convenient for patient transport situations when the needle valve adjusts the flow rate. As it is opened,
tank cannot remain upright. more gas flows into the tube.
Caution must be taken when using the Bourdon The uncompensated Thorpe tube flowmeter reads
gauge flowmeter. Any increase in pressure distal to the inaccurately in the presence of back-pressure. If pres-
fixed orifice, such as that caused by kinks in the oxygen sure exists distal to the Thorpe tube, as it would if the
tubing, causes the flowmeter to read inaccurately. The oxygen tubing had a kink, the Thorpe tube becomes
presence of back-pressure may cause this flowmeter to pressurized. This effect decreases the pressure gradient
indicate a higher flow than is actually being delivered. between the top and the bottom of the ball float,
In fact, this gauge may indicate flow even if the outlet is causing the float to drop in the tube. The indicated flow
completely occluded! rate may be lower than the flow rate actually being
The Thorpe tube flowmeter can either be uncompen- delivered.
sated or compensated. In a back-pressure-compensated Thorpe tube flowme-
In the uncompensated Thorpe tube flowmeter ter (Figure 20-20B), the needle valve is positioned distal
(Figure 20-20A), the needle valve is proximal to the to the Thorpe tube. The pressure in the tube is equal to
Thorpe tube. The pressure in the tube is equal to working pressure (50 psi) when the flowmeter is
ambient pressure. The Thorpe tube gradually increases connected to a gas source, rather than to ambient
in diameter from the bottom to the top of the tube. pressure as in the uncompensated tube. Back-pressure
The ball float indicates flow rate. As the needle valve is applied distal to the tube does not affect the perfor-
opened, the gas pressure overcomes the force of gravity, mance of the Thorpe tube. Further back-pressure
pushing the ball float up the tube. The higher the ball restricts the flow rate, but this restriction is indicated
float is in the tube, the more gas is needed to flow by the position of the ball float. Even in the presence
around the float in order to keep it in a stable position of back-pressure, the compensated Thorpe tube
because of the widening diameter of the tube. The flowmeter reads accurately.
Tube Tube
Ball float Ball float
Needle valve
(proximal position to tube) Needle valve

(proximal position to tube)
(A)
B. (B)
C.
FIGURE 20-20 Thorpe tube flowmeters: (A) Uncompensated. (B) Back-pressure-compensated. (continues)
Therapeutic and Diagnostic

Uses of Oxygen
The respiratory therapist needs to be well versed in
both the therapeutic and diagnostic uses of oxygen.
The practitioner must be able to assess the need for
oxygen therapy and to recognize the indications and
hazards of therapy. Monitoring the patient during
oxygen therapy and assessing its outcome are equally
important.
GOALS AND OBJECTIVES OF OXYGEN THERAPY

The broad goal of oxygen therapy is to maintain
adequate tissue oxygenation. Specific objectives of
oxygen therapy are to:
• Correct acute hypoxemia.
• Alleviate the symptoms associated with chronic
hypoxemia.
• Decrease the workload of the cardiopulmonary
system.
Correction of Acute Hypoxemia. Hypoxemia is the

(C) term used to describe a low level of oxygen in the
FIGURE 20-20 (continued) (C) The Thorpe arterial blood. Table 20-6 lists the three levels of
flowmeter. hypoxemia according to PaO2.
Increasing the concentration of inspired oxygen
usually increases the level of oxygen in the blood.
Exceptions are discussed later in the chapter.
Alleviation of Symptoms of Chronic Hypoxemia.

Best Practice The dyspnea that occurs with both obstructive and
restrictive lung disease can be somewhat alleviated
Identifying a Back-Pressure- with oxygen therapy. The alleviation of dyspnea may
result in a decreased work of breathing and, over time,
Compensated Flowmeter an improved tolerance to exercise.
The following three methods should be used to
identify a back-pressure-compensated Thorpe Decrease in the Work of the Cardiopulmonary
tube flowmeter (Figure 20-20 C): System. The cardiac system compensates for hypox-
emia by increasing cardiac output. Because of the low
• Check the label for one of two statements: blood oxygen level, the heart must pump more blood
“Calibrated at 760 mm Hg, 70°F, 50 psig to maintain tissue oxygenation. The results are height-
inlet and outlet pressure” or “pressure ened blood pressure and heart rate. Increasing the
compensated.” blood oxygen level with oxygen therapy decreases the
• Connect the flowmeter to the gas source work of the left ventricle.
with the needle valve closed. The ball float Chronic hypoxemia, over time, causes certain
rapidly jumps up the tube if it is back- physiological changes. One physiological effect of
pressure compensated.
• Completely occlude the tubing or outlet
after turning on the flowmeter. The flow- TABLE 20-6 Levels of hypoxemia
meter should read 0. (adult values)
Technically, if the needle valve is distal to Level PaO2
the Thorpe tube, the flowmeter is back-pressure Mild 60–80 mm Hg
compensated. However, determining the position Moderate 40–60 mm Hg
of the needle requires dismantling the flowmeter.
Severe < 40 mm Hg
hypoxemia is constriction of the pulmonary arterioles, Diffusion Impairment. Certain pulmonary diseases,
which leads to pulmonary hypertension and eventually such as interstitial fibrosis, cause the alveolar-capillary
cor pulmonale (right ventricular failure). Continuous membrane to thicken, resulting in a diffusion impair-
low-flow oxygen therapy may alleviate the vasoconstric- ment. This may result in inadequate time for oxygen to
tion, decreasing the work of the right ventricle. equilibrate across the alveolar-capillary membrane.
Another physiological change of chronic hypox- Diseases that result in a loss of surface area for
emia is polycythemia, an excess or increased number diffusion, such as emphysema, also result in a dimin-
of red blood cells. Although polycythemia has various ished transfer of oxygen from the alveoli to the blood.
causes, when it results from chronic hypoxemia, it is a
compensatory response. Oxygen that is carried in the Ventilation/Perfusion Mismatch. When pulmonary
blood is either dissolved, as indicated by the PaO2, or V ), low
perfusion exceeds alveolar ventilation (Q A
bound to hemoglobin (a constituent of red blood ventilation/perfusion ratio exists, producing a shunt
cells), as indicated by the SaO2. Red blood cells carry effect. Shunt effect is a condition in which the PaO2 is
almost all transported oxygen in its bound form. decreased because pulmonary perfusion is greater than
Chronic hypoxemia stimulates the bone marrow to alveolar ventilation. This effect can be caused by an
increase production of red blood cells by the release of accumulation of mucus, bronchospasm, or any cause
erythropoietin (EPO) by the kidneys. This is a compen- of uneven distribution of ventilation. In shunt effect,
satory mechanism designed to increase the oxygen- the pulmonary perfusion is in contact with ventilated
carrying capacity of the blood. This increase in red alveoli, but the ventilation is inadequate to provide
enough oxygen to the blood. V /Q
blood cells increases the viscosity of the blood, present- mismatch is the most
ing as an increase in hematocrit (Hct, see Chapter 6). common cause of hypoxemia. Shunt effect readily
More driving pressure is needed to pump high-viscosity responds to oxygen therapy.
blood, resulting in an increase in work of both the
right and left ventricles, and increasing afterload. True Shunt. True shunt (absolute shunt) is a
Polycythemia can be alleviated by increasing the blood condition in which ventilation is absent to certain
oxygen level with oxygen therapy, thereby decreasing alveoli or to a section of the lung (see Chapter 6). True
the work of the heart. shunt is caused by conditions such as alveolar collapse,
atelectasis, or consolidation. In this condition, pulmo-
nary perfusion is in contact with alveoli that are not
CAUSES OF HYPOXEMIA ventilated at all. The perfusion that is in contact with
normal alveoli cannot pick up more oxygen because
Hypoxemia, a low oxygen concentration in the arterial
the blood is already fully saturated. For these reasons,
blood, must be differentiated from hypoxia, an
true shunt conditions are refractory (not responsive) to
inadequate amount of oxygen available for cellular
oxygen therapy.
metabolism at the tissue level. Tissue hypoxia can be
categorized as hypoxic, anemic, circulatory, or histo-
toxic. The broad category of tissue hypoxia is discussed ASSESSMENT OF HYPOXEMIA
in Chapter 6. The focus here is on hypoxic hypoxia, or
The assessment of hypoxemia and of the need for
hypoxemia.
oxygen therapy is accomplished by a thorough patient
There are four major causes of hypoxemia: low
assessment, combined with laboratory data indicating
alveolar PO2 (PAO2), diffusion impairment,
hypoxemia. Table 20-7 lists the common physical signs
ventilation/perfusion mismatch (V/Q), and true shunt.
and laboratory findings of hypoxemia.
Low Alveolar PO2. The arterial blood level of oxygen
depends on the alveolar level of oxygen. If the alveolar TABLE 20-7 Clinical signs of hypoxemia
level of oxygen (PAO2) is low, the result is a low arterial Respiratory Cardiac Neurological Laboratory
level of oxygen (PaO2). A low PAO2 can be caused by Dyspnea Tachycardia Headaches Decreased
hypoventilation (such as from a drug overdose), PaO2
COPD, neuromuscular disease, or the effects of anes-
Tachypnea Hypertension Restlessness Decreased
thesia. Other causes include ascent to high altitudes
SaO2
where the partial pressure of oxygen is lower than
159 mm Hg, and breathing gas mixtures less than Cyanosis* Confusion Decreased
21% oxygen, as occurs during a fire. CaO2
Hypoxemia caused by a low PAO2 readily responds Polycythemia
to oxygen therapy. In most cases, an increase in the *Cyanosis presents as a pale or bluish tint of the lips and extremities,
PAO2 results in an increase in the PaO2. caused by 5 or more grams of unbound hemoglobin.
INDICATIONS FOR OXYGEN THERAPY

Obviously, the primary indication for oxygen therapy Best Practice
is documented hypoxemia. According to the American
Association for Respiratory Care clinical practice Chronic Hypercapnea and
guideline for oxygen therapy in the acute care hospital, Hypoxemia
the level of hypoxemia that indicates the need for
COPD patients, or any patients with suspected
oxygen therapy is a PaO2 below 60 mm Hg or an SaO2
chronic hypercapnea and hypoxemia, should
below 90%.1 Other indications for oxygen therapy
have an arterial blood gas performed to verify
include acute myocardial infarction, trauma, postop-
PaO2 and PaCO2. These patients should be
erative recovery, and any condition in which hypox-
placed on an oxygen delivery system that ensures
emia is suspected.
practitioner control of the FIO2 and should be
maintained at an FIO2 just high enough to ensure
adequate oxygenation. Oxygen levels should be
HAZARDS OF OXYGEN THERAPY
titrated to achieve acceptable baseline values for
There are four major hazards of oxygen therapy: these patients.
absorption atelectasis, ventilatory depression, oxygen
toxicity, and retinopathy of prematurity. All are related
to a high fraction of inspired oxygen (FIO2), pro-
longed exposure to a high FIO2, or a high PaO2. the peripheral chemoreceptors, responding to hypox-
emia, are the primary stimulus to breathe. These
Absorption Atelectasis. Absorption atelectasis occurs as patients are breathing on what is termed hypoxic
a result of nitrogen washout. Two factors increase the drive. Peripheral chemoreceptors are significantly
risk for absorption atelectasis: a high FIO2 (greater than activated when the PaO2 is below 60 mm Hg, resulting
0.50) and the presence of partially obstructed alveoli. in an increase in ventilation. Patients with a chronic
Nitrogen exists in equilibrium in the alveoli and in the PaCO2 above 50 mm Hg and a PaO2 below 60 mm Hg
blood, acting as a filler gas. When a person is breathing are at risk of oxygen-induced hypoventilation if
high concentrations of oxygen, the nitrogen is rapidly administered an FIO2 that results in a PaO2 above
washed out of the alveoli and replaced by oxygen. A 60 mm Hg. Although oxygenation should never be
pressure gradient for oxygen exists between the alveoli compromised, these patients need to be treated with
and the blood; therefore, oxygen diffuses into the caution.
blood. However, owing to a partial or full obstruction,
the oxygen is diffusing into the blood faster than it is Oxygen Toxicity. During the normal metabolism of
being replaced in the alveoli. The alveolar pressure oxygen, O2 splits and forms oxygen free radicals. In
falls, deflating the alveoli in the areas of obstruction. response, the body produces enzymes and antioxidants
in defense against the free radicals. However, prolonged
Ventilatory Depression (Oxygen-Induced exposure to a high FIO2 can overwhelm the body’s
Hypoventilation). Ventilation is controlled primarily natural defenses. Alveolar cell damage occurs, espe-
by central chemoreceptors that respond indirectly to a cially to type I pneumocytes (see Chapter 6), which are
rise in PaCO2 and by peripheral chemoreceptors that primarily responsible for alveolar wall integrity.
respond directly to a low PaO2. The central chemorecep- Thickening of the alveolar-capillary membrane and
tors are located in the medulla oblongata; the peripheral interstitial edema follow. Eventually, pulmonary
chemoreceptors are in the aortic arch and the carotid fibrosis develops. In response to the cellular damage,
artery. the immune system is activated, releasing neutrophils
The normal physiological stimulus to breathe is a and macrophages (see Chapter 6). The chemical
rising PaCO2; the secondary stimulus is a low PaO2. As mediators of these immune cells actually worsen the
the PaCO2 rises, the concentration of H+ in the cerebro- damage and release free radicals of their own. Lung
spinal fluid (CSF) increases. The increase in H stimu- compliance, diffusing capacity, and vital capacity all

lates the central chemoreceptors, resulting in an decrease. Worsening of the V/Q mismatch occurs as
increase in ventilation. The PaCO2 of some patients pulmonary shunting increases. These effects, in turn,
with COPD or neurological disorders is chronically worsen the hypoxemia, creating the need for an even
high. Bicarbonate (HCO3) eventually buffers the higher FIO2.
increase in H+ in the blood and cerebrospinal fluid in
order to normalize the pH (see Chapter 4). This Retinopathy of Prematurity. Retinopathy of prematurity
buffering blunts the central chemoreceptors. So, in the (ROP), previously known as retrolental fibroplasia
patient with chronic hypercapnea (increased PaCO2), (RLF), is a condition that sometimes occurs in
patient receives is much higher than that indicated on

Best Practice the flowmeter. The amount of air entrained by a
high-flow system is controlled by the delivery device,
Limiting High FIO2 Exposure which is set by the practitioner, making the delivered
FIO2 fixed. Air is entrained into a high-flow system by
Try to limit exposure to 100% oxygen to fewer
the viscous shearing that occurs at the jet orifice of the
than 24 hours. Strive to keep the FIO2 below
system. Viscous shearing and Bernoulli’s and Venturi’s
0.50 while maintaining adequate oxygenation.
principles are discussed in Chapter 3.
Consider balancing FIO2 with the application of
The FIO2 is changed by varying the size of the
positive pressure in the form of continuous posi-
entrainment ports or the jet size. In most systems, the
tive airway pressure (CPAP) for spontaneously
jet size is fixed by the manufacturer, but the practitio-
breathing patients or positive end-expiratory
ner can vary the size of the entrainment ports. Simply
pressure (PEEP) for mechanically ventilated
stated:
patients. These methods aid in keeping the
FIO2 as low as possible. • The larger the air entrainment port is, the more
air is entrained—the lower the FIO2, the higher
the total flow.
• Conversely, the smaller the air entrainment port
is, the less air is entrained—the higher the FIO2,
Age-Specific Competency the lower the total flow.
The patient’s inspiratory flow needs must be
Values for Infants approximated to determine whether a system is
In infants, maintain a PaO2 between 50 and delivering gas flow in excess of the patient’s inspiratory
80 mm Hg or an SaO2 of 88–92%. Attempt to needs. A patient breathing at a tidal volume of 500 mL,
avoid wide fluctuations in PaO2. FIO2 should be a breathing rate of 20 bpm, and an I/E ratio of 1:2
kept below 0.50. (see Chapter 6), has the following inspiratory flow
requirements:
60 seconds/20 bpm
premature infants receiving supplemental oxygen cycle time __________________
3 seconds
(see Chapter 29). In this case, a high PaO2 or a wide
fluctuation in PaO2, more than the FIO2, causes the I:E 1:2
hyperplasia of the retina.2 High blood levels of oxygen I time 1 second
cause constriction of the blood vessels in the retina. 0.5 L (VT) 60 seconds
These blood vessels eventually turn necrotic, and new
30 Lpm
vessels form (a process called neovascularization). The
new vessels tend to hemorrhage and cause scarring
behind the retina, which can result in blindness. The • Although the patient’s minute ventilation (V E) is
infant is at risk for this condition until about 1 month 10 Lpm, expiration constitutes two-thirds of the
of age. At that time, the arteries of the retina are mature. ventilatory cycle. Ten liters is only one-third of
the total flow required. A minimum flow of
30 Lpm is required to satisfy the patient’s peak
OXYGEN DELIVERY SYSTEMS inspiratory flow requirements.
Oxygen delivery systems are commonly categorized as • Next, the total flow of the system must be
high-flow, low-flow, reservoir, or enclosure systems. known. The first step in this process is to
Categorization as high- or low-flow does not refer to compute the air-to-oxygen ratio. The following
the liter flow of the device but rather to whether the equation is applied:
outflow of the device satisfies the entire inspiratory liters of air entrained
demands of the patient. air:oxygen ratio ___________________
liters of oxygen
1.0 (100%) FIO2
_________________
High-Flow Systems. High-flow oxygen systems use FIO2 0.21 (21%)
various methods to entrain room air. The air then
mixes with the source gas, and the system delivers Using an FIO2 of 0.50, substitutions are made:
enough gas to completely satisfy the patient’s inspira- 1.0 0.50
air:oxygen ratio ___________
tory flow needs. The total flow of a high-flow oxygen 0.50 0.21
delivery system meets or exceeds the patient’s total inspira- air:oxygen ratio _____ 1.7
0.50 ___
tory flow requirements. The actual flow rate that the 0.29 1.0
TABLE 20-8 Air-to-oxygen ratios for

common FIO2s Best Practice
FIO2 Air/Oxygen Peak Inspiratory Flow
0.24 25:1
Requirements
0.28 10:1
A quick and easy method used to approximate a
0.30 8:1 patient’s peak inspiratory flow requirements is to
0.35 5:1 multiply the patient’s VE by 3: 10 Lpm 3
0.40 3:1 30 Lpm, the minimum flow required.
0.50 1.7:1
0.60 1:1
1.00 0:1 Best Practice
• The air-to-oxygen ratio of a device set at 50% Minimum Total Flow
is 1.7:1. In other words, for every liter of oxygen It is common practice to ensure a minimum total
from the input source, 1.7 L of air is entrained. flow of 60 Lpm for a high-flow system.
Table 20-8 lists the air-to-oxygen ratios for
common FIO2s from 0.24 to 1.0.
• To calculate the total flow from the system,
simply add the air and oxygen parts and multi- commonly called Venturi masks, or venti-masks, the
ply by the source oxygen input flow. Again, name “Venturi” is really a misnomer. These devices
using an FIO2 of 0.50 and an oxygen input flow do not use a Venturi tube to entrain gas; rather they
rate of 10 Lpm: utilize the principle of viscous shearing (described in
Chapter 3). Figure 20-21 depicts a Venturi mask.
1.7 parts air 1 part oxygen 2.7 total parts Although the mask contains side exhalation ports,
2.7 10 Lpm 27 Lpm room air is not entrained by the patient as long as the
total flow exceeds the patient’s peak inspiratory needs.
This system is providing a total flow of only 27 Lpm. There is little concern at FIO2s of 0.35 or less, but at
This is not enough to satisfy the patient’s inspiratory higher FIO2s, total flow drops significantly.
flow needs, which are a minimum of 30 Lpm. The
source input flow rate must be increased, or a double Air Entrainment Nebulizers Air entrainment nebulizers
system or specialized nebulizer must be employed. have a fixed jet orifice. Air entrainment and FIO2 are
A less commonly used calculation, but one adjusted by varying the size of the entrainment port.
included for completeness, is calculating the resulting These nebulizers have the added options of delivering
FIO2 from a fixed air/oxygen ratio. A device having a additional humidification in the form of an aerosol
fixed air/oxygen ratio of 5:1 delivers the following FIO2: and of delivering heat. For these reasons, air entrain-
ment nebulizers are commonly used for patients with
(air parts 0.21) (oxygen parts 1.0) intact upper airways and those with artificial airways.
FIO2 ____________________________________
total parts For patients with intact upper airways, the desired FIO2
(5.0 0.21) (1.0 1.0) is delivered via an aerosol mask or face tent. For
FIO2 ________________________ patients with artificial airways, such as a tracheostomy
6.0
2.05 or an endotracheal tube, oxygen is delivered via a
FIO2 ____ tracheostomy collar or a T-tube (see Chapter 20).
6.0
Most nondisposable air entrainment nebulizers
FIO2 0.34
(Figures 20-22 and 20-23) have preset, fixed FIO2
settings, such as 0.40, 0.70, and 1.0. Most disposable
A device with a fixed air-to-oxygen ratio of 5:1 will
nebulizers have a much wider or a continuous range.
deliver gas at an approximate FIO2 of 0.34.
Examples of high-flow systems are aerosol masks, • Because of the function of aerosol production,
trach collars, trach tubes, and mist tents. the jet size of most air entrainment nebulizers is
very small. Consequently, they are designed to
Air Entrainment Masks High airflow with oxygen entrain- function properly at a limited range of source
ment (HAFOE) masks, by the principle of viscous flows, usually between 10 and 15 Lpm, depend-
shearing, utilize specific combinations of entrainment ing on the manufacturer. Although increasing
ports and jet sizes to deliver specific FIO2s. Although the source input flow rate is not an option to
P1 c
Exhaled
P2
air a
b
c

FIGURE 20-21 A venturi mask: (a) High-velocity jet.

(b) Area of viscous shearing (c) Air entrainment. Image not available due to copyright restrictions
increase total flow, there is rarely a problem at

FIO2s of 0.35 and below because of the relatively
large air entrainment port opening. However,
increasing the FIO2 decreases the size of the
entrainment port, decreasing the total flow. At
FIO2s above 0.35, the system must be assessed to
ensure that it is meeting the patient’s peak
inspiratory flow needs. To make this assessment,
calculate the patient’s inspiratory flow needs and
the total flow from the system, making sure that
the system flow exceeds the patient’s require-
ments. A quick and simple method of assessing
adequate flow is by visual inspection.
• Another method is to install a 6-in. (50–75-mL)
The total flow can be increased in several ways.
length of large-bore corrugated tubing in the
• One method is to connect 50–150 mL of aerosol exhalation holes of an aerosol mask. These
tubing, which acts as a reservoir, to the expira- “tusks” provide a 100–150-mL reservoir.
tory side of the system. This method is routinely • A third common method is to connect two
used, but it can be used only with a T-tube. nebulizers, both set at the prescribed F O . This
Low-Flow Oxygen Systems. Low-flow oxygen

Best Practice systems provide only part of the patient’s inspiratory flow
requirements. The remainder of the flow is room air that is
Assessing the Flow of an Air entrained by the patient. The amount of air entrained by
the patient cannot be controlled; thus, the delivered FIO2
Entrainment Nebulizer varies with changes in the patient’s ventilatory pattern.
Observe the aerosol mist at the exhalation area of Delivered FIO2 is dependent on the patient’s tidal
the system. If the mist is continuous throughout volume, respiratory rate, and peak inspiratory flow rate.
the patient’s inspiration, the flow is adequate and In a typical low-flow system, supplemental oxygen is
the delivered FIO2 is stable. If the aerosol mist is delivered directly to the patient’s airway, commonly at
broken during the inspiratory cycle, the system liter flows of 6 Lpm or less. Because low-flow systems do
flow is inadequate. The patient is entraining an not satisfy the patient’s entire inspiratory demands and
uncontrolled amount of room air, and the deliv- require room air entrainment by the patient, the FIO2 is
ered FIO2 is lower than the FIO2 setting. variable (but it can be estimated). Some low-flow systems
incorporate a reservoir system that collects oxygen.
• For a patient with a low tidal volume, a higher
Age-Specific Competency percentage of each breath is delivered by the
system, resulting in a higher FIO2.
• Conversely, a patient with a large tidal volume
Pediatric Air Entrainment has a smaller percentage of each breath delivered
Masks by the system and a larger amount of room air
Air entrainment masks are also available in pedi- being entrained, resulting in a lower FIO2.
atric sizes; however, they are not recommended High respiratory rates and high inspiratory flow rates
for children younger than 3 years of age. also result in a lower FIO2 owing to more room air
entrainment by the patient. Examples of low-flow
systems are nasal cannulas, simple O2 masks, and
setup doubles the total flow delivered to the partial-rebreathing and nonrebreathing masks.1
patient (see Chapter 21).
Nasal Cannula The nasal cannula (Figure 20-24) is a
• A fourth method is to set the nebulizer to a lower
disposable plastic device with two curved prongs that
FIO2 than prescribed and bleed in supplemental
oxygen. The lower FIO2 setting on the nebulizer
increases the size of the air entrainment port,
increasing the total flow. The bled-in oxygen
compensates for the lower FIO2 setting. Although
the FIO2 of the system is being monitored via
oxygen analysis, the system can be adjusted to
deliver the prescribed FIO2 with enough flow to
exceed the patient’s inspiratory flow requirements.
Care should be taken to document the settings
that ensure adequate flow and an accurate FIO2,
assuming the patient’s ventilatory pattern remains
constant. All staff should be notified that both
flowmeters are supposed to be running.
• A fifth method is to use a specialized nebulizer
such as the Misty Ox Hi-Fi nebulizer or the Misty
Ox Gas Injection nebulizer (GIN).4 Both nebu-
lizers are designed to provide a high total flow
output that exceeds the patient’s peak inspiratory
requirements at any FIO2. The Misty Ox Hi-Fi
nebulizer uses air entrainment as the mechanism
for increasing total flow. The Misty Ox Gas

Injection nebulizer is not an entrainment device
but a closed system that uses two gas sources and
gas injection. Both nebulizers can provide high
total flows at high FIO2s. These nebulizers are
discussed in more detail in Chapter 21. FIGURE 20-24 Nasal cannula.
TABLE 20-9 Approximate FIO2s from a

nasal cannula
Liters of 100% Oxygen Approximate FIO2
per Minute
1 0.24
2 0.28
3 0.32
4 0.36
5 0.40
6 0.44
Table 20-9 lists approximate FIO2s according to
liter flow from a nasal cannula. Note that each addi-
tional liter per minute adds 0.40 to the FIO2. The FIO2s
are approximations only and are contingent on the
Anatomic reservoir patient’s tidal volume, respiratory rate, and inspiratory
flow rate being consistent and within normal range.
FIGURE 20-25 The anatomic reservoir.
Nasal Catheter A nasal catheter is a disposable plastic

tube with small holes at its tip. It is inserted through
are positioned in the nasal passage. The cannula rests the nostril until the tip is visualized behind and slightly
on the upper lip, and the tubing is connected directly above the uvula. The catheter is then taped to the
to the flowmeter or to a bubble humidifier. Humidifi- bridge of the nose for stabilization. If the catheter is
cation is typically used at liter flows above 4 Lpm. inserted too deeply, it stimulates the gag reflex and thus
Humidification is discussed in Chapter 21. can increase the risk of aspiration. Figure 20-26 illus-
The nasopharynx and the oropharynx constitute the trates the proper placement of a nasal catheter.
anatomic reservoir, as illustrated in Figure 20-25. This Oxygen is delivered directly into the oropharynx. FIO2s
reservoir has a volume of approximately 50 mL in a
normal adult. During the normal pause between expira-
tion and inspiration, this reservoir fills with 100% oxygen.
Therefore, at the beginning of the next inspiration, the
patient receives 50 mL of 100% oxygen. The remainder of
the inspiration consists of oxygen mixed with room air.
For example, a patient on a nasal cannula at 5 Lpm has an
inspired tidal volume of 500 mL. Of the 500 mL, 50 mL is
100% oxygen from the anatomic reservoir. The liter flow
of 5 Lpm is converted to seconds as follows:
5000 mL 83 mL/s
________
60s
Assuming a 1-second inspiratory time, 83 mL of 100%
oxygen is added to the breath. The remaining 367 mL
of the inspiration is room air at 21%, adding an
additional 77 mL of oxygen to the breath.
367 mL 0.21 77 mL
This patient is receiving approximately 42% oxygen,
computed as follows:
50 mL (oxygen from anatomic reservoir) 83 mL

(oxygen from source flow) 77 mL (oxygen from
room air) 210 mL of 100% oxygen
210 mL of 100% oxygen
_____________________ 0.42 FIO2
500 mL tidal volume FIGURE 20-26 The placement of a nasal catheter.
and liter flows are similar to those of the nasal cannula.

Nasal catheters are rarely used for simple oxygen
administration and have mostly been replaced by
nasal cannulas.
Transtracheal Catheter A transtracheal catheter is a

Tefl on catheter that is surgically inserted directly into
the trachea at the second cartilaginous ring (also
referred to as transtracheal oxygenation). In addition to
the upper airway, the anatomic reservoir now includes
part of the trachea, necessitating much less oxygen
flow. Compared with the nasal cannula, approximately
50% less oxygen is needed; in fact, some patients need
as little flow as 0.25 Lpm to maintain adequate oxygen-
ation. Cosmetically, the catheter is much less obtrusive
than the nasal cannula. Another advantage, especially
for the mobile patient, is that the time that a portable
system lasts between changes is greatly extended, in
some cases, quadrupled. FIGURE 20-28 OxyArm.
Courtesy of Southmedic, Inc
However, great care needs to be taken in patient
selection. Rigorous patient education is needed because
this system requires much care, maintenance, and comfort-related complications, such as nasal dryness
preventive measures. Hazards are infection, subcutane- and irritation. Several options have become available
ous emphysema, catheter obstruction, decannulation, in the last few years, including the Oxy-Arm and the
and hemoptysis (expectoration of blood). Figure 20-27 Oxy-View.
illustrates the transtracheal catheter and its anatomic • The Oxy-Arm is an oxygen delivery device that
placement. looks like a telephone operator’s headset (Fig-
ure 20-28). It delivers oxygen flow to the tip of
New Devices Nasal cannulas have been an available the device, called the diffuser, and creates a
option since 1956 for the delivery of oxygen. How- so-called oxygen cloud in front of the patient.
ever, the cannulas do not come without their own The range of liter flow is 1–15 Lpm. There is no
physical contact between the patient and the
device.4
• The Oxy-View is a pair of eyeglasses with tubes
that curl downward and loop into each nostril
in a J-shape (Figure 20-29). This range is also
1–15 Lpm. Both options can be connected to a
patient’s current oxygen source.
Reservoir Systems. Reservoir systems incorporate a small

reservoir that collects and holds oxygen. The patient
draws on this reservoir during inspiration whenever the
inspiratory flow demand is greater than that supplied by
the source flow. This system reduces air entrainment,
resulting in an overall higher FIO2. Reservoir systems
also conserve oxygen use because comparable FIO2s can
be achieved with lower flows. Examples of such systems
are reservoir cannulas and pendants, simple masks, and
partial and nonrebreathing masks.
Reservoir and Pendant Oxygen Cannulas Reservoir and

pendant cannulas store approximately 20 mL of oxygen
during the expiratory cycle. This gas is available for use
during inspiration, resulting in lower flows needed for
a given FIO2. Figure 20-30 depicts a reservoir and a
FIGURE 20-27 A transtracheal catheter and its placement. pendant cannula. The cannula is very noticeable, and
(A)
FIGURE 20-29 Oxy-View.

Courtesy of Oxy-View, Inc.
some patients object to using one because of its

(B)
appearance. The reservoir pendant can be concealed
beneath the clothing, but the weight of the pendant FIGURE 20-30 (A) Reservoir cannula. (B) Pendant cannula.
may put pressure on the ears. Courtesy of Chad Therapeutics
Simple Mask A simple mask (Figure 20-31) is a plastic

unit designed to fit over both the nose and mouth,
with open ports on both sides of the mask. These 0.55, but they are variable because of room air
openings serve as air entrainment ports for the entrainment. Because the patient exhales into the
amount of inspiratory flow gas not provided by the mask, carbon dioxide rebreathing may become a
source. They also serve as exhalation ports and problem. The simple mask must therefore have
function as an access for inspiration should flow to adequate gas flow in order to flush out any accumu-
the mask cease. lated carbon dioxide.
The body of the mask serves as a reservoir, filling
with oxygen between breaths. The oxygen is then
available to the patient during the next inspiration. Best Practice
During the beginning of inspiration, most of the gas
inspired is high-FIO2 gas that has filled the reservoir.
During the later part of inspiration, room air is Simple Mask Flow Rate
entrained through the side ports of the mask. Always operate a simple mask at a minimum flow
Simple masks are designed to operate at liter rate of 6 Lpm in order to flush out the reservoir.
flows of 6–12 Lpm. Typical FIO2s range from 0.35 to
ensured, and carbon dioxide rebreathing is negligible.

Because of air dilution from the exhalation ports and
from the loose fit of the mask itself, the FIO2 is vari-
able, with an upper limit of approximately 0.60 being
delivered.
Nonrebreathing Mask The nonrebreathing mask is

similar in design to the partial rebreather. The nonre-
breather also has a 1-L reservoir bag that collects and
stores oxygen, but it also has strategically placed,
one-way leaf valves to prevent rebreathing.
• A one-way valve between the reservoir bag and
the mask allows gas to flow in one direction
only, from the bag to the mask.
• Another valve, covering one of the exhalation
ports on the outside of the mask, allows gas to
flow only from the mask to the outside.
FIGURE 20-31 Simple oxygen mask.
During inspiration, the valve between the reservoir
bag and the mask opens, allowing gas delivery to the
patient. The patient’s inspiratory effort closes the valve
Partial Rebreathing Mask The partial rebreathing mask on the expiration port, preventing air entrainment
(Figure 20-32) is a mask with a 1-L reservoir bag. from that port. During expiration, the valve on the
During inspiration, oxygen from the gas source enters expiration port opens, allowing the patient’s exhaled
the mask via the small-bore tubing. During expiration, gas to exit. At the same time, the valve between the
source oxygen fills the reservoir bag. Because there is reservoir bag and the mask closes because of the slight
no valve to separate the mask and the reservoir bag, the back-pressure created by the patient’s expiratory effort.
first third of the patient’s exhaled gas also enters the The closing of this valve prevents any exhaled gas from
bag. Although the patient rebreathes this gas (hence entering the reservoir bag. One of the side expiration
the name, partial rebreather), the level of carbon ports is commonly left open as a safety feature, to ensure
dioxide is negligible. The first third of the patient’s an access for inspiration should the source gas fail.
expiration consists of the high-FIO2 gas that filled the The addition of the two one-way leaf valves
anatomic reservoir at the end of the previous inspira- increases the delivered FIO2. However, owing to the air
tion. As the reservoir bag is filled with this gas, plus dilution resulting from the open exhalation port and
oxygen from the source, the last two-thirds of the the loose fit of the mask itself, realistically, the deliv-
patient’s expiration, which is high in carbon dioxide, ered FIO2s are in the range of 0.70.
exits through the side ports of the mask. As long as the
flow rate of the source gas is high enough to prevent Oxygen Enclosures. Oxygen enclosures are environmen-
the reservoir bag from collapsing, safe operation is tally controlled head- or body-surrounding reservoir
systems. Surrounding the head or the entire body with
oxygen-enriched air was one of the first approaches to
oxygen therapy. Currently, these systems are used
primarily with infants and children.
Best Practice
Nonrebreathing Masks
On both the partial and the nonrebreathing sys-
tems, always maintain a high enough source gas

flow rate to ensure that the reservoir bag does not
collapse. Proper functioning of the system is veri-
fied by the visualization of slight fluctuations in
the reservoir bag during inspiration.
FIGURE 20-32 Partial rebreather mask.
FIGURE 20-33 An incubator.
Incubators An incubator (Figure 20-33), or Isolette, is a
total body enclosure that provides convection heat
with supplemental oxygen (see Chapter 29). Supple-
mental humidity is also provided by an external heated
humidifier or nebulizer. A neutral thermal environ- FIGURE 20-34 An oxygen hood.
ment is important because cool gas over the infant’s
face significantly increases oxygen consumption, and
incubators are the best choice to ensure a neutral
thermal environment. The incubator is directly con-
• Also monitor the infant’s oxygenation status.
nected to an oxygen flowmeter by way of the humidi-
Oxygenation can be monitored continuously
fier or nebulizer.
with either pulse oximetry or transcutaneous
Because the incubator is opened often to adminis-
monitoring.
ter care to the infant, delivered FIO2s are variable and
generally less than 0.40. If a controlled or high-FIO2 is
Mist Tents As its name suggests, a mist tent is generally
required, an Oxyhood can be used inside the incubator.
used to administer aerosol therapy (see Chapter 21).
Mist tents, or croupettes, are plastic tents that are large
Oxyhoods An Oxyhood (Figure 20-34) is a transparent
enough to enclose a child, usually powered with a
box designed to enclose the infant’s head (see
high-output aerosol device, and air-conditioned. Older
Chapter 29). It can be used alone or inside an incuba-
models were generally cooled by ice. Oxygen can be
tor. The Oxyhood leaves the infant’s body free for
bled in from a flowmeter or another nebulizer. FIO2s
nursing care without disturbing the delivered FIO2. The
are variable and generally low owing to constant leaks
gas that enters the Oxyhood is premixed, humidified,
and opening of the tent.
and heated. A minimum total flow of 7 Lpm should be
Mist tents are primarily used to provide aerosol
set to prevent the accumulation of carbon dioxide
therapy to children with croup or cystic fibrosis. Fire
inside the hood.
safety measures must be strictly adhered to because
When an Oxyhood is in use:
mist tents pose a significant fire hazard.
• Analyze the oxygen concentration at the infant’s
face, near the bottom of the hood. At higher
FIO2s, the hood has a layering effect on oxygen, OXYGEN-CONSERVING DEVICES
with the highest concentration at the bottom of The primary goal of long-term oxygen therapy (LTOT) is
the hood. The difference in FIO2s at the top and to treat hypoxemia, thereby increasing the survival in
the bottom of the hood can be as much as 20%. hypoxic patients with COPD and, in turn, leading to a
decreased number of hospitalizations and/or lengths of (1 atm) while breathing 100% oxygen either continu-
stay. Very often this goal is obtainable, but only ously or intermittently. Clinically, this exposure is
through the continuous use of this oxygen therapy after accomplished by means of a compression, or hyperbaric,
the patients return to their homes. chamber. Pressures used in hyperbaric medicine are
Many options are available to make sure the needs expressed in multiples of atmospheric pressure absolute
of each and every patient are individually met. In (ATA): 1 ATA is equal to 760 mm Hg, normal sea level
addition to the longstanding oxygen concentrator or barometric pressure.
liquid vessels, today’s options include a number of
oxygen-conserving devices (OCDs): Physiological Effects. The physiological effects of
hyperbaric oxygen therapy are caused by either
• Pulse dose oxygen delivery devices (PDOD)
increased pressure or increased oxygen tensions in the
• Demand oxygen delivery systems (DODS)
body fluids and tissues. Although very little oxygen can
• Portable oxygen concentrators (POC)
be added to the bound portion of the blood once
• Liquid filling oxygen concentrators.
saturation is 97%, the quantity of dissolved oxygen rises
The PDOD and DODS are electronic or pneumatic linearly with increases in PaO2.
(mechanical) devices that are used with the com-
pressed cylinders or liquid vessels to extend their • Bubble reduction. Any trapped gas bubbles
usable time. Portable oxygen concentrators, such as the decrease in size when exposed to an increase in
Sequal Eclipse, Inogen One, Air Sep Lifestyle, and pressure, an effect supported by Boyle’s law. This
Respironics’ EverGo, are more limiting; however, when effect accounts for the success of hyperbaric
appropriate, they allow users the freedom to travel and therapy in treating disorders such as decompres-
ambulate as they did prior to the initiation of therapy.3 sion sickness, commonly known as the bends.
The portable concentrators offer patients the ability Nitrogen bubbles form in the blood and tissues
to manage their power options rather than their oxygen when a diver ascends too quickly from an area of
contents. All are available with AC power supply, high pressure (the depths) to an area of low
mobile power charger (to be used in cigarette lighter pressure (the surface). The rapid decrease in
outlet), and an internal battery for unlimited options pressure causes the bubbles to form as gas
due to the fact that they are also FAA (Federal Aviation expands. The increase in pressure that results
Administration) approved. Users must be aware of each from hyperbaric oxygen therapy decreases the
manufacturer’s limitations. For instance, some portable size of the bubbles, and the increase in oxygen
oxygen concentrators offer only pulse dose flows, and tension helps flush nitrogen from the body. Gas
others offer continuous along with pulse dose but only embolism that occurs from central line place-
up to a limited liter flow. The options certainly benefit ment or other procedures can be treated in the
patients’ quality of life, but they need to be used in same manner.
connection with a knowledgeable home care company • Supersaturation of blood and tissues. Vast increases
that will accommodate each’s specific needs. in PaO2 can occur during hyperbaric oxygen
therapy. Under hyperbaric conditions, the PaO2
can get as high as 1500 mm Hg. This increase
HYPERBARIC OXYGEN THERAPY greatly improves oxygen transport even to areas
Hyperbaric oxygen therapy (HBO) is the exposure of poor perfusion.
of a patient to a pressure greater than one atmosphere • Generalized vasoconstriction. Although vasocon-
striction may decrease perfusion, the decrease is
offset by the greatly increased PaO2. Vasocon-
Age-Specific Competency striction may help reduce tissue edema in
conditions such as burns.
• Elimination of other gases. Nitrogen and carbon
Oxygen Delivery to Infants monoxide can be eliminated from the body
Blended, humidified gas is the preferred method more quickly with high oxygen pressures.
of oxygen delivery for infants rather than air Carbon monoxide has a strong affinity for
entrainment nebulizers. Nebulizers should be hemoglobin and, once bound, unbinds very
avoided because they produce an aerosol particle slowly. The half-life of carbon monoxide when a
that increases the risk of bacterial contamination person is breathing room air is over 5 hours.
and infection, especially if the aerosol is heated. Under hyperbaric conditions of 3 ATA, this
In addition, nebulizers can generate excessive half-life is reduced to 23 minutes.
noise levels, which can further stress an infant. • Enhanced immune function. The increase in
available oxygen may help the white blood cells
TABLE 20-10 Indications for hyperbaric oxygen therapy

Vascular Insufficiency Defects in Oxygen
Gas Diseases States Infections Transport
Decompression sickness Radiation necrosis of bone Clostridial myonecrosis Carbon monoxide poisoning
Gas embolism or soft tissue (gas gangrene) Cyanide poisoning
Severe acute anemia or Necrotizing soft tissue
hemorrhage infections
Diabetic microangiopathy Chronic refractory
Crush wounds osteomyelitis
Ischemic skin grafts or Refractory anaerobic
tissue transplants infections
Acute traumatic ischemias
Thermal burns
perform their immune functions. The high PaO2 only one patient. Because the chamber is pressurized
aids in wound healing. with 100% oxygen, the patient does not have to wear a
• Neovascularization. Hyperbaric oxygen therapy mask. However, 100% oxygen throughout the entire
promotes neovascularization (the formation of pressurized chamber greatly increases the fire hazard
new capillary beds) to poorly perfused tissues. and the need for strict precautions. Another disadvan-
The increased oxygenation promotes the forma- tage of the monoplace chamber is the necessity to
tion of osteoblasts, fibroblasts, granulocytes, and depressurize the chamber in order to manage an
collagen, which, in turn, promote capillary emergency situation.
budding. This physiological effect is beneficial in
treating conditions such as gas gangrene and Complications and Hazards. The complications and
difficult-to-heal wounds. hazards of hyperbaric oxygen therapy are related to:
Indications. The indication for hyperbaric oxygen • High pressures, causing barotrauma.
therapy is any condition that would benefit from an • The effects of oxygen toxicity.
increase in ambient pressure or in oxygen tension. • Decompression.
Table 20-10 summarizes the conditions that benefit • Fire.
from hyperbaric oxygen therapy. Table 20-11 summarizes the hazards of hyperbaric
oxygen therapy.
Mode of Administration. A specialized chamber is
required to administer hyperbaric oxygen therapy. The
Safety Considerations. The risk of fire is great with the
chamber is either a multiplace chamber or a mono-
use of hyperbaric chambers because of the vast increase
place chamber.
in the partial pressure of oxygen, which supports
combustion. Safety considerations during hyperbaric
Multiplace Hyperbaric Chamber The multiplace hyper-
oxygen therapy are directed toward fire prevention:
baric chamber is large enough to accommodate more
than one patient. The chamber is pressurized with air, • Use only cotton materials.
and oxygen is delivered to the patients individually by • Prevent static electricity.
way of a nonrebreather mask or other oxygen adminis- • Use no alcohol- or oil-based products.
tration device. Oxygen is delivered via a closed system • Patients and health care workers are not to wear
because O2 leakage into a pressurized chamber poses a make-up, deodorant, hair sprays, or jewelry.
significant fire hazard. The multiplace chamber has the • Use adequate fire suppression systems.
advantage of being large enough to accommodate the
patients and the health care team (who must take care
to avoid decompression sickness). Multiplace chambers MONITORING OXYGEN THERAPY
are very expensive to purchase and maintain. Objective outcomes must be measured and docu-
mented to ascertain whether oxygen therapy is effec-
Monoplace Hyperbaric Chamber The monoplace tive. Monitoring oxygen therapy can be accomplished
hyperbaric chamber (Figure 20-35) accommodates by both invasive and noninvasive methods.
FIGURE 20-35 Hyperbaric chamber.

Courtesy of Perry Baromedical
TABLE 20-11 Hazards of hyperbaric oxygen In general, invasive methods of monitoring carry a
therapy much greater risk of complications than noninvasive
monitoring.
Oxygen Toxicity Barotrauma Other
Pulmonary toxic Sinus trauma Fire Noninvasive Methods. Although noninvasive methods
reaction Tympanic of monitoring oxygenation status may not be as
membrane accurate as arterial blood gas analysis, they have certain
rupture advantages.
Central nervous Pneumothorax Sudden • The most obvious advantage is patient comfort.
system toxic reaction Air embolism decompression • The risk of complications is minimal.
• Noninvasive monitoring can provide the practi-
tioner with a continuous display of the patient’s
Invasive Methods. The most accurate assessment of
oxygenation status, rather than isolated static
oxygenation status is the arterial blood gas analysis,
measurements.
which not only gives a direct measurement of PaO2, but
also data needed to derive values for SaO2 and CaO2.
Pulse Oximetry Pulse oximetry is the most common
SaO2 and CaO2 can be measured directly by co-oximetry,
noninvasive method to monitor a patient’s
which is also used to measure total hemoglobin and to
oxygenation status, either intermittently or continu-
recognize and quantify dyshemoglobins
ously. Oximetry is a technique used to measure the
(discussed in the following section, where it is
oxygen saturation of hemoglobin in the blood by
contrasted to pulse oximetry). Although arterial blood
absorption of different wavelengths of light.
gas analysis is more accurate than noninvasive means,
it is an isolated and static measurement. It cannot
Principles of Operation The principles of operation
reflect continuous changes in oxygenation status.
of pulse oximetry are spectrophotometry and
An indwelling arterial line (A-line) has certain
plethysmography.
advantages over the arterial puncture. An arterial line
spares the patient from having to undergo repeated • Spectrophotometry is the generation of light at
punctures, and, when connected to a monitor, it a known intensity going into a solution and the
provides a continuous display of arterial blood pres- measurement of the intensity of light that leaves
sure and heart rate. (Arterial blood gas sampling and the solution. The solution in this instance is the
analysis are discussed in greater detail in Chapter 16.) arterial blood.
• Plethysmography is the study of changes in the • Optical shunting (light passes from the LED to
shape or size of an organ. It is used to separate the photodetector by passing around the body
static from dynamic components; in other words, part rather than through it).
plethysmography measures pulsatile waves. • Vascular dyes, such as methylene blue or
cardiogreen.
These two principles enable pulse oximeters to measure
• Deeply pigmented skin.
different wavelengths of light in pulsatile waves, giving
• Nail polish, especially dark colors such as black,
them the specific ability to focus on arterial, or pulsatile,
blue, or green.
blood.
Modern pulse oximeters use two wavelengths of Physiological factors that can cause inaccurate
light: red and infrared. The wavelengths are transmitted readings are:
from a light-emitting diode (LED) through the body
• Very low saturations. False high readings can be
part (artery) to a photodetector.
produced at SaO2s below 80%, and inaccurate
• At the wavelength of 660 nm, red light passes readings result at SaO2s below 65%.
through oxyhemoglobin (HbO2) and is • Low-perfusion states. Low-perfusion states that can
absorbed by reduced hemoglobin (RHb), or cause inaccurate readings include cardiac arrest,
deoxyhemoglobin (RHbO2). hypothermia, peripheral shunting, vasoconstric-
• At the wavelength of 940 nm, infrared light tion, and shock.
passes through reduced hemoglobin and is • The presence of dyshemoglobin.
absorbed by oxyhemoglobin.
Also, the oxyhemoglobin dissociation curve
Pulse oximeters compare oxyhemoglobin and flattens out at PaO2s above 60 mm Hg (SaO2 90%).
reduced hemoglobin, using the two wavelengths of light: There is a wide range of PaO2s between 60 and 100 mm
HbO2 Hg with relatively little change in SaO2. For this reason,
_______________ 100
RHbO2 HbO2 arterial blood gas analysis is more accurate than pulse
oximetry.
This is a measure of functional saturation.
Pulse oximetry does not take into account the Clinical Applications The clinical applications of pulse
presence of dyshemoglobin. Dyshemoglobin is an oximetry are:
abnormal type of hemoglobin, such as carboxyhemo-
globin (COHb), methemoglobin (MetHb), or sulfhe- • Continuous monitoring of oxygenation during
moglobin (SulfHb). Dyshemoglobins interfere with anesthesia.
the binding of oxygen, greatly decreasing the oxygen- • Adjusting FIO2 or titrating oxygen liter flow
carrying capacity of hemoglobin and significantly lower- during oxygen therapy
ing the arterial oxygen concentration (CaO2). Because • Documenting SaO2 during long-term oxygen
the hemoglobin is bound in the presence of dyshemo- therapy for purposes of Medicare requirements,
globin, the pulse oximeter reading is falsely high. reimbursement, or disability benefits.
Co-oximetry must therefore be used to obtain a • Continuous monitoring of oxygenation during
truly accurate measurement of oxygen saturation. weaning from mechanical ventilation.
Co-oximetry uses four wavelengths of light and does • Prevention of retinopathy of prematurity (ROP)
measure dyshemoglobins. The co-oximetry result is a in neonates, although transcutaneous monitor-
measure of fractional saturation. Oxyhemoglobin is ing is more sensitive.
compared with total hemoglobin. • Monitoring oxygenation during diagnostic
procedures such as bronchoscopy, sleep studies,
HbO2
_________________________________ 100 and exercise testing.
HbO2 RHbO2 COHb Met Hb
Unfortunately, an arterial blood sample must be Transcutaneous Monitoring Transcutaneous monitor-
obtained; therefore, this is an invasive procedure. ing measures the partial pressures of the gases that are
Co-oximetry is usually performed in conjunction with diffusing through the skin. The transcutaneous partial
arterial blood gas analysis. pressures of both oxygen (TcO2) and carbon dioxide
Limitations The limitations of pulse oximetry are both (TcCO2) can be measured simultaneously by incorpo-
technological and physiological. Technological factors rating the Clark electrode for measuring PO2 and the
that can cause inaccurate readings are: Severinghaus pH electrode for measuring PCO2 into the
same probe. The probe is secured to the skin and
• Motion artifact. connected to a monitor for continuous readings. A
• Sources of ambient light, such as xenon lamps heater and a thermistor inside the probe are connected
and fluorescent and infrared lights. to an external heat source to control skin temperature.
Principles of Operation The skin is heated to 44°–45°C Hazards The most important hazard of transcutaneous
to promote vasodilation of the capillary bed and to monitoring is burns caused by the sensor. The risk of
increase perfusion to the area. The increased perfusion burns increases greatly during conditions of low
increases the diffusion of oxygen and carbon dioxide. perfusion because the diminished blood flow prevents
The resulting TcO2 and TcCO2 measurements should be adequate dissipation of the heat.
positively correlated with PaO2 and PaCO2, assuming
conditions are optimal.
OXYGEN THERAPY PROTOCOLS
TcO2 Correlation with PaO2 Correlation of transcutane- Advances in noninvasive monitoring and bedside
ous values with arterial blood gas values are currently patient assessment make oxygen therapy well suited for
limited to PO2 measurements. Various factors deter- a therapist-driven protocol. Protocols ensure that
mine how well TcO2 is correlated with PaO2: immediate changes can be made in oxygen delivery
without the lapse time involved in contacting the
• Skin thickness. The thicker the skin, the larger the
physician for an order change. Protocol-based therapy
diffusion pathway for oxygen. The correlation is
ensures that the patient receives bedside assessments,
not accurate; the TcO2 is lower than the actual
individual treatment based on need, and the timely
PaO2.
discontinuance of therapy when it is no longer
• Oxygen consumption. Regional oxygen consump-
tion in the area of the sensor site affects correla-
tion. The TcO2 is lower than the PaO2.
• Perfusion status. Adequate perfusion, or even
hyperperfusion, must exist for an accurate Best Practice
correlation. This is the rationale behind heating
the skin. In low-perfusion states—such as a Transcutaneous Probe
decreased cardiac output, vasoconstriction, or These precautions help prevent burns:
hypothermia—the TcO2 is substantially lower
than the PaO2. If adequate perfusion exists • The sensor site for the transcutaneous
(a cardiac index of 2 Lpm/m2), the TcO2:PaO2 probe must be rotated every 2–4 hours.
ratio is 70% 12%. • The probe should never be placed over a
• Temperature. If the skin temperature is too low, bony area.
adequate peripheral perfusion is not present,
and the TcO2 is lower than the PaO2. If the skin
temperature is too high, the TcO2 is higher than
the PaO2 (as temperature increases, pressure
increases).
• Age. Transcutaneous monitoring is used almost Age-Specific Competency
exclusively in neonates and newborns. Their
skin is much thinner than an adult’s, so the Monitoring Oxygenation
diffusion pathway is smaller. Under proper
conditions, the correlation of TcO2 and PaO2 is in Neonates
excellent. TcO2 can actually equal PaO2 if the Transcutaneous monitoring is the preferred
proper temperature is maintained, adequate method of monitoring oxygenation status in
perfusion exists, and the infant is younger than infants younger than 2 weeks of age. The skin
2 weeks old. This positive correlation decreases composition is such that the correlation of TcO2
with age. and PaO2 is excellent. Transcutaneous monitor-
ing is more sensitive than pulse oximetry. There
Clinical Applications Transcutaneous monitoring of is a much wider range in PaO2 relative to SaO2.
PO2 is typically used to monitor oxygenation status Pulse oximetry is unable to reflect hyperoxia,
and oxygen therapy in neonates and newborns. It is because a large increase in PaO2 presents only as
much more sensitive than pulse oximetry. a small increase in SaO2 above a PaO2 of 80 mm
Transcutaneous monitoring of PO2 can also serve Hg. Transcutaneous monitoring is a great benefit
to reflect cardiopulmonary compromise. Whenever in preventing conditions such as ROP, for which
the TcO2 is decreased, an arterial blood gas should be oxygenation should be monitored continuously.
drawn. If the PaO2 is normal but the TcO2 is decreased, Source: From American Association of Respiratory Care. AARC
a perfusion or circulatory impairment should be clinical practice guideline: transcutaneous blood gas monitoring for
suspected. A decrease in both the TcO2 and the PaO2 neonatal and pediatric patients. Respir Care. 1994;39:1176–1179.
reflects a pulmonary impairment.
required. The oxygen protocol in Figure 20-36, for greater oxygen concentration cools, causing a current
example, was adopted by Saint Clare’s Hospital change that is proportional to the oxygen concentra-
(Denville, New Jersey).5 tion. The electrical oxygen analyzer can measure only
air–oxygen combinations. It does not work with other
gases because the reference wire is limited to compari-
ANALYZING OXYGEN CONCENTRATIONS sons with room air.
An integral part of oxygen therapy is the analysis of
oxygen concentration. Oxygen analysis is the only way Electrochemical Oxygen Analyzers. Electrochemical
to verify that the desired FIO2 is being delivered to the oxygen analyzers produce a current from a chemical
patient. reaction. There are two types of electrochemical oxygen
All oxygen analyzers should be calibrated before analyzers: galvanic and polarographic.
use. Calibration is accomplished by exposing the
sensor to a source of 100% oxygen and then to a source Galvanic Oxygen Analyzers The galvanic oxygen analyzer
of 21% oxygen (room air), making slight adjustments (Figure 20-39) utilizes the reduction reaction that
as necessary. After calibration, if the analyzer does not occurs when oxygen combines with water and electrons
function to within 2% at both the 21% and 100% from the cathode (negative electrode), forming
points, the equipment should not be used. hydroxyl ions (OH–). These ions migrate to the anode
Oxygen systems should be analyzed as close to the
patient’s airway as possible. Although analyzing the
system near its source verifies the system FIO2 delivery, it
does not indicate leaks in the system or air entrainment
by the patient.
Physical Oxygen Analyzers. Physical oxygen analyzers SAINT CLARE’S HOSPITAL

utilize the principle of paramagnetism to measure RESPIRATORY CARE SERVICES
oxygen concentrations. If a gas is paramagnetic, its
POLICY AND PROCEDURE MANUAL
molecules align themselves with the north-south lines
in a magnetic field. Diamagnetic gases do not. Oxygen
is a paramagnetic gas, so it responds to a magnetic
OXYGEN PROTOCOL
field. POLICY
The physical oxygen analyzer (Figure 20-37) It is the policy of Saint Clare’s Hospital to administer oxygen, utilizing the Oxygen Protocol,
consists of two magnets separated by a dumbbell filled based on the following guidelines.
Goals of Oxygen Therapy
with nitrogen. The dumbbell is suspended by a thin Correct documented or suspected hypoxemia
quartz wire. As oxygen is drawn into the sensor, its Relieve or prevent dyspnea
Decrease symptoms associated with chronic hypoxemia
molecules align themselves with the magnetic field. Decrease workload imposed on the cardiopulmonary system by hypoxemia
The dumbbell rotates, and its degree of rotation is
PROCEDURE
proportional to the oxygen partial pressure. The
I. DECISION MAKING (Refer to the Oxygen Protocol Flowchart)
analyzer measures partial pressure but displays both 1. After receiving an order for oxygen therapy or oxygen protocol, the patient is evaluated for
partial pressure and FIO2. oxygen needs and type of device, based on:
a. Relevant medical history
b. Baseline assessment
c. Degree of consciousness, alertness
Electrical Oxygen Analyzers. Electrical oxygen d. Stability of minute ventilation and airway
analyzers (Figure 20-38) utilize the principle of thermo- e. SpO2 obtained via pulse oximetry
f. PaO2 / PaCO2 obtained via arterial blood gas
conductivity to measure oxygen percentages. A molecule g. Severity/cause of hypoxemia
h. Chronic CO2 retention
with a large mass conducts more heat than a molecule 2. High-flow vs. low-flow oxygen therapy devices:
with a smaller mass. Oxygen has a greater mass than ⇒ High-flow systems provide a flow of oxygen sufficient to meet and/or exceed
nitrogen, which is the main gas in ambient air. There- the patient’s inspired flow rate needs; therefore the FIO2 is predictable and stable.
fore, the more oxygen there is in a mixture, the greater ⇒ Low-flow systems provide a flow which supplements the pateint’s inspired flow rate
needs; therefore the FIO2 is variable, depending on the patient’s size, minute volume, and
the heat transfer will be. The electrical oxygen analyzer respiratory pattern.
utilizes a special electrical circuit known as a Wheat-

stone bridge, which can detect small changes in resis-
tance. The small change in resistance causes a
measurable change in current. One limb of the Wheat-
stone bridge is exposed to ambient air, and the other FIGURE 20-36 Oxygen protocol. (continues)
limb is exposed to the sample gas. The side with the Reprinted with permission from Saint Clare’s Hospital, Denville, New Jersey
Physician order for oxygen

Initiate protocol
Assess patient
Determine appropriate device
Relevant Rspiratory
cardiac or Stable COPD distress and/or
medical history; with known unstable COPD
non-COPD CO2 status status
High-flow system
Nasal cannula Nasal cannula
FI02 based on severity
2 Lpm 1–2 Lpm
of distress
Measure SpO2 Measure SpO2 Draw ABG

within 30 minutes within 30 minutes within 30 minutes
Titrate O2 to Titrate O2 to Notify physician of

maintain SpO2 maintain SpO2 ABG results and
≥ 94% 90%–92% patient status
Titrate O2 to
maintain SpO2
≥ 92%
SpO2 within
Yes specified range? No
Recheck SpO2 within Increase FIO2 to

8 hours, then daily obtain desired SpO2;
and as needed notify physician if
based on clinical flow > 5 Lpm or FIO2
assessment > 40% is needed
Yes Decreasing O2
needs? No Monitor SpO2 Q shift and
as needed based on
clinical assessment;
Wean oxygen as Continue to check ABGs with signs
tolerated; check follow protocol of respiratory distress
SpO2 on room air
when tolerated
No
Yes SpO2 ≥ 92 on
room air
D/C O2
or keep PRN if indicated;
notify physician
FIGURE 20-36 Oxygen protocol. (continues)

Saint Clare’s Hospital Saint Clare’s Hospital

RESPIRATORY CARE SERVICES RESPIRATORY CARE SERVICES
POLICY AND PROCEDURE MANUAL POLICY AND PROCEDURE MANUAL
OXYGEN PROTOCOL OXYGEN PROTOCOL
3. Classification of Oxygen Devices: 6. In a stable patient with decreasing oxygen needs, oxygen may be weaned as tolerated,
Device Flow Range (Lpm) FIO2 Range(%) Flow Type unless specified otherwise by the physician. Oxygen may be discontinued on a patient
1 who maintains a satisfactory SpO2 on room air and shows no signs of increased work
Nasal cannula – –6 22–45 Low of breathing or respiratory distress. Oxygen may need to be kept PRN in the following
4
Simple mask 5–12 35–50 Low situations: a history of COPD, congestive heart failure, chest pain, nocturnal dyspnea,
Partial rebreather 6–10 35–60 Low dyspnea on exertion.
Nonrebreather 10–15 55–95 Low/High
Air entrainment mask Variable 24–50 High 7. In a patient who will be discharged with oxygen for use in the home, the goal may
Large-volume nebulizer 10–15 28–100 High not necessarily be to discontinue the oxygen device, but to optimize the level of
Note: The FIO2s listed for low-flow devices are approximate and are based on normal oxygen needed prior to discharge. The inability to maintain an SpO2 > 88% on room
breathing patterns. Settings on these devices should be reported in Lpms, air, at the time of discharge, is an indication for home oxygen therapy. If the physician
not as an FIO2. is not already aware of this situation, he or she should be notified.
4. Low-Flow vs High-Flow Criteria: III. GUIDELINES

Low-Flow Criteria High-Flow Criteria 1. The physician must be notified in the following circumstances:
a. Tidal volume: 300–700 mL a. Tidal volume: <300 mL ⇒ a. Abnormal ABGs: pH <7.30 or >7.50 ; PaCO2 <30 mm Hg or >50 mm Hg;
b. Respiratory rate: <25 bpm b. Respiratory rate: >25 bpm PaO2 <55 mm Hg
c. Regular ventilatory pattern c. Alveolar hypoventilation/CO2 retention ⇒ b.F IO2 >40% or >5 Lpm is required to achieve targeted SpO2
d. Required FIO2 <40% d. Required FIO2 >40% ⇒ c. Unexpected changes in clinical status
II MONITORING / TITRATION ⇒ d. Patient remains in respiratory distress after appropriate level of oxygen
has been initiated
1. Upon initiation of O2 device, titrate liter flow/FIO2 to meet targeted SpO2 range: ⇒ e. Patient is being discharged and still needs supplemental O2 to maintain
a. Patients utilizing low-flow devices <6 Lpm will be titrated in increments of 1 Lpm. an adequate SpO2
b. Patients utilizing low-flow devices >6 Lpm or high-flow devices will be titrated in
5%–10% increments. 2. If oxygen has been discontinued and patient presents with a change in status
indicating a need for oxygen, the Oxygen Protocol may be reinstituted based on
2. The SpO2 will be measured 30 minutes after the initiation of an O2 device for evaluation the original order.
of appropriate FIO2, liter flow and/or device. Arterial blood gases will be drawn if
IV. DOCUMENTATION
respiratory distress is noted. Clinical signs of respiratory distress include tachypnea,
use of accessory muscles of ventilation, tachycardia, erratic or excessively high minute 1. A written order and/or standing order for oxygen must be on the patient’s chart on a
ventilation, cyanosis, alterations in level of consciousness. physician’s order sheet.
3. Once an appropriate device has been selected and SpO2 is within an acceptable 2. The device, flow rate, and/or FIO2 will be documented on the patient’s chart on the
range, the RN assigned to the patient will be notified of the patient’s oxygen status. Respiratory Care Graphic Sheet and on the patient’s pathway sheet if applicable.
This should also occur as changes are made in the device or liter flow/FIO2 setting.
Arterial blood gas results will be reported to the physician. 3. SpO2 results will be charted on the Respiratory Care Graphic Sheet.
4. In a stable patient who is responding appropriately to the device selected, SpO2 will 4. A sticker will be placed on the oxygen device indicating the current liter flow and/or
be reevaluated within 8 hours, and then on a daily basis. SpO2 can be FIO2 setting.
reevaluated as needed, based on clinical evaluation.
5. A sticker will be placed in the Progress Notes section of the chart notifying the physician
5. In an unstable patient, or one with increasing oxygen needs, SpO2 will be monitored a
when the oxygen is discontinued.
minimum of once per shift and as-needed based on clinical evaluation. Arterial blood
gases should be reevaluated with continuing signs of respiratory distress to confirm Reviewed: Value-based Content Date Reviewed:
adequacy of ventilation. Revised:
Prepared by: Sharon Shenton, RRT 4/99
FIGURE 20-36 Oxygen protocol. (continued)
Calibration
Magnets N N
Quartz fiber
Dumbbell
Mirror
S S
Meter
Reference chamber Sample chamber

Scale
Light source Battery
FIGURE 20-37 A physical oxygen analyzer. FIGURE 20-38 A schematic of an electrical oxygen analyzer.
Meter Best Practice

Calibrating an Oxygen Analyzer
When analyzing a system with a high FIO2, such
as 0.80, use 100% as the final calibration point.
When analyzing a system with a low FIO2, such
as 0.35, use 21% as the final calibration point.
An FIO2 of 0.60 can be used as the point of
Lead anode Gold cathode change.
Membrane
FIGURE 20-39 A schematic of a galvanic electrochemical
oxygen analyzer.
CASE STUDY 20-1

R. T. was admitted to the hospital through the Mr. T.’s oxygen therapy orders were changed to an
emergency room. Mr. T. is a 56-year-old male who aerosol mask at an FIO2 of 0.60. The respiratory
was in apparent good health until 3 days ago, when therapist set up the aerosol mask as ordered and
he developed a fever, chills, chest pain, and a analyzed the system at the nebulizer outlet. Oxygen
cough productive of thick yellow sputum. analysis confirmed an FIO2 of 0.60.
Upon arrival in the emergency room, Mr. T. was Two hours later Mr. T. was again dyspneic and
dyspneic and tachypneic and had a temperature of tachypneic. Another ABG was obtained with the
103°F. An arterial blood gas analysis, a complete following results:
blood count, and a sputum specimen were pH: 7.45
obtained. Mr. T. was started on IV therapy with
PaO2: 60 mm Hg
broad-spectrum antibiotics and placed on a
nonrebreathing mask. PCO2: 30 mm Hg
The complete blood count revealed most values HCO3: 24 mEq/L
within normal range, with the exception of the white Mr. T.’s FIO2 was increased to 0.70, with orders
blood cell count, which was greatly elevated. for another ABG to be obtained in 1 hour.
Arterial blood gas values were as follows: Mr. T. continued to be dyspneic and tachypneic.
pH: 7.47 One hour later, ABG results were as follows:
PaO2: 44 mm Hg pH: 7.45
PCO2: 30 mm Hg PaO2: 50 mm Hg
HCO3: 24 mEq/L PCO2: 30 mm Hg
Mr. T was admitted to the hospital. The sputum HCO3: 24 mEq/L
culture revealed pneumococcal pneumonia.
Mr. Tyler’s antibiotics were changed to a narrow- Questions
spectrum antibiotic according to the sensitivity 1. Were the respiratory therapist’s actions in
results. He was kept on a nonrebreather mask. The setting up the aerosol system and analyzing the
next set of ABGs revealed the following results: system correct? Explain your answer.
pH: 7.40 2. How can you explain the drop in the patient’s
PaO2: 100 mm Hg PaO2 after an increase in the FIO2?
P CO2: 35 mm Hg 3. What would you have done differently with
HCO3: 24 mEq/L regard to Mr. Tyler’s oxygen therapy?
(positive electrode) through a semipermeable mem-

brane that allows only oxygen to pass through. The Meter
change in current is proportional to the partial pressure
of oxygen. Although the analyzer measures partial
pressure, it displays the percentage of oxygen. Battery
Polarographic Oxygen Analyzers The polarographic

oxygen analyzer (Figure 20-40) utilizes the same prin-
ciple of operation and the same chemical reaction as
the galvanic oxygen analyzer. The polarographic oxygen
analyzer, however, uses a battery to polarize the system; Silver anode Platinum cathode
polarizing speeds up the reduction reaction, resulting
in a faster response time. Like the galvanic analyzer, the
polarographic oxygen analyzer measures the partial
pressure of oxygen and displays it as the percentage of
oxygen. Polarographic oxygen analyzers can be used for Membrane
continuous oxygen analysis, such as in-line with a FIGURE 20-40 A schematic of a polarographic electro-
mechanical ventilator. chemical oxygen analyzer.
CASE STUDY 20-2

E. G., a 65-year-old woman, arrived in the emer- respiratory rate dropped to 16 bpm. Arterial blood
gency room with acute shortness of breath. She had gases on 100% oxygen were as follows:
a history of COPD. Mrs. G. had a respiratory rate of
pH: 7.32
30 bpm; she was using accessory muscles and
PaO2: 80 mm Hg
pursed-lip breathing. A complete blood cell count
P CO2: 78 mm Hg
and arterial blood gas analysis were performed. The
HCO3: 38 mEq/L
results of the CBC were within normal range, and
the ABG results were as follows: Mrs. G. became lethargic and hard to rouse. Her
respiratory rate decreased even further, to 10 bpm.
pH: 7.40
PaO2: 50 mm Hg Questions
PCO2: 68 mm Hg
1. Was the oxygen therapy order appropriate?
HCO3: 38 mEq/L
Explain your answer.
A diagnosis of exacerbation of COPD was made. 2. Explain the resulting PaCO2, respiratory rate,
Mrs. G. was placed on 100% oxygen via a nonre- and neurological reaction.
breathing mask. Her oxygen saturation improved, as
3. Suggest an alternative method of oxygen
confirmed by continuous pulse oximetry, and her
delivery.
Therapeutic Use of Gas Mixtures This is the rationale for using carbon dioxide–oxygen
(carbogen) mixtures to treat hypoventilation and to
Certain gases can be combined with oxygen in specific augment lung inflation. However, this approach has
concentrations and administered to treat a variety of been found to be ineffective for hyperinflation because
conditions: carbon dioxide–oxygen, helium–oxygen, most patients treated with it preferentially increase
and nitric oxide therapy. their respiratory rate rather than their tidal volume.
Carbon dioxide–oxygen mixtures have also been
used to treat singulation (hiccups), although the efficacy
CARBON DIOXIDE AND OXYGEN (CARBOGEN) is questionable. Singulation is the spastic contraction
At a concentration of less than 10%, carbon dioxide of the diaphragm. Increased PCO2 levels increase
acts as a respiratory stimulant; indeed, the rise in phrenic nerve discharge (the phrenic nerve innervates
carbon dioxide acts as the normal stimulus to breathe. the diaphragm). Increasing the discharge of the phrenic
nerve may improve the coordination of diaphragmatic 80% helium and 20% oxygen. A mixture of 70%
contractions. helium and 30% oxygen can be used for patients with
More modern uses of carbogen include: hypoxemia.
When administering helium–oxygen mixtures,
• Early treatment of central retinal artery
remember that the oxygen flowmeter is inaccurate.
occlusion.
Oxygen flowmeters are calibrated for the density of
• In biology, to research in vivo oxygen and
oxygen. Helium’s density is lower; therefore, more gas
carbon dioxide flows.6
exits the source than the flowmeter indicates. The
• To increase cerebral blood flow by dilating the
correction factor for an 80:20 helium–oxygen mixture is
cerebral blood vessels. However, most patients
1.8. This means that for every liter of flow indicated on
respond by hyperventilation in an attempt to
the flowmeter, 1.8 L is actually being delivered. For
normalize the PCO2 because the brain indicates
example, if 10 Lpm of the mixture is needed, the flow-
an increase in CO2 as a decrease in O2.7
meter should be set at 5.6 Lpm (10 1.8). The correc-
Normally, the concentration of the administered tion factor for a 70:30 helium/oxygen mixture is 1.6.
carbon dioxide–oxygen mixture is 5% CO2/95% O2 for Also, due to its low density, helium–oxygen must be
10–15 minutes. Although low concentrations of carbon administered via a closed system to prevent gas escape.
dioxide are a respiratory stimulant, concentrations Side effects of helium–oxygen therapy are directly
above 10% result in respiratory depression. related to its low density: distorted voice pitch and
Side effects of carbon dioxide–oxygen therapy impaired cough. The helium should be washed out
include headache, palpitations, hypertension, dizzi- before the patient performs the cough maneuver.
ness, muscle tremors, and mental depression. Do not The lower density of the gas also reduces its aerosol-
leave the patient unattended during this treatment. carrying capacity.
HELIUM AND OXYGEN (HELIOX) NITRIC OXIDE THERAPY

The benefit of helium as a therapeutic adjunct is based Although nitric oxide therapy is no longer in the
on its low density. In areas of turbulent flow, higher investigation stage as a therapeutic modality, extensive
driving pressures are needed to maintain a given flow clinical trials have been performed with successful
(see Chapter 3). Turbulent flow exists in the larger results. FDA approval was obtained in December 1999.
airways. In the presence of large airway obstructions, a
patient, especially one compromised by pulmonary Physiological Effects of Nitric Oxide. The benefits of
disease, has a greatly increased work of breathing nitric oxide are due to its physiological effect of
(WOB). Administering a gas of lower density, such as capillary smooth muscle relaxation. By improving
helium, lowers the driving pressure needed to maintain blood flow to ventilated alveoli, it:
gas flow. A helium–oxygen mixture (heliox) can
• Improves V /Q
relationships.
substantially reduce a patient’s work of breathing.8 The
density of an 80:20 helium–oxygen mixture is only • Decreases pulmonary vascular resistance and
0.429 g/L as compared with the 1.29 g/L density of air. pulmonary pressures.
Keep in mind that helium–oxygen mixtures are effec- • Improves arterial oxygenation.
tive only in large airways, where turbulent flow exists.
There is no benefit in small airways because the flow in Indications and Potential Uses for Nitric Oxide
these areas is laminar; density is not a factor. Therapy. Indications for nitric oxide therapy are
Helium is inert; it must always be mixed with at conditions that would benefit from its physiological
least 20% oxygen. The most commonly used mixture is effects. Table 20-12 summarizes the indications and
TABLE 20-12 Indications and potential uses for nitric oxide therapy
Pulmonary Newborn/Pediatric Other
Primary pulmonary hypertension Congenital heart disease Heart transplant
Chronic pulmonary hypertension Pulmonary hypertension of Lung transplant
the newborn
Pulmonary fibrosis Hypoxemic respiratory distress Sepsis
of the newborn
Pulmonary embolism Pediatric chronic lung disease Sickle-cell disease
Adult respiratory distress syndrome
TABLE 20-13 Adverse and toxic effects

Spotlight
of nitric oxide therapy On
Effects Due to
Direct Effects By-Products I-NOvent
Paradoxical response Cell damage The I-NOvent delivery system (INO Therapeutics)
Worsening hypoxemia Hemorrhage is the only commercially available nitric oxide
(NO) delivery system that has FDA approval.
Platelet inhibition Pulmonary edema
However, the hospital must have an Investiga-
Increased left ventricular Formation of tional New Drug Number for INO administration.
filling pressures methemoglobin It is designed for mechanically ventilated
Pulmonary hypertension Formation of peroxynitrite patients.
The injection module is between the ventila-
tor output and the humidifier in the inspiratory
potential uses that are currently being investigated for circuit. Nitric oxide is injected in proportion to
inhaled nitric oxide therapy.2,9,10 the sensed inspiratory flow, providing the desired
dose of NO. The concentration of NO remains
Dose and Mode of Delivery. Effective doses of nitric accurate over a wide range of ventilator flows and
oxide have been reported in the range of 2–20 ppm desired NO concentrations.
(parts per million), with an optimal dose of 10 ppm. Source: From Hess DR, Hurford WE. Journal conference on inhaled
Doses less than 20 ppm show minimum adverse nitric oxide. Respir Care. 1999;44.(3);241–384.
effects.2,10
Nitric oxide can be inhaled spontaneously by
nonintubated patients, but therapy is more commonly
delivered by mechanical ventilation. A nitric oxide
injector and flow sensor are incorporated into the therapy must always be considered and recognized.
inspiratory limb of the ventilator circuit.2 These factors, along with documented outcomes
assessment, reflect not only a competent practitioner
Adverse and Toxic Effects of Nitric Oxide Therapy. but also a professional one who is able to interact
Adverse and toxic effects of nitric oxide therapy can be successfully with other members of the health care
due to its direct action or to its chemical by-products. team and to contribute actively to the diagnosis,
Nitrogen dioxide (NO2), which is produced whenever treatment, and recovery of the patient.
nitric oxide is exposed to oxygen, has very toxic effects
at concentrations greater than 10 ppm.2 Table 20-13 Study Questions
lists the adverse and toxic effects of nitric oxide therapy.
REVIEW QUESTIONS
Discontinuation of Nitric Oxide Therapy. Withdraw-
1. List the indications for oxygen therapy.
ing nitric oxide therapy must be done carefully to
prevent rebound effect. Take the following steps when 2. List and briefly explain the hazards of oxygen
withdrawing a patient from nitric oxide therapy.5 therapy.
3. List and briefly explain the causes of hypoxemia.
• Decrease the nitric oxide level to the lowest
effective dose, optimally at 5 ppm or less. 4. Describe the indications for a liquid oxygen
• Confirm that the patient is able to maintain delivery system versus gaseous oxygen.
adequate oxygenation on an IIO2 of 0.40 or lower. 5. Differentiate between a noncompensated and a
• The patient should be hyperoxygenated before back-pressure compensated Thorpe tube.
discontinuing nitric oxide. 6. Differentiate between a high- and a low-flow
oxygen delivery system.
Summary 7. Describe the physiological effects of hyperbaric
oxygen therapy.
Medical gas therapy is an integral part of respiratory
care practice. The competent, skilled practitioner is well 8. Differentiate between functional and fractional
versed in all aspects of therapy. Patient assessment and oxygen saturation.
critical thinking skills are vital, as are skills in equip- 9. Describe the physiological effects of the following
ment selection and troubleshooting. The goals, indica- medical gas mixtures: carbon dioxide–oxygen,
tions, physiological effects, hazards, and side effects of helium–oxygen, nitric oxide.
MULTIPLE-CHOICE QUESTIONS c. 70–80% of the PaO2.

d. higher than the PaO2.
1. The regulatory agency that is responsible for the
purity levels of medical gases is the: 8. The measurement that is taken by the use of two
a. DOT. wavelengths of light to compare oxyhemoglobin
b. OSHA. with deoxyhemoglobin is known as the:
c. FDA. a. fractional saturation.
d. CGA. b. wavelength saturation.
c. functional saturation.
2. Which of the following is not a low-flow delivery
d. hemoglobin saturation.
device?
I. Venturi mask 9. Which of the following factors may cause an
II. nasal cannula erroneous pulse oximetry reading?
III. high-volume nebulizer a. hyperperfusion
IV. simple mask b. hyperthermia
a. I and II c. an SaO2 of 78%
b. II and III d. the presence of carboxyhemoglobin
c. II and IV 10. The type of oxygen analyzer that utilizes oxygen’s
d. I and III property of paramagnetism is:
3. When checking on a patient wearing a nonre- a. physical.
breathing mask, the respiratory therapist notices b. electrical.
that the reservoir bag is deflating almost c. galvanic.
completely during inspiration. The appropriate d. polarographic.
action is to:
a. leave the system as is.
b. increase the flow of source oxygen.
c. decrease the flow of source oxygen. 1. A patient suffering from smoke inhalation is
d. change the patient to a simple mask. admitted to the emergency room. His PaO2 on
4. The best oxygen delivery device to administer the arrival is 42 mm Hg. He is placed on a nonre-
highest FIO2 as quickly as possible is a: breathing mask at 100%; his PaO2 rises to 80 mm
a. Venturi mask. Hg and his SaO2 via pulse oximetry is 95%. There
b. simple mask. is no apparent cyanosis; in fact, the patient’s
c. partial rebreather. coloring seems quite good. The patient remains
d. nonrebreather. tachypneic and lethargic despite the fact that his
PaO2 and SaO2 are within normal range. Discuss
5. A COPD patient requires an oxygen delivery system
the reason for the discrepancy between the
that provides a moderate concentration of oxygen.
patient’s normal blood values and his poor
The patient has a history of chronic hypoxemia
respiratory and neurological status. Describe how
and carbon dioxide retention. The most appropri-
you would treat and monitor this patient.
ate system for oxygen delivery is a:
a. simple mask. 2. A patient with COPD is suffering from an acute
b. nasal cannula. exacerbation of her condition. Arterial blood gas
c. Venturi mask. analysis reveals a PaO2 of 48 mm Hg and a PaCO2
d. partial rebreather. of 62 mm Hg. Describe how to treat and monitor
this patient.
6. A patient is wearing a HAFOE device set at an FIO2
of 0.50. When the therapist analyzes the system at 3. A patient is on a high-volume nebulizer and
the patient’s airway, the analyzer reads 35%. What aerosol mask at an FIO2 of 0.60. Oxygen analysis at
is the most likely reason for the large difference in the patient’s airway reads 30%. Why is there a
concentrations? discrepancy? Discuss appropriate alternative
a. The analyzer is malfunctioning. methods of delivering an FIO2 of 0.60.
b. The patient is breathing very shallowly.
c. The source gas outlet is faulty.
d. The patient is entraining room air. References
7. In an adult with proper skin temperature and 1. American Association for Respiratory Care. AARC
adequate perfusion, the TcO2 should be: clinical practice guideline: oxygen therapy in
a. 20–30% of the PaO2. the acute care facility-2002 Revision & Update.
b. equal to the PaO2. Respiratory Care. June 2002; 47(6);717–720.
2. Scanlon CL, et al. Egan’s Fundamentals of Respiratory 10. Hess DR, Hurford WE. Journal conference on
Care. 9th ed. Philadelphia: Mosby; 2008. inhaled nitric oxide, Respir Care. 1999;44.
3. American Association for Respiratory Care. AARC
clinical practice guideline: oxygen therapy in the
home or alternate site health care facility-2007 Suggested Readings
Revision & Update. Respiratory Care. August 2007; American Association for Respiratory Care. AARC
52(1)1063–1068. clinical practice guideline: in vitro pH and blood
4. White GC. Equipment Theory for Respiratory Care. gas analysis and hemoximetry. Respir Care.
3rd ed. Clifton Park, NY: Delmar Cengage 1993;38:505–510.
Learning; 1999. American Association for Respiratory Care. AARC
5. Shenton S. Oxygen protocol. Policy and Procedure clinical practice guideline: selection of an oxygen
Manual. Denville, NJ: Saint Clare’s Hospital; 1999. delivery device for neonatal and pediatric patients,
6. Arnold JF, Kotas M, Fidler F, Pracht ED, Flentje M, Respir Care. 1996;41:637–646.
Jakob PM. Quantitative regional oxygen transfer Burton GG, Tietsort JA. Therapist-Driven Protocols, A
imaging of the human lung. Journal of Magnetic Practitioner’s Guide. Los Angeles: Academy Medical
Resonance Imaging. 2007; 26,3:637–645. Systems Inc; 1993.
7. Walsh, RN. Higher Wisdom: Eminent Elders Explore Eubanks DH, Bone RC. Principles and Applications of
the Continuing Impact of Psychedelics. Albany, NY: Cardiorespiratory Care Equipment. Philadelphia:
State University of New York Press; 2005. Mosby; 1994.
8. Chevrolet J-C. Helium oxygen mixtures in the McPherson SP. Respiratory Care Equipment. 5th ed.
intensive care unit. Crit Care. 2001;5,4:179–181. Philadelphia: Mosby; 1995.
9. Hsu C-W, et al. The initial response to inhaled White GC. Basic Clinical Lab Competencies for Respiratory
nitric oxide treatment for intensive care unit Care, An Integrated Approach. 4th ed. Clifton Park,
patients with acute respiratory distress syndrome. NY: Delmar Cengage Learning; 2003.
Respiration. 2008; 75:288–295.
CHAPTER 21
Humidity and Aerosol Therapy

Dianne A. Adams
OBJECTIVES
• Differentiate between the physical properties of humidity and aerosol.
• Explain the understanding of physiologic mechanisms for airway hydration.
• Recognize the effect of underhydration and overhydration on the respiratory system.
• Evaluate the function and effectiveness of devices that provide supplemental humidification to the
respiratory system.
• Evaluate the function and effectiveness of devices that deliver aerosol particles to the respiratory system.
• Identify the appropriate clinical application of devices used to provide humidity and aerosol to patients who
require supplemental hydration or aerosol therapy.
CHAPTER OUTLINE
Concepts of Humidity Therapeutic Use of Humidifying Devices
Defining Humidity Indications for Humidity Therapy
Measuring Humidity Hazards
Effect of Temperature on Humidity General Principles of Humidifying Devices
Body Humidity Factors Affecting Effectiveness
Physiological Mechanisms of Airway Types of Humidifiers
Humidification Heating Systems
Maintaining Adequate Humidification Therapeutic Use of Aerosol-Generating Devices
Consequences of Underhumidification Indications for Aerosol Therapy
Consequences of Overhumidification Hazards
Concepts of Aerosols General Principles of Aerosol-Generating Devices
Defining Aerosol Factors Affecting Aerosol Distribution
Characteristics of Aerosols Types of Aerosol Generators
Effect of Aerosols on Airway Function
597
KEY TERMS
absolute humidity (AH) humidifier isotonic
aerosol humidity nebulizer
body humidity (BH) humidity deficit relative humidity (RH)
body temperature pressure satu- hygrometer stability
rated (BTPS) hygroscopic tonicity
deposition hypertonic water vapor content
homeostasis hypotonic water vapor pressure
T
he body’s systems require a certain amount of The water vapor content (the amount of water
hydration to maintain homeostasis, a state vapor present) of a given volume of a gas depends on
of relatively constant conditions. The respira- both the temperature of the carrier gas and the gas’s
tory system is no exception. Hydrating the water-carrying capacity. Water vapor content is
body is necessary to maintain adequate cellular expressed as the mass of water in a volume of gas, in
function and is usually associated with water or fluid either milligrams of water suspended in a liter of gas
consumption. External signs of dehydration are evident (mg/L) or in grams per cubic meter (g/m3). As the
to us: chapped lips, flaky skin, dry cracked elbows and temperature of a gas increases, the amount of water
heels. Hydration of the respiratory system is rarely a vapor the gas can carry also increases. When the water
concern until signs of dehydration appear: crusty nasal vapor content is at the maximum possible at a given
drainage, nosebleeds, dry mouth, scratchy throat, a dry temperature, the gas is considered fully saturated. As a
hacking cough. Overhydration can also cause problems gas cools, its capacity to hold water vapor decreases.
and lead to conditions associated with excess fluid This decrease causes condensation, in which the vapor
retention. Maintaining hydration of the mucociliary turns back into liquid form and “rains out” of the gas.
lining of the airway and subsequent humidification of Humidity, then, can be explained as the cumulative
inspired air are primary functions of the upper airway. effect of the evaporation of moisture into the air and
However, when an optimal balance cannot be met the condensation of moisture out of the air. A compari-
because of pathology or environmental conditions, son of water vapor content in the atmosphere at given
compromise of respiratory function is likely. Therefore, temperatures is shown in Table 21-1.
maintaining these conditions during altered states is Absolute humidity (AH) is the actual amount of
the primary goal of humidity and aerosol therapy. This water present in a given volume of gas, and it is usually
requires an understanding of humidification concepts expressed in the same terms as water vapor content
and their effect on airway function. (mg/L or g/m3). Because water vapor is in a gaseous
state and behaves like any gas, absolute humidity can
also be expressed by the amount of pressure exerted by
Concepts of Humidity the water molecules, or water vapor pressure, in
“Humidity” is a familiar term. The humidity of the millimeters of mercury (mm Hg). The water vapor
atmosphere affects people’s comfort whether they are content of fully saturated air at 21°C is 18.4 mg/L and
out- or indoors. In this section, humidity is defined exerts a pressure of 18.6 mm Hg (Table 21-1). There-
and ways of quantifying it are discussed, both in the fore, one could refer to the AH of that air sample as
atmosphere and in the respiratory system. 18.4 mg/L or as 18.6 mm Hg.
Relative humidity (RH) compares the actual
DEFINING HUMIDITY amount of water present in a given volume of gas
(content, or AH) with the amount the gas is capable of
Humidity is the amount of water vapor present in an
holding at that temperature (capacity). It is always
environment or substance. Water vapor (water in its
expressed as a percentage. The following formula
molecular, or gaseous form) enters the atmosphere
illustrates the relationship:
through evaporation and leaves it through condensa-
tion. Evaporation occurs when water changes from its absolute humidity
liquid form to its gaseous form; condensation occurs %RH _________________ 100
capacity
when water changes from its gaseous to its liquid form.
Both processes are temperature dependent, as is a When the AH of a gas equals the capacity, the gas is
carrier gas’s water-carrying capacity. fully saturated, and RH is 100%. If the AH of a gas at
CHAPTER 21 ■ Humidity and Aerosol Therapy 599
TABLE 21-1 Water vapor content and RH expresses how close the air is to becoming fully
pressure of a fully saturated air sample saturated. As RH reaches 100%, the rate of evaporation
is equal to the rate of condensation. Depending on the
at various temperatures season or geographic region, a dehumidifier might be
Water Vapor Water Vapor used to remove excess water vapor from the air, such as
Temperature Content Pressure in a damp, cool basement during the spring. Or a room
(°C) (mg/L) (mm Hg) humidifier might be run to increase the water vapor in
20 17.3 17.5 air that is dry due to home heating systems during the
winter months. Relative humidity can be measured in
21 18.4 18.6
such conditions with a hygrometer.
22 19.4 19.8
23 20.6 21.0
24 21.8 22.3
EFFECT OF TEMPERATURE ON HUMIDITY
25 23.0 23.7
The temperature of a carrier gas plays an important
role in determining the amount of water vapor a gas is
26 24.4 25.1 capable of carrying. At a given temperature, a gas has
27 25.8 26.7 its individual capacity to carry a certain amount of
28 27.2 28.3 moisture (Table 21-1). As the temperature increases,
29 28.8 29.9 the gas has a greater capacity for holding water vapor;
at lower temperatures, its water-holding capacity and
30 30.4 31.7
thus its water vapor content decrease. If the water vapor
31 32.0 33.6 content is kept at a constant volume, an increase in
32 33.8 35.5 temperature decreases RH because the higher tempera-
33 35.6 37.6 ture increases the gas’s water-holding capacity. Compar-
ing its content with its new capacity at the increased
34 37.6 39.8
temperature would then decrease RH, as shown in
35 39.6 42.0 the following situations.
36 41.7 44.4
37 (body 43.9 47.0
temperature) SITUATION 1
38 46.2 49.5
Temperature: 21°C
39 48.6 52.3
Capacity for water vapor content 18.4 mg/L
40 51.1 55.1 AH 18.4 mg/L
(content) 18.4 mg/L
%RH ___________________ 100 100%
(capacity) 18.4 mg/L
21°C is 9.2 mg/L and its capacity at that temperature is

known to be 18.4 mg/L, the RH is 50%.
9.2 mg/L SITUATION 2
%RH __________ 100 50%
18.4 mg/L
Temperature 26°C
Understanding the different ways of expressing Capacity for water vapor content 24.4 mg/L
humidity and the underlying concepts helps the AH 18.4 mg/L
respiratory therapist (RT) appreciate the differences in
capabilities of humidifying devices. These same (content) 18.4 mg/L
%RH ___________________ 100 75%
expressions also explain concepts of humidity as (capacity) 24.4 mg/L
related to the respiratory system.
The role of temperature on humidity must be

MEASURING HUMIDITY understood to appreciate the effect of body tempera-
In terms of our environment, relative humidity is a ture on inspired air. Using this knowledge of AH and
familiar method of measuring and reporting the the capacity of a gas to hold moisture helps in the
amount of moisture present in the air and is used to explanation of how temperature affects humidity and
monitor outdoor as well as indoor humidity levels. The airway function.
BODY HUMIDITY AH is 18.4 mg/L. The formula for BH shows a BH

The concepts of absolute and relative humidity can of 42%:
also be applied to conditions of inspired gases and
18.4 mg/L
humidity in alveolar air. Body humidity (BH) is the %BH __________ 100 42%
43.9 mg/L
water vapor content required to fully saturate alveolar
air at normal body temperature, expressed as a percent- Determining the humidity deficit with the following
age. At 37°C (normal body temperature), the capacity formula shows how much moisture the body has to
for water vapor content is 43.9 mg/L, or 47 mm Hg, give up to reach BTPS.
which represents normal BH. If the BH of inspired air
is 100%, the air is fully saturated. The condition of Humidity deficit BH (mg/L) AH (mg/L)
fully saturated alveolar air at normal body temperature Humidity deficit 43.9 mg/L 18.4 mg/L
and at barometric (atmospheric) pressure (760 mm Hg) 25.5 mg/L
is called body temperature pressure saturated (BTPS).
However, BH may not be 100% if the AH of an This difference becomes clinically significant as the
inspired air sample is low. Suppose the room deficit increases over an extended period of time.
temperature is 22°C and the water vapor content of Maintaining normal physiological function through
the room is 14 mg/L. The following formula shows proper hydration or by artificial administration of
that BH is 32%: supplemental humidity helps in avoiding a humidity
deficit and in restoring normal airway function.
content at 22°C 100
%BH _______________ Table 21-2 summarizes terms describing humidity
capacity at 37°C concepts and their mathematical expression.
14 mg/L
%BH __________ 100 32%
43.9 mg/L
At the room temperature in this example, the air is not Physiological Mechanisms of
fully saturated because the capacity for water vapor
content at 21°C is 18.4 mg/L. Furthermore, as the air is
Airway Humidification
inspired, the temperature changes to 37°C, increasing Humidification of the airways occurs naturally under
the capacity to 43.9 mg/L. These circumstances create a ideal conditions. The physiological mechanisms set in
humidity deficit, or a difference between the BH and place by the cellular layer and mucus blanket that make
the AH of inspired gas. If the inspired air is to become up the mucosal lining are designed to maintain a
fully saturated, the upper airway must make up the balance of moisture and heat exchange. Any alteration
difference by losing moisture. Even when the inspired in this state causes airway dysfunction and eventually
air is fully saturated at room temperature, the upper pulmonary compromise. The specific indications and
airway may still have to make up for a humidity deficit devices for humidity therapy are discussed later in this
to achieve BTPS. As in the previous example, suppose chapter. Here are some of the basic principles of
the inspired air is at 21°C. If the air is fully saturated, its humidification.
TABLE 21-2 Humidity terms and their mathematical expressions

Term Definition Mathematical Expression
Absolute humidity The actual amount of water vapor in a gas Content = mg/L
Pressure = mm Hg
Relative humidity The actual amount of water vapor in a gas compared AH 100
%RH ________
capacity
with the amount necessary to cause 100% saturation,
multiplied by 100
Body humidity The absolute humidity of inspired gas saturated at AH
%BH _______________ 100
capacity at 37°C
body temperature
Humidity deficit The difference (usually in mg/L) between the water Humidity deficit = BH – AH
vapor content of gas at BTPS (fully saturated air at
normal body temperature and pressure) and the water
vapor content of inspired gas
MAINTAINING ADEQUATE HUMIDIFICATION determines the ability of the mucociliary transport

The upper airway is designed to prepare inspired air for system to function adequately.2
gas exchange and to maintain efficient pulmonary The mucus gel layer is composed of mucus secreted
function by filtering and heating the inspired air to by goblet cells and submucosal glands. Mucus is 95%
37°C and providing 100% RH, or BTPS. This optimal water and 5% glycoproteins and lipids. The complex
gas conditioning continues from the initial inhalation bonding of these substances is critical in determining
by nose or mouth through the pharynx and usually has the viscosity of mucus and thereby its ability to be
been completed before the air reaches the trachea, the propelled by the cilia and function in mucociliary
beginning of the lower airways. The primary layers of transport. Any alteration, such as water loss or gain,
the airway mucosa responsible for gas conditioning are disturbs this delicate balance and impairs the mobility
the cellular layer (epithelial lining) and the aqueous sol of mucus.
layer and mucus gel layer, which make up the mucus The upper airway is responsible for conditioning
blanket (Chapter 6). A change in either the tempera- the inspired air and for maintaining clearance of
ture or the moisture of the inspired air affects the contaminants. Under normal circumstances, such as
function of each layer. breathing room air that is 22°C and has an RH of 50%,
The aqueous sol layer is a low-viscosity fluid that gas conditioning occurs by reaching 31–33°C and
bathes the cilia. When the cilia are fully extended, 59–73% RH at the larynx, 34°C and 77% RH in the
microhooks at their tips reach through the aqueous sol trachea, and 37°C and 100% RH in the mainstem bron-
layer to engage the mucus gel layer above. With each chi. These conditions can be achieved only when the
stroke, the mucus gel layer is moved toward the body and the respiratory system are adequately
pharynx. The depth of this aqueous layer is the result hydrated. Depleting the body of the needed water—
of the amount of water evaporation that occurs during whether a result of improper oral intake, exposure to
inspiration and water condensation that occurs with dry gases, or artificial bypass of the upper airway—can
exhalation. lead to detrimental consequences, as can excessive
water accumulation in the respiratory tract.
• When air that is less than BTPS is inspired, water
evaporates from the mucus gel layer in an
attempt to reach full saturation at 37°C. This CONSEQUENCES OF UNDERHUMIDIFICATION
phenomenon is part of what is known as When the respiratory tract is exposed to anhydrous
insensible water loss and under normal conditions gases, physiological changes occur in the primary layers
amounts to a net loss of 250 mL of water and 35 of the airway mucosa. The degree of decreased humid-
kcal of heat from the lungs each day.1 Water that ity and the length of exposure time to dry gases deter-
is lost in this layer is replaced by the secretory mine the severity of these changes.
cells found in the cellular layer. As cool, dry gas is inspired, heat and moisture are
• Conversely, during exhalation, some heat and given up by the mucus gel layer and then by the
moisture are given back to the mucosal lining, aqueous sol layer, leading to changes in the system.
preparing the lining for the next inspiration.
Condensation during exhalation occurs when • The most noticeable change begins with the
gas exiting the airways comes into contact with thickening of the mucus gel and the retention of
the mucosal lining, which is now cooler as a secretions. The mucociliary transport is greatly
result of heat loss during inspiration. compromised owing to the change in viscosity of
the gel layer and depletion of the fluid layer.
Likewise, heat is transferred from the exhaled gas, • The beat frequency of the cilia is also affected by
warming the mucosal lining for the next inspiration. the decreased temperature of the gas, adding to
Under certain conditions, water gained by condensa- the inability of the cilia to participate in secre-
tion can increase the depth of this fluid layer, thus tion movement.2
decreasing the function of the mucociliary transport. • As the dehydrated state continues, the mucus
The activity of the cilia is also dependent on the gas blanket becomes encrusted, increasing the
temperature and the RH. When the temperature of the likelihood that mucus will plug smaller airways.
inspired gas is not at 37°C and the RH is less than Plugging of the airways may lead to atelectasis
100%, the beat frequency is affected. These conditions and impaired pulmonary function.
may occur because of changes in the viscosity of the • Exposure to cold, dry air may be responsible for
gel layer above the mucosal lining or as a result of the the impairment of pulmonary function and
change in depth of the aqueous sol layer. The depth bronchoconstriction among asthmatic patients.3
of the aqueous sol layer represents an equilibrium • Histological changes that occur with prolonged
between water loss and water gain and greatly impairment of the mucociliary transport include
the destruction of cilia, damage to mucus glands, function. The therapeutic use and design of aerosol-
and the destruction of the epithelial lining and generating devices are discussed later in the chapter.
basement membrane.
Of all the changes that occur in the airway as a DEFINING AEROSOL
result of underhumidification, thickening and reten-
An aerosol is any liquid or solid particle that is
tion of secretions are the hallmark signs of dehydration
suspended in a gas. Whereas humidity involves water
of the respiratory tract.
in its molecular (gaseous) form, aerosols contain actual
droplets of liquid water. Thus, aerosols are visible to
CONSEQUENCES OF OVERHUMIDIFICATION the naked eye. Aerosols can occur naturally in the
external environment (e.g., fog), can be a result of a
The airways can also be overhumidified. Too much
chemical reaction (e.g., a by-product of combustion),
humidity occurs when the insensible water loss
or can be artificially created. Smoke and smog are
decreases, such as when either the temperature of the
composed of solid particles suspended in a gas; they
inspired gas is higher than body temperature or
result from combustion. Liquid aerosols are in aerosol-
inspired gas contains aerosols (droplets). Both of these
ized cleaning solutions, spray deodorants, and hair
conditions can lead to excess body fluid retention and
sprays. Likewise, in medical use, aerosols are created as
intoxication.
a delivery system for medication or for hydration to a
When the inspired gas temperature is higher than
desired location. Producing aerosols for this purpose
37°C and the gas is 100% saturated:
requires an in-depth understanding of them and the
• Condensation rather than evaporation occurs, delivery systems used to deposit the aerosol particles
adding water to the mucosal lining. at the intended site.
• As exhaled gas passes over the mucosal lining,
condensation continues to reduce the amount of
normal insensible water loss and results in an CHARACTERISTICS OF AEROSOLS
increase in the depth of the aqueous sol layer. How an aerosol behaves is determined by factors such
as the physical nature and activity of the particle.
Inspired air that contains aerosols can lead to
The size of an aerosol particle and its ability to
overhumidification:
remain in suspension dictate whether the aerosol
• The presence of aerosols increases the risk of reaches the intended site in the airways and thus affects
adding water to the mucosal lining. The change how therapeutic the aerosol administration will be.
in depth affects the efficiency of the cilia because Size depends on several factors. Ambient conditions,
their microhooks can no longer reach the mucus such as temperature and RH, determine whether an
gel layer above and propel it forward. aerosol particle gets larger, gets smaller, or remains the
• The mucus gel layer is also affected because the same size in its suspended state.
balance between its substances has now changed,
• If aerosol particles are introduced to a cooler
resulting in a less viscous layer that cannot be
and less humid gas stream, the aerosol particle
cleared with the rhythmic motion of the cilia.2
evaporates and decreases in size as the gas
• Added moisture may also dilute surfactants at the
warms.
alveolar level, leading to decreased surface tension
• If introduced to a warmer gas stream that is
and thereby affecting pulmonary function.
more humid, small aerosol particles coalesce,
• Histologically, degeneration and adhesion of
forming fewer, but larger, particles.
cilia result.
• Ideally, to maintain a steady size, aerosol
Eventually these changes lead to increases in secretions, particles should be introduced into a main gas
decreases in ventilation, and compromise of oxygen- stream that has the same temperature and
ation. The hallmark signs of overhumidification are humidity as the carrier gas.
weight gain in neonates, crackles on auscultation,
Aerosols that absorb moisture from the surround-
and radiographic changes that suggests pulmonary
ing environment are called hygroscopic. Aerosols can
congestion.
absorb moisture when they are exposed to a humidi-
fied environment such as that within ventilator circuits.
Concepts of Aerosols The tonicity of an aerosol is its tendency to absorb
water.
Humidification therapy often involves aerosols. This
section explains how aerosols can be used in the • Hypertonic aerosols, such as hypertonic saline
respiratory system and what effect they have on airway solutions, have a greater tonicity than body
fluids, so they absorb water from the surround- • The kinetic activity of the aerosol affects when
ing tissues and increase in size. deposition (the landing of the particle on a
• Hypotonic aerosols have less tonicity than body surface) occurs. All molecules are in continuous
fluids and tend to evaporate and decrease in size. motion and often collide with one another.
• An isotonic aerosol is one that neither gains nor These collisions cause even more rapid, random
loses water but maintains a steady size. motion, referred to as Brownian movement, which
mainly involves particles of less than 0.1 μm. As
Because of the way they are created, therapeutic
an aerosol particle decreases in size, it becomes
aerosols contain a range of particle sizes. The design of
more subject to Brownian movement and to
equipment that produces aerosols determines the
collisions with other molecules. The collisions
initial size. How the equipment is powered (gas or
cause particles to coalesce (join together) and
ultrasonic) and the use of structural objects (baffles)
eventually fall out of suspension.
can produce a variety of particle sizes.
• As the concentration of aerosol particles increases,
In the clinical setting, the concern is to create an
the chances are greater that the particles collide,
aerosol that delivers an average-sized particle that
coalesce to form larger particles, and fall out of
guarantees distribution to the intended site. The term
suspension.
mass median aerodynamic diameter (MMAD) describes
the average size of aerosol particles generated,
EFFECT OF AEROSOLS ON AIRWAY FUNCTION
expressed in micrometers (μm). MMAD divides the
range of aerosol particles generated in half. If the Aerosol delivery is designed to target three specific
MMAD of an aerosol device is 5 μm, 50% of the areas: the upper airway, the lower airways, and the lung
aerosol particles produced are smaller than 5 μm parenchyma. The aerosols may be categorized as either
and have less mass, and 50% of the aerosol particles bland aerosols or pharmacologically active (medicated)
are larger than 5 μm and have greater mass. aerosols. The site of deposition and the type of aerosol
Knowing that aerosol particle size is affected by administered determine the effect of the aerosol on
the temperature and RH of the gas, the tonicity of airway function.
the particle, and the equipment design helps the The initial size of the aerosol being generated
respiratory therapist to choose appropriate devices, usually determines the approximate area for deposition
set correct temperatures, and select the proper (the site of aerosol action). The first step in ensuring
solutions to achieve the desired results. appropriate deposition in the airway is knowing the
The ability of an aerosol particle to remain sus- location of aerosol deposition according to particle size
pended in a gas is its stability. Aerosol stability is influ- and the MMAD production of the available aerosol-
enced by several factors such as size, activity, and generating device, or nebulizer.
concentration. Although the choice of aerosolized agent is usually
the responsibility of the physician, the respiratory
• The size of the aerosol particle determines how therapist must still know the various agents available
much influence gravity imposes because a large and understand their use as therapeutic or diagnostic
particle is more affected by gravity than a small adjuncts to respiratory care. Aerosolized agents can be
one is; it has a greater tendency to fall out of its bland (not containing medication) or pharmacologically
carrier gas and be deposited on the surface. The active (containing medication designed to elicit a
effect of particle size on deposition is summa- biological effect when topically applied in aerosol form
rized in Table 21-3. to the airways). Bland aerosols can be sterile water and
hypotonic, isotonic, or hypertonic saline; they can also
TABLE 21-3 Particle deposition in the be either cooled or heated. Successful results require
respiratory tract that the respiratory therapist be familiar with the
solution agents, delivery devices, and desired site of
Particle Size (μm) Deposition Site deposition. Table 21-4 summarizes the uses of bland
50 Is filtered out before it enters and pharmacologically active (medicated) aerosols.
the respiratory tract Pharmacologic agents are discussed further in Chapter 7.
5–50 Mouth, nose, pharynx
2–5 Respiratory tract proximal to Therapeutic Use of Humidifying
alveolar ducts Devices
0.5–3 Lung parenchyma: alveoli
The decision to use clinical humidifying devices
0.5 Remains in suspension and is (humidifiers) is typically left to the discretion of
exhaled the respiratory therapist. More often than not, a
TABLE 21-4 Uses of bland and medicated aerosols

Type of Nebulizer Type of Solution Desired Effect
Cool bland aerosols
Small-volume nebulizer (SVN), Hypotonic saline Induce sputum without added sodium
ultrasonic nebulizer (USN)
SVN, USN Isotonic saline Induce sputum
SVN, USN Hypertonic saline Induce sputum
Large-volume nebulizer (LVN), Babbington Sterile water Reduce upper airway swelling
Heated bland aerosols
LVN Sterile water Reduce humidity deficit
Medicated aerosols
Dry powder inhaler (DPI), metered-dose Bronchoactive agents Reduce smooth muscle spasm
inhaler (MDI), SVN
SVN Mucokinetic agents Promote clearance of secretions
MDI, SVN Glucocorticoids Reduce airway inflammation
MDI, SVN Anti-asthmatics Prevent allergic airway reactions
SVN, small-particle aerosol generator (SPAG) Antimicrobial agents Reduce and inhibit microbial growth
Best Practice
Choosing a Nebulizer
A particle’s deposition in the respiratory tract The response to aerosol administration depends
depends on its size. To optimize delivery of aerosol on the deposition site of the particle and on the
particles to the targeted site, choose a nebulizer for activity—bland or medicated—of the agent.
the particle size range it produces.
• If deposition occurs in the upper airway, as
• If the targeted site is the nasal cavity, choose is the intended site when using nasal sprays,
a nebulizer that generates particles in the size the activity of the aerosol is then directed to
range of 5–50 μm, according to Table 21-3. the mucosal lining or to the vasculature of
• If the desired site is the lower airway, the the nasal cavity.
particle size range should be 2–5 μm, and • When aerosol deposition occurs in the lower
the device of choice would have an MMAD of airways, the activity is directed to the mucus
2–5 μm. layer, submucosal cells, or nerve endings.
• In some cases, deposition must occur at the • Aerosols whose site of action is the lung
alveolar level to promote systemic absorption. parenchyma stimulate a response through
The particle size required for this location is systemic absorption of a pharmacologic
0.5–3 μm. agent.
physician’s order for humidity is not forthcoming. INDICATIONS FOR HUMIDITY THERAPY
Hospital policy on the application of these devices Clinical indications for providing humidity therapy
varies from institution to institution; therefore, the include the administration of dry medicated gases and
decision to provide supplemental humidity requires altered BTPS. When a patient is breathing dry gas
that the respiratory therapist be proficient in this supplied from a cylinder or central supply system, a
treatment modality. The respiratory therapist must humidity deficit may result, causing further respiratory
be able to recognize the need for humidity therapy complications for the already compromised patient.
and to choose the most appropriate device for the Humidity therapy is not limited to patients whose
patient. upper airway is bypassed; it must also be considered
Spotlight
On
Aerosol Delivery of Macromolecules
Until recently, injection or ingestion was thought to • Aerosol therapy provides a more rapid onset
be necessary for delivering drugs to the systemic of the desired results. Macromolecules that
circulation because most bioengineered drugs are currently being tested for administration
consist of macromolecules too large for entry in any by inhalation are insulin, morphine, hor-
other way. Currently, aerosolizing devices are being mones, calcitonin, and vaccines.
designed to provide inhalation delivery of these
Device design appears to be the key to the ef-
drugs for systemic therapy.
fective delivery of these drugs to the lung periphery.
• Inhaling macromolecules provides a direct Currently, several companies are conducting clinical
route of entry for systemic absorption without and preclinical trials of aerosol devices to deliver
the problems associated with traditional drug macromolecules. The development of systemic drug
therapy, such as inconvenience, pain, and delivery by inhalation will dramatically change the
gastrointestinal upset, all of which result in way medication is delivered for many patients.
poor patient compliance. Source: Corkery K. Inhalable drugs for systems therapy. Respir Care.
2000;45:831–835.
for the spontaneously breathing patient receiving increased hydration for such patients is thick tenacious
medicated gas therapy. The type of gas flow device also secretions, mucus plugging, increased airway resistance,
indicates whether supplemental humidity is necessary: and increased work of breathing.4 A patient who
presents with any of those signs requires delivery of
• A low-flow device, such as a nasal cannula, can
humidified gas at a temperature of at least 30°C,
be humidified in an attempt to supplement a
according to the relevant American Association for
spontaneously breathing patient’s humidity
Respiratory Care (AARC) clinical practice guideline
level. But, because the room air and humidity
(CPG) for providing humidity to a patient during
are being entrained with each breath on these
mechanical ventilation.5 Standards for the humidity
devices, supplemental humidity may not be
output of any humidifying device for medical use have
required.
been established by the American National Standards
• A high-flow device, such as a mechanical ventila-
Institute (ANSI). Their report states that:
tor, requires supplemental humidity delivery to
meet BTPS because the gas delivered is fully • The minimum output of 10 mg/L is the lowest
supplied by the medical gas system, which is acceptable humidity level for devices that deliver
anhydrous. gas to the upper airway.
• A minimum output of 30 mg/L is necessary
Hospital policies on humidity therapy attempt to
when gas delivery bypasses the upper airway.6
set guidelines for the respiratory therapist to follow. For
example, a hospital’s policy may state that supplemen-
tal humidity is not necessary with oxygen devices at HAZARDS
flows of less than 3 Lpm. However, the respiratory
In addition to the physiological hazards associated
therapist must recognize signs and symptoms of
with under- and overhumidification, the technical
inadequate humidification and the need for humidity
hazards associated with humidity therapy are related
therapy. If a spontaneously breathing patient on
to the functioning of the humidity devices.
oxygen therapy presents with a dry nonproductive
cough, nasal bleeding, and complaints of throat • Unheated humidification devices, such as
dryness or discomfort, a lack of humidity may be the bubble humidifiers and heat and moisture
cause. the respiratory therapist has the responsibility of exchangers, are simple in their design and
providing an appropriate humidification device. require minimal assembly. The respiratory
The RT must also recognize whether a patient with therapist should inspect these devices for
a mechanically ventilated artificial airway is receiving cracks or manufacturing defects before setting
poorly humidified gas. Evidence of the need for them up.
• Once a device has been connected to the oxygen patient’s airway. If heated wire circuits are used
delivery device, it must be checked for proper in conjunction with a heated humidifier, the
functioning, and the patient must be assessed for respiratory therapist must ensure that the
any discomfort or adverse effects. temperature settings are correct and that
• Heated units that provide humidification to the circuit is properly eliminating excess
patients receiving medicated gas therapy can condensation.
impose a risk if they are incorrectly set up or
improperly monitored.
General Principles of
Before connecting a patient to any electrical
humidity device, the respiratory therapist should Humidifying Devices
inspect the humidifier for damaged or worn parts to Many humidifying devices are available, and they
reduce the risk of electrical shock. have a variety of designs and offer a range of humidity
capabilities. The respiratory therapist needs to be
• Equipment that is powered by electricity must
familiar with the basic designs and to know how
meet the Underwriters Laboratory (UL) compli-
each affects performance in order to make appropriate
ance for power specifications, conduction, and
selections in various clinical situations.
leakage current before being approved for
medical use.
• The power plug should be grounded, intact, and FACTORS AFFECTING EFFECTIVENESS
unmodified.
Several factors determine the effectiveness of a humid-
• The device should have an up-to-date inspection
ity device. The goal may be to achieve the same RH
label from the hospital’s biomedical engineering
as that of the ambient air when delivering dry medi-
department, which certifies that the equipment
cated gases to a spontaneously breathing patient or to
has passed the minimum standards for electrical
provide heated humidity that is near BTPS when
safety as set by the National Fire Protection
bypassing the upper airway. Whatever the goal,
Association (NFPA). The NFPA 1999 norms
the humidification system has to meet certain
require that electrical leakage be less than
requirements:
300 microamps and that the electrical ground
be less than 0.5 ohms.7 • It should comply with ANSI standards.
• The device should be cleaned and properly • The humidity output is determined, in part, by
packaged to discourage cross-contamination. the temperatures of the water and of the carrier.
• Once a heated humidifier is in place, the RT’s Heating the water increases the gas’s water-
responsibility is to monitor its functioning. carrying capacity. Thus, a heated humidifier is
much more effective at achieving BTPS than
The respiratory therapist has other responsibilities
is a cool humidifier.
when using humidifying equipment.
• The length of time that the water and gas are in
• Most of the humidity devices used today are contact with each other also affects humidity
fully disposable or have disposable components, output. Exposing the gas to water for a longer
such as the humidity chamber used with heated period of time gives the water molecules a better
humidifiers. The respiratory therapist must chance of being picked up by the carrier gas.
inspect all disposable as well as nondisposable So, if the time a gas is in contact with water is
equipment to avoid risks associated with increased, the water vapor content is increased.
defective or damaged parts. • Contact time is regulated by the liter flow of gas
• Continuous water feed systems and the level of through a humidifying device. So, as liter flow is
water in the humidifier chamber must be increased through a humidifying device, the
checked, and the amount of condensation exposure time is decreased and the less saturated
occurring in the circuit must be monitored. Any the gas is when it reaches the patient.
build-up of water in the circuit can cause an • Humidifier design, such as depth of the water
increase in the patient’s work of breathing and reservoir, also affects exposure time.
add to the risk of inadvertent lavage of the • The surface area between the gas and the water
patient’s airway when the circuit or the patient is has its effect. The greater the surface area is of the
repositioned. gas-liquid interface, the greater is the chance of
• The temperature of the chamber and of the increasing humidity levels. Devices that encour-
circuit proximal to the airway must be moni- age increased surface area can deliver fully
tored to prevent overheating or underheating the saturated gases.
TYPES OF HUMIDIFIERS water and carried on to the patient via a low-

Humidifiers can be categorized according to the type of flow oxygen-delivery device, usually a nasal
gas flow system with which they are used. cannula.
• Low-flow humidifiers are used with low-flow The design of the capillary tube may vary and affect
oxygen-delivery devices and are limited in the the amount of RH delivered. The simplest of bubble
amount of humidity they provide. Because a humidifier designs and the lowest in humidity output
patient on a low-flow oxygen device still entrains is the capillary tube with an open end. RH is also
room air with each breath, the low-flow humidi- affected by the liter flow of the gas and the temperature
fier is only partially providing humidification. In of the room. As flow rates are increased or room
these systems, the volume of dry medical gas temperature is increased, the RH of the gas delivered
that is being humidified represents only a to the patient is decreased.
portion of the patient’s total inspired volume
of air; the remainder is entrained from the Diffuser Humidifier. The diffuser humidifier is based on
surrounding room air. the principles of the bubble humidifier but has a
• High-flow humidifiers are used with high-flow different capillary tube design. The diffuser humidifier’s
oxygen-delivery devices and are responsible for capillary tube has a plastic or porous metal diffuser at
providing the total volume of inspired gas going the end. The diffuser increases the number of bubbles
to the patient. Therefore, they should meet the created below the water surface, thereby increasing the
patient’s total needs for RH. surface area of the liquid-gas interface. Because of the
larger surface area of the liquid-gas interface, this
Table 21-5 lists the devices available for use with humidifier is more efficient in providing humidity
low-flow and high-flow systems. with a low-flow oxygen device than is the bubble
humidifier (Figure 21-1A and B).
Bubble Humidifier. The bubble humidifier is designed
to create bubbles below the surface of water; the Jet Humidifier. The jet humidifier, available as a
bubbles increase the contact time and surface area of nondisposable or disposable bubble humidifier,
the liquid-gas interface. It is the most commonly used applies Bernoulli’s principle (Chapter 3) with an
disposable humidifier with low-flow devices. Several underwater jet. The capillary tube is designed to direct
designs are available; all achieve an RH range of gas to the bottom of the reservoir bottle, passing
about 33–40%. through the jet and creating an aerosol. The bubbles
All bubble humidifiers incorporate a capillary tube containing the aerosol droplets now pass through a
submerged in a reservoir of water. diffuser before floating to the surface and being carried
• The reservoir bottle cap is fitted with a connector to the patient. This design enhances the efficiency of
that attaches to a gas source, such as a flowmeter. this type of humidifier by increasing both the time and
• Gas flows through the capillary tube and is amount of the gas and water interface. The jet humidi-
directed to the bottom of the bottle, where fier is designed for use with a low-flow device.
bubbles are created.
• As the bubbles travel upward, they pick up water Passover Humidifier. The passover humidifier, a high-
vapor, which is released at the surface of the flow humidifier, is the simplest in design. As its name
implies, gas simply passes over the surface of a con-
tainer of water. The gas is not diverted beneath the
TABLE 21-5 Types of humidifiers by flow water to increase the amount of contact time, nor is the
delivery gas-liquid interface surface area increased. Humidifica-
tion occurs through simple evaporation; molecules of
Low-flow humidifiers water simply move from the surface of the water into
Bubble humidifier the gas flowing above it. This type of humidifier has a
Diffuser humidifier very low efficiency and cannot provide gas at BTPS.
The humidity output from a passover humidifier is not
Jet humidifier
suitable for humidification when the upper airway
High-flow humidifiers has been bypassed. Furthermore, humidity can be
Passover humidifier increased only by reducing the flow, or heating
Heated, high-flow, high-humidity device the water, or both.
Wick humidifier
Wick Humidifier. Modifications to the earlier design of
Heat and moisture exchanger the simple passover humidifier have led to several
Inlet
Outlet
Reservoir
Diffuser
(A) (B)
FIGURE 21-1 (A) Bubble humidifier with diffuser. (B) Schematic of a diffuser humidifier.
CASE STUDY 21-1

The night shift therapist in a 200-bed community 2.5 Lpm. Her respiratory rate is 25 breaths per minute,
hospital has just been called to the third floor to and her breathing is mildly labored. The therapist
assess a patient who is complaining of breathing introduces himself while taking note of the pulse
discomfort. oximetry readings, which show a pulse of 110 and
T. S. is a 65-year-old female who was admitted an SpO2 of 91% (SpO2 is oxygen saturation as
two nights ago through the emergency department measured by a pulse oximeter). The RT observes
with a diagnosis of acute exacerbation of COPD. A dried bloody secretions around her nares and on the
review of her chart for current respiratory orders nasal cannula. Her breath sounds are diminished
reveals an order for oxygen therapy at 2.5 Lpm via a but free of wheezing or rhonchi. When asked to
nasal cannula. She is also receiving bronchodilator cough, she explains that her throat is very dry and
therapy every 3 hours. The last treatment was given irritated and that it hurts to cough.
1 hour ago.
Questions
Her most recent arterial blood gas analysis
shows pH 7.37, PaCO2 60 and PaO2 58, HCO3 34, 1. On the basis of the RT’s assessment, what is
SaO2 89% when on a nasal cannula at 2 Lpm. causing Ms. Simpson’s breathing discomfort?
Upon entering the room, the therapist notes 2. According to the hospital policy, oxygen orders
that Ms. Simpson appears mildly short of breath. for flow rates of less than 3 Lpm do not require
The nasal cannula is directly connected to the additional humidification. On the basis of this
nipple adaptor on the flowmeter, which is set at policy, what do you recommend?
Reservoir feed
system
Inlet Outlet
Wick Wick
Heaters Heaters
Float Constant
water
level
FIGURE 21-2 A Bird wick humidifier.
models of humidifiers that provide greater humidity

outputs and higher RH, making them ideal for use with
mechanical ventilation when the upper airway is
bypassed.
The so-called wick humidifiers are designed for
high-flow devices. The addition of heat from an
electrical plate or heating element increases the water-
carrying capacity of the dry gas, which enters the wick
chamber. Porous absorbent paper or water-saturated
cloth in the chamber provides greater surface area and
good conditions for humidifying dry gas (Figure 21-2).
The Inspiron Vapor-Phase humidifier, for example, uses
a hydrophobic wick that allows only water vapor to
pass through it and efficiently provides 100% RH. The
liquid chamber remains separate from the gas chamber,
preventing any water from passing through the wick. FIGURE 21-3 Heated wick humidifier.
This design offers some protection against microbial Courtesy of Fisher & Paykel Healthcare, Inc.
growth.
Other wick humidifiers are designed for use with
wick paper that is fully saturated with water. A continu-
ous water feed system keeps the paper wick moist, All these units incorporate nondisposable heating
thereby providing continuous humidity to the airways. elements with servocontrols to regulate temperature
The Fisher & Paykel Model MR 850 heated humidifier and disposable humidification chambers.
is a wick humidifier with these features; it can provide
100% RH (Figure 21-3). Heat and Moisture Exchanger. Heat and moisture
Some wick humidifiers also include spiral vanes to exchangers (HMEs) use the effects of airway physiology
increase surface area and to enhance humidification to provide humidification with high-flow systems to
capabilities (Figure 21-4). The Bear VH-820 humidifier patients with an artificial airway. Sometimes referred
uses this spiral design to increase the surface area and to as passive humidifiers or artificial noses, HMEs mimic
contact time of water to gas in the chamber, enabling the airway’s exchange of heat and moisture during
this humidifier to provide 100% RH. inspiration and expiration. An HME is placed close to
Humidified
gas
Dry gas
Humidity
chamber
Sensor port FIGURE 21-5 A heat and moisture exchanger (HME).
Vanes
out, of the exhaled gas because of the cooler
temperature and is absorbed by the HME. Thus
the HME is prepared to heat and humidify the
Refill Chamber cool, dry incoming gas for the next inspiration
Heater rod
(Figure 21-5).
A study by Vitacca and coworkers showed that
HME use improves the viscosity of secretions and
FIGURE 21-4 A wick humidifier with spiral vanes. reduces bacterial colonization in chronically tracheos-
tomized patients who breathe spontaneously.8 Use of
these devices during mechanical ventilation, however,
is contraindicated in certain situations, according to the
AARC CPG for humidification during mechanical
the patient’s artificial airway in line with a high-flow
ventilation.5
device. As gas travels from the high-flow device and
Heat and moisture exchangers are available in four
through large-bore tubing, it must pass through the
basic designs:
HME before being delivered to the patient.
• The one that uses the physical principles of heat
• During inspiration, as gas passes through the
and moisture exchange as just described is
HME, it picks up the heat and moisture pro-
simply called an HME.
duced by the previously exhaled breath, thereby
• Another, called a hygroscopic condenser humidifier
warming and humidifying the dry gas coming
(HCH), includes hygroscopic material.
from the high-flow system. The gas delivered to
• The design that functions as a filter is known as a
the patient is at 30°C and has as high as 100%
heat and moisture exchanging filter (HMEF).
RH at this temperature, depending on the design
• The fourth design incorporates both hygroscopic
of the HME.
properties and filtration: the hygroscopic condenser
• Upon exhalation, gas (which is at body
humidifier filter (HCHF).9
temperature) travels back through the HME,
this time giving up heat to the cooler HME. Table 21-6 compares terms that identify the
At the same time, water condenses, or rains different types of HMEs by material and by function.
TABLE 21-6 Terminology for heat and moisture exchanger devices

Type of Device Classified by Material Used Classified by Function
A device that uses physical methods Heat and moisture exchanger (HME) Heat and moisture exchanger (HME)
to exchange heat and moisture
A device that uses material treated Hygroscopic condenser humidifier Hygroscopic heat and moisture
hygroscopically (HCH) exchanger (HHME)
An HME device with a filter Heat and moisture exchanging filter Heat and moisture exchanging filter
(HMEF) HMEF)
An HCH device with a filter Hygroscopic condenser humidifier filter Hygroscopic heat and moisture
(HCHF) exchanging filter (HHMEF)
humidifying chamber. Whether the heat source

Best Practice is immersed, wrapped around, or beneath the
humidifying chamber, an RH of 100% can be
Contraindications to HME Use achieved.
The use of a heat and moisture exchanger during Still other types of heating systems provide heat
mechanical ventilation is or may be contraindi- and hydration with high-flow air or oxygen by nasal
cated for patients with: cannula. Traditionally, the use of a nasal cannula
implied low-flow delivery of supplemental oxygen in
• Thick, copious, or bloody secretions.
connection with a bubble humidifier. (These devices
• An expired tidal volume of less than 70%
are not heated and not capable of producing high
of the delivered tidal volume.
humidification.) However, advances in humidification
• A body temperature of less than 32°C.
technology and cannula design have led to the devel-
• A high spontaneous minute volume
opment of humidification systems that combine the
(10 Lpm).
advantage of 100% RH at body temperature with the
comfort of a nasal cannula.
In 2002, Vapotherm introduced the first high-flow
humidification system that accomplished this. Their
Best Practice newest device—Precision Flow, shown in Figure 21-6—
is capable of delivering a set temperature of 33–43o C
at gas flows of 1–40 Lpm with the use of a triple-lumen
HMEs with Inline Nebulizers
Heat and moisture exchanger devices must be
removed from the ventilator circuit during aerosol
drug therapy when the nebulizer or metered-dose
inhaler (MDI) is placed inline. Otherwise, the
HME filters and traps the aerosol, resulting in
little if any deposition of aerosolized medication
to the airway and interference with the therapeu-
tic effect.
HEATING SYSTEMS
Adjuncts to heated humidifiers are heating elements,
temperature control units, and heated wire circuits.
Their combined use improves the humidity output of
any humidifying device and reduces condensation in
the tubing.
Heating Elements. Several types of electrical heating

sources are available for heating the water contained in
the humidifier’s reservoir. Three basic designs are
described in terms of their location.
• Immersion heaters extend a heating element into
the water reservoir.
• Other heating elements, such as the Hudson RCI
Concha, wrap around the humidity chamber. In
this design, an aluminum cylinder (the Concha-
Column) that contains a column of water is
surrounded by a heating element.
• In other designs, heating plates located at the
base of a heating chamber provide the heat,
which is transferred by conduction between the FIGURE 21-6 Vapotherm Precision Flow.
heating plate and the base of the aluminum Courtesy of VapoTherm Precision FlowTM
patient delivery tube and integrated nasal cannula. temperatures. Temperature probes are placed as
Humidification is supplied using a continuous feed close to the airway connection as possible on the
reservoir of sterile water to a membrane cartridge that inspiratory limb of the ventilator circuit so that
incorporates a permeable membrane. Molecular water the monitored temperature reflects the condi-
vapor is permitted to pass into the gas stream, produc- tions closest to the patient.
ing an output of 95–100% RH. The triple-lumen • Nonservocontrolled units are capable of monitoring
patient delivery tube maintains gas temperature and the temperature of the heater but are not
minimizes condensation in the nasal cannula. Simi- influenced by the temperature at the patient’s
larly, Smith’s Medical AquinOx high-flow system airway. In these units, power to the heating
provides heated humidified oxygen therapy at flows of element will shut off if the temperature reaches
15–35 Lpm. This system utilizes a heating unit that 40°C. The temperature at the patient’s airway can
mounts directly to bottled sterile water. The particulate be monitored with an external probe, but the
recovery system reclaims large particles and returns respiratory therapist is responsible for adjusting
them to the humidification system, so only molecular the temperature of the heating element.
humidity reaches the patient through a nasal cannula.
Both servocontrolled and nonservocontrolled units
Both systems vary in alarm features and digital moni-
incorporate heater alarms to alert the RT of tempera-
toring, but only the Vapotherm device allows the use of
ture changes in the heating chamber, in addition to an
flows between 1 and 8 Lpm with the use of their
alarm-activated heater shutdown.
low-flow cartridge, which is suitable for neonatal and
pediatric use.10
Heated Wire Circuits. The advancement of humidifier
design has led to improvements in humidity output
Temperature Control Units. The temperature of these
through heating systems but has increased condensa-
heating elements is regulated by either servocontrolled
tion in the ventilator circuits tubing. As gas leaves the
or nonservocontrolled units.
humidifying chamber, it begins to cool because of the
• A servocontrolled unit is a microprocessor ambient temperature on the outside of the tubing. The
closed-loop system that allows a set parameter, distance between the heating chamber and the patient
such as temperature, to be compared with a connection can be more than 5 feet, which allows for
measured parameter and that makes an auto- significant cooling before the gas reaches the patient.
matic adjustment to maintain the preset value. The heating chamber temperature may be set as high as
Power to the heating element is adjusted when a 39°C, a temperature that allows for some cooling while
difference exists between the set and measured still providing gas near body temperature when it
CASE STUDY 21-2

The day-shift therapist is assigned to the surgical During the morning assessment, the therapist
intensive care unit (SICU). The patient in room 4 has notes that the patient’s heart rate is 100, total
been mechanically ventilated for the past 3 days. respiratory rate is 16 (10 mechanical breaths and 6
B. C. is a 55-year-old male who was admitted to spontaneous breaths), breath sounds reveal rhonchi
the SICU after a right upper lobectomy that required bilaterally, and the SpO2 is reading 96%. When the
postoperative mechanical ventilation. He has a RT attempts to suction, the secretions are thick,
history of emphysema and congestive heart failure. yellow, and difficult to clear from the airway.
His chart reveals a 50-pack-year smoking history. Inspection of the ventilator reveals that the humidi-
He has failed two weaning attempts and remains on fier has been bypassed, and an HME is in line with
the ventilator with an endotracheal tube in place. the ventilator circuit. The daily ventilator flow sheet
Respiratory orders include daily weaning shows that an HME has been used since the patient
parameters and ventilator settings to be adjusted was received in the SICU 3 days ago.
according to weaning protocol.
The morning arterial blood gases reveal pH
Questions
7.38, PaCO2 45, PaO2 88, HCO3– 28, and SaO2
95%, and an FIO2 of 50%. (SaO2 is the oxygen 1. What immediate action should you take to
saturation of arterial blood. FIO2 is the fractional rehydrate this patient’s airway?
concentration of oxygen; see Chapter 3.) 2. When is it appropriate to use an HME device?
reaches the patient’s airway. However, the drop in Both are primarily used to deliver water that is in
temperature decreases the capacity of the gas to carry aerosol form to the patient who presents with upper
water vapor thus causing water molecules to rain out airway swelling or who has a humidity deficit. Sterile
within the tubing. water is the solution of choice for continuous bland
Heated wire circuits attempt to maintain the set aerosols, whether cool or heated.
temperature throughout the circuit, preventing any A cool, bland aerosol with sterile water is usually
cooling and rainout in the tubing. Heating wires indicated when upper airway swelling is present. It has
wrapped inside the ventilator circuit are electrically been shown that breathing cool air causes a decrease in
connected to the heating unit close to where the tubing airway mucosal blood flow, resulting in vasoconstric-
leaves the heating chamber, and they continue to the tion and reduction in swelling that may occur postextu-
patient connection so that the tubing is unaffected by bation, or with upper airway disorders such as croup.13
the ambient temperature. Servocontrol guarantees In this situation, the cool aerosol is the most efficient if
regulation of the set temperature throughout the delivered continuously.
circuit. Reducing the condensation in the tubing Heated, bland aerosol is primarily used when
eliminates the need for frequent draining and lessens a humidity deficit exists or during hypothermic
the risk of infection for the patient and the respiratory situations.
therapist. Current practice has promoted the use of continuous
bland aerosols with sterile water to promote secretion
thinning and spontaneous removal of secretions
Therapeutic Use of Aerosol- through coughing or suctioning. However, studies to
determine the efficacy of continuous bland aerosol
Generating Devices delivery have concluded that there is no scientific
Aerosol-generating devices, called nebulizers, are evidence that bland aerosol therapy aids in the removal
selected for the delivery of bland or medicated aero- of airway secretions.14 The AARC CPGs for bland
sols. The choice of nebulizer is usually made by the aerosol administration and humidification during
ordering physician because of the varying therapeutic mechanical ventilation support these findings and
effects of such devices. A bland aerosol with sterile recommend use of cool bland aerosol for upper airway
water can be administered for 15 minutes every 4 hours swelling and heated bland aerosol for situations in
with an ultrasonic nebulizer, or it can be delivered by which a humidity deficit may occur.5,13
continuous administration with a large-volume Aerosolized saline administered intermittently is
nebulizer. Both would provide hydration to the airway; primarily indicated for sputum induction or as a
however, the deposition and thus the therapeutic effect diluent for aerosolizing pharmacologic agents. The
of the two devices differ significantly. AARC CPG for bland aerosol administration recom-
A physician who writes a request for aerosolized mends hypotonic or hypertonic salines for inducing
medication should state the method of delivery sputum specimens.12 Isotonic or normal saline is used
preferred for the patient. In some cases, hospital policy as a diluent, with medication being delivered in aerosol
on the type of nebulizing devices used may allow the form. In this situation, the saline, which is added to the
respiratory therapist to convert a patient from the medication in the appropriate aerosol-generating
initial device ordered to one that is equal in therapeutic device, acts as a carrier for the medication. Because
outcome or more clinically appropriate. As shown on dosages of respiratory drugs are so small, the saline
Table 21-4, bland or medicated aerosols can be created extends the aerosol delivery time and promotes
with a variety of nebulizing devices. Although the respi- deposition to the lower airway.
ratory therapist may not make the initial selection of Medicated aerosols deliver drugs that:
the aerosol-generating device, the RT is responsible for
• Reduce inflammation of the mucosal lining.
knowing the indications for use of each device in a
• Decrease bronchospasm of the airway smooth
given situation and whether another device is more
muscle.
appropriate and must be capable of evaluating a
• Prevent allergic response by inhibiting mediator
patient’s response to the therapy selected.11,12
release.
• Restore airway patency by promoting expectora-
INDICATIONS FOR AEROSOL THERAPY tion and clearance of secretions.
• Treat infectious processes through absorption of
The clinical indications for aerosol therapy are best
anti-infectious drugs.
explained on the basis of the type of agents used for
aerosolization. Most medicated aerosols are delivered intermit-
Bland aerosols can be delivered as either cool or tently and require fewer than 10 minutes to nebulize.
heated aerosols on a continuous or intermittent basis. Other therapeutic modalities require continuous
nebulization of certain drugs by means of special • The administration of bland aerosols can also
devices. Furthermore, medicated aerosol delivery to the lead to increased airway resistance due to
upper and lower airway is far more desirable than bronchoconstriction in patients with preexisting
systemic delivery because it allows for rapid onset of respiratory disease, such as asthma. Because the
the desired results without much of the systemic side airways of asthmatic patients are hyper-reactive,
effects that occur with oral or intravenous routes. The the mere administration of aerosol particles can
selection of a device that delivers aerosolized medica- induce bronchospasm.
tion to the lung parenchyma should be based on the • Cool aerosols tend to cause more airway reactivity
ability of the device to produce aerosol particles with than heated aerosols, presumably by the same
an MMAD of 0.5–3 μm.15 mechanism that causes exercise-induced
bronchospasm.
• Furthermore, aerosolized hypertonic saline is
HAZARDS known to be irritating to the airway and respon-
Infection from contamination should always be a sible for inducing bronchospasm in asthmatic
concern for the respiratory therapist but especially patients.16 A pretreatment administration of a
when aerosol therapy is administered. bronchodilator medication to reduce the likeli-
Aerosols can carry microorganisms to the patient hood of bronchospasm is recommended.
and deposit them in the airway. Therefore:
Hazards associated with medicated aerosols are
• The RT must follow aseptic technique when related to the side-effects of the specific drugs. Respira-
handling aerosol equipment during the initial tory therapists must be aware of the pharmacologic
set-up and when refilling the nebulizer reservoir. effect of any drug they administer on airway function,
• Tubing should be drained away from the nebu- cardiovascular response, onset, duration, clearance, and
lizer to prevent any microorganisms from compatibility with other drugs. See Chapter 7 for
contaminating the sterile water inside the specific drug information.
reservoir. Electrical hazards exist with electrically powered
• Water traps placed at the dependent portion of nebulizers. The respiratory therapist is responsible for
the tubing encourages drainage of excess water inspecting the device and monitoring its operation, as
away from the patient and away from the with any electrical device.
nebulizer, and they can aid in removal without
contamination.
Hazards associated with aerosol therapy may also General Principles of Aerosol-
occur as a result of the agent being aerosolized or the Generating Devices
nebulizer being employed. Aerosolization of bland
Aerosol generators are available in a variety of designs
agents delivers additional water to the airway’s mucosal
that determine the physical features, including the
lining. The amount of water delivered is based on the
particle size, of the aerosol. Nebulizer performance,
output of the nebulizer and the duration of exposure,
airway integrity, and the patient’s breathing pattern
which is related to the incidence of hazards. When
affect how and where the aerosol is deposited in the
deposition occurs in airways with dried retained
airway and thus determine the efficacy of the therapeu-
secretions, the dried secretions tend to absorb water,
tic intervention.17
causing the mucus to swell. This swelling usually does
not pose a problem if measures are taken to promote
mobilization and expectoration of the secretions after FACTORS AFFECTING AEROSOL DISTRIBUTION
aerosol therapy:
Several factors are involved in determining the distribu-
• Proper coughing techniques tion of aerosol particles in the respiratory system.
• Postural drainage and percussion
• Patient-related factors are the patient’s ventila-
• Possibly aspiration of secretions from the airway
tory pattern and airway integrity.
The continuous inhalation of aerosols with sterile • Device-related factors are nebulizer design and
water and normal saline presents possible hazards. type of delivery device.
• The nature of the aerosol particles and the effect of
• It can lead to overhydration, fluid weight gain,
the RH of the carrier gas determine aerosol
and electrolyte imbalance. Patients especially at
stability and the effect on distribution in the lungs.
risk are infants, patients with existing fluid
imbalances such as those in renal or congestive A very important factor in the distribution of
heart failure, and patients in pulmonary edema. aerosols in the lungs is the ventilatory pattern of the
spontaneously breathing patient. In the ideal breathing • Patients who are unable to use a mouthpiece,
pattern, inspiration is slow and deep, lasts 3–4 seconds, such as small children or unresponsive patients,
and is twice the normal tidal volume; at the end of may require a face mask, which delivers the
the inspiration, there is a 3–5-second breathhold aerosols to the airway but cannot eliminate nose
followed by a passive exhalation. The breathhold breathing.
slows the forward movement of the aerosol, making • A face tent or blow-by delivery device delivers
deposition into the distal airways possible. This aerosols to the immediate space surrounding the
pattern, although ideal, is difficult to achieve with a patient’s mouth, but the patient inhales a much
patient who is short of breath, but the RT can achieve it smaller amount of aerosol than with a mouth-
with mechanical manipulation of an artificially piece because the device is open to the room,
ventilated patient. allowing aerosol to escape.
The type of flow created during inspiration is • When the aerosol is delivered to an artificial
an aspect of the ventilatory pattern that affects airway, the gas flows directly into the patient’s
distribution. lungs. In this situation, the filtering effects of the
nose are bypassed as is any potential rainout in
• A laminar flow, which is achieved with slower
the oropharynx.
flow rates, promotes deeper deposition and
better distribution of aerosols. The performance of the nebulizer and the delivery
• A turbulent flow, which is achieved with faster device in which the aerosol particle is introduced to the
flow rates, causes inertial impaction of larger airway is enhanced by the respiratory therapist’s
aerosols into the upper airways. interaction with the patient. Although the initial choice
of nebulizer may be the responsibility of the physician,
Airway integrity also determines the distribution of
appropriate breathing instructions and the correct
aerosols in the lungs. A decrease in the lumen of the
choice of a delivery device are the sole responsibility of
airway restricts inspiratory flow, causing aerosol
the respiratory therapist.
deposition to occur in the upper airways, and hinders
lower airway distribution. Airway size may be decreased
in bronchospasm, in inflammation of the mucosal TYPES OF AEROSOL GENERATORS
lining, or in the presence of excess secretions. The
Aerosols can be generated from nebulizers that are
respiratory therapist can encourage lower airway
pneumatically, electrically, or manually powered. A
deposition by first assessing the airways for signs of
range of particle sizes can be produced from the
increased production of mucus. By employing methods
various types of nebulizers. The nebulizer reservoir size
for secretion clearance and following an ideal breath-
varies from a small, 5-mL container to one large
ing pattern, the RT can enhance aerosol distribution
enough to hold 1000 mL. Knowing how each nebulizer
even when bronchospasm is present.
operates and understanding the clinical use for each
Nebulizer design determines the initial size range of
help the respiratory therapist to properly administer
the aerosols. Certain nebulizers are designed to create
aerosol therapy to the patient who requires respiratory
particles between 2 and 5 MMAD, thereby delivering
care.
aerosols primarily to the lower airway. The internal
design of some nebulizers includes structures such as
Bulb Nebulizer. The bulb nebulizer has earned its place
baffles, which shatter the aerosol particles into smaller
in history as the first hand-held nebulizer that is
and smaller sizes, thereby preventing larger particles
from entering the main stream of gas flow to the
patient. The effect is to promote distribution in the
lower airway.
Best Practice
The delivery device used also affects aerosol distribu-
tion. These devices deliver aerosols through the mouth, Ideal Breathing Pattern
the nose and mouth, or an artificial airway. When administering aerosol therapy, the respira-
• Mouth breathing is encouraged because it lacks tory therapist should encourage the patient to
the filtering effects of the nasal cavity and follow an ideal breathing pattern by instructing
thereby prevents the filtering out of the aerosols the patient to:
that would occur if the patient were breathing • Inhale slowly and deeply through the
through the nose. Mouth breathing is usually mouth for 3–4 seconds.
accomplished with a mouthpiece. If necessary, • Hold the breath for 3–5 seconds.
noseclips are used to guarantee breathing • Exhale.
entirely through the mouthpiece.
manually powered. To use this nebulizer, the patient

must be able to squeeze a rubber bulb that forces Age-Specific Competency
airflow through a jet in the reservoir, which contains
the medicated solution. This action produces an Dry Powder Inhalers
aerosol that is directed out of the reservoir through the The dry powder inhaler is appropriate for patients
mouthpiece and to the patient. This nondisposable who can achieve an inspiratory flow greater than
device is designed for single-patient use and is ideal for or equal to 50 Lpm. Because children under the
home use. Patient instruction and coordination are age of 6 cannot achieve this inspiratory flow,
important. The bulb nebulizer has lost popularity since the use of a DPI for this age group is not recom-
the introduction of smaller devices, such as metered- mended.
dose inhalers, which eliminate the need for mixing Source: American Association for Respiratory Care. AARC clinical
solutions and are capable of producing smaller par- practice guideline: selection of an aerosol delivery device for neona-
ticles. Its use today is limited mostly to the nasal or tal and pediatric patients. Respir Care. 1996;40:1325–1335.
oropharyngeal application of medications.
Dry Powder Inhaler. Dry powder inhalers (DPIs) are

small, portable, manual nebulizing devices that are
Metered-Dose Inhaler. Metered-dose inhalers (MDIs)
activated by the patient’s inspiratory effort. Medication
are small pressurized canisters that are manually
supplied in a powder capsule is inserted into the DPI
activated to release medication suspended in a gas
container. The DPI is designed to break the capsule
propellant. The canister contains 80–300 doses of
open so that, when the patient places the mouthpiece
medication. When the patient depresses the canister, a
into the mouth and begins to inhale, the powdered
valve opens, releasing the medication particles with an
medication is available for delivery (Figure 21-7). This
MMAD of 2–4 μm (Figure 21-8). The gas propellant
device produces particles of 2–6 μm. The patient must
used until recently was chlorofluorocarbon (CFC),
generate enough inspiratory flow (greater than 1 L per
but, because of environmental concerns, CFC has
second) to guarantee delivery of medication to the
been replaced with other propellants such as
lower airways. These devices are especially popular for
hydrofluoroalkanes (HFAs). Once released from the
home use and are ideal for patients who cannot
canister, the propellant that carries the medication
coordinate activation and inspiration, as is necessary in
evaporates into the air, leaving the medication
other devices.
suspended as an aerosol.
Mouthpiece Drug exit port Non-CFC

Strip lid peeled Metered Dose Inhalers
Manifold from pockets
Index wheel
Hydrofluoroalkane
Empty Body Stronger
propellants
strip aluminium
can Salt form of drug
Base Contracting
wheel wheel substance
Novel valve features

Lever Reformulated
Innovative elastomers
canister filling
Dose indicator process
Coiled strip wheel
Thumbgrip
Pockets Outer case Unchanged
containing drug actuator
FIGURE 21-7 A cross-section of the discus inhaler, a FIGURE 21-8 The functional design of a non-CFC
commonly used dry powder inhaler. metered-dose inhaler.
Reprinted with permission of Glaxo Wellcome Reprinted with permission of Glaxo Wellcome
Baffle
Jet
Reservoir
FIGURE 21-9 Spacer used with a metered dose inhaler. Inlet

FIGURE 21-10 A small-volume nebulizer.
The use of MDIs for spontaneously breathing

patients requires proper patient instruction and
coordination of inspiration and activation to achieve
optimal deposition. Additional devices, referred to as
spacers or chambers, create a reservoir in which the
aerosol particle is held until being inspired by the
patient (Figure 21-9). Spacers eliminate the need for
synchronizing inspiration and activation. Most spacers
incorporate a one-way valve to ensure the flow of
medication from the canister through the reservoir to
the patient. Some have a signaling device that alerts the
patient to reduce inspiratory flow to prevent deposition
in the upper airway. Because MDIs are often needed for
mechanically ventilated patients, some spacers are
made for use with ventilator circuits.
Small-Volume Nebulizers. Small-volume nebulizers

(SVNs) come in a variety of designs that produce an FIGURE 21-11 Aero Eclipse II Breath Actuated Nebulizer.
aerosol with a particle size range of 1–5 μm. They are Courtesy of Monaghan Medical Corporation
primarily used in short-term intermittent delivery of

aerosolized medication, but they can also be used for
delivery of bland aerosols such as hypotonic saline for designed to decrease aerosol waste during exhalation
sputum induction. SVNs require a pneumatic source with the use of a one-way valve that directs gas flow
either from a central piping system or a cylinder to a away from the nebulizer chamber. This design prevents
flowmeter or from an electrical air compressor. Flow medication from being nebulized rather than the
rates of 6–8 Lpm are recommended to achieve optimal traditional practice of using an extension reservoir
particle size and aerosol output. Directing the gas flow tubing to trap medication during exhalation. BANs
through a jet within the 5–6-mL reservoir container nebulize only when the patient inhales, making them
causes a shearing effect of the liquid solution, produc- ideal for reduction in therapy time and wasted medica-
ing an aerosol that enters the mainstream of gas flow to tion (Figure 21-11).18 SVNs can be used for the patients
the patient (Figure 21-10). They are used in both of any age—from neonatal to geriatric patients. Com-
clinical and home settings. mon delivery devices are a mouthpiece attached to a
An SVN can be used as a handheld nebulizer for a Briggs T-adaptor, aerosol face mask, aerosol face tent,
spontaneously breathing patient or incorporated into a trach collar, and inline adaptation for IPPB and
ventilator circuit for delivery to a patient requiring ventilator circuits.
mechanical breaths. Additionally, SVNs are available as The Marquest Respigard II is an SVN that is
breath-actuated devices (BANs), such as the AeroEclipse designed to create a particle size with an MMAD of
II Nebulizer by Monahan Medical. These devices are 0.93 μm, which deposits more deeply in the lung
One-way
valve
Filter
Mouthpiece
One-way
valve Nebulizer
Reservoir
FIGURE 21-13 Large-volume nebulizer.
Courtesy of CareFusion
FIGURE 21-12 The small-volume nebulizer assembly of the

Marquest Respirgard II. concentration (FIO2; see Chapters 3 and 20) to the
patient. Air-to-oxygen ratios are fixed for each oxygen
percentage. For example, the air-to-oxygen ratio for
delivering an FIO2 of 40% is 3:1. This FIO2 setting
parenchyma than larger particles do. The SVN’s design allows 3 parts of air to be entrained for every 1 part of
is ideal when delivery of anti-infectious agents is oxygen. If the oxygen flowmeter is set at 10 Lpm, the
required (Figure 21-12). Within its nebulizer reservoir, amount of room air being entrained is 30 Lpm, making
this SVN produces an aerosol that is directed to the a total flow of 40 Lpm. Table 21-7 lists air-to-oxygen
patient through a circuit containing one-way valves. ratios of commonly used FIO2s.
The valves act as baffles to trap large particles and to Bland aerosol delivery is the most common use for
direct exhalation to a bacteria-filtering system on the LVNs. Most LVNs incorporate a jet venturi to entrain
expiratory limb. The system is designed to prevent any gas from the oxygen source and room air, allowing
aerosolized medication from escaping into the sur- precise mixing to achieve the desired FIO2. Medical
rounding environment. Molding Corporation’s Misty Ox Hi-Flo nebulizer is
an example of a disposable LVN capable of meeting
Large-Volume Nebulizers. Large-volume nebulizers flow rates of 42–77 Lpm at FIO2 ranges of 60–90%
(LVNs) are designed to provide long-term and continu- (Figure 21-14). The nebulizer is designed to fit a
ous nebulization of cool or heated bland aerosols as standard reservoir bottle. Depending on the flow rate
well as medicated aerosols. A variety of designs are
available, all with a large reservoir capable of holding
240–1000 mL of solution. Most LVNs are designed for TABLE 21-7 Air-to-oxygen ratios at
use with large-bore tubing connected to an aerosol commonly used fractional oxygen
delivery device such as an aerosol mask, face tent, concentrations
tracheostomy collar, or Briggs T-adaptor. Disposable
nebulizers are available for use with or without sterile Room Air/Oxygen Fractional Oxygen
water, such as the AirLife Prefilled Nebulizer or the Ratio Concentration (%)
Portex Unfilled Nebulizer (Figure 21-13). 25:1 24
The oxygen percentage varies among devices. Some 10:1 28
provide a range of 40–100%; others provide a range of
8:1 30
21–100%. A flow rate that exceeds the patient’s inspira-
tory flow rate is required for adequate aerosol delivery 5:1 35
and to meet the desired FIO2, usually above 25 Lpm. 3:1 40
The total flow through an LVN that incorporates a jet 1.7:1 50
venturi uses flow from the source gas (oxygen flowme-
1:1 60
ter) plus room air that is being entrained. The two
gases are mixed to provide a precise fractional oxygen 0:1 100
(A)
A. (B)
B.
FIGURE 21-14 The Misty Ox Hi-Flo large-volume nebulizer: (A) Assembly.
(B) Functional diagram.
and the set FIO2, this LVN can provide an aerosol

output of 30–50 mg/L with an MMAD of 3 μm. Age-Specific Competency
In certain situations, one nebulizer may not be
enough to meet a patient’s inspiratory demand. If the Nebulizer Interfaces
patient’s inspiratory demand is being met, the aerosol Depending on a patient’s age, which determines
continually flows from the delivery device even when ability and coordination, various devices can be
the patient increases inspiratory volume. If the aerosol used in conjunction with the SVN and MDI to
disappears when the patient inhales, there is not optimize drug delivery. These devices, referred to
enough gas flow through the device, and the patient as interfaces, are spacers, accessory devices with
draws from the surrounding room air to meet inspira- mouthpieces, and face masks. Patients younger
tory needs. The patient’s needs for humidification and than 3 years of age may not be able to use a
for oxygen are affected. mouthpiece; therefore, a face mask with a spacer
A solution to this situation, while maintaining the device for MDI use or a face mask for SVN use
same FIO2 setting, is to pair two oxygen flowmeters and may be necessary. Cooperative children over the
two LVNs with large-bore tubing that is connected to a age of 3 can receive aerosol therapy via an SVN
wye adaptor. Large-bore tubing is then attached to the with a mouthpiece and extension reservoir or via
third port of the wye, and the delivery device of choice an MDI with a mouthpiece and spacer.
can be used at the proximal end of the tubing. This
Source: American Association for Respiratory Care. AARC clinical
arrangement is referred to as a tandem set-up (Figure 21-15). practice guideline: selection of an aerosol delivery device for neona-
The two flowmeters should be set at the same flow rate, tal and pediatric patients. Respir Care. 1995;40:1325–1335.
and the two LVNs must be set at the same FIO2.
O2 inlet O2 inlet
Air
entrainment
Wye
adaptor
Large-volume Large-volume
nebulizer nebulizer
To patient
delivery device
FIGURE 21-15 Assembly and functional design of a tandem
large-volume nebulizer set-up.
FIGURE 21-16 HEART Nebulizer.

Continuous medicated aerosol delivery is indicated
Reprinted with permission of Westmed, Inc.
when aggressive care of bronchospasm is required. The
Vortran High Output Extended Aerosol Respiratory
Therapy (HEART) nebulizer is used during continuous that time, the design of ultrasonic nebulizers (USNs) has
bronchodilator nebulization therapy (CBNT). The medica- been perfected, and their use has been expanded from
tion and solution are placed inside a standard reservoir the hospital to the home. Ultrasonic nebulizers are
container capable of holding 240 mL. A mini unit with used in the hospital setting to deliver bland aerosols on
a 30-mL reservoir is also available. The HEART nebu- an intermittent basis. Smaller, more portable units are
lizer produces an aerosol particle size of 3.5–2.2 available for medication delivery in the home.
MMAD, which is optimal for the continuous delivery The USN is an electrically powered device that
of aerosols to the lower respiratory tract for up to 8 sends electrical current to a radio frequency generator.
hours (Figure 21-16), if the flow rate is set at 10 Lpm. The generator produces electromagnetic energy, which
Albuterol with normal saline solution is the recom- is conducted to a transducer through a shielded cable.
mended bronchodilator for CBNT. Medical centers In the transducer, a piezoelectric crystal converts
with the highest emergency room discharge rate and electrical energy from the radio frequency to mechani-
the lowest length of stay for patients treated for moder- cal energy in the form of sound waves. These high-
ate to severe asthma are using the following dosages of frequency sound waves travel through a water-filled
albuterol: chamber that acts as a medium for the sound waves,
transmitting them to the surface of water in the nebu-
• 3 mL or more per hour for status asthmaticus
lizer chamber, where they break the water into a fine
cases
aerosol (Figure 21-17).
• 2 mL per hour for severe asthma cases
Particles generated by a USN can range from 1 to
• 1 mL per hour for moderate asthma19
10 μm with an MMAD of 3 μm. The aerosol output
The patient should be reevaluated 1 hour after initia- from a USN can range from 60 to 100 mg/L. A fan in
tion of CBNT for improvement in bronchospasm and the USN creates the gas flow necessary to move the
pulmonary mechanics. The physician’s order must aerosol from the nebulizing chamber to the patient
include dosage, medication, flow rate, and duration of through large-bore tubing attached to a delivery device,
treatment. usually an aerosol mask or a mouthpiece. To increase
the aerosol output, adjust the amplitude of the sound
Ultrasonic Nebulizer. The use of ultrasonic sound waves by selecting an appropriate setting on the dial.
waves to produce aerosols began in the 1960s. Since The frequency of the sound waves, which determines
Inlet Outlet
Membrane Glass
sphere
Water reservoir
Outlet
Piezoelectric Inlet
Radio frequency Baffle
crystal
Generator
Radio frequency
cable Solution
FIGURE 21-17 An ultrasonic nebulizer.

FIGURE 21-19 A Babbington nebulizer.
the particle size produced, is preset by the manufac-

turer and cannot be adjusted. The DeVilbiss Ultra-Neb
continually bathed with a bland solution from the
99 is a USN used in the hospital setting for intermittent
reservoir above, an aerosol is produced (Figure 21-19).
use. Its fine aerosol and high-density output make it
Gas enters the hollow sphere from an inlet connected
ideal for lower respiratory tract hydration of dried
to a 50-psig (pounds per square inch gauge) source.
retained secretions and for sputum induction
The pressure in the inlet channel activates a siphoning
(Figure 21-18).
system in an adjacent channel that draws liquid in the
form of small bubbles up a capillary tube to the
Babbington Nebulizer. The Babbington nebulizer,
reservoir above the glass sphere. The bubble escalator
designed for long-term continuous use with aerosol
continually fills the reservoir and bathes the surface of
tents, is a pneumatically powered nebulizer that
the sphere with the solution to be aerosolized. Gas
incorporates a pressurized glass sphere. As the sphere is
pressure exits the sphere through a very small hole,
rupturing the thin sheet of water that coats the sphere,
creating a fine aerosol. A baffle positioned in the flow
of the aerosol further reduces the particle size.
The Maxi Cool nebulizer uses two glass spheres to
produce a high-density output of 60–70 mg/L with an
MMAD of 4 μm. Flow rates generated by the Maxi Cool
can be as high as 250 Lpm, making the unit ideal for
providing a moisture-rich enclosed environment, such
as a croup tent, while flushing out heat and exhaled
carbon dioxide.
Small-Particle Aerosol Generator. The small-particle

aerosol generator (SPAG) is a nebulizer specifically
designed for the administration of ribavirin, an antivi-
ral medication used in the treatment of respiratory
syncytial virus (RSV). This pneumatically powered
nebulizer is used in conjunction with an aerosol tent,
hood, or mask or in conjunction with a mechanical
ventilator. The source gas flows into a regulator set at
FIGURE 21-18 UltraNeb. 26 psig, and the regulator is connected to two flowme-
Courtesy of DeVilbiss Healthcare, Inc., Somerset, Pa. ters. One flowmeter directs gas into the nebulizer flask,
CASE STUDY 21-3

Outflow Drying
The respiratory therapist is covering a medical chamber
step-down unit in a university hospital. One of Nebulizer
the patients has been successfully weaned from
Pressure
mechanical ventilation and is currently on a 60%
regulator
LVN to a tracheostomy collar.
The patient, M. W., is a 60-year-old male who
was admitted 3 months ago in respiratory failure Compressed
due to Guillain-Barré syndrome. He was intubated Nebulizer gas Dryer
and placed on mechanical ventilation at that airflow airflow
time. He required a tracheostomy after 2 weeks FIGURE 21-20 The functional design of a small-particle
of mechanical ventilation. After a slow weaning aerosol generator.
process, he was placed on a 60% continuous
bland aerosol with an LVN to a tracheostomy
collar 24 hours ago.
The respiratory orders state that the patient
is to remain on a 60% LVN as tolerated. The Summary
physician wants to be notified if the respiratory Humidity is described in terms of its presence in our
therapist feels that an increase in FIO2 is environment as absolute humidity (AH) and relative
necessary. humidity (RH), according to the amount of water
The patient’s morning arterial blood gas vapor present and expressed as water vapor content or
analysis revealed pH 7.39, PaCO2 50, PaO2 55, water vapor pressure. Temperature affects a gas’s ability
HCO3 –29, SaO2 88%. to carry moisture: As temperature increases, a gas can
During the morning assessment, the RT carry more water vapor; as a gas cools, its capacity to
notices that Mr. W. appears to be short of breath carry water vapor decreases and condensation, or
and has a respiratory rate of 30 breaths per rainout, occurs.
minute. His pulse oximetry readings show a pulse This relation also pertains to inspired gas as it
rate of 102 and an SpO2 of 88%. Although the travels through the respiratory system. Humidity in our
LVN is set up correctly, all of the aerosol disap- respiratory system, body humidity, is the water vapor
pears from the exhalation port of the tracheos- content required to fully saturate alveolar air at normal
tomy collar when the patient inhales. The body temperature. The difference between the body
therapist calculates the total flow from the LVN humidity and the absolute humidity of inspired air is
based on the air-to-oxygen ratio of 1:1 at a flow called the humidity deficit.
rate of 15 Lpm. Maintaining adequate humidity in the respiratory
system is the role of the respiratory mucosal lining.
Questions When inspired gases are underhumidified, such as
1. What is the total flow being delivered to the those that occur in the delivery of anhydrous gases, the
patient? Is the flow meeting the patient’s mucosal lining must give up water to the inspired gas
inspiratory demand? to reach body temperature pressure saturated (BTPS).
2. How can the RT maintain the same FIO2 Over time, this humidity deficit can lead to the reten-
setting and guarantee a flow rate that meets tion of thick dried secretions, atelectasis, pneumonia,
the patient’s inspiratory demand? and pulmonary compromise. When inspired gas is
overhumidified, as may occur when the gas contains
aerosols or is at a temperature higher than body
temperature, water drops out of suspension onto the
which holds approximately 300 mL of the medication mucosal lining, and excess body fluid is retained. This
solution. Here, the aerosol particles are produced and fluid retention leads to an increased depth of the
travel to a drying chamber. The other flowmeter directs aqueous sol layer and affects ciliary action in the
gas into the drying chamber, which functions to removal of secretions.
dehumidify and reduce the size of the aerosol particle Aerosols are liquid or solid particles that are
to approximately 1.3 μm within the drying chamber. suspended in a gas or a substance that contains such
The aerosol is then directed through large-bore tubing particles. Aerosols can occur naturally in the environ-
to the delivery device (Figure 21-20). ment or in a chemical reaction, or they can be created
influenced by the kinetic activity of the aerosol particle

CASE STUDY 21-4 and the concentration of the particles. The instability of
an aerosol particle in the respiratory tract leads to
The respiratory therapist is called to the emer- deposition in the upper or lower airway or in the lung
gency room of a large university hospital for a parenchyma. Where deposition occurs and the type of
patient diagnosed as status asthmaticus. When agents being used determine the therapeutic effective-
the RT arrives, the nurse assigned to the patient ness of the aerosolized solution.
advises that the patient received three broncho- The use of humidity devices in the clinical setting
dilator treatments by SVN while in transit to the is the responsibility of the respiratory therapist and
hospital. must be considered when administering dry medical
Ms. K. M. is a 40-year-old woman with a gases. Supplemental humidity in low-flow systems that
long history of asthma who has required two deliver gas to the upper airway should provide a
intubations in the past 2 years. Ms. M. is unable minimum output of 10 mg/L, whereas a high-flow
to speak because of her extreme shortness of system delivering gas that bypasses the upper airway
breath, but the nurse states that the patient uses should provide a minimum of 30 mg/L. Hazards of
her MDI bronchodilator four times a day. She humidity therapy include excessive delivery of heat and
stopped using her corticosteroid inhaler 2 weeks moisture, electrical malfunctions, and risk of infection.
ago because she felt she didn’t need it. The effectiveness of humidity devices depends on the
The emergency room physician has asked temperature of the water and gas, the length of contact
the RT to measure peak flows pre- and time, and the surface area of the liquid-to-gas interface.
postbronchodilator and to administer an aerosol The types of low-flow humidity devices are various
treatment with a bronchodilator via an SVN types of bubble humidifiers such as the diffuser and jet
every 30 minutes. humidifier. High-flow devices are the passover and
No lab orders are available. wick humidifiers and the heat and moisture exchang-
The patient is obviously unable to perform a ers. These systems can deliver humidity that is cool or
peak flow maneuver. As the therapist begins heated using heating elements that are servocontrolled
administration of the aerosolized medication, the or nonservocontrolled. Systems such as the Vapotherm
patient is taking rapid shallow breaths at a rate and Aquinox are high-flow, high-humidity, heated
of 40 per minute. Her breath sounds are very systems designed for use with a nasal cannula. Heated
diminished, with posterior lower lobe wheezing wire circuits are an adjunct to humidification systems
bilaterally. The patient’s cough is weak, dry, and that attempt to eliminate the excess condensation due
nonproductive. Before it is time for the next to changes in temperature within the ventilator circuit.
treatment, the nurse calls the RT again, explain- The use of aerosol-generating devices in the clinical
ing that the patient is extremely short of breath. setting requires a physician’s order in most hospitals or
The patient’s dsypnea is slightly relieved during a respiratory care department protocol to allow the
the second treatment, but the bronchospasm respiratory therapist to choose the type of nebulizer
persists, and the physician calls for another that will meet the patient’s needs. Aerosols are deliv-
treatment. ered as bland solutions or as medicated solutions, for
intermittent therapy or continuous therapy, to achieve
Questions a variety of desired effects. Hazards of aerosol therapy
1. What alternative treatment should the are contamination, overhydration, swelling of dried
therapist suggest at this time? secretions, medication side effects, and shock from
2. What equipment is needed to administer a electrically powered devices. Aerosol deposition in the
CBNT, and what information should the airway is determined by the patient’s ventilatory
physician’s order include? pattern, the integrity of the airway, nebulizer design,
and delivery device. The types of aerosol generators are
bulb nebulizers, dry powder inhalers, metered-dose
inhalers, small-volume nebulizers, large-volume
artificially. How long an aerosol particle can remain in nebulizers, ultrasonic nebulizers, Babbington nebuliz-
suspension depends on its size. Size, in turn, is affected ers, and small-particle aerosol generator (SPAG) units.
by the temperature and RH of the carrier gas and by the The respiratory therapist must understand the
tonicity of the solution being aerosolized. Equipment principles of hydration of the respiratory tract to
design determines the mass median aerodynamic maintain a humidity balance in a patient’s airways and
diameter (MMAD) of the artificially created aerosol, must determine the need for medication delivery to the
thus determining its initial size. Aerosol stability is also airways of the compromised patient. In aerosol and
humidity therapy, selecting the most appropriate device, 5. If inspired gas in the lower airway contains
monitoring the functioning of the device, assessing the 43.9 mg/L water vapor and the absolute humidity
patient, and making any necessary changes are the of the room at 21°C is 9 mg H2O/L, what is the
responsibilities of the respiratory therapist. humidity deficit between the alveolar and
ambient air?
a. 43.0 mg H2O/L
Study Questions b. 34.9 mg H2O/L
REVIEW QUESTIONS c. 52.9 mg H2O/L
d. 61.2 mg H2O/L
1. What are the differences between providing humidifi-
6. What is the RH if the water vapor content of room
cation and delivering an aerosol to a patient’s airway?
air at 24°C is 21.8 mg/L and the AH is 12.8 mg
2. When dehydration of the mucosal lining occurs, H2O/L?
what conditions may result? a. 50%
3. Which low-flow humidification device provides the b. 55%
greatest amount of relative humidity? c. 59%
4. Which aerosol device provides the greatest amount d. 60%
of absolute humidity?
5. What are the benefits of providing supplemental CRITICAL-THINKING QUESTIONS
humidity to a patient receiving oxygen therapy?
1. J. A. is a frequently admitted patient with a long
6. What are the benefits of administering aerosolized history of cystic fibrosis. His current chief com-
medication via the inhaled route? plaint is an increased production of thick secre-
tions that he is unable to clear. The physician
would like to supplement his oxygen on the basis
of an oxygen saturation of 88%. What device
1. Which of the following heating devices could be would you recommend?
used to increase the temperature of water in a 2. J. A.’s condition deteriorates, and he requires a
nondisposable large-volume nebulizer? higher FIO2. The physician orders an oxygen
a. hot plate concentration of 60% but does not order a specific
b. immersion rod device. What devices could deliver a 60% FIO2?
c. heating chamber Which device would the RT recommend, and why?
d. heated wire circuit
3. J. A. now requires intubation and mechanical
2. Which aerosol delivery device cannot be used to ventilation. What devices can be used in conjunc-
administer medication? tion with a mechanical ventilator, and which
a. small-volume nebulizer device would be most suited for this patient?
b. metered-dose inhaler with spacer
4. After selecting a humidification device to be used
c. ultrasonic nebulizer
with mechanical ventilation, what should the RT
d. Babbington nebulizer
inspect? What precautions should the RT take
3. Which of the following devices is capable of before connecting this device to the patient?
delivering 100% RH with the use of a nasal can-
nula?
a. bubble humidifier References
b. ultrasonic nebulizer 1. Jackson C. Humidification in the upper respiratory
c. Vapotherm hydration system tract: a physiological overview. Intensive Crit Care
d. Fisher & Paykel wick humidifier Nurs. 1996;12:27–32.
4. Heated wire circuits are used with mechanical 2. Williams R, Rankin N, Smith T, Galler D, Seakins P.
ventilation for all of the following reasons except to: Relationship between the humidity and tempera-
a. reduce the amount of condensation in the ture of inspired gas and the function of the airway
tubing. mucosa. Crit Care Med. 1996;24:1920–1929.
b. maintain an even temperature from the exit port 3. Omari C, Schofield BH, Mitzner W, Freed AN.
of the humidifier to the patient connection. Hyperpnea with dry air causes time-dependent
c. prevent overhydration. alterations in mucosal morphology and
d. eliminate the need for frequent drainage of bronchovascular permeability. J Appl Physiol.
excess water in the circuit. 1995;78:1043–1051.
4. Ronnestad I, Thorsen E, Segadal K, Hope A. 19. Ferrante S, Painter E. Continuous nebulization: a

Bronchial response to breathing dry gas at 3.7 Mpa treatment modality for pediatric asthma patients.
ambient pressure. Eur J Appl Physiol. 1994;69:32–35. Pediatr Nurs. 1995;21:327–331.
clinical practice guideline: humidification during
mechanical ventilation. Respir Care. 1992;37: Suggested Readings
887–890. American Association for Respiratory Care. AARC
6. Chatburn R, Primiano FP. A rational basis for clinical practice guideline: selection of an aerosol
humidity therapy. Respir Care. 1987;32:249–254. delivery device for neonatal and pediatric patients.
7. National Fire Protection Association. NFPA 1999: Respir Care. 1995;40:1325–1335.
Standard for Health Care Facilities. Quincy, MA: Branson RD, Davis Jr K. Evaluation of 21 passive
American National Standards Institute/National humidifiers according to the ISO 9360 standard:
Fire Protection Association; 1999. moisture output, dead space, and flow resistance.
8. Vitacca M, Clini E, Foglio K, Scalvini S, Marangoni Respir Care. 1996;41:736–743.
S, Quadri A, Ambrosino N. Hygroscopic condenser Branson RD, Davis Jr K, Brown R, Rashkin M. Compari-
humidifiers in chronically tracheostomized son of three humidification techniques during
patients who breathe spontaneously. Eur Respir J. mechanical ventilation: patient selection, cost, and
1994;7:2026–2032. infection considerations. Respir Care. 1996;41:
9. Branson R. Humidification for patients with 809–816.
artificial airways. Respir Care. 1999;44:630–641. Branson RD, Campbell RS, Johannigman JA, Ottaway
10. Walsh, B. Comparison of High Flow Nasal Cannula M, Davis Jr K, Luchette FA, Frame S. Comparison of
Devices. Respir Care. 2006 AARC Open Forum conventional heated humidification with a new
Abstract. active hygroscopic heat and moisture exchanger in
11. American Association for Respiratory Care. AARC mechanically ventilated patients. Respir Care.
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administration of bronchodilator, and evaluation Chatbaurn, R. A new system for understanding nebu-
of response to therapy in mechanically ventilated lizer performance. Respir Care. 2007:52:1037–1050
patients. Respir Care. 1999;44:105–113. Corkery K. Inhalable drugs for systemic therapy. Respir
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blood flow responses to temperature and humidity Chew N, Cole CH, Dhand R, Fink JB, Gross NJ, Hess
of inhaled air. Respir Physiol. 1996;105:235–239. DR, Hickey AJ, Kim CS, Martonen TB, Pierson DJ,
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CHAPTER 22
Hyperinflation Therapy
John A. Rutkowski
OBJECTIVES
• State the physiological basis for hyperinflation therapy.
• List the indications for and discuss the appropriateness of the three hyperinflation therapy modalities: sus-
tained maximal inflation, continuous positive airway pressure, and intermittent positive pressure breathing.
• Identify the hazards and contraindications of the various modalities used for hyperinflation therapy.
OUTLINE
Key Definitions, Concepts, and Contraindications
Professional Standards Hazards and Complications
American Association for Respiratory Care Clinical Positive Airway Pressure
Practice Guidelines
Procedure
Historical Perspectives
Contraindications
Development of Positive Pressure Breathing
Hazards and Complications
Hyperinflation Therapy Limitations
Physiologic Basis
Intermittent Positive Pressure Breathing
Collateral Channels
Procedure
Deep Breathing Techniques Specific Indications
Glossopharyngeal Breathing Contraindications
Sustained Maximal Inflation Hazards and Complications
(Incentive Spirometry)
Limitations
Procedure
Outcomes Assessment
Specific Indications
626
CHAPTER 22 ■ Hyperinflation Therapy 627
KEY TERMS
atelectasis glossopharyngeal breathing pleural pressure
biofeedback (GPB) positive airway pressure (PAP)
collateral ventilation hyperinflation surface tension
continuous positive airway incentive spirometry (IS) sustained maximal inflation
pressure (CPAP) inspiratory capacity (IC) (SMI)
elastic recoil intermittent positive pressure total lung capacity (TLC)
functional residual capacity (FRC) breathing (IPPB)
P
eriodic deep breaths are essential for Key Definitions, Concepts, and
maintaining adequate bronchial hygiene.
A normal breathing pattern incorporates Professional Standards
periodic deep breaths called sighs. Patterns A hyperinflation maneuver is a breathing pattern that
of shallow, monotonous tidal ventilation without emphasizes an inflation to total lung capacity (TLC)
deep breaths lead to a gradual collapse of alveoli, and maintenance of a normal functional residual
beginning within an hour. If the pattern is maintained capacity (FRC). Ideally, high alveolar inflating pres-
for several hours, gross atelectasis develops, and sure is exerted for a long period of time, resulting in the
reinflation may be difficult.1 The collapse of alveoli largest possible inhaled tidal volume.1 The alveolar
leads to impaired gas exchange and retention of inflating pressure can be achieved with positive or
secretions. If allowed to progress, pneumonia may negative pressure. The inhaled volume should be
result. measured with either method.
This chapter reviews therapeutic modalities The relationship among three forces determines
collectively referred to as hyperinflation therapy. Most the functional residual capacity.2
patients can achieve adequate hyperinflation without
assistance. Some patients may achieve better results • Pulmonary atelectasis is the collapse of lung
with the use of a biofeedback device; others may tissue.
require the assistance of a device capable of generating • The elastic recoil of the lungs and chest wall,
positive pressure. The selection of appropriate interven- combined with surface tension, tends to cause
tions based on patient assessment in conjunction with collapse of the lung.
multidisciplinary care plans is a vital role of the respira- • Pleural pressure (normally negative) provides a
tory therapist. countering force that tends to expand the lung.
Unfortunately, these interventions are all too These concepts are illustrated in Figure 22-1.
often considered routine. Effective hyperinflation Atelectasis may occur owing to decreases in
therapy demands that patients are assessed and appro- distending pressure (compressive atelectasis) or as the
priate interventions initiated, coached to achieve the result of airway obstruction (obstructive atelectasis).
best results, and monitored to determine clinical
impairment and adjustments in care plans. Positive • Compressive atelectasis is seen in patients who
outcomes may shorten length of stay, reduce admis- have suffered pleural effusion, pneumothorax,
sion or readmission to critical care units, improve hemothorax, or similar conditions.
patient satisfaction, and contribute to reduced • Obstructive atelectasis is the result of a complete
expenses. obstruction of an airway.
Although hyperinflation therapy has application in Atelectasis is associated with increased physiologic
bronchial hygiene, this chapter generally addresses the shunting and reduced FRC. Although atelectasis has a
prophylaxis and treatment of alveolar collapse. Because number of causes, it is frequently associated with the
airway obstructions can result in the development and postsurgical period. If atelectasis is caused by mucus
progression of atelectasis, bronchial hygiene therapies obstruction of the airway, the techniques utilized to
often play a significant role in the prophylaxis and enhance the removal of secretions (see Chapter 23) may be
treatment of alveolar collapse. helpful in correcting conditions that lead to lung collapse.
Negative pleural Surfactant lining

pressure Elastic recoil
Gas Collateral
diffusion ventilation
A. Forces in the normal lung B. Lack of distending forces on the lung C. Localized airway obstruction
−P
Increased
surface
tension
D. Insufficient surfactant E. Negative airway pressure F. Increased lung elastic recoil

FIGURE 22-1 Models illustrating mechanisms involved in pulmonary atelectasis.
Courtesy of Respiratory Care, Dallas, Texas
AMERICAN ASSOCIATION FOR RESPIRATORY Historical Perspectives

CARE CLINICAL PRACTICE GUIDELINES
Over the years, a number of approaches have been
A clinical practice guideline (CPG) is a systematically
taken to prevent or reverse lung collapse. These tech-
developed statement to help practitioners deliver
niques include:
appropriate care in specific clinical circumstances.
The guidelines serve to improve consistency and • Rebreathing of carbon dioxide or breathing of gas
appropriateness of care and as guides for education mixtures with concentrations of carbon dioxide
and research.3 CPGs dealing with hyperinflation great enough to stimulate increased minute venti-
therapy include the following: lation. The inhalation of gases with increased
carbon dioxide levels induces hyperventilation
• Directed Cough4 but primarily with increased respiratory rate.
• Incentive Spirometry5 • Resistive breathing devices (blow bottles), as
• Use of Positive Airway Pressure Adjuncts to shown in Figure 22-2.9 The patient must exhale
Bronchial Hygiene Therapy6 with sufficient force to move the water from the
• Intermittent Positive Pressure Breathing7 first container to the second. Resistive breathing
• Perspectives in Disease Prevention and Health devices are more likely to be successful if a deep
Promotion Update: Universal Precautions breath and a prolonged exhalation are incorpo-
for Prevention of Transmission of Human rated into the maneuver.9
Immunodeficiency Virus, Hepatitis B Virus, and
Other Bloodborne Pathogens in Health Care
Settings8
DEVELOPMENT OF POSITIVE
PRESSURE BREATHING
The guidelines review indications, contraindications, Intermittent positive pressure breathing (IPPB)
hazards/complications, and assessment of outcomes. was introduced into clinical practice in 1947.10 In the
To patient
Capillary
FIGURE 22-2 System to create resistance breathing. Pore of Kohn
years after its introduction, it attained broad accep-

Type l cell
tance, and its application increased with little regard
for its appropriateness. In 1974 at the Conference on
the Scientific Basis for Respiratory Therapy (the so-
called Sugarloaf Conference),11 it was generally con-
cluded that the clinical evidence could not support the
widespread use of IPPB, and the participants recom-
mended continued investigation into its effectiveness
and appropriateness. A few years later, at a conference Macrophage
on the use of in-hospital respiratory therapy,12 IPPB
was again identified as overused.
Subsequently, the Respiratory Care Committee of Type ll cell
the American Thoracic Society13 released guidelines for
FIGURE 22-3 Collateral ventilation channels: pores of
the use of IPPB, and the American Association for
Kohn.
Respiratory Care provided an assessment of its effec-
tiveness14 and clinical practice guidelines7 for its use.
• Bronchiole-alveolar channels called the canals of
Hyperinflation Therapy Lambert (Figure 22-4).
• Interbronchiolar communications.
Hyperinflation therapies are utilized primarily for the
prevention and treatment of pulmonary atelectasis. A number of investigators have related that complete
obstruction of an airway is not always followed by
alveolar collapse and that ventilation and gas exchange
PHYSIOLOGIC BASIS distal to an obstruction could be well preserved by
The physiologic basis for lung reexpansion or for the collateral ventilation.16
prevention of atelectasis depends on the relationship
between distending pressure and the resulting change Deep Breathing Techniques
in lung volume. The key factor in preventing atelectasis
Essential elements of most care plans aimed at the
or in the reexpansion of small areas of collapsed lung
prevention or resolution of pulmonary atelectasis are
appears to be a deep, prolonged inspiratory effort.15
deep breathing techniques. In most instances when
This factor should be included when preparing treat-
patients have a reduced lung compliance or shallow
ment plans for the prevention or reversal of lung
breathing patterns, they are at risk for atelectasis and
collapse.
the retention of secretions. These problems can often
be reversed by voluntary or assisted lung expansion,
COLLATERAL CHANNELS provided the large airways remain patent. Spontaneous
deep breathing using the diaphragm and chest wall
Alternate pathways for the movement of air in the lung
tends to better expand the dependent areas of the lung
may be provided by:
where atelectasis is likely to occur.17
• Interalveolar communications such as the pores How the deep breathing is carried out may also be
of Kohn (Figure 22-3). important. Multiple short, deep breaths have little
Terminal effect on altering lung volume and function; sustained

bronchial tree inspiratory efforts are more effective.
(cut-away)
• The patient should be coached to inspire slowly
from the normal end-expiratory level to total
Alveoli lung capacity.
• The breath should be held at total lung capacity
for approximately 5 seconds.
• Exhalation should not be forced.
• The patient should be allowed to rest.
• The maneuver should be repeated 5–10 times
each hour.
Canals of Lambert
Terminal
bronchiole Deep-Breathing Exercises
Young children can be taught to perform deep-
breathing exercises. Many activities can be
utilized to encourage lung expansion and can
also be enjoyable for the patient.18 Providing the
child with a surgical glove, which can be easily
inflated, makes the sessions more enjoyable. As

the child inflates the toy or glove, the caregiver
should coach the child to take deep inspira-
tions with an inspiratory hold prior to inflating
the glove. If the child is to have elective surgery,
FIGURE 22-4 Collateral ventilation channels: canals of deep breathing instruction and practice should
Lambert. occur prior to surgery. Also, provide adequate
supervision and avoid potential hazards for
aspiration (small balloons or broken pieces).

Deep-Breathing Exercises E. D., a 65-year-old woman, was admitted to the
hospital for treatment of cholecystitis. On the
When indicated, sequential deep breaths (5–10)
second day of her hospital stay, a cholecystec-
are necessary to increase compliance. Each
tomy was performed. The surgery and recovery
breath should be held at or near total lung ca-
were uneventful, and she was returned to her
pacity for 5 seconds to allow inflation of poorly
room for postoperative care. On the second day
ventilated areas through collateral ventilation
after surgery, the nurse observed that her heart
channels. Exhalation should not be forced and
rate and respiratory rate were increased and that
should end at the normal end-expiratory level
she had an increased temperature. Auscultation
(not continued into the FRC). This sequence
revealed a decrease in breath sounds in the
should be repeated once every hour while the
bases and inspiratory crackles.
patient is awake. After thoracic or upper abdomi-
nal surgery, the management of pain during the Questions
postoperative period is important in maximizing
1. What clinical process(es) might have brought
success with voluntary deep breathing exercises.
about the sudden change in this patient’s
Preoperatively, the respiratory therapist should
vital signs?
instruct the patient in the splinting of incisions,
as well as in the sustained maximal inflation 2. How should the RT assess this patient?
maneuver and use of incentive spirometer when 3. What elements would the RT include in the
indicated. plan of care?
Glossopharyngeal Breathing Exhalation

Spirometer
Glossopharyngeal breathing (GPB) (sometimes
referred to as frog breathing or glossopharyngeal insuffla- Bag intake
tion) is a method of increasing the lung volume at
end-inspiration (Figure 22-5). This method utilizes the
muscles of the mouth and pharynx to add additional From patient
air to the volume already inspired by gulping boluses
of air into the lungs. GPB was first described in the Air Stacking
1950s when it was used by patients with weak inspira- Spirometer (Inhalation)
tory muscles to augment tidal volumes and to prolong
the time they were able to remain off mechanical Bag intake
ventilator support.19
The technique may be useful in patients with a
reduced vital capacity due to inspiratory muscle paraly- To patient
sis or weakness. It is a form of positive pressure ventila- FIGURE 22-6 Air is delivered via the manual resuscitator
tion produced by the patient’s voluntary muscles, in (bottom) to full lung expansion, with the exhalation port
which boluses of air are forced into the lungs. To of the spirometer manually covered so that the insufflated
breathe in, a series of pumping strokes are produced by air does not exit the patient (or enter the spirometer) until
the action of the lips, tongue, soft palate, pharynx, and its exhalation port is uncovered at maximally tolerated
larynx. Air is held in the chest by the larynx, which acts lung inflation (top).
as a valve, as the mouth is opened for the next gulp.20
An alternative to glossopharyngeal breathing for
patients who have glottis dysfunction is passive lung
insufflation with breath stacking. This is accomplished
using a manual resuscitator with a closed expiratory Sustained Maximal Inflation
port. The closed expiratory port mimics a closed glottis (Incentive Spirometry)
(Figure 22-6). Expanding the lungs beyond inspiratory
capacity: The rationale for using sustained maximal inflation
(SMI), or incentive spirometry (IS), is precisely the
• Increases lung distention. same as for spontaneous deep breathing. The incentive
• Improves the ability to cough. spirometer is an adjunct device to improve patient
• Can decrease atelectasis. success in accomplishing the maneuver.
• Can improve lung compliance.21
PROCEDURE
Sustained maximal inflation (SMI) with incentive
Volume spirometry is a modality that depends on the patient’s
GIV
ability to generate an adequate hyperinflation maneu-
ver. Recall that the ideal maneuver generates a high
inflating pressure (40–60 cm H2O) over a long period
VC
VC04 of time (5–15 seconds), resulting in the largest possible
TLC01 inhaled volume (6–10 times tidal volume).1
TLC
The incentive spirometer gives an indication of the
inspired volume and provides biofeedback to the
patient. Commonly available devices utilize the flow of
RV inhaled air and volume displacement (Figure 22-7 A and B).
The use of an incentive spirometer provides the patient
FIGURE 22-5 Schematics of lung volumes (V) achieved and caregiver with immediate feedback regarding the
with normal breathing (TLC, RV, and vital capacity, VC), ability to accomplish the maneuver. The incentive
and with glossopharyngeal insufflation and GI (glos- spirometer also provides an objective assessment of the
sopharyngeal insufflation volume, GIV). GI adds air to patient’s progress or regression and may provide
lungs. The individual steps in the GIV represent separate guidance as to the need for more aggressive therapy. The
boluses of air injected with each cycle. Volume (V ), total use of a prediction nomogram (Table 22-1) for inspira-
lung capacity (TLC).
tory capacity is useful in setting goals for patients and as
Modified from Lindholm P, et al. A fluoroscopic and laryngoscopic study of
glossopharyngeal insufflations and exsufflation. Respiratory Physiology and an indicator that more aggressive therapy is needed
Neurobiology. 2009:167:189–194. (that is, intermittent positive pressure breathing).
(A) (B)
FIGURE 22-7 (A) Incentive spirometer with “volume” indication markings (B) In-Flow Incentive Spirometer
Courtesy of Teleflex Incorporated
Flow-dependent incentive spirometers provide a • The patient’s vital capacity is less than 10 mL/kg
visual indication of activity only until flow ceases. The or the inspiratory capacity is less than one third
incentive to hold the breath, an essential element of of predicted capacity.
the maneuver, is negated and must be emphasized in
other ways; a spirometer is required to assess vital
capacity or inspiratory capacity. HAZARDS AND COMPLICATIONS
Typical incentive spirometers with volume dis- If performed correctly, the maneuver is relatively safe.
placements of approximately 4 L may not get the best The patient should be observed and coached not to
results when working with children. Generally, children maintain the hyperinflation by closing the glottis and
respond better when smaller volume displacements contracting the expiratory muscles. This is a Valsalva-
result in greater movement of the indicators. Pediatric like maneuver.
incentive spirometers require about half the volume
displacement and therefore provide the patient with
increased satisfaction and motivation.
Positive Airway Pressure
A widely recognized and significant mechanism
SPECIFIC INDICATIONS
leading to postoperative pulmonary complications is
Indications for the use of incentive spirometry are: the reduction in functional residual capacity (FRC) that
• The presence of any condition that predisposes a occurs during the postoperative period. The FRC
patient to atelectasis. reduction leads to the collapse of peripheral airways
• The presence of atelectasis. in dependent areas of the lung and atelectasis.22
Positive airway pressure (PAP) may be added to
treatment plans for the prevention or resolution of
CONTRAINDICATIONS atelectasis. The various methods of application differ
Patient cooperation is essential for the effective utiliza- owing to the method by which positive pressure is
tion of this modality. Consider other modalities if: generated:
• The patient cannot be instructed or is unwilling • Positive expiratory pressure (PEP) therapy. The
or unable to cooperate. patient exhales against a fixed orifice resistor
TABLE 22-1 Inspiratory capacity prediction nomogram

Male
Height
58 in. 60 in. 62 in. 64 in. 66 in. 68 in. 70 in. 72 in. 74 in. 76 in. 78 in.
Age 147 cm 152 cm 158 cm 163 cm 168 cm 173 cm 178 cm 183 cm 188 cm 193 cm 198 cm
20 2.35 2.55 2.70 2.90 3.05 3.25 3.40 3.55 3.75 3.90 4.10
25 2.30 2.50 2.65 2.85 3.00 3.20 3.35 3.55 3.70 3.90 4.05
30 2.30 2.45 2.60 2.80 2.95 3.15 3.30 3.50 3.65 3.85 4.00
35 2.25 2.40 2.60 2.75 2.95 3.10 3.30 3.45 3.65 3.80 4.00
40 2.20 2.35 2.55 2.70 2.90 3.05 3.25 3.40 3.60 3.75 3.95
45 2.15 2.35 2.50 2.70 2.85 3.05 3.20 3.35 3.55 3.70 3.90
50 2.10 2.30 2.45 2.65 2.80 3.00 3.15 3.35 3.50 3.70 3.85
55 2.10 2.25 2.40 2.60 2.75 2.95 3.10 3.30 3.45 3.65 3.80
60 2.05 2.20 2.40 2.55 2.75 2.90 3.10 3.25 3.45 3.60 3.80
65 2.00 2.15 2.35 2.50 2.70 2.85 3.05 3.20 3.40 3.55 3.75
70 1.95 2.15 2.30 2.50 2.65 2.85 3.00 3.15 3.35 3.50 3.70
75 1.90 2.10 2.25 2.45 2.60 2.80 2.95 3.15 3.30 3.50 3.65
80 1.90 2.05 2.20 2.40 2.55 2.75 2.90 3.10 3.25 3.45 3.60
Female
Height
58 in. 60 in. 62 in. 64 in. 66 in. 68 in. 70 in. 72 in. 74 in.
Age 147 cm 152 cm 158 cm 163 cm 168 cm 173 cm 178 cm 183 cm 188 cm
20 2.25 2.40 2.55 2.75 2.90 3.05 3.20 3.35 3.50
25 2.20 2.35 2.50 2.65 2.80 2.95 3.10 3.25 3.40
30 2.10 2.25 2.40 2.60 2.75 2.90 3.05 3.20 3.35
35 2.05 2.20 2.35 2.50 2.65 2.80 2.95 3.10 3.25
40 1.95 2.10 2.25 2.45 2.60 2.75 2.90 3.05 3.20
45 1.90 2.05 2.20 2.35 2.50 2.65 2.80 3.00 3.10
50 1.80 1.95 2.10 2.30 2.45 2.60 2.75 2.90 3.05
55 1.75 1.90 2.05 2.20 2.35 2.50 2.65 2.80 2.95
60 1.65 1.82 1.95 2.15 2.30 2.45 2.60 2.75 2.90
65 1.60 1.75 1.90 2.05 2.20 2.35 2.50 2.65 2.80
70 1.50 1.65 1.80 2.00 2.15 2.30 2.45 2.60 2.75
75 1.45 1.60 1.75 1.95 2.05 2.20 2.35 2.50 2.65
80 1.35 1.50 1.65 1.85 2.00 2.15 2.30 2.45 2.60
Source: Courtesy of DHD Healthcare, Wampsville, New York.
(Figure 22-8A and B). The pressure returns to All three appear to be effective in increasing FRC in
ambient on inspiration. spontaneously breathing patients. CPAP appears to be
• Expiratory positive airway pressure (EPAP) therapy. more effective in increasing FRC.22
The patient exhales against a threshold resistor When PEP or EPAP therapy is used appropriately,
(Figure 22-9). The pressure returns to ambient the positive pressure on exhalation encourages collateral
on inspiration. ventilation. The positive pressure is developed when
• Continuous positive airway pressure (CPAP) the patient exhales against a resistance. The pressure
therapy. Positive pressure is maintained during generated on exhalation ranges from 10 to 20 cm H2O.
inspiration and expiration (Figure 22-10). PEP or EPAP therapy can be self-administered if the
FIGURE 22-10 Ez PAP Positive Airway Pressure with

(A) nebulizer.
Courtesy of Smiths Medical
The effectiveness of CPAP in increasing FRC seems

well documented, and CPAP may increase collateral
ventilation.23 Both phenomena should be beneficial in
the resolution of atelectasis. Positive airway pressure
techniques should incorporate diaphragmatic breath-
ing with significantly increased inspiratory volumes
and long exhalation times. The increased tidal volumes
(B) assist in the recruitment of collapsed alveoli. The
expiratory pressure assists in keeping the recruited
FIGURE 22-8 (A) PEP device with small volume aerosol alveoli inflated.
nebulizer. (B) PEP device close-up showing flow direction
and selected PEP level.
Courtesy of Mercury Medical PROCEDURE
Intermittent CPAP can be applied to the airway by
using a face mask. The patient breathes through a
pressurized circuit against a threshold resistor capable
of developing 5–20 cm H2O. Effective administration
requires a gas flow sufficient to maintain the desired
inspiratory pressure. FIO2 should be regulated accord-
ing to the patient’s needs.
The frequency of therapy ranges from once per
hour to twice per day for 10 minutes or more. It may be

beneficial for the patient to take two or three maximal
inhalations periodically during the CPAP sessions.
CONTRAINDICATIONS
FIGURE 22-9 Threshold devices incorporate flow-independent As noted in the AARC clinical practice guidelines, there
one-way valves to ensure consistent resistance and feature are no absolute contraindications to the administration
adjustable specific pressure settings. of positive pressure therapy; however, this modality
should be used with careful evaluation in the following
patient is given proper instruction. When used with
situations:
directed cough techniques, secretion removal may also
be enhanced. Small-volume nebulizers may also be • Patients unable to tolerate the therapy due to
used to simultaneously deliver and perhaps improve increased work of breathing.
the distribution of medications throughout the lungs • Elevated intracranial pressure.
(Figure 22-10). • Hemodynamic instability.
• Facial trauma. management of atelectasis where other approaches

• Acute sinusitis. have failed to correct the problem.24 The use of an
• Hemoptysis. end-inspiratory hold or expiratory retard may have a
• Nausea. positive impact on the results achieved with IPPB.15
• Middle ear pathology. IPPB treatments can be administered either
• Untreated pneumothorax. passively or actively. Most of the literature characterizes
• Esophageal surgery. the routine therapy session as passive.
• During passive IPPB, the patient initiates
HAZARDS AND COMPLICATIONS inspiration and is coached to relax and allow the
Although therapy is generally benign and well toler- “machine” to fill the lungs. The patient should
ated, several complications may arise, which should be be instructed to hold the inspired volume in for
monitored, and therapy should be modified if possible. several seconds before exhaling without force.
The documented complications are: • During an active therapy session, the patient is
required to inhale to maximum inflation. Peak
• Hypoventilation and hypercarbia secondary to pressure is increased gradually as tolerated. Active
increased work of breathing. therapy sessions appear to result in the greatest
• Increased intracranial pressure. post-treatment inspiratory capacity (IC).25
• Decreased venous return and myocardial isch-
emia secondary to cardiovascular compromise. The effectiveness of IPPB requires a tidal volume
• Gastric insufflation. greater than is possible for the spontaneously breathing
• Claustrophobia. patient. Tidal volumes and pressure should be moni-
• Skin irritation and breakdown from the mask. tored during therapy and incorporated into assess-
• Pulmonary barotrauma. ments. The increased tidal volumes achieved with IPPB
necessitate that the respiratory rate be reduced to
maintain a normal minute ventilation for the patient
LIMITATIONS and to avoid side effects that hyperventilation may
CPAP requires additional equipment and skilled cause.
personnel. Other methodologies, if appropriate, would IPPB should not be the therapy of first, or only,
have a lower cost. Additionally, patients must be able choice for lung expansion or aerosol delivery. Gener-
to breathe effectively without mechanical assistance. ally, patients who can demonstrate a vital capacity
greater than 10 mL/kg might not benefit from IPPB.
IPPB therapy is generally more costly to administer
Intermittent Positive Pressure than other therapies. It requires additional equipment,
Breathing supplies, monitoring, and time for instruction of
patients; however, when appropriate, it must be included
Intermittent positive pressure breathing (IPPB) is utilized to in care plans. At this time, one device is being manufac-
provide short-term ventilatory support in an effort to: tured and sold for single-patient use (Figure 22-11).
• Augment lung expansion.
• Improve delivery of aerosolized medication
when other methodologies have been ineffective.
• On occasion, assist ventilation.
Few modes of therapy have been more controver-
sial than IPPB. Most of the criticism has been due to its
overuse, especially with regard to the belief that aerosol
medication administration improved with the addition
of IPPB. An indication that appears to respond to Image not available due to copyright restrictions
effective IPPB administration is pulmonary atelectasis
when bronchial obstruction has been excluded. 24 The
effectiveness of IPPB may be the direct result of its
potential to inflate the lungs to volumes greater than
what the patient could achieve without mechanical
assistance.
The use of IPPB to provide large inspiratory
volumes when patients will not or cannot take a
deep breath has been found to be beneficial in the Text not available due to copyright restrictions
PROCEDURE SPECIFIC INDICATIONS

• The patient should be seated comfortably in a IPPB is the most useful when:
chair or in bed. Avoid a slouched position, • The patient’s ability to take deep breaths or to
which limits diaphragmatic excursions. generate an effective cough is impaired due to
• Vital signs and breath sounds should be pathology or the inability to cooperate fully.
recorded. • Other methods of lung expansion have not been
• The patient should be encouraged to relax and effective in preventing or correcting atelectasis.
breathe slowly through the mouth. If a
mouthpiece is used, it should be positioned IPPB may be valuable for:
between the teeth with the lips sealed tightly • The administration of aerosolized medications
around the mouthpiece. Nose clips may be used, in patients with muscle weakness or conditions
if required, to minimize air leak. that limit the effectiveness of breathing patterns
• Inspiratory pressure should be initiated at low important to the effective deposition of aerosol-
pressure. The pressure should be increased ized medication.
gradually until the desired volume is achieved • Short-term support of ventilation as an alterna-
(10–15 mL/kg of body weight). Auscultation tive to tracheal intubation and continuous
should reveal improved expansion of the mechanical ventilatory support.25–26
dependent areas of the lungs.
• The patient should be coached to perform 2 to 3
inspiratory holds periodically. CONTRAINDICATIONS
• Pulse rate should be measured periodically. If In addition to the relative contraindications noted for
the heart rate changes to greater than 20% of , CPAP, the AARC clinical practice guidelines recom-
discontinue the therapy and reassess. mend a careful evaluation prior to initiating IPPB
• If signs of hyperventilation are present therapy for patients who have any of the following:
(dizziness, nausea, tingling), suspend therapy
• Active untreated tuberculosis.
and reevaluate.
• Evidence of bleb on X-ray.
• At midway and at the end of the session, the
• Singultation (hiccups).
patient should be instructed to rest, and then
deep breathe and cough.
• At the completion of the session, vital signs and HAZARDS AND COMPLICATIONS
breath sound data should be collected and the In addition to the complications that may be associ-
outcome assessed. ated with CPAP, the AARC clinical practice guidelines
note that careful monitoring of the patient should
Age-Specific Competency include observation for the following:
• Hospital-acquired infection.
IPPB Treatment • Hemoptysis.
IPPB may be effectively taught to young children. • Impaction of dessicated secretions.
If necessary, and when possible, the patient • Cardiovascular embarrassment.
should become familiar with the device, the • Air trapping and overdistention of alveoli.
procedure, and the caregivers prior to surgery. • Increased mismatch of ventilation and perfusion.
The child should be encouraged to handle the • Psychological dependence.
equipment to reduce fear and anxiety. If possible,
observation of another child receiving a treatment LIMITATIONS
can be very effective in gaining cooperation. The effectiveness of the IPPB therapy is short-lived. If
Uncooperative patients and patients who are the patient returns to an ineffective pattern of ventila-
unable to cooperate must never be forced to tion, lung collapse begins within an hour after the
undergo the procedure. For small children, the therapy session.
equipment used should have the smallest
mechanical deadspace (rebreathed gas)
possible. The treatments should always be Outcomes Assessment
initiated at minimal pressure. The pressure
Post-treatment assessment should be made in two steps.
can be increased gradually until adequate tidal
volumes are achieved. • First, evaluate the therapy session, comparing
breath sounds, vital signs, and mental status to
the baseline assessment. Note any unexpected or Summary

undesirable.
• Second, collect post-treatment data to evaluate Pulmonary atelectasis is a condition characterized
progress toward meeting the goal(s) of therapy. by areas of the lung that have collapsed. Although
atelectasis is generally associated with upper abdomi-
Post-treatment and daily progress should include nal and thoracic surgery, it can occur anytime when
references to the following: lung expansion is limited. Factors that predispose a
• Sputum production and characteristics. patient to atelectasis are obesity, general anesthesia,
• Breath sounds. and preexisting pulmonary disease. Atelectasis can
• Patient’s subjective response. result from three mechanisms that may act indepen-
• Vital signs. dently or in combination: inadequate lung distending
• Chest radiograph. forces, airway obstruction, and loss of pulmonary
• Oxygen saturation. surfactant.
Patients must be assessed for the presence of any of
the risk factors prior to surgery, before procedures that
require sedation, or before procedures that result in
Best Practice extended periods of immobilization. The RT must also
assess when possible therapy should begin preopera-
Atelectasis tively when risk factors are present. Appropriate
therapy should continue postoperatively until the
Atelectasis can be the result of multiple factors.
patient is ambulating. The patient’s condition and
Evaluation of patients for all factors that place
effectiveness of the treatment plan must be assessed
them at risk for the development and progression
often and therapy adjusted accordingly.
of atelectasis must be thorough. Hyperinflation
therapy alone may not be effective in the pre-
vention or reinflation of atelectasis. The factors Study Questions
that predispose the patient to atelectasis must
be addressed in the treatment plan. Control and REVIEW QUESTIONS
removal of excessive secretions, adequate pain 1. What are the general indications for hyperinflation
control, and other appropriate interventions must therapy?
be considered.
2. What is atelectasis? Differentiate between
compressive and obstructive atelectasis.
3. What are the key factors for the prevention or
reversal of atelectasis?
CASE STUDY 22-2 4. Under what circumstances would IPPB be
recommended as an alternative to incentive
A day after initiating SMI therapy with an spirometry?
incentive spirometer and cough instruction, the
respiratory therapist is called to evaluate E. D., a
postop cholecystectomy patient. On arrival you
note that Ms. D. is awake and oriented. The 1. What inspiratory capacity goal should be set
patient complains of dyspnea, and inspiratory for a male patient 45 years old and 5 feet
capacity is decreased to 800 mL. The respiratory 8 inches tall?
rate is 28/min and heart rate is 120/min, both a. at least 500 mL
increased from an earlier visit. She is febrile. b. at least 1000 mL
Auscultation reveals diminished breath sounds c. approximately 3000 mL
in the bases and inspiratory crackles. SpO2 is d. approximately 5000 mL
92% on 6 Lpm of oxygen via nasal cannula. 2. Incentive spirometry is most effective if the
maneuver is performed at least:
Questions
a. twice/day for 10 repetitions each session.
1. What is the RT’s assessment after the first b. four times/day for 10 repetitions each session.
day of treatment? c. at least every hour for 10 repetitions each
2. What changes in the treatment plan should session.
the RT suggest? d. Frequency and repetitions have no relationship
to effectiveness.
3. Key factors in the prevention or correction of 2. Develop a rational approach to decision making
atelectasis include: with regard to recommendations of modality for
a. depth of inspiration and duration of inspiration. the prevention or correction of atelectasis.
b. depth of inspiration and respiratory rate. 3. When coaching a patient to perform sustained maxi-
c. maximum inspiratory flow rate and tidal volume. mal inflation maneuvers, the therapist notes that the
d. FIO2 and vital capacity. inspiratory capacity being achieved has decreased by
4. CPAP is valuable in the correction of atelectasis 500 mL since the previous day. Is this significant?
because of its ability to: Discuss the RT’s assessment of the therapy.
a. increase tidal volume. 4. When coaching a patient to perform sustained
b. increase functional residual capacity. maximum inflation maneuvers, the respiratory
c. increase inspiratory capacity. therapist notes that the patient coughs with each
d. decrease residual volume. attempt, has a rapid shallow breathing pattern,
5. Which of the following may be an indication of a poor quality of breath sounds on auscultation of
patient’s inability to tolerate intermittent CPAP the basal lung fields, and increased oxygen require-
therapy? ments. What should the RT recommend to the
a. a 10% reduction in respiratory rate physician?
b. a 10% reduction in heart rate
c. a 10% increase in tidal volume
d. a 25% increase in heart rate References
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reevaluated if: tory maneuvers to prevent postoperative pulmo-
a. during the first 5 minutes of the session the nary complications. JAMA. 1973;224:1017–1021.
patient has no improvement of aeration to the 2. Johnson NT, Pierson DJ. The spectrum of pulmo-
posterior basal lung fields. nary atelectasis: pathophysiology, diagnosis, and
b. during the treatment session, the patient’s heart therapy. Respir Care. 1986;31:1107–1120.
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collateral ventilation except: 7. American Association for Respiratory Care. Inter-
a. canals of Lambert. mittent positive pressure breathing. Respir Care.
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c. sustained maximum inflation maneuvers. 8. Centers for Disease Control. Perspectives in disease
d. eustachian tube. prevention and health promotion update: Univer-
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a. functional residual capacity should remain MMWR. 1988;37:377–388.
unaffected. 9. Colgan FJ, Mahoney MC, Fanning GL. Resistance
b. inspiratory capacity is likely to be increased breathing (blow bottles) and sustained hyperinfla-
after the therapy session. tions in the treatment of atelectasis. Anesthesiology.
c. heart rate should always be increased by 15%. 1970;32:543–550.
d. coughing and expectoration of secretions 10. Motley HL, Werko L, Cournand A, and Richardo
should never be encouraged. DW. Observations on the clinical use of intermit-
tent positive pressure. J Aviation Med. 1947;18:417.
11. Pierce AK, Saltzman HA. Conference on the
1. Discuss the relationship between distending scientific basis for respiratory therapy. Am Rev
pressure, surface tension, and elastic recoil of the Respir Dis. 1974;110.
lungs as they relate and interact to determine 12. Pierce AK. Scientific basis of in-hospital respiratory
functional residual capacity. therapy. Am Rev Respir Dis. 1980;122.
13. The Respiratory Care Committee of the American pulmonary complications after heart and
Thoracic Society. Guidelines for the use of intermit- pulmonary surgery. Intensive Care Med (1993)
tent positive pressure breathing. Respir Care. 19:294–298.
1980;25:365. 23. Pontoppidan H. Mechanical aids to lung expan-
14. American Association for Respiratory Care. The sion in non-intubated surgical patients. Am Rev
pros and cons of IPPB. AARC Times. 1986;10:48. Respir Dis. 1977;109–119.
15. Martin RJ, Rogers RM, Gray BA. The physiologic 24. O’Donahue WJ. Maximum volume IPPB for the
basis for the use of mechanical aids to lung management of pulmonary atelectasis. Chest.
expansion. Am Rev Respir Dis. 1980;122:105–107. 1979;76:683–687.
16. Menkes HA, Traystman RJ. Collateral ventilation. 25. Welch MA, Shapiro BJ, Mercurio P, Wagner W.
Am Rev Respir Dis. 1977;116:287–309. Methods of intermittent positive pressure breath-
17. Donohue WJ. Postoperative pulmonary complica- ing. Chest. 1980;78:463–467.
tions. Postgraduate Medicine. 1992;91:157–165. 26. De Troyer A, Deisser P. The effects of intermittent
18. Lester MK, Flume PA, Airway clearance guidelines positive pressure breathing on patients with muscle
and implementation. Respiratory Care, weakness. Am Rev Respir Dis. 1981;124:132–137.
2009:54(6)733–753.
19. Lindholm P, et al. A fluoroscopic and laryngoscopic
study of glossopharyngeal insufflations and
exsufflation. Respiratory Physiology and Neurobiology. Suggested Readings
2009:167:189–194. Farzan F. A Concise Handbook of Respiratory Disease. 2nd
20. Pryor JA, et al. Physiotherapy for airway clearance ed. Reston, VA; Reston; 1985.
in adults. European Respiratory Journal. Shapiro BA, Kacmarek RM, Cane RD, et al. Clinical
1999:14,6:1420. Application of Respiratory Care. 4th ed. St. Louis:
21. Bach JR, et al. Lung insufflations capacity in neuro- Mosby-Yearbook; 1991.
muscular disease. American Journal of Physical White GC. Equipment Theory for Respiratory Care. 3rd ed.
Medicine and Rehabilitation. 2008;87(9):720–725. Clifton Park, NY: Delmar Cengage Learning; 1999.
22. Ingwersen UM, et al. Three different mask physio- Wilkins RL, Dexter JR. Respiratory Disease: Principles of
therapy regimens for prevention of post-operative Patient Care. Philadelphia: FA Davis; 1993.
CHAPTER 23
Pulmonary Hygiene and Chest Physical

Therapy
John A. Rutkowski
OBJECTIVES
• Understand the rationale for pulmonary hygiene and chest physical therapy.
• Identify diseases and conditions for which pulmonary hygiene and chest physical therapy might be
appropriate.
• Assess the need for pulmonary hygiene and chest physical therapy.
• Assess the results of pulmonary hygiene and chest physical therapy.
• List and describe the characteristics and limitations of various pulmonary hygiene modalities.
CHAPTER OUTLINE
Key Definitions, Concepts, and Professional Chest Physical Therapy
Standards Breathing Retraining
Goals and Objectives of Pulmonary Hygiene and Postural Drainage, Chest Wall Percussion, and
Chest Physical Therapy Chest Wall Vibration
Normal Mucociliary Clearance Forced Exhalation Technique
Functions of Airway Mucus Active Cycle Breathing
Characteristics of Mucus Autogenic Drainage
Mucociliary Escalator Mechanical Adjuncts to Chest Physical Therapy
Cough Positive Airway Pressure Adjuncts to Bronchial
Diseases and Conditions Associated with Hygiene Therapy
Abnormal Mucus Clearance Intrapulmonary Percussive Ventilation Therapy
Assessment of Pulmonary Hygiene Combined Mechanical and Acoustical Vibration
Mucus Continuous Lateral Rotation (Kinetic Therapy)
Breathing Pattern Selection of Mucociliary Clearance Technique
Effectiveness of Cough Complications and Adverse Effects of Chest
Physical Therapy
Improving Pulmonary Hygiene
Coughing
640
CHAPTER 23 ■ Pulmonary Hygiene and Chest Physical Therapy 641
KEY TERMS
active cycle breathing (ACB) high-frequency oscillation proprioceptive
autogenic drainage (HFO) rheology
collateral ventilation intrapulmonary percussive spinnability
continuous lateral rotation ventilation (IPV) transudate
therapy (CLRT) mucociliary escalator vibration
elasticity mucokinesis viscosity
high-frequency chest wall mucostasis
oscillation (HFCWO) percussion
T
he word “hygiene” is derived from the Greek of Respiratory Care. Periodic additions and revisions
word for “healthful.” It is a general reference continue to occur on an annual basis. The guidelines
to the science of health and the prevention of with application to bronchial hygiene are:
disease or conditions and procedures
• Directed cough.
promoting or preserving health. Pulmonary, or
• Postural drainage, percussion, and vibration
bronchial, hygiene is the promotion or preservation of
therapy.
healthy lungs. Exercise, nutrition, avoidance of air-
• Humidification during mechanical ventilation.
borne pollutants, and immunization are all vital
• Incentive spirometry.
components of bronchial hygiene and the maintenance
• Use of positive airway pressure adjuncts to
of pulmonary health.
bronchial hygiene therapy.
An understanding of how pulmonary hygiene
might be achieved requires an awareness of the natural
mechanisms for maintaining lung health. Normal Goals and Objectives of
airway clearance requires that two processes operate
optimally and in coordination: (1) mucus manufacture
Pulmonary Hygiene and Chest
and transport and (2) an effective cough. Physical Therapy
Submucosal glands and the goblet cells produce
The goals of treatment with all airway clearance
pulmonary secretions with contributions from the
methods are to improve the removal of secretions,
Clara cells and tissue fluid transudate. The diaphragm,
thereby decreasing obstruction of the airways with the
intercostals, and abdominal muscles generate the forces
hope of improving the distribution of ventilation and
required for the effective movement of air and the
gas exchange.2
generation of forceful coughs. The brain is responsible
for coordination of all of the events required for
clearance of the airways. Normal Mucociliary Clearance
The clearance of mucus from the airways is normally
Key Definitions, Concepts, and achieved by a combination of factors, most important
of which are the mucociliary escalator and cough.3 In
Professional Standards healthy individuals, estimates for the volume of mucus
Bronchial hygiene therapies have been collectively secreted are 10–100 mL per day. When the rate of
referred to as chest physical therapy (CPT), which is mucus production or the characteristics of the mucus
usually a reference to postural drainage, percussion, and produced change, clearance mechanisms become less
vibration (PDPV). Recently, new techniques have effective, mucus accumulates in airways, and respira-
expanded the capabilities and requirements placed tory function is impaired. Mucostasis is a frequent
on caregivers and further complicated decision making complication of such diseases as bronchitis, pneumo-
regarding the application of therapy. nia, cystic fibrosis, and bronchiectasis.
In 1990 the American Association for Respiratory
Care began the development of clinical practice
guidelines. The guidelines provide a broad, but limited, FUNCTIONS OF AIRWAY MUCUS
context within which specific departmental procedures, Under normal circumstances, the secretion of mucus
policies, and protocols can be developed.1 The first five into the airway serves as a defense against inhaled
guidelines were published in the December 1991 issue irritants that are breathed in to the lungs. Inhaled
Surfactant layer Mucus gland
Mucus flow
Inhalation
Mucus flow
Surfactant Airflow
layer
Mucus gland
FIGURE 23-1 Physiology of airway mucus clearance.
irritants, including dust, microbes, and gases, may Mucus gland

damage the airway epithelium. After entrapment in the
airway mucus, the irritants are removed through a
process termed mucociliary clearance. These alterations
can result in the retention of secretions in the lungs
and subsequent increased work of breathing and other
complications.4
Exhalation
Mucus flow
CHARACTERISTICS OF MUCUS Surfactant
Airflow
layer
Respiratory airway mucus is a complex mixture of
glycoproteins, proteoglycans, lipids, other proteins, and
sometimes DNA. The glycoproteins and proteoglycans
associate closely to form the main structural compo-
nent of the viscoelastic hydrophylic mucus gel. The
lipids interacting with the glycoproteins also contribute
to the formation of a viscoelastic gel. Other proteins
that are present have a role in protection against
FIGURE 23-2 Cephalad airflow bias: With normal mucocili-
microorganisms. 5 The mucus blanket consists of two ary function, greater energy is applied to the mucus layer
layers, separated by a layer of surfactant.3 The layer during expiration than during inspiration, because of
adjacent to the epithelium, the sol layer, is less viscous airway narrowing during expiration.
than the gel layer (Figure 23-1).
MUCOCILIARY ESCALATOR Factors having a significant role in bronchial hygiene

and its effectiveness are:
The transport of mucus depends on the mechanical
forces of cilia beating and airflow.6 Normally the • The rheologic (ability to flow or be deformed)
cilia move through the sol layer in a wavelike fashion properties of the mucus layers.
with the tips striking the lower surface of the gel • The various factors that can alter those proper-
layer at rates of 8–15 Hz.6 As the cilia penetrate the ties.
viscous gel layer, they propel it toward the larger • The functional status of the cilia and airflow
bronchi. (Figure 23-2).
Tidal breathing and forced exhalation also propel
mucus cephalad.6 During normal breathing, the
diameter of flexible airways increases during inspira- COUGH
tion and narrows during exhalation. The narrowing of Cough is an important defense mechanism that helps
the airways during exhalation increases the velocity of to clear excessive secretions and foreign material from
exhaled air, assisting with the movement of mucus.7 the airways. The effectiveness of a cough depends on its
Irritation Inspiration Compression Expulsion
FIGURE 23-3 The four phases of a normal cough.
ability to achieve high gas flows and velocities through Potential hazards and complications of cough that
the airways. The sequence of events during a typical have been identified in the literature and listed in the
cough have been well described.4–8 AARC clinical practice guidelines for directed cough are:
There are four phases of the cough mechanism
• Reduced coronary artery perfusion.
(Figure 23-3):
• Reduced cerebral perfusion.
• A deep inspiration. • Incontinence.
• A pause at peak-inspiration to improve the • Fatigue.
distribution of inspired air. • Headache.
• A compressive phase, which is the closure of the • Paresthesia or numbness.
glottis, accompanied by active contraction of the • Bronchospasm.
expiratory muscles. • Muscular damage or discomfort.
• The expiratory phase, which is the opening of • Spontaneous pneumothorax, pneumomediasti-
the glottis with an explosive release of air from num, subcutaneous emphysema.
the lungs. • Cough paroxysms.
• Chest pain.
An ineffective cough can result from any condition
• Rib or costochondral junction fracture.
that interferes with the inspiratory or expiratory phases
• Incisional pain, evisceration.
of cough:
• Anorexia, vomiting, and retching.
• Pain. • Visual disturbances, including retinal
• Weakness. hemorrhage.
• Neuromuscular disorders. • Central line displacement.
• Artificial airways. • Gastroesophageal reflux.
• Pulmonary diseases that reduce expiratory flow.
Coughing is a source of droplet nuclei and is
Cough can be a symptom of an underlying prob- associated with the transmission of airborne patho-
lem that requires treatment. Cough can have a benefi- gens, including tuberculosis. Risk of exposure to these
cial effect on bronchial hygiene, and directed coughing airborne pathogens must be minimized. The most
may have a significant role in therapy. If the cause of a effective method for reducing the transmission of
cough is unknown or if the coughing has no beneficial droplet nuclei is to have patients cover their mouths
function, the complications that might result from the with a tissue or handkerchief when coughing. Personal
coughing may represent a potential hazard, and protective equipment and effective air exchange
symptomatic treatment should be considered.4–8 systems should also be used.
Diseases and Conditions BREATHING PATTERN

Patients with shallow, monotonous breathing patterns
Associated with Abnormal are subject to the retention of secretions and alveolar
Mucus Clearance collapse. The normal breathing pattern incorporates
intermittent deep breaths (sighs) at a rate of 6–10 per
The American Association for Respiratory Care (AARC)
hour. These sigh breaths are generally considered an
has published generally accepted indications for CPT
important part of adequate bronchial hygiene.
or PDPV and for adjunctive devices in the form of
clinical practice guidelines. In general, indications
for CPT or PDPV are: EFFECTIVENESS OF COUGH
• Evidence or suggestion of difficulty with secre- Several techniques can be used to assess a patient’s
tion clearance as indicated by: Difficulty clearing ability to cough.
secretions with expectorated sputum production • Subjective assessment, based on quality of the
greater than 25–30 mL/day in adults. Evidence sound generated and the perceived adequacy of
or suggestion of retained secretions in the the cough to dislodge secretions, can be classi-
presence of an artificial airway. fied as weak or strong.
• Presence of atelectasis caused by, or suspected • Peak flow rates and FVC are often reduced in
of being caused by, mucus plugging. patients with an ineffective cough.
• Diagnosis of diseases such as cystic fibrosis, • The measurement of maximum expiratory
bronchiectasis, or cavitating lung disease. pressure (MEP) at the mouth appears to be an
excellent indicator for the capacity to generate
peak flow transients.11 The MEP should be
Assessment of Pulmonary measured at total lung capacity and repeated
until reproducible results are achieved.
Hygiene
Although subjective assessment and FVC measure-
Assessment of the need for and the effectiveness of
ments are routinely used to evaluate patients, the
pulmonary hygiene generally focuses on the ability of
findings presented by Szeinberg and colleagues suggest
the patient to cough effectively and expectorate secre-
that MEP is a more accurate measurement of cough
tions. Factors that alter the effectiveness of coughing
strength. Patients with an MEP value of 60 cm H2O or
include the characteristics of the mucus, the breathing
more are able to generate transients of peak flow
pattern, and the mechanics of the cough.
during coughing and should be able to cough effec-
tively. Evidence suggests that a peak cough flow (PCF) of
MUCUS at least 160 L/min is the minimum required to clear
airway debris. Peak cough flows of greater than 270 L/
Mucokinesis (mucus movement) depends on two
min may be necessary to prevent upper respiratory
factors: ciliary activity and the production of mucus.
tract infections.12
Ciliary dyskinesis, or abnormal ciliary function, may
be the result of many pulmonary and nonpulmonary
stresses. Examples are smoking, high oxygen concentra- Improving Pulmonary Hygiene
tions, dehydration, and general anesthesia. Mucus
Efforts to improve pulmonary hygiene are generally
rheology (or movement) can be adversely impacted by
focused on two primary objectives: altering the physical
many other factors:
properties of mucus and improving the distribution of
• Inflammatory processes involving the pulmo- air in the lungs.
nary epithelium.
• Alterations in the physical properties of mucus.
• Abnormalities of the serous or mucus secreting
Mucus transport can be altered by changes in
glands.
the physical properties of mucus. Viscosity
• Dehydration.
(resistance to flow in a fluid), elasticity
Inadequate humidification of inspired air when (tendency to return to original shape), and
artificial airways are used can lead to desiccation of spinnability (the capacity to form threads under
secretions.10 traction) are considered to be the most impor-
Bronchial hygiene is dependent on adequate tant of the properties. Decreases in viscoelasticity
mucokinesis. Any abnormality in the production or and spinnability have been shown to correlate
transport of mucus can result in the retention of with increases in secretion mobilization. Main-
secretions with the potential for further complications. taining adequate hydration, the administration
of mucolytic agents, and the utilization of Diaphragmatic breathing is taught and coached
techniques and devices discussed later in this with the patient in a relaxed position. The patient is
chapter can all have positive impacts on the seated, with the head and neck well supported; if in
characteristics of mucus. bed, the patient is semirecumbent with the knees
• Alterations in airflow and air distribution. Abnor- slightly flexed and supported. The therapist’s hands rest
mal patterns of ventilation and distribution of lightly on the anterior-costal margins to stimulate and
air in the periphery of the lungs can lead to palpate the costal movement.
retention of secretions. Effective air distribution
is essential for the clearing of mucus from the • The upper chest and shoulders are relaxed.
respiratory tract. Techniques that improve Instructions should be short and precise. Do not
volume and distribution of inspired air are an confuse the patient with a complicated series of
important factor in prophylaxis and therapy of commands. Demonstrating the technique is
secretion retention. beneficial.
• Instruct the patient to breathe out quietly,
relaxing the shoulders and chest.
COUGHING • Then tell the patient to breathe in gently and
An effective cough is essential for clearing mucus from “feel the air coming in around the waist” or to
the airway. Coughing may be ineffective when the “push away the therapist’s hands.” A method
mucus blanket is abnormal or when the essential that may encourage the early movement of the
mechanical components necessary to generate an diaphragm is to have the patient initiate inspira-
effective cough are not intact. If necessary, cough may tion by sniffing.
be encouraged, simulated, or assisted mechanically. In The therapist should observe a normal sequence of
postoperative patients, the incision site must be inspiratory muscle movements:
supported to minimize the stress that an adequate
cough exerts on the wound. Proper support of an • The diaphragm contracts, resulting in the upper
incision minimizes pain and reduces the complications abdomen rising.
that might occur owing to stress at the incision site. • Lateral-costal expansion occurs.
• The upper chest expands.
Chest Physical Therapy The inspiration occurs in a 1-2-3 sequence with the
upper chest wall moving slightly, if at all. If the upper
Chest physical therapy consists of a group of generally
chest wall moves, it should move after the diaphragm
accepted procedures to improve airflow and distribu-
contracts and lateral-costal expansion occurs. Observe
tion of air in the lungs that utilizes gravity and a variety
the patient to note and correct some common errors:
of physical maneuvers to assist in the movement and
expectoration of mucus. • Forced expiration should be avoided.
• Prolonged expiration should be discouraged.
• The patient should not be “bloating” the abdo-
BREATHING RETRAINING
men or arching the back to give the appearance
When performed effectively, breathing exercises can of abdominal expansion.
greatly assist patients in obtaining the best possible • Overuse of the upper chest and accessory
lung function. The patients are instructed and coached muscles should be discouraged.
with the purpose of:
The exercises can be gradually advanced to include
• Promotion of a normal, relaxed pattern of the necessary use of other skeletal muscles. A good
breathing. progression is moving from the bed to sitting to
• Minimizing the effort required to breathe. standing to walking to climbing stairs.
• Assisting the removal of secretions. The techniques used in the training of the dia-
• Aiding the reexpansion of lung tissue. phragm can also be applied to improve the movement
• Mobilizing the thoracic cage. of the rib cage and can assist further in the removal of
The effectiveness of these techniques requires the secretions. These exercises, often referred to as localized
frequent and regular performance of the exercises. The expansion exercises, segmental breathing exercises, or
patient should be advised to carry out each of the lateral-costal breathing, may be valuable when address-
exercises 18–24 times in groups of 6, resting between ing specific problem areas in the lungs. Examples are
groups to avoid hyperventilation. The exercises should atelectasis, pneumonia, muscle splinting from pain
be repeated 2 to 5 times a day, depending on the often observed after cardiothoracic surgery, tight chest
patient’s condition.13 walls, or kyphoscoliosis.14
The therapist’s hand is placed over the area of the for each of the segmental bronchi and its correspond-
chest wall to be emphasized. The hand is used to provide ing area of the lung (Figure 23-4). Nine different
proprioceptive input for the selected muscle movement. positions are employed to assist in the drainage of
At the end of exhalation, hand pressure is increased secretions from the segmental bronchi (Figure 23-5).
slightly and the patient is instructed to push up against Questions that should be answered prior to
the therapist’s hand. Some resistance to inspiration may initiating therapy are:
encourage the patient to inhale more completely.
• Which area(s) of the lung are to be emphasized
The areas that are most often selected to encourage
during therapy sessions?
segmental expansion are:
• What is the patient’s general condition?
• Lateral-costal, unilateral or bilateral, anterior at Also before beginning therapy, the respiratory
the lower ribs. therapist:
• Posterior at the lower chest and midchest for the
lower lobes. • Gathers sufficient information to determine
• Midaxillary for the right middle lobe and lingula. which areas of the lung should be emphasized
by thoroughly examining the patient’s chest,
Repeated contractions should be encouraged, conferring with the physician, and reviewing
along with deep breathing and an end-inspiratory the medical record for chest X-ray reports and
breath-hold. During the breath-hold phase, the other notes.
patient is encouraged to breathe deeper, deeper, • Considers any cardiopulmonary instability, the
deeper to provide a stretch. A technique suggested by ability of the patient to cooperate and tolerate
Frownfelter that may be helpful in teaching the stretch the therapy, and coexisting conditions that might
is to ask the patient to mimic a sneeze. The patient limit the positioning of the patient.
can usually relate to the deep breath, holding it, and • Determines the best time for the administration
then ah-ah-ah-ah-choo! of therapy. (The RT avoids therapy sessions
These exercises can be helpful if done several times immediately after meals, including tube feed-
prior to coughing to increase the distribution of ventila- ings. If the patient is experiencing pain, therapy
tion and to promote the movement of secretions. sessions should be coordinated after the admin-
istration of pain medications.)
POSTURAL DRAINAGE, CHEST WALL Each of the positions employed should be main-
PERCUSSION, AND CHEST WALL VIBRATION tained for 5–10 minutes or longer if the patient can
This group of techniques is often collectively referred tolerate the time and has a large volume of secretions
to as chest physical therapy (CPT), or postural drainage, or thick secretions.
percussion, and vibration (PDPV). In general, these
techniques are employed to improve mucociliary
clearance, increase expectorated sputum volume,
and improve airway function.
An analogy for the fundamental concepts of PDPV CPT or PDPV Sessions
is getting ketchup out of a bottle. The first step in the Children and infants may be positioned effec-
procedure is to position the bottle with the open end tively by supporting them on the upper legs or
down; next the bottle gets a few thumps on its , cradling them in the arms of the caregiver. Older
followed by some vigorous shaking. If there is any children may benefit by performing CPT or PDPV
ketchup in the bottle, some may be deposited on independently; however, some assistance is
the dinner plate.15 advisable to treat some of the segments.
PDPV utilizes a combination of gravity and CPT or PDPV sessions have an additional
mechanical energy in the form of percussion and benefit for children. The regular sessions can
vibration to assist the natural movement of secretions often provide a “special time” for the child.
from the periphery of the lung to the larger segmental This time may be enhanced if the sessions are
bronchi. When the secretions are transported to the scheduled to coincide with a favorite television
segmental bronchi, they can then be expectorated by program. A favorite tape or CD can be played,
coughing. or a game can be played or created to make
the sessions more enjoyable.
Postural Drainage. The postural drainage component These techniques may also be beneficial
of CPT is an attempt to make the best use of gravity. with adolescents and adults. The sessions can be
This is analogous to turning the open end of the quality time for the patient and caregiver.
ketchup bottle down. There is a recommended position

Apical 1 Upper division
Posterior 2 Apical/Posterior 1&2
Anterior 3 Anterior 3
Middle lobe Lower division (lingular)

Lateral 4 Superior lingula 4
Medial 5 Inferior lingula 5

Superior 6 Superior 6
Medial basal 7 Anterior medial basal 7&8
Anterior basal 8 Lateral basal 9
Lateral basal 9 Posterior basal 10
Posterior basal 10
1 1 -2
2 3
Posterior
6 views
4 6
8
10 9 8 9 10
1 2
1
1 3
1-2
2
2 3 4 3
3 5 6
Lateral 4 4 Lateral
view 6 5 6
4 6 view
5
5 8 7 8
10 8 9 10
9 7
9 10 8
10 9
1-2
1
2 3
3 1
1-2
Anterior 2
4
view 4 5 3 Anterior
3 6 5 view
8 4 8 © Delmar/Cengage Learning
10
5 7 5
10 Medial
Medial 7-8
view 8 9 9 view
FIGURE 23-4 Lung segments.
Percussion. Percussion, or clapping, is performed with compressed and then used to transmit a wave of
a cupped hand (Figure 23-6) over the area of the chest mechanical energy through the chest wall and
corresponding to the segment being drained. The purpose into the lung parenchyma.
of the percussion is to loosen and mobilize secretions that • The percussion should be applied rhythmically
are adhering to the bronchial walls. Percussion is analo- and vigorously throughout inspiration and
gous to the thumping of the ketchup bottle. expiration.
• The percussion should not be painful or result in
• The cupped hand must be formed in a manner
erythema and should not be applied over bare
that traps a cushion of air, which can be
skin or bony prominences.
UPPER LOBES
Apical Segment
A.
UPPER LOBES
Anterior Segment
B.
UPPER LOBES
Posterior Segment
C.
LEFT UPPER LOBE

Lingular Segment 14"
Superior/Inferior
D.
RIGHT MIDDLE LOBE

Lateral Segment 14"
Medial Segment
E.
LOWER LOBES
Superior Segment
F.
LOWER LOBES
Anterior Basal 18"
Segment FIGURE 23-6 Cupped hand for manual percussion.
G.
LOWER LOBES
Lateral Basal 18"
Segment Ulnar surface
(vibration)
H.
LOWER LOBES
Posterior Basal 18"
Segment
I.
FIGURE 23-5 Segmental bronchial drainage positions.
FIGURE 23-7 Flat hand for vibration.
• The percussion should be applied for 3–5

minutes continuously in each of the positions the other, pressing the upper hand and lower
utilized. hand into each other for vibration.
• The therapist presses the hands firmly against the
chest wall, sending the vibrations to the chest wall
Vibration. Vibration is also a technique that may
and through to the lung parenchyma by pressing.
stimulate the movement of secretions.
• The hands are flattened and contoured to the
• The therapist places a hand firmly on the chest chest wall (Figure 23-7), not cupped as in
wall over the lung segment being treated and percussion.
tenses the muscles from the shoulders to the • The vibrations are applied at the end of inspira-
hands, producing vibrations. Some therapists tion and continuously throughout a prolonged
may be more comfortable placing one hand over and complete exhalation.
• The therapist should be mindful of the normal

movement of the rib cage and follow the rib cage
movement when applying the vibrations.
PDPV can be followed with deep breathing and Image not available due to copyright restrictions
coughing to assist the movement and expectoration of
secretions.
FORCED EXHALATION TECHNIQUE

The forced exhalation technique (FET) consists of:
• One or two huffs (forced expirations), from Text not available due to copyright restrictions
midlung volume to low lung volume, followed
by a period of relaxed, controlled diaphragmatic
breathing.
• Bronchial secretions mobilized to the upper
airways are then expectorated. facilitating the movement of mucus. The method
• The process is repeated until maximal bronchial allows for improved airflow at lower lung volumes than
clearance is obtained. would be utilized for coughing and active breathing.
• The patient can reinforce the forced expiration The patient is trained to breathe at three lung volumes
by self-compression of the chest wall, using a in phases (Figure 23-8):
brisk adduction movement of the upper arm.16
• Breathing at low lung volume to loosen
secretions.
ACTIVE CYCLE BREATHING • A series of breaths at midlung volumes to move
Active cycle breathing (ACB) incorporates the FET secretions to larger airways.
and two additional components: thoracic expansion • Then a series of high-volume breaths to expel
exercises and diaphragmatic breathing. The three secretions.
components are combined in a set cycle:
The patient must be instructed to balance maximal
1. Relaxation and breath control expiratory flows against collapse of unstable airways.
2. Three to four thoracic expansion exercises The goal is to achieve a mucus rattle, not a wheeze.
(possibly with percussion, vibration, chest Auditory, visual, and tactile feedback are essential to
compressions) the effective teaching of this technique.
3. Relaxation and breathing control
4. Three to four thoracic expansion exercises Biofeedback and Breathing Retraining. One of the
(possibly with percussion, vibration, chest concerns regarding the use of these techniques is the
compressions) difficulty in teaching the breathing patterns to
5. Relaxation and breathing control patients. Biofeedback devices may be useful in achiev-
6. One or two forced expirations (huffs) ing adequate performance of the maneuvers and in
7. Relaxation and breathing control coaching patients who may not be able to pay atten-
Theoretically, the ACB technique includes the tion during therapy sessions. Biofeedback technology
benefit of the FET and the improvement of alveolar adds additional cost to therapy sessions; however, the
aeration. Benefits of ACB are: long-term outcomes may improve enough to offset
this added cost.
• Independence for patients who are capable of
performing the maneuver.
• The absence of desaturation, or physical MECHANICAL ADJUNCTS TO CHEST PHYSICAL
compromise during its performance. THERAPY
• No need for costly equipment. A wide variety of devices are useful adjuncts to CPT.
The technique is not useful for infants, young Mechanical percussors, vibrators, and positioning
children, and others who cannot follow instructions or appliances allow for improved consistency and may
who are otherwise unable to perform the maneuver. increase compliance with the plan of care.
Mechanical Percussion and Vibration. Traditionally,

AUTOGENIC DRAINAGE PDPV has been performed using manual techniques
Autogenic drainage is a breathing training technique for percussion and vibration. Some of the negatives of
that theoretically improves airflow in the small airways, manual percussion and vibration are fatigue and
Continuous Positive Airway Pressure. During continu-

ous positive airway pressure (CPAP) therapy, the patient
breathes through a system that is capable of maintain-
ing positive pressure throughout the breathing cycle.
There should be very little fluctuation in airway
pressure during inhalation and exhalation. The primary
goal of CPAP therapy is to achieve a normal functional
residual capacity (FRC). The improved FRC is usually
accompanied by an increase in PaO2, decreased intra-
pulmonary shunt, work of breathing, and oxygen
consumption. CPAP increases collateral ventilation to
collapsed lung regions and assists in the inflation of
collapsed regions and removal of secretions.17
Positive Expiratory Pressure Therapy. After its

introduction in Scandinavia in the late 1970s, positive
expiratory pressure (PEP) therapy has gained wide
acceptance in Europe, Canada, and the United States.
The original application was for patients who had
difficulty clearing secretions, and it is now used as an
alternative or adjunct to traditional bronchial hygiene
modalities.
When used appropriately, PEP therapy can improve
FIGURE 23-9 Palm cup percussors. airway patency and airflow into and out of partially
Courtesy of Smiths Medical obstructed airways. The improved airflow enhances
mucus clearance. The positive pressure during exhala-
tion encourages collateral ventilation, which allows
inconsistencies in application when different therapists air to enter collateral ventilation channels and open
provide the therapy. Partial solutions include the use of airways behind mucus obstructions (Figure 23-10).
mechanical adjuncts to supplement the PDPV. An additional effect of the positive pressure during
A number of devices are available and used as exhalation is the splinting (Figure 23-11) of airways,
mechanical adjuncts to PDPV. These devices are which acts to oppose the premature collapse of airways.
generally referred to as percussors and vibrators. Percussors With the airway splinted open, the expiratory airflow
are motor-driven (electrical or pneumatic) pistons to can move secretions into larger airways, from which
which a cushioned rubber cup is attached. There are they can be coughed.
also manual models (Figure 23-9). The percussor can The positive expiratory pressure is developed when
be applied in the usual PDPV positions. the patient exhales against a resistance, provided by
either a fixed-orifice resistor or a threshold resistor. The
Tilt Table. A drainage table or board may provide an pressures generated during expiration range from 10 to
advantage in positioning patients. These commercially
available devices are constructed to adjust angles and
heights for optimal therapy sessions. They are also
helpful in achieving comfortable positioning of the
patient and the caregiver. When these are not conve-
nient, pillows, foam wedges, or cushions can be used
to optimize positioning.
POSITIVE AIRWAY PRESSURE ADJUNCTS TO

BRONCHIAL HYGIENE THERAPY
Positive airway pressure adjuncts are used to mobilize
secretions and to treat atelectasis. They include
continuous positive airway pressure (CPAP) and
positive expiratory pressure (PEP), with or without
vibration. These techniques are used with cough FIGURE 23-10 Collateral ventilation.
techniques and other bronchial hygiene therapies. Courtesy of DHD Healthcare. Canastota, New York
Elevated intrathoracic pressure can Pursed-lips breathing (or use of a fixed

compress unstable airways during exhalation. orifice resistor such as a PEP device)
creates back pressure that splints the
airway open during exhalation.
FIGURE 23-11 Splinting of airways during exhalation with PEP.
Courtesy of DHD Healthcare, TheraPEP ® PEP Therapy System
20 cm H2O; additionally, no pressurized gas source is traditional therapies and does not require precise
required. positions that are often uncomfortable or painful for
A distinct advantage to PEP therapy as an adjunct the patient. When used in conjunction with FET, or
or alternative to traditional therapy is that it can be huff coughing, it appears to be an effective therapy
self-administered. It is not as time-consuming as for enhancing secretion removal (Figure 23-12).
FIGURE 23-12 TheraPEP® Therapy System.

Courtesy of Smiths Medical
Positive Expiratory Pressure with High-Frequency Movement of mucus

Oscillation (Vibratory Positive Expiratory Pressure
Therapy). Two commercially available devices, the
Flutter® (Axcan Scandipharm) (Figure 23-13) and the
Acapella® Smiths Medical (Figure 23-14) incorporate
PEP therapy and high-frequency oscillation (HFO) Bronchus
and deep breathing to improve mucus clearance. The wall
Pressure
waves
FIGURE 23-15 Vibration of airway with loosening of mucus.
addition of oscillation at frequencies 6–20 Hz theoreti-

cally vibrates the airways to loosen secretions.
• The Flutter device consists of a hardened plastic
pipe with a mouthpiece at one end and a steel
(A)
ball resting in a cone at the other end. As the
patient exhales through the Flutter, the steel ball
rolls and bounces up and down. The motion of
Perforated the ball and the resultant intermittent opening
protective cover
Circular cone and closing of the tube cause oscillations that
High-density resonate and are amplified in the airways
stainless steel ball
(Figure 23-15).
• The Acapella device directs exhaled air through
an opening that is periodically closed by a
pivoting cone. As air passes through the opening,
Mouthpiece the cone alternately closes and opens the airflow
(B) path. The result is a vibrating pressure waveform.
FIGURE 23-13 (A) Flutter valve. (B) Schematic of flutter
Acapella is available in two flow rate ranges for
valve. patients who can achieve greater than 15 Lpm.
(A) Courtesy of CareFusion
The other device is available for patients who are
capable of achieving less than 15 Lpm. The
frequency of vibration can be adjusted by
turning a dial on the exhalation port.
Intermittent Positive Pressure Breathing. After

gaining wide acceptance without benefit of controlled
studies,18 the intermittent positive pressure breathing
(IPPB) mode of therapy is now infrequently used.
However, in some conditions it is considered a useful
intervention:
• In disease states in which the patient’s inspira-
tion is limited.
• When the patient’s vital capacity is less than
15 mL/kg, owing to an acute illness or chronic
condition that has caused a temporary deteriora-
tion in the patient’s overall respiratory state.19
Assisted Cough Techniques. Pulmonary complica-

FIGURE 23-14 Acapella Vibratory PEP Therapy System tions are major causes of morbidity and mortality for
(green for high flow and blue for low flow). patients with severe expiratory muscle weakness. The
Courtesy of Smiths Medical vital capacity, forced vital capacity, and peak cough
(A) (B)
FIGURE 23-16 (A) Manually assisted cough via thoracic compression. (B) Manually
assisted cough via abdominal thoracic compression.
expiratory flows are diminished during respiratory tract

infections because of fatigue, weakening of inspiratory
and expiratory musculature, and mucus plugging.
PDPV techniques are often problematic or ineffective
in patients with severe musculotedinous contractures,
skeletal injury, or limited mobility20 (Figure 23-16).
Cough efforts can be improved with devices and
techniques that simulate natural coughing. Manual
thrusts applied to the anterior chest wall or abdominal
thrusts may be adequate to prevent pulmonary compli-
cations. However, these techniques must be used with
caution in patients with fragile chest walls and indwell-
ing abdominal or pelvic catheters. They should not be
used on patients with Greenfield filters.20
Manual ventilators have also been utilized to
simulate the cough mechanism. The manual ventilator
FIGURE 23-17 Philips Respironics Cough Assist device.
is used to deliver a deep breath and inspiratory hold. A
sudden release of pressure allows expiration at higher
velocities than what the patient may develop without
assistance. The positive pressure on inspiration may clearing retained bronchopulmonary secretions by
also be applied with intermittent positive pressure gradually applying a positive pressure to the airway,
breathing devices. and then rapidly shifting to a negative pressure
[mechanical insufflation and exsufflation with negative
Mechanical Insufflation and Exsufflation with pressure (EWNP)]. This rapid shift in pressure produces
Negative Pressure. The Philips Respironics Cough a high expiratory flow rate from the lungs, simulating
Assist (Figure 23-17) is used to assist patients in a cough.
The indication for the use of this device is the mechanisms for the improvement in mucus clearance
inability to cough or clear secretions effectively owing have been proposed. Most are associated with:
to reduced peak expiratory flow (less than 5–6 Lps).
• An increase in mucus-airflow interaction that
This indication is often associated with high spinal
appears to decrease the sputum viscosity.
cord injuries, neuromuscular deficits, or severe fatigue
• And a shearing mechanism resulting from the
associated with intrinsic lung disease.
oscillatory airflow, which loosens and mobilizes
The Cough Assist is usually applied by giving the
secretions.
patient 4–5 coughing cycles in succession, and then
allowing the patient to rest for 20–30 seconds. The During HFCWO, small gas volumes alternately
resting period helps avoid the hyperventilation that flow into and are withdrawn from an inflatable vest
may result from the cough cycles. During the resting (Figure 23-18) by an air-pulse generator at user-con-
period, any visible secretions should be removed. trolled frequencies of 5–25 Hz. These pressure pulses
The cycles can be repeated 6–10 times for a full are superimposed on a small positive pressure back-
treatment. ground (0.0125 psi). The mean pressure exerted on the
chest wall is also user controlled. HFCWO produces:
• Pressures are allowed to build up slowly over
2–3 seconds. • Transient increases in airflow.
• Then the device is switched to “exhale” to induce • Coughlike shear forces.
cough. • Alterations in the physical properties of mucus.
• The exhalation pressure is maintained for 1–2 • Increases in mucus mobilization.
seconds. Indications for the utilization of HFCWO generally
• The machine can be left in the “neutral” position follow the guidelines established by the AARC for
for a few seconds or switched to positive pres- airway clearance therapies. The decision to utilize
sure for another cough cycle, depending on the HFCWO therapy requires a patient-specific assessment
patient’s preference. of the potential benefits versus the potential risks.
Individual patients require special settings for Absolute contraindication to the use of HFCWO are:
maximum positive and maximum negative pressures. • Head and/or neck injury not yet stabilized.
For patients using the device for the first time, begin • Active hemorrhage with hemodynamic instability.
with lower pressures to let them get the feel of
EWNP. Subsequent treatment pressures can then be
increased as necessary to achieve adequate secretion
clearance. Maximum positive pressure with the device
is 60 cm H2O, and maximum negative pressure is
60 cm H2O.
Potential contraindications to the use of EWNP are
bullous emphysema, susceptibility to pneumothorax or
pneumomediastinum, and recent barotrauma. Patients
with cardiac instability should be monitored for pulse
and oxygen saturation very closely.
High-Frequency Chest Wall Oscillation. High-

frequency chest wall oscillation (HFCWO) is also
referred to as:
• External chest wall oscillation (ECWO).
• External oscillation of the chest.
• High-frequency chest compression (HFCC).
• High-frequency chest wall compression
(HFCWC).
• High-frequency transthoracic ventilation (HFTV).

In 1966, Beck demonstrated the effectiveness of
so-called thoracic vibrocompression in chronic bron-
chial asthma and emphysema.21 Further investigations
have documented the effectiveness of HFCWO and
its ability to enhance mucus clearance. Possible FIGURE 23-18 Vest airway clearance system.
Relative contraindications are:

• Subcutaneous emphysema.
• Recent skin grafts on the thorax.
• Burns, open wounds, and skin infections of the
thorax.
• Recently placed transvenous or subcutaneous
pacemaker.
• Suspected pulmonary tuberculosis.
• Lung contusion. Image not available due to copyright restrictions
• Complaint of chest wall pain.
Therapy should be reevaluated and/or modified if
the following circumstances are present:
• Pulmonary hemorrhage.
• Hypoxemia.
• Increased intracranial pressure.
• Vomiting and aspiration.
• Acute hypotension during the procedure.
• Bronchospasm. Text not available due to copyright restrictions
• Pain or injury to muscles, ribs, or spine.
• Dysrhythmias.
aerosols is also available. The PercussiveTech HF is
designed to oscillate primarily on exhalation. Please
INTRAPULMONARY PERCUSSIVE VENTILATION note that in general the devices discussed above also
THERAPY oscillate as the patient exhales. The PercussiveTech HF
Intrapulmonary percussive ventilation (IPV) is a provides intrapulmonary percussion at 360–840 cycles
form of physical therapy administered to the airways per minute at a maximum pressure of 20 cm H2O
by a pneumatic device called a percussionator or intrapul- when operated according to the manufacturer’s instruc-
monary percussive device. tions (Figure 23-19).
• The patient breathes through a mouthpiece and COMBINED MECHANICAL AND ACOUSTICAL
the percussionator delivers high-flow-rate bursts VIBRATION
of gas into the lungs 100–300 times per minute.
The Frequencer is described as a digitally controlled
• During the percussive bursts of gas into the
electroacoustical transducer device. It has a control unit
lungs, continuous positive pressure is main-
(digital frequency generator and amplifier) and a
tained while the pulses progressively dilate the
transducer that applies mechanical and acoustical
airways.
stimulation to the chest wall. Typical frequency of
• At the end of the percussive interval (5–10
vibration is 30–70 Hz depending on the patient needs
seconds), a deep exhalation is performed with
(see Figure 23-20).
resultant mucus transport; then the cycle is
The manufacturer has set a default frequency at
repeated. Coughing is performed as necessary
30 Hz. However, the recommendation is to find the
to clear secretions.
“best” setting by adjusting the volume and frequency
The therapy period lasts approximately 20 minutes. to a level that the patient finds comfortable. Indications
The device is also capable of delivering a medicated
or nonmedicated aerosol.
A recently introduced device, the MetaNeb System,
(Hill-Rom Services, Inc.) is capable of providing lung
expansion with medicated aerosol and continuous
positive pressure, or secretion clearance with medicated
aerosol while oscillating the airways with continuous
pulses of pressure. The device can also automatically
alternate between these modes.
A single-patient device capable of delivering
high-frequency intrapulmonary percussive ventilation FIGURE 23-20 Frequencer.
with simultaneous administration of medicated Courtesy of Dymedso, Inc.
CASE STUDY 23-1

B. T. is an 8-year-old girl who was hospitalized
for the sixth time in the past 8 months. All of
the previous admissions were for the treatment
of various pneumonias. The X-ray on admission
is consistent with bronchiectasis and
atelectasis of the lower lobes. Traditional
methods of CPT or PDPV have resulted in
minimal improvement of the patient’s
pulmonary status.
Questions
1. Evaluate the effectiveness of the therapy
provided.
2. What, if any, alternatives to traditional CPT
FIGURE 23-21 Placement of device for frequencer. or PDPV might be considered?
Courtesy of Dymedso, Inc.
3. How else might bronchial hygiene be
improved in this case?
that optimal frequency is being reached are a desire to

cough and a change in voice. Since sound moves better
through relaxed muscle, the patient is instructed to relax
care of immobilized patients. This movement ensures
the shoulder and chest muscles. The patient should also
that one lung is raised above the other. The constant
take deeper breaths than usual, exhale through pursed-
changes in position may enhance secretion clearance,
lips and use abdominal muscles to increase diaphragm
resulting in effective therapy for the treatment and
excursion slightly. The transducer is applied to the six
prevention of pulmonary complications. There may
regions, as shown in Figure 23-21. The default treatment
also be some benefit with respect to the prevention
time is set at 20 minutes, after which the device auto-
of thrombophlebitis, pulmonary embolus, and
matically stops. The default treatment time can be
decubitus ulcer.
adjusted to accommodate physician prescription or
In recent years, specialty beds have become avail-
patient comfort. The Frequencer can be applied in
able that can rotate patients several times an hour at
either a seated or reclining position.
angles up to 67 degrees from the horizontal.23 This
Airway clearance devices generating vibrations that
mechanical turning of the body to 40 degrees or greater
can penetrate into the airways have the ability to alter
on each side is known as continuous lateral rotation
mucus rheology. The Frequencer is capable of generat-
therapy (CLRT), or kinetic therapy (KT). CLRT is a
ing higher frequencies than other devices (30–70 Hz).
method of providing constant turning of patients who
Theoretically, the more mucus that is agitated, the
have decreased mobility and who are unable to
more liquid it becomes.
reposition themselves (Figure 23-22).
CONTINUOUS LATERAL ROTATION (KINETIC)

SELECTION OF MUCOCILIARY CLEARANCE
THERAPY
TECHNIQUE
Immobilization is associated with hypoxemia, pooling
Selection of the mode, or combination of modes,
of secretions, and atelectasis in the dependent lung.
of therapy is largely based on a thorough evaluation
These conditions have the potential to promote
of the patient’s respiratory status. The primary indica-
pneumonia, and all appear to be diminished by
tion for pulmonary hygiene therapy must be defined.
mobilization. Frequent changes in position for
immobilized patients have been recognized as • Is the indication for prophylaxis?
beneficial in the treatment and prevention of pulmonary • Is the location of the pulmonary problem central
complication for many years. In 1954, Baker noted its or peripheral?
value in the treatment of poliomyelitis.22 For decades, • Can the patient cough and deep breathe?
half-hour rotations to alternating lateral positions • Can the patient cooperate to improve the
have been a standard of care in postoperative care and effectiveness of therapy?
TABLE 23-2 Recommendations for

airway clearance techniques in specific
conditions*
Cystic fibrosis, cilial Infants—PDPV
syndromes, bronchiectasis 3–12 years—exercise,
(require ACT) PEP, PDPV, ACB, HFCC
(HFao or flutter valve)
⬎ 12 years—exercise,
ACB, AD, PEP, PDPV,
HFCC
Atelectasis, abdominal PEP, PDPV
surgery
Prevention of postoperative PEP, ACB
atelectasis
Asthma (with mucus PEP, PDPV
FIGURE 23-22 Roto Rest.
plugging but without airleak)
RotoRest™ Delta Advanced Kinetic Therapy System. Courtesy of KCI Licensing, Inc.
Neurologic abnormalities PDPV, suction
(spasticity, bulbar palsy,
• Does the patient have complicating or limiting aspiration-prone)
factors that question the appropriateness of Musculoskeletal weakness PEP, negative and
some modes of therapy? (muscular dystrophy, positive-assist devices
myasthonia, poliomyelitis)
All such questions should be answered prior to initiat-
ing therapy (Tables 23-1 and 23-2). *ACT ⫽ airway clearance technique; PDPV ⫽ postural drainage,
Respiratory therapists should also consider percussion, and vibration; PEP ⫽ positive expiratory pressure;
ACB ⫽ active cycle of breathing; HFCC ⫽ high-frequency chest wall
that individual patient responses to therapy are compression; HFao ⫽ high-frequency compression at the airway opening;
extremely variable and that there is no evidence yet and AD ⫽ austogenic drainage
that any single treatment is superior to another. It Source: From Hardy KA. A review of airway clearance: new techniques,
may be necessary to try several airway clearance indications, and recommendations. Respir Care. 1994; 39:450.
techniques to find the one that works well for the
Best Practice
TABLE 23-1 Factors to be considered when
selecting an airway clearance technique Bronchial Hygiene
• Motivation In addition to determining the most effective tech-
• Patient’s goals nique for clearing secretions, the patient’s underly-
• Physician’s/caregiver’s goals ing problems must also be considered. Techniques
or therapies that benefit the underlying problems
• Effectiveness (of considered technique) often enhance the effectiveness of bronchial
• Patient’s age hygiene. The coordination of other appropriate
• Patient’s ability to concentrate therapies can also benefit the patient. For example:
• Ease (of learning and of teaching) • Dehydration has a negative effect on the
• Skill of therapists/teachers mobilization of secretions, and a bronchodi-
• Fatigue or work required lator, if indicated, can help in this respect.
• Physical therapy and rehabilitation might
• Need for assistants or equipment
be more effective if the patient has cleared
• Limitations of technique based on disease type and secretions prior to the session.
severity • Sleep patterns should be considered when
• Costs (direct and indirect) preparing a schedule for therapy sessions.
• Desirability of combining methods A rational approach to all relevant aspects of
Source: From Hardy KA. A review of airway clearance: new techniques, patient care must be a part of the treatment plan.
indications, and recommendations. Respir Care. 1994; 39:449.
Most of the hazardous situations noted are the

CASE STUDY 23-2 result of the position required for optimal CPT or
PDPV. Patients who have responses to CPT or PDPV
M. S., a 20-year-old patient, was admitted to the that are unexpected or that may limit its effectiveness
emergency department after a high-speed motor may benefit from techniques that are not position
vehicle accident. On his arrival, the injuries dependent (PEP therapy with/without vibration,
noted were a fractured right femur and right high-frequency chest wall oscillation, and the like).
forearm. There were no complaints of difficulty When utilizing modalities that require pressure to
breathing, and his level of consciousness did not augment lung expansion, the respiratory therapist has
appear to be altered. Mark later complained of to consider additional complications and hazardous
increasing breathing difficulty. The attending situations.
physician suspected a fat embolism. • Tension pneumothorax is the only absolute
During the ensuing two weeks. Mark’s contraindication cited with regularity.
condition deteriorated and required mechanical • Cardiovascular side effects that are often associ-
ventilation. A tracheostomy was performed to ated with increased intrathoracic pressure are
improve pulmonary hygiene and airway care. reduced venous return, reduced cardiac output,
Mark was noted to have atelectasis. and tachycardia.
Questions • Increased intracranial pressure is also a concern.
• Pulmonary barotrauma is a potential complica-
1. Evaluate the effectiveness of the therapy tion of positive pressure generation.
provided.
2. What recommendations might optimize
pulmonary hygiene? Summary
3. How else might bronchial hygiene be
Under normal conditions pulmonary hygiene is
improved in this case?
ongoing, and individuals are generally unaware of the
processes involved. When chronic or debilitating
illnesses develop, patients often need assistance to
individual patient. The RT must also recognize that maintain pulmonary hygiene, ranging from education
individual patients may prefer to utilize airway and encouragement to complex devices and regimens.
clearance techniques that are self-administered.24 The chapter reviewed a number of techniques
and devices that are used to promote the removal of
retained secretions and to reduce the likelihood of
COMPLICATIONS AND ADVERSE EFFECTS progressive worsening of pulmonary function. Proper
OF CHEST PHYSICAL THERAPY nutrition and fluid balance, as well as the incorpora-
Complications that may be the result of cough efforts tion of physical conditioning into the care plan, should
have already been noted. Adverse effects that may be not be neglected. The use of pharmacologic agents to
related to PDPV are: improve air distribution and alter the physical charac-
teristics of mucus must also be considered when
• Bronchospasm. appropriate. Additionally, the caregiver must be
• Transient hypoxemia. prepared to remove secretions by performing
• Increased intracranial pressure. tracheal aspiration when necessary.
• Hypotension. The selection of therapy modalities and develop-
• Pain. ment of a care plan must be based on the nature of
• Vomiting. the problems being addressed; the patient’s ability or
• Dysrhythmias. desire to comply with proposed regimens, and the
In the event of a significant change in clinical complexity of equipment and associated expenses.
status during therapy:
• Stop the session.
• Return the patient to the prior or a comfortable Study Questions
position. REVIEW QUESTIONS
• Contact the physician.
• If necessary, consider increasing the inspired 1. List the three general indications for CPT or PDPV.
oxygen concentration, and call for assistance if 2. An analogy often used to illustrate the concept of
needed. CPT or PDPV is the ketchup bottle. Discuss the
similarities between getting ketchup out of the 6. Active cycle breathing is sometimes described as a
bottle and mucus clearance. combination of the FET maneuver and:
3. List the four phases of an effective cough. Give one a. diaphragmatic breathing and intrapulmonary
illustration of a disorder that would compromise percussive ventilation (IPV).
each of the four phases. b. thoracic expansion exercises and PEP
therapy
4. Discuss the rationale for continuous lateral rota-
c. intrapulmonary percussive ventilation (IPV)
tion therapy (CLRT) or kinetic therapy (KT).
and postural drainage (PD).
d. thoracic expansion exercises and diaphragmatic
breathing.
MULTIPLE-CHOICE QUESTIONS 7. PEP therapy may be helpful in promoting the
1. An ineffective cough is often associated with: expectoration of mucus by:
a. maximum expiratory pressures greater than a. allowing peripheral airways to collapse during
80 cm H2O. exhalation.
b. weakened abdominal muscles. b. improving air distribution with positive
c. vital capacity greater than 80% of predicted pressure during inhalation.
vital capacity. c. minimizing collateral ventilation.
d. inspiratory capacity greater than 80% of d. generating a slight increase in pressure during
predicted inspiratory capacity. inspiration.
2. Percussion of the chest wall should always: 8. Continuous lateral rotation therapy (CLRT):
a. be performed with a cupped hand, or a. is a method of providing constant turning of
mechanical adjunct. patients to minimize complications that might
b. be performed over bare skin. result from immobilization.
c. be performed for a maximum of 30 seconds to b. has no application in preventing pulmonary
1 minute in each position. complications in immobilized patients.
d. be performed during inspiration only. c. has its greatest effect on secretion clearance if
the rotation is limited to less than 20 degrees
3. Drainage of the posterior basal segments is best from horizontal.
accomplished with the patient in which of the d. should never be used with patients who have
following positions? decreased mobility.
a. the foot of the bed elevated 30 degrees, lying on
the abdomen, head down
b. the foot of the bed elevated 15 degrees, lying
on the back, head down CRITICAL-THINKING QUESTIONS
c. the head of the bed raised to a 30-degree angle,
lying on back 1. A patient presents with a consolidation of the left
d. the bed flat, lying on the abdomen lower lobe. The respiratory therapist auscultates the
chest and hears bronchial breath sounds over the
4. Indications for CPT or PDPV include all of the
left posterior basal region. A recent chest X-ray
following except:
indicates the presence of an air bronchogram. How
a. difficulty expectorating secretions with expected
would the RT develop a bronchial hygiene plan for
sputum production greater than 25 mL/day in
this scenario?
adults.
b. presence of an artificial airway and evidence of 2. The therapist receives an order to perform CPT or
retained secretions. PDPV on a child. The right middle lobe appears to
c. bilateral pleural effusions. be one of the regions that needs to be addressed.
d. cystic fibrosis. How would the RT develop a bronchial hygiene
plan? What postural drainage position(s) would
5. When instructing a patient to cough effectively
be utilized?
during the immediate postoperative period, you
should instruct the patient to: 3. A patient presents with a consolidation of the
a. support the incision with a pillow. right lower lobe. The therapist auscultates the
b. inspire at low tidal volumes to control pain. chest and hears coarse crackles over the right
c. minimize abdominal muscle contraction posterior basal region. A recent chest X-ray indi-
during exhalation. cates that no air bronchogram is present. How
d. minimize movement of the rib cage during would the RT develop a bronchial hygiene plan for
inspiration. this scenario?
4. A physician asks the respiratory therapist for input 15. Murray JF. The ketchup bottle method. N Eng J
on developing a bronchial hygiene plan for a Med. 1979;300:1155–1157.
patient. The patient is expected to be immobilized 16. Pryor JA, Webber BA, Hodson ME, Batten JC.
for a prolonged period of time owing to injuries Evaluation of the forced expiration technique as an
suffered in a motor vehicle accident. How would adjunct to postural drainage in treatment of cystic
the RT proceed in developing a bronchial hygiene fibrosis. Br Med J. 1979;2:417–418.
plan for this scenario? 17. Branson RD, Hurst JH, DeHaven CB. Mask CPAP:
State of the art. Respir Care. 1985;309:846–857.
18. Pierce AK, Saltzman HA. Conference on a scientific
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Respir Care. 2007;52:1150–1158. prevention of respiratory complications during
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cough and autogenic drainage. Respir Care. 1447–1457.
2007;52:1210–1223. 24. Main E, Prasad A, van der Schans CP. Conventional
8. Irwin RS, Rosen MJ, Braman SS. Cough: A chest physiotherapy compared to other airway
comprehensive review. Arch Intern Med. 1977;137: clearance techniques for cystic fibrosis (Review).
1186–1191. Cochrane Database of Systematic Reviews 2009;2.
9. Shapiro BA, Kacmarek RM, Cane RD, et al. Clinical
Application of Respiratory Care. 4th ed. St. Louis:
Mosby-Yearbook; 1991. Suggested Readings
10. Judson MA, Sahn SA. Mobilization of secretions in Bills GW, Soderberg RC. Principles of Pharmacology for
ICU patients. Respir Care. 1994;39:213–227. Respiratory Care. 2nd ed. Clifton Park, NY: Delmar
11. Szeinberg A, Tabachnik E, Rashed N, et al. Cough Cengage Learning; 1998.
capacity in patients with muscular dystrophy. Sorenson HM, Thorson JA. Geriatric Respiratory Care.
Chest. 1988;94:1232–1235. Clifton Park, NY: Delmar Cengage Learning; 1998.
12. Bach JR, Ishikawa Y, Heakyung K. Prevention of Whitaker K. Comprehensive Perinatal and Pediatric
pulmonary morbidity for patients with Duchenne Respiratory Care. 3rd ed. Clifton Park, NY: Delmar
Muscular Dystrophy. Chest 1997;112:1024. Cengage Learning; 2001.
13. Gaskell DV, Webber BA. The Brompton Hospital White GC. Equipment Theory for Respiratory Care. 3rd ed.
Guide to Chest Physiotherapy. 2nd ed. London: Clifton Park, NY: Delmar Cengage Learning; 1999.
Blackwell Scientific Publications; 1973.
14. Frownfelter DL. Chest Physical Therapy and Rehabili-
tation: An Interdisciplinary Approach. Chicago: Year
Book Medical Publishers; 1978.
CHAPTER 24
Airway Management
Doug McIntyre
OBJECTIVES
• List and describe the two basic classifications of airway obstructions.
• List the indications for artificial airways.
• Describe a Carlens tube.
• List the advantages and disadvantages of the oroendotracheal tube versus the nasoendotracheal tube.
• Describe the difficult airway and identify the equipment and techniques used to manage the difficult
airway.
• Differentiate between a tracheostomy and a laryngectomy.
• Describe the Passy-Muir valve, and define the function of the valve.
• Differentiate between low-volume, high-pressure cuffs and high-volume, low-pressure cuffs.
• List the complications associated with airway suctioning.
• Explain the suction technique for the Trach Care suction device.
• Describe how to safely handle patients with artificial airways.
CHAPTER OUTLINE
Airway Management Tracheostomy Tubes
Artificial Airways Artificial Airway Cuffs
The Difficult Airway Airway Suctioning
Emergency Airway Adjuncts Artificial Airways and Patient Safety
Cricothyrotomy
KEY TERMS
airway obstruction cricothyrotomy endotracheal intubation
airway suctioning cuff fiberoptic intubation
artificial airways difficult airway tracheostomy tube
blind nasotracheal intubation emergency airway adjuncts
661
T
he upper airway does most of the condition- When acute airway obstruction occurs, the airway
ing of the ambient air; cleaning, warming and has to be opened.
humidifying, before it reaches the carina. They
condition the inspired air by correcting the
temperature and humidity and by cleansing it. Think of ARTIFICIAL AIRWAYS
the temperature of ambient air on a dusty road in a Artificial airways are indicated for:
desert being 112°F with a 10% relative humidity.
• The prevention or relief of airway obstruction.
Without conditioning, ambient air with those character-
• Providing an access to the airway for the purpose
istics would destroy the respiratory system. The upper
of suctioning.
airway filters out the dust, cools the air-to-body tem-
• Prevention of aspirating foreign substances into
perature, and humidifies the air-to-body humidity.
the airway.
The vocal cords are responsible for generating the
• Creating a closed system for mechanical
sounds of vocalization, and the upper airways are respon-
ventilation.
sible for phonation. The structure and movement of the
upper airways actually form the quality of the sounds Several different types of artificial airways are in use
that we use to communicate by speaking, singing, today. Each type has a specific application in airway
screaming, whispering, and making other sounds. management.
The most important function of the upper airway is
conducting air to and from the lower airways. Ventila- Nasopharyngeal Airways. Nasopharyngeal airways
tion is defined as the mass movement of air to and (Figure 24-1) are designed with a flared proximal tip,
from the lower airways. much like a trumpet. They are sometimes referred to as
This chapter focuses on the upper airway when a nasal trumpet. Nasopharyngeal airways are commonly
function is impaired. Impaired function necessitates manufactured from a soft flexible polyvinyl chloride
the use of artificial airways and adjunct therapy to material that contours to the nasopharyngeal structure.
mimic normal function. Discussed in this chapter are Nasopharyngeal airways are indicated for the
the numerous types of special-purpose artificial airways conscious patient who has difficulty maintaining a
and their applications. patent upper airway or who needs frequent suctioning.
The airway must be properly sized with the outside
diameter smaller than the nasal passage and well
Airway Management lubricated for insertion to prevent trauma to the nasal
mucosa. The advantages of the nasopharyngeal airway
The goal of airway management is to maintain an open are as follows:
airway to ensure adequate ventilation.
There are two basic classifications for airway • It provides relief for upper airway obstruction.
obstructions, or blockage: partial and complete. • It is better tolerated than the oropharyngeal
airway.
• With partial airway obstruction, some air is • It provides an easily accessible route for suction-
allowed to move, and the patient can cough and ing with less trauma to the nasal mucosa.
produce breath sounds.
• Complete airway obstruction differs in that there
is no movement of air, even with marked
inspiratory efforts.
The causes of airway obstruction are:
• The tongue occluding the airway (the most
common cause).
• Aspiration of foreign objects.
• Thick mucus in the airway.
• Laryngeal edema.
• Laryngospasm.
• Glottic edema.
• Subglottic edema.
Airway obstruction of the unconscious patient is
usually the result of loss of muscle tone in the tongue,
allowing the tongue to fall back and occlude the
airway. FIGURE 24-1 Nasopharyngeal airways.
CHAPTER 24 ■ Airway Management 663
The disadvantages of the nasopharyngeal airway are as

Best Practice follows:
• It is difficult to insert.
Opening the Airway • It should be alternated between the nares every
The preferred technique for opening the airway is 24 hours.
the head lift with the anterior movement of • Drainage for sinuses and eustachian tubes can be
the jaw by chin lift and jaw thrust, if indicated obstructed, potentially causing congestion or
(Figures 24-2 and 24-3). The jaw thrust is infection.
performed by placing the fingers behind the
mandible while the hands are on each side of the Oropharyngeal Airways. Oropharyngeal airways
patient’s face and then thrusting the jaw forward. (Figure 24-4) are available in two basic designs: the
If neck injury is suspected, begin with the chin Berman airway and the Guedel airway.
lift without the head tilt. If the airway is still
• The Berman airway has two horizontal plates
obstructed, the head tilt is gradually and very
connected by one ridge in the center of the
slowly incorporated until the airway opens.
airway. Each side of the ridge serves as a channel
Safety Note: Don’t use techniques that rotate or
to pass a suction catheter through to the laryngo-
extend the head until the “head and neck are
pharynx. The two horizontal plates provide a flat
cleared”; that is it is determined that there are
surface for the teeth to contact. The smooth
no head or spinal injures.
rounded tip prevents trauma to the soft tissue of
the upper airway.
• The Guedel airway is designed with one smooth
channel through the center. Suction catheters are
passed through the center channel into the
laryngopharynx.
Oropharyngeal airways are indicated for the
unconscious or nonresponsive patient who has diffi-
culty maintaining a patent upper airway. The size of the
airway to be inserted is determined by measuring from
the angle of the jaw to the tip of the chin.
The advantages of the oropharyngeal airway are that:
• It may be used with endotracheal tubes to
prevent problems associated with biting the tube.

• It can be used with seizure patients to prevent
the tongue from being bitten.
FIGURE 24-2 Head tilt, chin lift maneuver.

FIGURE 24-3 Jaw thrust maneuver. FIGURE 24-4 Oropharyngeal airways.

of a handle and a curved or straight blade, is used to

aid in the insertion by the oral route and sometimes by
the nasal route. The blade is gently inserted through
the mouth into the oropharynx until the vocal cords
are visualized. A light at the distal tip of the blade
facilitates vocal cord visualization. Then the endotra-
cheal tube is guided through the vocal cords and into
the trachea.
Verification of Placement Immediate verification of

endotracheal placement in the trachea is still a prob-
FIGURE 24-5 Endotracheal tube. lem. Verification is often necessary before an X-ray
machine is on the scene.
• The most common method is by auscultation of
The disadvantage of the oropharyngeal airway is the thorax for bilateral and equal breath sounds.
that conscious patients have difficulties tolerating it When breath sounds are unequal and present on
because of the gag reflex. one side only, main stem intubation must be
suspected. The tube must be withdrawn until
Endotracheal Airways. Endotracheal tubes (Figure 24-5) breath sounds are present on both sides.
are probably the most commonly used artificial • Auscultation of the thorax should be concurrent
airways. Historically, endotracheal tubes were manufac- with auscultation of the stomach. If sounds of
tured using red rubber. The cuff was supplied separately air are being introduced into the epigastrium
and required installation by the user. These cuffs were and not into the lungs, esophageal intubation
all low-volume, high-pressure cuffs inflated with high must be suspected.
pressures at low volumes by design. The invention of a
The introduction of disposable colorimetric CO2
clear polyvinyl chloride (PVC) endotracheal tube brought
detectors provides another method of placement
with it the advantage of being able to visualize secre-
verification (Figure 24-7). The presence of CO2 turns
tions in the tube. Originally, the cuff on the PVC tube
the media in the detector yellow. The color change
was also low volume, high pressure. The high-volume,
must be consistent with each exhalation because the
low-pressure cuff (i.e., high inflation volume at low
detectors are not 100% accurate. CO2 may not be
pressures) was introduced shortly after the advent of
present in sufficient quantities to change the color if
the PVC endotracheal tube.
cardiac output is insufficient to provide adequate
Endotracheal Intubation Endotracheal intubation pulmonary circulation.
is the introduction of an endotracheal tube into the The introduction of radiopaque lines placed in endo-
trachea, by either the oral or the nasal route. The oral tracheal tubes changed the standard for verification of
route is used most commonly in the acute situation. A tube placement (see Chapter 14). The radiopaque line
laryngoscope (Figure 24-6), an instrument that consists should be in place from the proximal end to the distal


FIGURE 24-6 Laryngoscope and blades.
tip and centered in the posterior curve of the endotra- Other considerations are as follows:
cheal tube. The use of a simple radiographic examina-
• Cloth tape performs better than silk or some of
tion of the chest became, and continues to be, the
the newer types of tape.
standard. With radiographic examination of the chest,
• The endotracheal tube should be retaped each
the radiopaque line can be visualized to determine the
shift.
placement of the distal tip of the endotracheal tube.
• If the skin is extremely moist, tincture of
The radiopaque line has been incorporated into the
benzoin is sometimes useful to ensure a secure
design of other devices used for insertion into the
bonding between the skin and the tape.
body. It improves the clinician’s ability to ascertain the
• Care must be taken to monitor the skin for signs
appropriate placement of tubes and other medical
of sensitivity and reactions to the tape. The tube
devices.
should be moved from one side of the mouth to
the other during retaping to avoid tissue break-
Tube Securing Methods Accidental extubation is a
down in the corner of the mouth.
common problem when the tube is not secured
properly. The therapist must therefore secure endotra- Manufactured securing devices are available for
cheal, tracheostomy, and laryngectomy tubes after the securing an endotracheal tube during a code. The
proper placement is verified. Advanced Cardiac Life Support Standards recommends
Securing tubes has been accomplished in a number several of such devices, which come in some creative
of ways. The widespread and first method ever used is styles and configurations. Most are effective; some are
taping endotracheal tubes in place. better than others.
Twill ties have been the mainstay of securing
• One-inch-wide tape, sufficient in length to reach
methods for tracheostomies and laryngectomies.
around the patient’s head with each end extend-
ing 6 inches past the tube, is used to secure the
tube.
• Another length of tape, sufficient to reach from
ear to ear behind the patient’s head, is placed in Spotlight
the center of the first length of tape. This makes a On
non-stick surface for the tape behind the
patient’s head that does not adhere to the Tube Holders
patient’s hair.
• The tape is placed around the patient’s head, and Several tube holders that have become available
both ends are split in the middle. One half of in recent years vary in design and methodology.
the split tape, on each side, is secured across the • One of these uses a piece of Velcro, which
patient’s upper lip under the nose or across is secured on the tube at the level of the
the chin, and the other split is wrapped around lip. The neckband attaches directly to the
the tube, with the sticky side to the tube. tube via the Velcro fastening method.
• Another holder secures the tube by placing
Patients who are conscious and alert should not be the holder component of the device to the
taped across the chin to avoid inadvertent extubation chin with adhesive. The tube is placed in
by movement associated with the chin. the holder and secured with a tying band
that resembles a plastic electrician tie.
• Still another has a bite block incorporated
into the holder and is secured with rubber
Best Practice straps.
Holders for tracheostomies and laryngec-
Endotracheal Intubation tomies are also available. Most of them are
Sometimes endotracheal intubation may take designed with a neckband made of soft material.
several attempts before the tube is properly On each end is a tab, manufactured from Velcro-
placed. The attempts must not exceed 30 sec- like material, that threads through the tracheos-
onds without reoxygenating the patient. If the tomy tube plate and folds back to attach to the
person attempting the intubation is unsuccessful neckband. Even though the neckband stretches
after two attempts, the patient should be returned for comfort and safety, the tabs can be removed
to 100% oxygen bag-and-mask ventilation, and and reattached repeatedly due to the Velcro-like
another rescuer should attempt the intubation. material.
I.D
.4
.0
Z7
9-
I.T
.
5
O
ra
l/N
as FIGURE 24-9 Double-lumen endobronchial tube.
al
O
.D
.
FIGURE 24-8 Tube markings.

Endotracheal Tube Sizes
Endotracheal tubes are available in sizes rang-
ing from 2.5 to 9.5 mm in diameter. The tube
Endotracheal Tubes Markings on an endotracheal tube size and cuff application are determined by the
may include the following (Figure 24-8): patient’s age and size (Table 24-1).
• IT indicates that the material used to manufac-
ture the tube has been implant-tested in living
tissue for toxic reactions. Stylet The stylet is a smooth, malleable metal or plastic
• Z79 indicates that the tube meets the standards rod that is placed inside an endotracheal tube to adjust
established by the American Materials Standard the curvature, typically into a the shape of a J or hockey
Institute’s Z79 committee. stick to allow the tip of the endotracheal tube to be
• Centimeter markings are used as a guide to directed through a poorly visualized or unseen glottis
determine how far the distal tip is inserted into (Figure 24-10).1 To avoid potential airway injury, the
the airway. stylet must not project beyond the end of the endotra-
• The size of the endotracheal tube in millimeters is cheal tube.
expressed in terms of internal diameter (ID) and
outside diameter (OD). Gum Elastic Bougie The gum elastic bougie is a blunt-
• The name of the manufacturer. ended, malleable rod that may be passed through the
Endotracheal tubes are manufactured to maintain poorly visualized or nonvisualized larynx by putting a
a curvature that resembles the curvature of the upper J-shaped bend at the tip and passing it blindly in the
airway, which aids in the intubation procedure. How- midline upward beyond the base of the epiglottis. The
ever, sometimes a small stylet, a thin rodlike device, endotracheal tube can then be advanced over the
must be placed in the lumen of the tube to change the bougie, which is then withdrawn.
curvature to facilitate a difficult intubation.
Specialty endotracheal tubes, designed for specific Lighted Stylet The lighted stylet is a malleable fiberoptic
uses, are also available. The double lumen endobronchial light source on which an endotracheal tube can be
sometimes refer to as a Carlen’s tube. (Figure 24-9) tube
has a double lumen design complete with two cuffs
TABLE 24-1 Endotracheal tube sizes
and two pilot balloons. It is used to intubate the right
mainstem bronchus with the distal cuff resting inflated Age Recommended Internal Diameter (mm)
in the right mainstem bronchus above the right upper Premature infant 2.5–3.0 uncuffed
lobe bronchial opening. The second cuff rests inflated
Full-term infant 3.0–3.5 uncuffed
in the distal end of the trachea. The purpose is to
perform independent lung ventilation. These tubes are 6 months–1 year old 3.5–4.5 uncuffed
also available in a left mainstem bronchial orientation. 1–6 years old 4.5–5.5 uncuffed
Both versions of these tubes have a carinal hook that 6–10 years old 5.5–6.5 uncuffed or cuffed
straddles the carina and prevents overly deep insertion 10 years old–adolescent 6.5–8.0 cuffed
of the tube and the blockage of segmental or lobar
bronchi openings. Adolescent–adult 7.0–9.0 cuffed
The disadvantages of the nasoendotracheal tube are that:

• The individual inserting the tube must exhibit a
high degree of skill to attempt the procedure.
• Size limitations of the nasal passage require the
use of a tube at least 0.5 mm smaller than for
oral intubation.
• The curvature of the tube is greater owing to the
insertion path.
• The size limitation and the increased curvature
of the tube makes it more difficult to suction the
patient, increases the work of breathing, and
raises airway resistance.
• Tissue necrosis may occur in the nasal passage
owing to the pressure exerted by the tube.
• Though less likely than with oral intubation,
FIGURE 24-10 Malleable stylet.
vagal stimulation still occurs.
• Drainage for sinuses and eustachian tubes can be
obstructed, potentially causing congestion or
infection.
mounted and subsequently advanced into the trachea • Laryngeal trauma is possible, just as is true for
when the light source has passed beyond the glottis. oral intubation.
The result is a greater intensity of light visible through
anterior soft tissues of the neck as the light source passes The advantages of the oroendotracheal tube are that:
beyond the vocal cords. The lighted stylet facilitates • It is the airway of choice in an emergency
blind tracheal intubation by distinguishing the tracheal situation because of ease of insertion.
lumen from the (more posterior) esophagus.2 • Size limitations are not as limiting as with the
A potential disadvantage is the need for low nasal route, thus allowing a tube at least 0.5 mm
ambient light, which may not be desirable (or easily larger.
achieved) in a critical care setting. Light wand devices • The curvature of the tube is not as great as with
may be contraindicated in patients with known nasal insertion because of the increased size of
abnormal upper airway anatomy and those in whom the insertion path (the complications associated
detectable transillumination is unlikely to be ade- with suctioning, work of breathing, and airway
quately achieved.3 resistance are of less significance than with nasal
intubation).
Endotracheal Tube Insertion Routes With appropriate • There is no interference with drainage from the
training, endotracheal intubation can be performed, and sinuses and eustachian tubes.
it is not restricted to use in the hospital environment.
There are two routes of insertion: nasoendotracheal The disadvantages of the oroendotracheal tube are that:
(nasal) and oroendotracheal tubes (oral). When the two • A laryngoscope is required for insertion, increas-
are compared, each has its advantages and disadvantages. ing the possibility of lacerating the lip or break-
The advantages of the nasoendotracheal tube are that: ing teeth if the procedure is improperly
• It can be inserted without the aid of a laryngo- performed.
scope in some instances. • Tube stabilization is more difficult than with the
• Once inserted, it can be stabilized easily. nasal route, with occasional resultant skin
• It is tolerated better by the patient because it irritation or trauma.
does not pass through the mouth. • Patients conscious enough to realize the pres-
• The patient can close the mouth and swallow. ence of the tube have a very low tolerance for the
• It is easier to provide oral hygiene. tube because of gag reflex, dry mouth, and
• Communication is better because the patient can general discomfort associated with having a
form words with the mouth. secured foreign object in the oral cavity.
• Connection to a ventilator or other equipment is • The patient’s mouth cannot be closed com-
easier. pletely, and swallowing becomes difficult.
• Turning and nodding pressures on the trachea • Oral hygiene is extremely difficult to provide.
are less likely. • Communication is difficult because of difficulty
• Inadvertent extubation is less likely. in forming words with the mouth.
• Vagal stimulation is more common than with

nasal intubation. Best Practice
• The tube may become dislodged more easily
than with nasal intubation. ET Tubes
• Inadvertent extubation is more common with
Neither the naso- nor the oroendotracheal tube
oral intubation.
should be ruled out for insertion until an assess-
• Ventilator and equipment connection and
ment of the patient’s airway is completed. The
stabilization is often more difficult.
individual performing the intubation may need to
• The tube forms a channel for secretions from
change from one type of endotracheal tube to the
the mouth to travel into the area above the cuff
other at the last second. Therefore, a variety of
and hence to the lungs, causing aspiration
tube sizes and types must be readily available at
pneumonia.4
the procedure site.
Endotracheal Tube Removal When the endotracheal
tube is no longer needed for ventilation, airway
stability, or secretion management, it can be Specialized Endotracheal Tubes Several types of special-
removed. Before extubation occurs, the patient’s ized endotracheal (sometimes called endobroncheal tubes)
airway above and below the cuff must be suctioned are used for specific purposes, one of which is used for
well to remove any secretions that may migrate into differential lung ventilation. In differential lung ventila-
the lung when the tube is removed. If secretions are tion, each lung is ventilated differently than the other.
already present in the lungs, care must be taken to These differences may result in different volumes, in
remove as many of the secretions as possible before different pressures, or perhaps in no ventilation at all in
removing the tube. one lung while the other lung is being ventilated
Then perform the following steps rapidly: mechanically or manually. The Carlen’s tube (a type of
endobroncheal tube) is a double-lumen, double-cuffed
• Remove the endotracheal securing device. endobrocheal tube with two pilot balloons, two infla-
• Oxygenate the patient well. tion lines, and two cuffs. In addition to the double
• Insert a suction catheter. lumens and double cuffs, Carlen’s tubes differ from
• Apply suction. other endotracheal tubes in that they come with either a
• Deflate the cuff while instructing the patient to right or a left orientation, each of which has color-coded
cough. inflation lines, pilot balloons, and lumen shafts as a
• Remove the endotracheal tube. safety measure to prevent accidental misconnections.
Once the patient is extubated, remember that cuff Due to its unique structure, the Carlen’s tube
pressures low enough to prohibit the necrosis of the provides the opportunity to perform procedures that
trachea might be high enough to reduce the normal would be otherwise impossible, extremely dangerous,
flow of the lymphatic system. The glottic and subglottic or even life-threatening to the patient. Table 24-2 lists
edema associated with these pressures may create some of the indications for and contraindications of
problems when the tube is removed. use of a Carlen’s tube.
• If the patient experiences difficulties, the first The Laryngeal Mask Airway The laryngeal mask airway
action is to start humidified oxygen to prevent (LMA) (Figure 24-11) is a small mask with an inflat-
resultant hypoxemia. able rim on the end of a tube. Developed in 1982 by
• If there is no sign of improvement or if Archie Brain, MD and approved for use in the US by
worsening is noted, it may become necessary the FDA in 1991, it comes in four sizes.5 It is inserted
to administer racemic epinephrine 2.25% and blindly with the mask facing the tongue until
normal saline in a small volume nebulizer. resistance is met. The mask is then inflated to cover
Racemic epinephrine has a vasoconstriction the opening of the trachea, providing a route for
action and produces shrinkage of the tissue in ventilation.
the larynx and vocal cords to reduce airway The LMA works well in approximately 90% of
resistance. cases. However, it is not without limitations, which
• Should symptoms of the edema persist, be include the following:
prepared to reintubate the patient.
• Ventilation may not be adequate because the
After extubation, the patient may exhibit cuff fails to seal the larynx, the tongue pushes
hoarseness, sore throat, and vocal cord trauma over the larynx, or the epiglottis flips over the
or paralysis. larynx.
TABLE 24-2 Indications and

contraindications for Carlen’s tubes
Lung isolation (separate access to each lung)
Indications:
Infection (prevent contamination of the nonaffected
lung)
Pulmonary hemorrhage
Control of the distribution of ventilation
Prevent air volume loss through the fistula due to
bronchopleural fistula
Prevent air volume loss through the fistula due to
bronchopleural cutaneous fistula
Surgical opening of major conducting airway
Giant unilateral cyst or bulla
Life-threatening hypoxemia from unilateral pulmonary
process
Unilateral bronchopulmonary lavage
Relative indications:
Surgical exposure (strong indication)
Thoracic aortic aneurysm
Pneumonectomy
Upper lobectomy
Mediastinal exposure
FIGURE 24-11 Insertion and placement of the laryngeal
Thoracoscopy
mask airway.
Surgical exposure (moderate indication)
Middle and lower lobectomy
Subsegmental resection
Esophageal resection • Laryngospasm can occur when the mask
Procedures on the thoracic spine is inserted or removed without adequate
Post-C-P bypass status after removal of totally anesthesia.
occluding chronic unilateral pulmonary emboli • It cannot protect against aspiration of gastric
content. (The operator must remember this.)
Severe hypoxemia from unilateral pulmonary
process
Requirement for differential ventilation for Esophageal-Tracheal Combitube The esophageal-tracheal
critical care combitube (ETC) (Figure 24-12) is a double-lumen tube
that is blindly inserted into the pharynx. One lumen is
Contraindications open to the end, similar to an endotracheal tube. The
Absolute contraindications: other lumen ends blindly with holes that wind up in
Patient refusal the vicinity of the opening of the larynx when the tube
Airway (especially laryngeal or tracheal) mass that is inserted into the esophagus. Once the tube is
may be occluding, dislodged, traumatized, or inserted, the operator inflates the small balloon on the
hemorrhaging end of the tube and the large, 100 mL balloon, which
occludes the pharynx. Verification of placement in the
Relative contraindications:
trachea is determined by the operator. If it is deter-
Patients requiring rapid intubation to prevent mined to be properly placed, the tube can then be used
aspiration of gastric contents for ventilation much like the endotracheal tube.
Patients who are likely to be difficult to intubate If the tube is determined to be in the esophagus,
ventilation can be accomplished by using the other
opening.
spontaneously breathing patients but is contraindi-

cated for patients with bleeding disorders. The nasal
mucosa should be prepared with phenylephrine
or oxymetazolone (Afrin) prior to the procedure.
Local anesthesia should be considered, especially
in the awake, sedated patient. The procedure is as
follows:
• Place the patient’s head and neck in the “sniffing
position,” if it is not contraindicated.
• The appropriate tube size for the nasal intuba-
A tion route is the same as used for the oral route.
Position the naso endotracheal tube connector
in a position that corresponds to the curvature of
the endotracheal tube to provide a reference for
guiding the endotracheal tube.
• Slowly advance the endotracheal tube along the
floor of the nose. Using the endotracheal tube
connector as a reference, guide the endotracheal
tube toward the larynx. This is slightly to the
opposite side of the nares that a tube is entering
(i.e., left for the right nares and right for the left
B nares).
FIGURE 24-12 (A) Combitube in the esophageal position. • Listen for breath sounds as the tube is advanced.
(B) Combitube in the tracheal position. • When the tube is correctly positioned in the
trachea, breath sounds will continue and the
patient will cough through the tube.
• Auscultate the breath sounds bilaterally, confirm
Sealing the esophagus with the small balloon tube placement and secure the tube. The absence
allows the evacuation of gastric contents through that of breath sounds and cough through the tube,
lumen. The ETC thus provides ventilation similar to while the tube is still being advanced, indicates
that accomplished with the endotracheal tube while that the tube is inappropriately placed in the
preventing gastric content aspiration. esophagus.8
The ETC has two major limitations:
• It comes in one size, which limits the applica-
tion to adults. THE DIFFICULT AIRWAY
• The trachea is not accessible for suctioning if the The difficult airway can result from:
tube is in the esophagus.
• An inability to open the mouth.
• Abnormal facial anatomy.
Fiberoptic Intubation. The fiberoptic scope can be
• Cervical immobility,
used in the unanticipated difficult airway but only if it
• Pharyngeal abnormality.
is readily available and the operator is skilled.6
• Laryngeal abnormality.
Fiberoptic intubation is usually more straightforward
through the nasal route instead of the oral route. The All can contribute to difficult tracheal intubation.
scope is advanced to the midtracheal level, and the Difficult tracheal intubation is tracheal intubation
carina is visualized. The endotracheal tube may then be that requires multiple intubation attempts. It may result
placed carefully through the nasal cavity and into the from difficulty in visualization of the larynx, a situation
trachea. Occasionally, passing the endotracheal tube termed difficult direct laryngoscopy.9 Visualization of the
through the vocal cords is difficult. Withdrawing the larynx is described using the Cormack and Lehane
endotracheal tube, rotating it 90 degrees counterclock- grades (Table 24-3).10 Grades 3 and 4 indicate difficult
wise, and readvancing it usually allows passage with direct laryngoscopy, and a nondirect laryngoscope may
less difficulty. The endotracheal tube should be posi- be required to obtain an airway.
tioned approximately 3 cm above the carina.7 Nondirect techniques are available. However, the
clinician must have the necessary equipment and
Blind Nasotracheal Intubation. Blind nasotracheal supplies to perform them. The recommended items for
intubation is especially valuable for intubating a difficult airway cart are listed in Table 24-4.
TABLE 24-3 Grades of Difficult Laryngoscopy Endotracheal Tube Removal in Patients with a
Difficult Airway. Patients with a difficult airway can be
Mallampati
problematic when it is time to remove the endotracheal
airway scale
tube. If there is a need for reintubation, the difficulty level
Grade I Most of glottis is is higher than the initial intubation. Reintubating these
seen. patients can be exceptionally difficult. The procedure for
removing the endotracheal tube from the difficult airway
patient is similar to removal from a patient intubated
without difficulty. The difference is that a plan must be in
place in the event that the patient requires reintubation.
And the plan should include a difficult airway cart and
Grade II Only posterior
skilled staff capable of reestablishing the airway.
portion of glottis
can be seen.
EMERGENCY AIRWAY ADJUNCTS
Approximately 30 years ago a category of devices was
created to fill the void presented when circumstances
Grade III Only epiglottis made it impractical or impossible to insert an endotra-
may be seen cheal tube. The category is known as emergency airway
(none of glottis adjuncts, and it includes the esophageal obturator
seen). airway and the esophageal gastric tube airway.
Esophageal Obturator Airway. The esophageal obturator

airway (EOA) (Figure 24-13) is a tube that looks a lot
Grade IV Neither epiglottis
like an endotracheal tube with a mask attached. It has a
nor glottis can be
cuff with small holes above the cuff and is designed to
seen.
be inserted into the esophagus, not the trachea. Once
inserted, the cuff is inflated to block the esophagus, the
mask seals the patient’s airway, and air blown into the
tube passes through the holes in the tube into the
Source: Cormack and Lehane patient’s lungs, not the stomach.
TABLE 24-4 Recommended items for EOA

difficult airway cart
• Bag mask ventilator with oxygen supply source
• Oropharyngeal airways, various sizes
• Nasopharyngeal airways, various sizes
• Endotracheal tubes, various sizes
• Endotracheal tube stylet
• Lighted stylet, if available
• Gum elastic bougie
• Laryngoscope with various type and size blades
• Laryngeal mask airway, various sizes
• Esophageal-tracheal Combitube, various sizes
• Endotracheal tube carbon dioxide detectors
• Cricothyroidotomy kit
• Tracheostomy mini kit

• Oxygen supply source with required connectors and
supply tubing
• Suction catheters and Yankauer suction device
• Spare bulbs and batteries as required FIGURE 24-13 Esophageal obturator airway.
Best Practice
Esophageal Obturator Airway
The end of the airway tube is sealed. If inadver-
tent intubation of the trachea occurs, the patient
cannot breathe. Also, tracheal intubation must
be done before the esophageal obturator airway
is removed to prevent aspiration when the patient
regurgitates.
FIGURE 24-14 Tracheostomy tubes.
The esophageal obturator airway is used primarily The disadvantages are the potential for:
by health care providers outside the hospital setting
when intubation efforts have failed or when personnel • Hemorrhage.
cannot intubate because of licensure or training • Thyroid, vocal cord, and esophageal tissue
limitations. The advantages of the esophageal obturator trauma.
airway are: • Pneumothorax and subcutaneous emphysema
related to the incorrectly performed
• Ease of insertion. procedure.
• Security of the airway from the aspiration of • The increase of airway resistance due to the small
gastric juices. diameter of the airway.11
• Prevention of gastric distention from air intro-
duced into the stomach.
The disadvantages of the esophageal obturator airway
TRACHEOSTOMY TUBES
are as follows:
Tracheostomy tubes (Figure 24-14) were common
• It is indicated for short-term use only. before a nucleus of professionals became adequately
• Esophageal trauma is possible. trained to insert endotracheal tubes. A tracheostomy
• The trachea can be inadvertently intubated. is primarily performed for use in long-term ventila-
• Regurgitation can occur when the tube is tion or in the case of permanent upper airway
removed. obstruction.
Nontoxic soft materials such as Teflon, silicone
Esophageal Gastric Tube Airway. The esophageal rubber, nylon, and PVC are used in the construction of
gastric tube airway (EGTA) has a gastric tube lumen in tracheostomy tubes and other artificial airways. PVC is
the center to permit decompression of the stomach the most common material in tracheostomy and
after bag and mask ventilation. Its use is compared endotracheal tubes. The Z79 committee of the
with the that of the EOA. The level of ventilation American Materials Standards Institute establishes the
provided by these devices is generally less than that standards for the composition of the materials that
provided by intubation of the patient. manufacturers use in the construction of medical
products.
The advantages of tracheostomies are that:
CRICOTHYROTOMY
• Suctioning is much easier than it is with endo-
The cricothyrotomy is an emergency airway procedure
tracheal tubes.
performed when upper airway obstruction renders it
• Trauma to the larynx is not a concern.
impossible to intubate or otherwise ventilate the
• The tube is secured easily, using ties around the
patient. A small opening is made between the cricoid
neck.
cartilage and the thyroid cartilage, allowing the patient
• Communication is facilitated.
to breathe below the obstruction.
• The oropharynx is free of foreign objects, which
The advantage of the cricothyrotomy is that an
allows the patient to eat or drink. thus making it
airway can usually be established quickly when other
more tolerable.
efforts fail.
The disadvantages of tracheostomies are twofold:

• Problems associated with the surgical
tracheotomy procedure, such as:
• Bleeding.
• Damage to the thyroid.
• The possibility of pneumothorax, subcutane-
ous emphysema, and air embolism associated
with air leaks.
airway
• Problems that occur after the stoma is com- esophagus
pletely healed, such as:
• Infection.
vocal cords
• Tracheal esophageal fistula. larynx
hole
• Erosion of the innominate artery. trachestomy (fenestration)
• Hemorrhage. tube
• Obstruction from mucus plugs. to ventilator cuff
• Inadvertent insertion into the subcutaneous
tissue. FIGURE 24-15 Fenestrated trach tube.
• Often constipation associated with the inability
to increase abdominal pressures influenced by
the vocal cords, which are bypassed.
Under normal circumstances, tracheostomy tubes Best Practice
should need to be changed only once a week. The tube
may need to be changed if the cuffed tube is too small, Fenestrated Tracheostomy
the cuff develops a leak, or the tube becomes Tubes
obstructed. Cleaning should be daily, and the ties are
Fenestrated tracheostomy tubes equipped with
to be cleaned or changed when they become soiled.
cuffs must have the cuff deflated before the plug
Ties are not too tight or loose if you can place two
is inserted into the outer cannula.
fingers between the ties and the neck.
Tracheostomy tubes are designed for specific
functions. Most have:
• An outer cannula with a neck plate to affix ties Silver Tracheostomy Tube. A number of silver tracheos-
for stability in the stoma. tomy tubes are still in use. It is constructed of sterling
• An obturator used to guide the tube into the silver and has an inner cannula matched to the indi-
stoma. vidual tube. A cuff must be installed externally when a
• An inner cannula, usually with a standard cuff is indicated. A fenestrated version of the silver
15 mm connector. The inner cannula can be tracheostomy tube is also manufactured.
removed for cleaning or eliminating obstruction The disadvantages of the silver tracheostomy are that:
without removing the outer cannula.
• Its rigid construction contributes to patient
The most common tracheostomy tube is the cuffed discomfort and pressure necrosis.
tracheostomy tube designed with the standard 15-mm • The metal can be irritating to the skin and
connector for ease of connecting equipment or ventila- contribute to the production of secretions.
tors. A low-profile tracheostomy tube is available for the
active patient concerned about cosmetic appearance. Laryngectomy Tubes. The laryngectomy tube
(Figure 24-16), designed much like the tracheostomy
Fenestrated Tracheostomy Tube. Another type is the tube, is shorter and usually has a larger internal
fenestrated tracheostomy tube (Figure 24-15), designed diameter. It is intended for use after a laryngectomy to
with a fenestration (hole) in the outer cannula of the maintain a patent airway. The most important thing to
tube that aligns with the tube’s distal opening. Remov- remember about the laryngectomy tube is that it
ing the inner cannula and plugging the outer cannula cannot be plugged. The larynx is absent, and the
allow the patient to breathe around the tube and patient cannot breathe through the oropharynx.
through the fenestration. This allows breathing through A respiratory therapist is a good resource for
the oropharynx and aids in the weaning process from providing instructions for appropriate care. Some
the tracheostomy tube. health care organizations provide support groups that
Best Practice
Laryngectomies
Patients with newly acquired laryngectomies or
permanent tracheostomies must receive appro-
priate instructions related to communicating,
eating, and caring for the new airway.
Trach-Button The Trach-Button (Figure 24-17) is a self-
retaining prosthesis for the maintenance of the tracheal
stoma. The Trach-Button is indicated for long- or short-
term patients who:
FIGURE 24-16 Laryngectomy tube. • May need to reinstate the use of a tracheostomy
in an emergency.
• Require repeated tracheostomies for conditions
such as myasthenia gravis, quadriplegia, polio-
myelitis, COPD, and sleep disordered breathing.
are beneficial to patients. Additional information is
• Must be evaluated during decannulation for
available from the American Lung Association and the
ability to cough and to manage secretions of the
American Cancer Society.
respiratory tract.
Airway Adjuncts for Tracheostomy Patients. Airway An expansion lock on the proximal end makes the
adjuncts for tracheostomy patients are available for Trach-Button self-retaining. Ties are not required to
different functions. secure the unit. The “petals” on the end of the cannula
Closure plug Hollow cannula

fits into cannula with expansion lock end
Ventilator adapter (optional) Spacers

fits into cannula in place of closure plug adjust cannula length
FIGURE 24-17 Trach-Button®.

Courtesy of Olympic Medical, Seattle, Washington
expand against the anterior wall of the trachea when cover the tube with a finger. Indications for the use of
the closure plug is inserted into the hollow cannula. special speech aids include but are not limited to:
This unique lock eliminates the danger of the unit
• Neuromuscular disease.
being ejected during violent coughing spells or hyper-
• Quadriplegia.
extension of the sternocleidomastoid muscles. The
• Head trauma.
cannula locks flush against the tracheal wall and does
• COPD.
not protrude into the tracheal lumen, allowing the
• Tracheomalacia.
patient to breathe through the mouth and nose, speak
• Mild tracheal stenosis.
normally, and expectorate more readily.
• Mild laryngeal stenosis.
The patient can be easily and conveniently suc-
• Vocal cord paralysis without airway obstruction.
tioned with the closure plug removed. A standard
• Nonobstructive laryngeal tumors.
15-mm fitting is available to replace the closure plug if
• Tracheostomized sleep apnea patient, used
mechanical ventilation becomes necessary.
instead of plugging while awake.
The Trach-Button is available in sizes of 9–14 mm
• Patients who cannot tolerate tracheal plugging,
in diameter and 15–40 mm in length. The length is
either psychologically or physically.
adjustable by using the spacers provided by the manu-
facturer, thus allowing adjustments as the length of the Trach-Talk Valves The Trach-Talk (Figure 24-18) allows
stoma changes. The device is constructed of Teflon and the patient to speak normally and cough more effective-
is comfortable, nonirritating, and well tolerated in ly. The device attaches directly to any standard trache-
long-term use. The external end of the device is small ostomy tube. The principal mechanism of the device is
and cosmetically unobtrusive.12 a one-way valve that is held in the open position by a
stainless steel spring.
Speech Aids Special speech aids are available to enable The valve remains open except during exhalation.
the tracheostomy patient to speak without having to The force of expiration closes the valve, allowing the
• Attaches to any trach tube.

• Patient does not have to
cover tube in order to speak.
• Triggered by patient's breathing.
Inhalation Exhalation
Spring-loaded, one-way valve One-way valve closes, forcing
remains open during inhalation. air and mucus up trachea and
past vocal cords.
FIGURE 24-18 Trach-Talk®.
Courtesy of Olympic Medical, Seattle, Washington
position except during inspiration. When the patient

breathes in, the valve opens, allowing air to enter the
airway. At the end of inspiration, the valve closes and
remains closed during the complete expiratory phase.
When the patient breathes out, the air is directed
through the larynx and pharynx, allowing the patient
to speak as air passes through the vocal cords and the
oral and nasal cavities. The positive closure design
creates a column of air in the tracheostomy tube,
FIGURE 24-19 Passy-Muir® tracheostomy and ventilator inhibiting secretions from entering the valve. The
speaking valve. normally closed position of the valve allows for a
Courtesy of Passy-Muir Inc., Irvine, California nearly normal closed respiratory system. The resultant
restoration of subglottic pressure facilitates a more
normal swallow, permits a stronger and more effective
expired air to flow through the larynx and enabling the cough that allows expectoration of secretions orally,
patient to speak. When exhalation stops, the spring and may reduce aspiration.
forces the valve into the open position again. The advantages of the valve are that it:
The use of Trach-Talk is indicated when mechani-
cal ventilation is no longer required and the patient is • Restores a closed respiratory system.
beyond the acute phase. It is not necessary to remove • Improves speech production.
the unit for suctioning, administering oxygen, or • Improves swallowing.
humidifying the inspired gases. Removing the cap from • Improves olfaction.
the distal end allows a suction catheter to be passed • Facilitates secretion management.
into the tracheostomy for suctioning. Oxygen or • Facilitates weaning.
humidity may be administered by connecting a large- • Reduces aspiration in some patients.
bore tubing to the inlets provided for this purpose.13 • Promotes hygiene.
• Is ventilator applicable.
Passy-Muir Valve The Passy-Muir tracheostomy and Ventilator dependency is an indication only for the
ventilator speaking valve (Figure 24-19) is likewise Passy-Muir valve. Trach-Talk valves are not suitable for
designed to eliminate the necessity of having to cover use with mechanically ventilated patients.
the tube with a finger to speak.14 The Passy-Muir valve
is designed for use by both short- and long-term
adult, pediatric, and neonatal patients with a trache- ARTIFICIAL AIRWAY CUFFS
ostomy or ventilator dependence. Patients must be
Cuffs (Figure 24-20) are commonly used with some
awake and alert and have adequate airflow around the
artificial airways in certain applications. A cuff is a
tracheostomy tube during exhalation. The valve can
balloonlike device consisting of three parts:
be connected to the standard 15 mm connector of
tracheostomy tubes in adults, pediatrics, and neo- • The pilot balloon.
nates, including fenestrated, nonfenestrated, cuffless, • The pilot balloon tubing.
metal, and air-filled cuffed with the cuff completely • The cuff.
deflated.
The application of the Passy-Muir valve is contrain-
dicated in the following situations:
• Unconscious or comatose patients.
• Inflated tracheostomy tube cuff.
• Foam-filled cuffed tracheostomy tube.
• Severe airway obstruction, which may prevent
sufficient exhalation.
• Thick and copious secretions.
• Severely reduced lung compliance that may

cause air trapping.
• Endotracheal tubes.
The Passy-Muir valve is a lightweight, one-way
valve, available in four configurations. It is designed
with positive closure that maintains a bias closed FIGURE 24-20 Artificial airway cuff.
Most cuffs are classified as either high-volume,

Best Practice low-pressure cuffs or as low-volume, high-pressure
cuffs.
Patient Assessment Before • The high-volume, low-pressure cuff, the cuff of
Using a Speaking Valve choice, requires a larger volume of air to inflate
The respiratory therapist must perform a thor- and has a larger surface area that comes into
ough assessment of the patient before using contact with the trachea, thus requiring less
any special speech aids. The assessment should pressure to seal the airway. It is often referred to
consider the following: as the floppy cuff because of the soft pliable and
loose-fitting material that surrounds the artificial
• The patient must be awake, alert, airway.
and making an effort to communicate. • Conversely, the low-volume, high-pressure cuff
• Lung mechanics must be sufficient to requires a smaller volume of air to inflate and
exhale around the tracheostomy has a smaller surface area, which requires higher
tube. pressures to seal the airway.
• The patient must be able to tolerate having
the cuff deflated. Cuffs originally were supplied separately from the
• There must be adequate space in the tubes and installation was the user’s responsibility. This
airway around the tracheostomy tube. was not an easy task, and many ingenious methods of
• There must not be thick and copious installation were attempted. Hemostats, Magill forceps,
secretions. and all types of lubricants were used to make the task
• Vital signs, work of breathing, breath easier. Many times, a seemingly successful attempt
sounds, and any change in the patient’s would result in producing a small hole in the cuff. Of
color or responsiveness to questions or course, the leak went undetected until it was the last
commands. available cuffed tube.
Assessment for the ventilator-dependent
patient includes the preceding list, plus Cuff Types. Low-volume, high-pressure cuffs were the
assessments, before and after, placement of only types available until manufacturers began to listen
the valve: and respond to users. In the interim, a multitude of
different low-volume, high-pressure designs were
• All ventilator settings. introduced in hopes of solving the problems. The list
• Alarm settings. included double-cuffed tubes with the ability to inflate
• Airway pressure levels. either or both cuffs to alternate pressure sites on the
trachea.
The advent of the high-volume, low-pressure cuffs
The cuff surrounds the distal end of the artificial eliminated most of the problems. This classification of
airway to provide an airway seal. Air is injected with a cuff includes two basic designs.
syringe into it through the pilot tubing that runs the
length of the endotracheal tube or tracheostomy tube • The air-filled cuff still sets the standards by being
to the cuff. the most commonly used.
• The foam-filled cuff reverses the methodology of
inflation. Before inserting the tube, a syringe is
Spotlight employed to withdraw all air from the cuff. Once
On the tube is inserted, the pressure in the cuff is
allowed to return to ambient pressure, causing
Speaking Valve the foam to expand to its original size. This
A new Passy-Muir tracheostomy tube speaking allows the cuff to expand to the wall of the
valve was recently introduced in 1985. The new trachea, sealing the airway.
low-profile valve is intended for use by both
The first generation of foam-filled cuffs had
short-term and long-term adult, pediatric, and
difficulties.
neonatal non-ventilator-dependent tracheosto-
mized patients. It can be used with the Bivona • Some cuffs developed leaks while in the airway.
non-foam-filled and Pilling-Weck metal Jackson • Air could not be withdrawn from the cuff, and
tracheostomy tubes. consequently removal of the tube became a
problem.
Subsequent design improvements reduced the recur-

rence of these problems. Best Practice
The three primary reasons to use cuffed artificial
airways are to: Airway Cuffs and Hyperbaric
• Provide a sealed airway for the application of Procedures
mechanical ventilators.
• Prevent aspiration of foreign materials into the An important exception to the filling of cuffs with
lungs. air is in hyperbaric procedures. Normal saline
• Maintain the artificial airway in the center of the is used to fill the cuffs of the tracheostomy and
trachea. endotracheal tubes. If air is used, the increased
pressure compresses the air, decreasing the cuff
Cuff Pressure Management. The cuff of a permanent volume. Normal saline is essentially incompress-
artificial airway is usually deflated and inflated as ible and maintains the required volume.
needed for eating or for connecting to a mechanical
ventilator. Conversely, cuffs used in the acute care
setting are usually inflated most of the time. There are
two commonly used methods of cuff inflation. is not available. Monitoring of cuff pressures is
• The minimal leak method is used when it is not always indicated but especially with the minimal
essential to maintain high levels of PEEP or peak occlusion inflation method. Cuff pressures and cuff
inspiratory pressures. This is accomplished by filling volumes should be included in the routine
adding air to the cuff until no leak can be heard documentation of airway management when a cuff is
during the inspiratory phase and withdrawing employed.
air until a minimal leak can be heard. Common problems identified with cuff pressure
• The minimal occlusion method is used during the monitoring are leaking cuffs and tubes that are too
use of high PEEP and peak inspiratory pressures. small for the patient.
This is accomplished by adding air to the cuff • If the cuff pressure is unaffected by adding more
during the inspiratory phase until no leak can be and more air, the cuff is leaking.
heard, withdrawing air until a leak is present, and • Conversely, if the pressure is higher with
gradually adding air until no leak can be heard. additional air and the leak around the cuff
continues, the tube is undersized for the patient.
Cuff Complications. The RT must be aware of possible
complications: In both cases, the tube must be changed.
• Cuff pressures greater than 5 mm Hg reduce AIRWAY SUCTIONING

lymphatic flow.
• Pressures greater than 18 mm Hg reduce venous Airway suctioning is indicated for patients who are
flow. unable to eliminate accumulated secretions without
• Pressures greater than 30 mm Hg reduce arterial assistance. Airway suctioning is performed to:
flow of the trachea. • Maintain a patent airway by removing secretions
• Sustained high cuff pressures cause ischemia of and other foreign objects.
the mucosa, hemorrhage, and ultimately stenosis • Stimulate a cough in patients who are unable or
of the trachea. unwilling to cough.
• Other complications are related to the esopha- • Collect specimens for diagnostic purposes.
gus and its position against the soft tissue of the
trachea, specifically, aerophagia (air swallowing) Complications associated with airway suctioning are:
and dysphasia (difficulty swallowing). • Hypoxemia associated with the removal of
oxygen from the lungs.
Cuff Monitoring. Cuff pressures can be measured by • Lung collapse associated with the removal of air
means of a simple pressure manometer with an adapter from the lungs.
to fit the fill port of the cuff or any one of the devices • Airway occlusion with suction catheters greater
specifically designed for measuring cuff pressures to the than one half the diameter of the artificial airway.
clinician can feel the pilot balloon while observing the • Arrhythmia associated with resultant hypoxemia.
pressure on a cuff pressure monitor and estimate the • Mucosal stripping associated with poor catheter
pressure in the cuff. This manual technique is useful design or greater-than-required vacuum levels.
to approximate cuff pressures when a pressure monitor • Cardiac arrest associated with vagal stimulation.
modifications to the whistle tip with little functional

Best Practice change from the original design.
Suction Catheters Argyle Airflow Catheter The Argyle airflow suction

catheter (Figure 24-21B) is designed with a doughnut-
Always remember that each millimeter is equal
shaped tip on the distal end. It differs from other
to approximately three French units. To deter-
suction catheters because one of the suction ports in
mine the appropriately sized suction catheter for
the distal end is in the center, and several are on the
use with an 8-mm artificial airway, divide the size
proximal side of the doughnut. The port placement is
of the artificial airway by 2 and then multiply the
part of the design to prevent contact with the mucosa
answer by 3 (i.e., 8 mm ⫼ 2 ⫽ 4, 4 ⫻ 3 ⫽ 12).
of the airways.
In this example, a 12 French suction catheter
is appropriate for use with the 8-mm artificial
Coudé Suction Catheter The distal tip of most suction
airway. Equally important, use the largest suction
catheters inserted for the purpose of secretion removal,
catheter allowable to facilitate the removal of
however, enters the right mainstem bronchus. The
secretions in the least amount of suctioning time.
Coudé directional suction catheter (Figure 24-21C) is
designed with a fixed-angle distal tip, which allows the
operator to rotate the proximal end of the suction
catheter using reference marks to guide the distal tip in
Airway suctioning to maintain a patent airway can
order to direct it into the left mainstem bronchus. The
be accomplished by using several devices.
Coudé directional suction catheter can be a useful
• Straight suction catheters device to facilitate the removal of accumulated secre-
• The Yankauer Suction Device tions from the left mainstem bronchus.
• Trach Care
Characteristics of Suction Catheters Characteristics of
Straight Suction Catheters. Suction catheters good suction catheters are that:
(Figure 24-21) are most commonly used for the
removal of secretions from the airway. Three of the • They must be manufactured from materials that
numerous suction catheter designs available are: are nonirritating to the airway mucosa.
• They must be of sufficient length to extend past
• Whistle tip
the distal tip of the artificial airway, usually
• Argyle airflow
20–22 inches.
• Coudé Suction
• They must be manufactured from a material that
does not produce frictional resistance on the
Whistle Tip Catheter The whistle tip suction catheter
airway when inserted.
(Figure 24-21A) is the most commonly used design in
• The finger port on the proximal end (Figure 24-22)
the clinical setting. It has a rounded distal tip with a
should be of sufficient size to minimize aspira-
hole in the center of the tip and a series of holes along
tion of air from the unoccluded lung.
the sides of the tip. Manufacturers have made several
• The tip of the catheter and all openings should
be molded and free of sharp edges to prevent
mucosal trauma.
Catheter Size Suction catheters must be less than

one half the diameter of the artificial airway being
suctioned to prevent excessive removal of oxygen and
potentially lung collapse. Determining the appropri-
ately sized suction catheter is sometimes difficult when
artificial airways are measured in millimeters and
catheters are measured in French units.
Finger port Tip of catheter
A. B. C.
FIGURE 24-21 Types of suction catheters: (A) Whistle tip.
(B) Argyle airflow. (C) Coudé directional. FIGURE 24-22 Suction catheter port.
Suctioning should be performed for need only. It Specimen Collection. Airway suctioning is indicated
should not be performed on a schedule except to for the purpose of specimen collection for sputum
obtain a specimen for analysis. analysis. The most common is specimen collection for
microbiological culture and sensitivity to determine the
Suction Technique An appropriate suction technique pathogen causing the disease process and the antibiotic
should include the following: sensitivity of the organism cultured. The technique for
suctioning for sputum specimen collection differs only
• Use a sterile technique using sterile equipment,
by the incorporation of a sterile inline suction trap,
gloves, and sterile rinse solutions.
between the suction catheter and the vacuum supply
• Set vacuum pressure within a range of
line, to collect the specimen.
80–120 mm Hg for adults.
• Oxygenate the patient well before, during, and
Trach Care Suctioning System. The Trach Care
after the airway suction procedure.
Closed Tracheal Suction System is a self-contained
• Insert the catheter into the artificial airway
device that can be incorporated into the mechanical
without applying suction.
ventilator circuit or continuous flow circuit.15 Trach
• Advance the catheter until resistance is felt.
Care is used for suctioning of the airway when a patient
• Withdraw it slightly.
has a tracheostomy or an endotracheal tube.
• Remove the catheter, slowly applying suction.
The Trach Care incorporates a self-contained
• Release the suction if resistance is felt, withdraw
suction catheter, enclosed in a clear plastic sleeve,
slightly, and reapply suction.
which passes through a modified T-piece into the
• Oxygenate the patient well, allowing a brief
airway. The lockable external suction control on the
resting period, if possible, before repeating the
suction catheter allows the application of suction only
procedure.
when the thumb control valve is depressed. The thumb
The application of suction to the airway should piece requires a 180-degree rotation from the locked
never exceed 15 seconds in adults. position to operate; the lock prevents the inadvertent
application of suction. There is an irrigation port to
Yankauer Suction Device. The Yankauer suction device instill fluid through to lavage the airway.
(Figure 24-23) is especially effective for the removal of Here is the suctioning procedure for the Trach
secretions accumulated in the oropharyngeal cavity. Care:
Sometimes referred to as the tonsil suction device, the
• Grip the T-piece with one hand.
Yankauer is rigid and designed to conform to the angle
• Advance the catheter with the other hand to the
of the oropharyngeal anatomy. The distal end has a
desired depth.
ball-shaped tip with a hole in the center large enough
• Depress the control valve to apply suction.
to facilitate thick copious secretion removal. Insertion
• Withdraw the catheter slowly until the black
is enhanced by the rigid design, and the smooth
marking on the catheter is visible on the back-
rounded distal tip reduces trauma to the oropharyngeal
side of the T.
cavity.
This is the procedure to lavage the airway:
• Insert the catheter approximately 4–5 inches
into the endotracheal tube or 1–2 inches into a
tracheostomy tube.
• Instill fluid through the irrigation port.
• Continue to advance the catheter to the desired
depth.
• Depress the control valve to apply suction.
• Withdraw the catheter slowly until the black
marking on the catheter is visible behind the T.
The therapist must keep several considerations in
mind during these procedures:

• Do not apply suction while instilling the fluid
during the lavage procedure.
• After suctioning, flush the catheter by depressing
the control valve and then slowly instill fluid
FIGURE 24-23 Yankauer and tonsil tip suction catheters. through the irrigation port.
TABLE 24-5 Actual published cases and

Best Practice monetary awards for injury and death as
a result of lack of caution
Safe Suctioning “Premature Extubation Following Gastric Bypass
Patient safety considerations should be para- Surgery—Respiratory Distress and Tracheotomy—
mount from the first signs and symptoms of Tracheotomy is permanent–$1 Million Verdict.”16
respiratory insufficiency until normal breathing
“Failure to Maintain Airway for Appendectomy—
is restored.
Brain Damage with Significant Disability–$35 Million
Settlement.”17
“Failure to Properly Monitor Woman in ICU—Self-
Extubation With Cardiac Arrest and Death–$1 Million
Best Practice Verdict”18
Artificial Airways and

Ventilator-Associated Most of these precautions are sufficiently addressed
elsewhere in this chapter or textbook.
Pneumonia Especially important, however, is taking steps to
The use of artificial airways, especially endotra- prevent the inadvertent obstruction or removal of the
cheal tubes, in mechanically ventilated patients artificial airway. The volume of references to the subject
is strongly related to ventilator-associated pneu- is relatively small in medical literature. One study
monia (VAP). reported 96 intubated ICU patients who underwent
101 episodes of unplanned extubation. Of these, 85%
were self-extubation and 15% were accidental. Overall,
57% required reintubation, and most were reintubated
• The thumb piece should be turned 180 degrees
within the first hour. Difficulty with reintubation was
to the locked position on the control valve until
common, and one patient who could not be reintu-
safely in the off position.
bated died.19 The medical literature usually chronicles
• The Trach Care has a cap on one side of the
the aftermath resultant from the lack of caution.
T-piece to provide a sealed system for mechani-
Unfortunately, almost as much is found in legal
cal ventilation. The cap must be removed from
journals publishing the monetary awards for injury or
the Trach Care before continuous flow therapy is
death as a result of the lack of caution (Table 24-5).
applied.
Safety concerns for patients with artificial airways
The advantages of the Trach Care are that the use of should include:
gloves is not indicated and sterile technique is ensured;
• Adequate staffing.
a new catheter is not necessary for every set-up. The
• Alarms.
manufacturer recommends not to resterilize the Trach
• Secretions and diaphoresis.
Care and not to use the unit for more than 24 hours.
• Airway securing devices.
However, some studies indicated no reduction of
• Restraining devices.
infection secondary to increased change intervals.
Adequate Staffing. Enough staff should be available
ARTIFICIAL AIRWAYS AND PATIENT SAFETY to accomplish any procedure safely anytime a patient
with an artificial airway, especially a mechanically
Patient safety considerations should be paramount
ventilated patient, is:
from the first signs and symptoms of respiratory
insufficiency until normal breathing is restored. Every • Pulled up in the bed or turned for a position
precaution must be adhered to including: change.
• Rolled for bathing or linen change.
• Maintaining ventilation before the introduction
• Lifted to be weighed.
of an artificial airway.
• Transferred to another bed or stretcher.
• Safely establishing a patent artificial airway.
• Transported on a bed or stretcher.
• Securing the artificial airway.
• Subjected to any movement that may compro-
• Using caution to prevent the inadvertent
mise the airway.
obstructing or removal of the artificial airway.
• Determining the appropriate time for safely In most cases, the respiratory therapist should be
removing the artificial airway. assisted by at least two nursing service staff members.
The respiratory therapist should monitor and maintain ventilation, and usually the patient needs suctioning.
the airway during the procedures. However, the alarm can also be warning of a problem
with the artificial airway, such as a kinked endotracheal
Alarms. Alarms on mechanical ventilators are there to tube. Regardless of the reason, when the alarms sound,
alert the staff that something is not right with the they are not to be ignored. The alarm may be a false
patient’s ventilatory status. The most common alarm one, but it may also mean the patient is at risk of injury
indicates that the patient is not receiving adequate or death.
CASE STUDY 24-1

J. C. is a 68-year-old white male with a history of Pulmonary status has worsened. Breath sounds:
COPD, CHF, and noncompliance. Additionally, in the crackles and slight rales on the right and markedly
past 10 months, he has been intubated and ventilated diminished on the left.
a total of 36 times for respiratory failure resultant from This patient historically was weaned and
his COPD and CHF and noncompliance. extubated within 8–10 hours after being intubated.
On this admission (at 0115, 03-23-2011) he It is unusual for his ABGs to have worsened after
presented with, as before, labored breathing, improving. All parameters were reassessed.
profuse sweating, slight cyanosis, four-plus pitted The following was observed after reassessing
edema, wet breath sounds bilaterally, and nonre- the endotracheal tube. The tape securing the tube
sponsiveness to verbal stimulus. ABG results on in place was wet because of the oral secretions. The
the aerosol treatment with oxygen as the driving endotracheal tube’s 29-mm mark was now at the
gas; PaO2 94 mm Hg, PaCO2 118 mm Hg, and patient’s lip.
pH 7.01. The problem: The patient’s endotracheal tube
He was intubated orally with an 8.0 endotra- was taped at the 25-mm mark on the tube at the
cheal tube and taped at the 25-mm mark on the patient’s lip. The moderate amount of oral secre-
tube at the lip. Radiographic examination of the tions moistened the tape and reduced its ability to
chest verified proper tube placement. hold the tube in place. The endotracheal tube
A PB 7200 mechanical ventilator was set up advanced farther into the lung until the tip was in
with settings as follows: CMV, Rate 12, VT 800, the right mainstem bronchus. In this position, the
FIO2 1.0, PEEP 10, PIP 45 (cm H2O). Lasix 40 mg left lung was deprived of ventilation.
was administered IV ⫻ 2, 40 mg on arrival and The solution: The patient was placed on a FIO2
40 mg 15 minutes after the first dose. (This drug of 1.0, the airway was suctioned with the Trach
and dose had been determined effective for this Care suction unit, and the oropharynx was suc-
patient during the previous ER admits.) tioned thoroughly with a Yankauer. With his airway
0200: The patient was transferred to the thoroughly cleared, the endotracheal cuff was
intensive care unit. Ventilator: CMV, Rate 12 vent/ deflated, the endotracheal tube was withdrawn to
5 pt, VT 800, FIO2 1.0, PEEP 10, PIP 34. ABG the 25-mm mark at the lip, the cuff was reinflated,
results: PaO2 359, PaCO2 44, pH 7.37. Ventilator and the tube was resecured. Breath sounds returned
changes: SIMV 12, pressure support 10, VT 800, to bilateral and equal. Weaning was continued.
FIO2 0.40, PEEP 10. 1030: The patient was extubated successfully.
0400: The Lasix has produced 1 L of urine.
Pulmonary status markedly changed. Breath
Questions
sounds: scattered crackles especially in bases.
Moderate amount of oral secretions. Ventilator: 1. What could the respiratory therapist do to
SIMV, Rate 12 vent/6 pt, VT 800 vent/ 560 pt., prevent the endotracheal tube from slipping
FIO2 .40, PEEP 10. ABG results: PaO2 150, PaCO2 into the right mainstream bronchus?
42, pH 7.39. Ventilator changes: SIMV 6, PS 10, 2. If a patient has had to be intubated 36 times
VT 800, FIO2 0.30, PEEP 5. over the last 10 months, what should the
0600: The Lasix has produced another 500 mL respiratory therapist recommend?
of urine. The patient was somewhat more restless 3. When the patient was initially intubated, what
and anxious. Ventilator: SIMV, Rate 6 vent/25 pt, kind of intubation would have been the easiest
VT 800 vent/ 300 pt, FIO2 .40, PEEP 5, PIP 49. to maintain during the patient’s short period of
ABG results: PaO2 78, PaCO2 56, pH 7.30. intubation?
Secretions and Diaphoresis. Patients who have management. Their duty is to be the most informed
copious amounts of secretions, either oral or nasal, member of the health care team and match the appro-
and/or diaphoresis should be monitored very closely. priate patient with the most effective modalities.
Both conditions contribute to the problems associated Numerous devices and techniques have not been
with securing artificial airways, arterial lines, IVs, as changed significantly since they were introduced to
well as with attaching devices for monitoring equip- clinical practice. The reason is that they are useful
ment. The moisture can interfere with the bonding as introduced and they blend in with the new
between the patient and the adhesive utilized to secure technologies to provide the tools necessary for airway
them. management.
Airway Securing Devices. Airway securing devices

designed to prevent unplanned or inadvertent extuba-
tion sometimes are contributing factors in the act they Study Questions
were designed to prevent. Usually the cause is that the
REVIEW QUESTIONS
device is firmly attached to the endotracheal tube and
inappropriately attached to the patient. Copious 1. List and describe two basic classifications of airway
amounts of secretions or extreme diaphoresis can obstruction.
prevent the device from attaching securely. Under these 2. List the indications for artificial airways.
conditions, the patient is vulnerable to unplanned or
3. Describe the double lumen endobronchial tube.
self-extubation. The therapist must closely monitor the
patient and ensure that the securing device is equally 4. Differentiate between a tracheostomy tube and a
well attached to the patient and to the endotracheal laryngectomy.
tube. 5. Describe the Passy-Muir valve, and define the
function of the valve.
Restraining Devices. Just the mention of restraining 6. List the complications associated with airway
devices for patients should raise a red flag. Legal, suctioning.
ethical, medical and moral issues arise with the
7. Explain the suction technique for the Trach Care
application of both chemical (drugs) or physical
suction device.
restraints to the patient’s freedom of motion and move-
ment. In most jurisdictions in the United States and 8. Define difficult tracheal intubation.
Canada, restraint orders must be renewed daily and 9. Describe the gum elastic bougie.
restraints themselves must be frequently checked for
comfort, appropriateness, and safety by the appropriate
personnel. The respiratory therapist must exercise
extreme caution with the use of any type of patient-
restraining device. Soft restraints on the patient’s upper 1. The most common cause of airway obstruction is:
extremities become necessary for most patients requir- a. the tongue occluding the airway.
ing mechanical ventilation. Even though some con- b. aspiration of foreign objects.
scious and alert patients do not intentionally c. laryngeal edema.
self-extubate, they may fall asleep and unknowingly do d. thick mucus in the airway.
so. If soft restraints are employed, the physician’s 2. The radiopaque line is used to:
orders have to be in compliance with standards set a. measure the distance for endotracheal
forth by regulatory agencies and clearly written on the intubation.
patient’s chart. b. measure the diameter of the trachea using X-ray.
c. determine proper placement of endotracheal
tube cuffs.
Summary d. determine proper placement of the distal tip of
Airway management is one of the areas of care that the endotracheal tube.
respiratory therapists perform so routinely that they 3. Endotracheal tube markings include all of the
sometimes overlook its importance. With the artificial following except:
airways, emergency airway adjuncts, airway adjuncts, a. Z79 committee.
and speech aids for tracheostomy patients, as well as b. centimeter markings.
suctioning capabilities, all constantly improving, RTs c. inhalation therapy (IT).
have the tools to be ever more effective with airway d. serial number.
4. Before removing an EOA, the respiratory therapist 12. The Trach-Talk valve is indicated in all of the
must: following patients except:
I. suction the oral cavity well. a. head trauma.
II. suction above the cuff before deflating. b. neuromuscular disease.
III. ensure that the endotracheal tube is properly in c. ventilator dependency.
place. d. tracheomalacia.
IV. ensure the proper deflation of cuff. 13. Passy-Muir valve is indicated in all of the following
a. all of the above patients except:
b. II and III a. quadriplegia.
c. III only b. tracheomalacia.
d. I and IV c. mild tracheal stenosis.
e. I only d. a comatose patient.
5. In an emergency situation in a hospital, the airway 14. Contraindications for use of the Passy-Muir valve
of choice is: include:
a. Guedel. I. conscious patients.
b. Berman. II. endotracheal tubes.
c. oroendotracheal tube. III. foam-filled tracheostomy cuff.
d. nasoendotracheal tube. IV. deflated tracheostomy tube cuff.
6. The length of a oropharyngeal airway can best be V. fenestrated tracheostomy tube.
determined by measuring: a. I and II
a. from the tip of the nose to the angle of the jaw. b. II and III
b. from the tip of the nose to the ear lobe. c. I and IV
c. from the center of the nare to the tip of the d. III and V
ear lobe. e. all of the above
d. from the jaw to the Adam’s apple. 15. The cuff of choice is:
7. The most appropriate artificial airway for the I. hydrofilled.
conscious patient is the: II. foam filled.
a. Guedel. III. high volume, low pressure.
b. Berman. IV. low volume, high pressure.
c. nasopharyngeal. V. floppy.
d. esophageal obdurator airway. a. I and II
8. The surgical procedure making an incision into the b. II and III
trachea is a: c. I and IV
a. cricothyrotomy. d. III and V
b. tracheostomy. e. all of the above
c. laryngectomy. 16. Cuff pressures should be monitored and should
d. appendectomy. not exceed:
9. The most commonly used material in the manufac- a. 5–10 cm H2O pressure
ture of artificial airways is: b. 11–15 cm H2O pressure
a. silicone. c. 16–20 cm H2O pressure
b. Teflon. d. 22 cm H2O pressure
c. nylon. 17. The following are characteristics of a good suction
d. polyvinyl chloride. catheter except:
10. The tracheostomy tube that is still manufactured I. construction from nonirritating material
but that can be irritating to the skin is: II. constructed from materials with low frictional
a. fenestrated. qualities
b. silver. III. maximum length of 12–15 inches
c. foam filled. IV. proximal finger port small enough to apply
d. plastic. suction at all times
V. molded catheter tip and openings
11. The Trach-Button does not allow the tracheosto-
a. I and II
mized patient to:
b. III and IV
a. breathe through the nose and mouth.
c. II and V
b. speak normally.
d. III and V
c. expectorate more normally.
e. none of the above
d. breathe through the stoma.
18. The suction device design most suitable for 5. Brain A I J. The Laryngeal Mask—A New
oropharyngeal suctioning is: Concept in Airway Management. Br J Anaesth
I. whistle tip catheter. 1983;55,8:801–5.
II. tonsil suction device. 6. Morris IR. Continuing medical education:
III. Argyle airflow catheter. fibreoptic intubation. Can J Anesth. 1994;41:
IV. Yankauer suction device. 996–1008.
V. modified oropharyngeal airway. 7. Jolliet P, Chevrolet JC. Bronchoscopy in the
a. I and II intensive care unit. Intensive Care Med.
b. III and IV 1992;18:160–169.
c. II and IV 8. Burkle CM, Walsh MT, Harrison BA, et al.
d. IV Airway management after failure to intubate
e. V by direct laryngoscopy: outcomes in a large
19. The most appropriate set vacuum pressure for teaching hospital. Can J Anaesth. 2005;52:
airway suctioning in adults is: 634–640.
a. 60–100 mm Hg. 9. Benumof, J. Management of the difficult airway.
b. 80–120 mm Hg. Anesthesiology. 75:1087–1210.
c. 90–140 mm Hg. 10. Cormac RS, Lehane J. Difficult tracheal intuba-
d. 100–180 mm Hg. tion in obstetrics. Anaesthesia. 1984; 39:1105–1111.
11. Cricothyrotomy. In: Finucane BT, Santora AH, eds.
20. The Trach Care closed suction device is designed
Advanced Cardiac Life Support Manual. Dallas, TX:
for suctioning:
American Heart Association; 1997:2–13.
a. the nasopharyngeal airway.
12. Trach-Button [product literature]. Seattle, WA:
b. a tracheostomy.
Olympic Medical; 1999.
c. the endotracheal tube.
13. Trach-Talk [product literature]. Seattle, WA:
d. b and c.
Olympic Medical; 1999.
14. Passy-Muir tracheostomy and ventilator speaking
CRITICAL-THINKING QUESTIONS valves. Instruction Manual. Irvine, CA: Passy-Muir
Inc.;1–14.
1. How would you determine whether to use an 15. Trach Care closed suction system [product
oropharyngeal airway or a nasopharyngeal airway? literature]. Des Moines, IA: Ballard Inc;1998.
2. In what situation should adjunct airways be 16. Medical Malpractice—Verdicts, Settlements &
considered for ventilation? Experts. 2006;22,7:3–4.
3. What should be monitored closely about cuffs 17. Medical Malpractice—Verdicts, Settlements &
when they are in use, and how can they be moni- Experts. 2006;22,7:4–5.
tored best? 18. Medical Malpractice—Verdicts, Settlements &
Experts. 2006;22,7:21.
4. When should patient safety with artificial airways
19. Christie JM, Dethlefsen M, Cane RD.
be considered?
Unplanned ETT extubation in the ICU unit. J
5. Under which circumstances should safety precau- Clinical Anesthesia. 1996;8,4:289–293.
tions be exercised for patients with artificial
airways?
Suggested Readings
References American Association for Respiratory Care. AARC
1. Finucane BT, Santora AH. Difficult intubation. clinical practice guidelines: management of
In: Principles of Airway Management, 3rd ed. St. airway emergencies. Respir Care. 1995;40(7):
Louis, MO: Mosby-Yearbook, 2009. 749–760.
2. Mehta S. Transtracheal illumination for optimal American Heart Association adjuncts for airway control
tracheal tube placement. A clinical study. Anaesthesia and ventilation. Circulation 2005;112:IV-51–IV-57.
1989;44:970–972. Originally published online November 28, 2005.
3. Hung OR, Stewart RD. Lightwand intubation: a http://circ.ahajournals.org/cgi/content/full/112/
new lightwand device. Can J Anaesth. 1995; 24_suppl/IV-51
42:820–825. American Heart Association. Advanced cardiac life
4. Kacmarek, R. The Essentials of Respiratory Care. support. www.americanheart.org/presenter.
4th ed. St. Louis, MO: Mosby; 2005. jhtml?identifier=3011775
ASA practice guidelines for management of the difficult Nasotracheal suctioning, revision & update. Respir Care.
airway. Anesthesiology 2003; 98:1269–1277. 2004;49(9):1080–1084.
Endotracheal suctioning of mechanically ventilated Patient-ventilator system checks. Respir Care.
patients with artificial airways. Respir Care. 1992;37(8):882–886.
2010;55(6):758–764. Removal of the endotracheal tube, 2007 revision &
Gavin GL, McCloskey BV. The difficult airway in adult update. Respir Care. 2007;52(1):81–93.
critical care. Crit Care Med. 2008;36,7:2163–2173. Suctioning of the patient in the home. Respir Care.
Posted August 12, 2008. http://www.medscape.com/ 1999;44(1):99–104.
viewarticle/578622
In-hospital transport of the mechanically ventilated
patient, 2002 revision & update. Respir Care.
2002;47(6):721–723.
CHAPTER 25
Physiological Effects of Mechanical

Ventilation
Chad J. Pezzano
OBJECTIVES
• Describe the difference between transairway, transpulmonary, and transthoracic pressures and how they
affect the process of gas movement through the pulmonary system.
• Explain the difference between intra-alveolar and intrapleural pressures.
• Discuss the difference between negative pressure ventilation, positive pressure ventilation, and
high-frequency ventilation.
• Describe the difference between static and dynamic lung compliance.
• Describe airway resistance and how it relates to the mechanically ventilated patient.
• Summarize the concept of time constants for mechanically ventilated patients.
• Discuss the complications that are associated with mechanical ventilation and how to minimize them.
CHAPTER OUTLINE
Pulmonary and Thoracic Pressure Gradients Pulmonary Dynamics
Transairway Pressure Lung Compliance
Transpulmonary Pressure Airway Resistance
Transthoracic Pressure Time Constants
Intra-Alveolar and Intrapleural Pressure Complications from Mechanical Ventilation
Modalities of Ventilation Volutrauma
Negative Pressure Ventilation Barotrauma
Positive Pressure Ventilation Disruption of Physiological Functions
High-Frequency Ventilation Other Considerations
687
KEY TERMS
barotrauma lung compliance transairway pressure
dynamic compliance negative pressure ventilation transpulmonary pressure
high-frequency ventilation positive pressure ventilation transthoracic pressure
intra-alveolar pressure static compliance volutrauma
intrapleural pressure time constant
M
echanical ventilation assists individuals oxygen level. When the medulla oblongata senses a
who are suffering from conditions that physiological change, a stimulus is sent through the
impair their ability to maintain adequate phrenic nerve to the diaphragm to begin the process of
ventilation and/or oxygenation. Even inspiration. This nerve signal causes the diaphragm to
with mechanical ventilation, complications may arise contract, creating changes in the pressure gradients
in the form of physiological side effects that occur with associated with respiration.1
the application of positive pressure ventilation. The Spontaneous breathing depends on many physi-
hemodynamic, renal, neurological, and pulmonary ological and physical changes occurring both in the
systems may all be at an increased risk. The respiratory pulmonary system and the thorax. During inspiration
therapist who is providing mechanical ventilation must and expiration, pressure gradient changes result, such as
be aware of the potential side effects and limit any ill transairway pressure, transpulmonary pressure, and
consequences that may result from the application of transthoracic pressures. These are responsible for some
positive pressure ventilation. of the physiological changes that deliver fresh gas to the
lower respiratory system and that remove expired gases.
Pulmonary and Thoracic Pressure
Gradients TRANSAIRWAY PRESSURE
Invasive mechanical ventilation is based on different Transairway pressure (Pta), also known as airway
physiological principles from those of spontaneous pressure, is the change in pressure gradient between the
breathing. Spontaneous respirations are initiated by barometric pressures at the mouth (Pm) and at the
means of a complicated series of nerve stimuli and alveoli (Palv). Transairway pressure is the driver of the
muscle contractions. Stimuli are sent from the medulla physiological movement of air from the upper respira-
oblongata in response to a physiological change, such tory system to the conductive airways (Figure 25-1).2
as an increase in carbon dioxide levels, a rise in hydro-
Pta Pm Palv
gen ions (acidosis), a decrease in pH, or a lowered
A Gas Flow Gas Flow B
Pm = 760 mm Hg Transairway Pm = 760 mm Hg

Pressure
+ 3 mm Hg
– 3 mm Hg
Palv = 757 mm Hg Palv = 763 mm Hg
Inspiration Expiration
FIGURE 25-1 Transairway pressure: The difference between the pressure at the mouth (Pm) and the
alveolar pressure (Palv). Even though the gas is moving in opposite directions in A and B, the
transairway pressure is 3 mm Hg in both examples. In this illustration, the pressure at the mouth
(Pm) is equal to the barometric pressure (PB).
CHAPTER 25 ■ Physiological Effects of Mechanical Ventilation 689
PB = 761 mm Hg
A B
Transpulmonary
Gas Flow Pressure Gas Flow
5 mm Hg
Ppl = 755 mm Hg Ppl = 758 mm Hg
FIGURE 25-2 Transpulmonary pressure: The difference between the alveolar pressure (Palv) and the
pleural pressure (Ppl). This illustration assumes a barometric pressure (PB) of 761 mm Hg.
TRANSPULMONARY PRESSURE TRANSTHORACIC PRESSURE

Transpulmonary pressure (Ptp) is the change in The last pressure gradient involved in respiration is
alveolar pressure (Palv) and pleural pressure (Ppl) of the transthoracic pressure (Ptt), which represents the
lungs, basically the change inside the lung versus difference between alveolar pressure (Palv) and body
outside it (Figure 25-2). surface pressure (Pbs) (Figure 25-3).
Ptp Palv Ppl Ptt Palv Pbs
Transpulmonary pressure is often referred to as Transthoracic pressure is the pressure required to

alveolar distending pressure. All of the processes of dilate and contract both the chest wall and the lungs
assisted mechanical ventilation attempt to increase simultaneously during the respiratory cycle. Transtho-
the transpulmonary pressure. During negative pressure racic pressure changes based on the patient’s weight,
ventilation, such as ventilation through a chest cuirass, restrictive disease processes, and during situations that
the ventilator attempts to decrease transpulmonary create a decrease in chest wall compliance.2,3
pressure to enable a larger gas volume to reach the
lungs. During positive pressure ventilation, the
mechanical ventilator likewise attempts to increase INTRA-ALVEOLAR AND INTRAPLEURAL PRESSURE
the transpulmonary pressure by delivering a volume The action of ventilation requires several changes in the
of gas to the alvoli.2,3 characteristics of the thoracic system. Intra-alveolar and
A B
Transthoracic
Gas Flow Pressure Gas Flow
– 3 mm Hg
+ 3 mm Hg
Pbs = 760 mm Hg Pbs = 760 mm Hg
FIGURE 25-3 Transthoracic pressure: The difference between the alveolar pressure (Palv) and the
body surface pressure (Pbs). In this illustration, the body surface pressure (Pbs) is equal to the
barometric pressure (PB).
intrapleural pressures change as a result of positive and pressure environment. In response to the change in
negative pressures being applied to the thoracic cavity. thoracic pressure, the intra-alveolar pressure becomes
negative as a result of a negative pressure generated at
• Intra-alveolar pressure is the pressure in the
the upper airway.2 Negative pressure ventilation mimics
alveoli during ventilation. This pressure changes
normal physiological respirations, though it has not
from approximately 1 cm H2O during expira-
been commonly used as a mechanically ventilated
tion to 1 cm H2O during inspiration.3 Intra-
device since the polio epidemic.
alveolar pressure changes in response to a
change in the intrapleural pressure.
• Intrapleural pressure is the pressure difference POSITIVE PRESSURE VENTILATION
between the visceral and parietal pleura. The Positive pressure ventilation is currently one of the
intrapleural pressure at end-expiration is most common methods of artificial ventilation. During
approximately 2 cm H2O; during inspiration, positive pressure ventilation, the ventilator delivers a
it can reach anywhere from 6 to 8 cm H2O.3 volume of gas through either an endotracheal tube or a
All of theses changes in pulmonary and thoracic noninvasive nasal or face mask to the patient’s lungs to
dynamics play a crucial role in the process of assist in ventilation. The volume of gas that the ventilator
spontaneous respirations. delivers to the lungs causes changes in the alveolar
During inspiration in a spontaneously breathing pressure, making the alveolar pressure gradient a positive
patient, the diaphragm and rib cage begin to increase pressure environment. This positive pressure is transmitted
the volume of the thoracic cavity. The result is a throughout the lungs, and gas exchange results.
decrease in intrapleural pressure and a resulting During expiration, the ventilator stops delivering
decrease in intra-alveolar pressure. The negative flow, and gas passively exits the lungs. The pressure at
intrapleural pressure results in a pressure difference the endotracheal tube or mask during expiration
(gradient) across the lung. Since atmospheric pressure returns to baseline. However, alveolar pressure remains
is higher than intra-alveolar pressure, air flows into the in a positive pressure state in response to positive
lung. Once the necessary inspiratory volume is reached end-expiratory pressure and ventilator pressure change.
and the thorax stops expanding, the difference between When a person requires the assistance of mechani-
atmospheric and intra-alveolar pressure becomes zero cal ventilation, the physiological process of respiration
and gas flow into the lungs stops. undergoes significant changes. As a breath is mechani-
Expiration is a passive process. The elastic property cally delivered to the patient, intra-alveolar and intra-
of the lung and thorax become prominent once the pleural pressures both increase above the atmospheric
muscular effort of the diaphragm and thoracic muscles pressure.1,2,3 The diaphragm is pushed downward in
ceases. This results in a positive intrapleural pressure response to the breath being delivered by the mechani-
and consequently an increase in intra-alveolar pressure. cal ventilator. Once the ventilator has delivered the
A pressure difference between the alveoli and atmo- mechanical breath, a no-gas state occurs in which both
sphere now exists. Intra-alveolar pressure is greater the intra-alveolar and intrapleural pressures are both
than atmospheric pressure and air begins to move greater than atmospheric pressure in response to the
out of the lung until the pressure gradient once volume, or pressure, of gas delivered to the individ-
again becomes zero. 2,3 ual.1,2,3 Diaphragmatic movement ceases at the end
of inspiration during mechanical ventilation.
Expiration for the mechanically ventilated patient
Modalities of Ventilation is a passive process in which the exhaled air causes
Artificial mechanical ventilation can be administered intra-alveolar pressure drops to normalize with atmo-
through three methods: negative pressure ventilation, spheric pressure. 1,2,3 Intrapleural pressure likewise
positive pressure ventilation, and high-frequency drops to a static level below atmospheric pressure, and
ventilation. the diaphragm relaxes and moves to a resting position.
At the end of expiration, a no–gas-flow state exists in
which intra-alveolar pressure is equal to atmospheric
NEGATIVE PRESSURE VENTILATION
pressure. Intrapleural pressure returns to a negative
Negative pressure ventilation attempts to mimic state below atmospheric pressure, and diaphragmatic
normal respirations. When an individual is receiving movement ceases.
negative pressure ventilation, the upper airway is
exposed to ambient pressure while the thoracic cavity
is placed in an airtight environment. When negative HIGH-FREQUENCY VENTILATION
pressure is applied to this airtight environment, the High-frequency ventilation provides ventilation
thoracic cavity pressure drops and becomes a negative that delivers a tidal volume less than deadspace and
respiratory rates anywhere between 60 and 900 breaths High-Frequency Flow Interruption Ventilation.
per minute.4 The three types of high-frequency High-frequency flow interruption ventilation (HFFIV) is
ventilation are high-frequency oscillation ventilation, similar to HFJV in that they both stream gas flow into
high-frequency jet ventilation, and high-frequency the patient’s lungs. In the HFFI ventilator is a ball that
flow interruption ventilation. interrupts the flow of gas, which causes this streaming
of gas into the airway.6 Respiratory rates can reach
High-Frequency Oscillation Ventilation. During as high as 600 breaths per minute. This form of
high-frequency oscillation ventilation (HFOV), the mechanical ventilation is not as commonly used
oscillating ventilator delivers a bulk flow of gas to the today with the advent of HFOV and HFJV.
airways, which provides fresh gas to the airways for
ventilation. Coupled with a high respiratory rate,
the HFOV delivers tidal volumes that are less then
deadspace; thus the pressure delivered to the lungs
Pulmonary Dynamics
is attenuated by the time it reaches the alveolar The lungs, in and of themselves, have characteristics
space.5 The mean airway pressure is constant that vary from patient to patient and that play impor-
throughout ventilation to keep the alveoli distended tant roles in how effectively mechanical ventilation can
and the lungs inflated in order to allow ventilation be delivered. Lung compliance and airway resistance
to occur. are two of the most important concepts that a respira-
HFOV relies on a number of physiological principles tory therapist must be aware of during mechanical
for effective ventilation and oxygenation such as the ventilation.
principles of Taylor dispersion (an effect in fluid
mechanics in which a shear flow can increase diffusivity),
molecular diffusion, bulk flow gas convection, LUNG COMPLIANCE
Pendelluft effect (the movement of air back and forth When a volume of gas is being delivered to the lungs,
between the lungs), gas flow streaming, and cardio- that air is working to open a lung unit against the force
genic mixing.4,5 HFOV is the only form of ventilation of the thoracic cavity.7 Lung compliance relates to
in which active exhalation occurs; the bellows, located how elastic the lungs are when a volume of gas is
in the oscillator, actively pulls the gas out of the lungs. applied to them. Lung compliance (CL) relates to the
Because expiration is active, the mean airway pressure change in volume (V) in liters (L) over the change
needs to be maintained to keep the alveoli open; if the in pressure (P) in centimeters of water pressure
mean airway pressure is decreased too much, atalectasis (cm H2O).8 This can be represented in the following
occurs, causing a disturbance in ventilation and expression CL V P.
oxygenation. Two types of compliance can be measured:
HFOV is commonly used for: dynamic compliance and static compliance.
Dynamic compliance (Cdyn) measures the
• Infant respiratory distress syndrome. changes in volume and pressure in the nonelastic
• Acute respiratory distress syndrome. airways. The normal dynamic compliance for a
• Pulmonary interstitial emphysema. nonintubated patient is 30–40 mL/cm H2O.8 When a
• Air leak syndromes. patient is intubated and mechanically ventilated, the
practitioner managing the patient should consider
High-Frequency Jet Ventilation. High-frequency jet using serial measurements to trend any changes
ventilation (HFJV), like HFOV, delivers tidal volumes occurring in the nonelastic airways. Dynamic
of 1–5 mL/kg with very high respiratory rates.4 Similar compliance is measured by taking the corrected
gas law principles apply to HFJV: Taylor dispersion, tidal volume from the patient in milliliters and
molecular diffusion, bulk flow gas convection, dividing that factor by the difference in peak inspiratory
Pendelluft effect, gas flow streaming, and cardiogenic pressure (PIP) subtracted by the positive end-expiratory
mixing.4,5 There are a few differences between HFJV pressure (PEEP).
and HFOV.
Vt
• HFJV can utilize additional support from a Cdyn ____________ 7
(PIP PEEP)
conventional ventilator to prevent atelectasis.
• HFJV uses passive exhalation instead of active A second type of compliance that measures the
exhalation, as HFOV does. elastic properties of the lungs, is known as static
• Passive exhalation makes HFJV a good choice for compliance (Cst). The normal static compliance of a
ventilation when hemodynamic status is of person who is spontaneously breathing and not
concern for the patient. receiving mechanical ventilation is 0.05–0.17 L/cm
H2O (50–170 mL/cm H2O).2 These normal values can

be affected by a variety of factors: Best Practice
• Mental status
• Patient position Lung Mechanics
• Abdominal girth Monitoring static compliance, dynamic
• Change in thoracic compliance such as burns compliance, and airway resistance in the
• Any factors that impede the work of the thoracic mechanically ventilated patient assists the
system health care provider in determining improve-
ment or deterioration in pulmonary status.
When an artificial airway is used to provide respira-
Static compliance, dynamic compliance,
tory assistance, compliance changes in relation to the
and airway resistance should be monitored
positive pressure ventilation and to the increase in
postintervention, such as suctioning and
airway resistance created by the artificial airway (dynamic
bronchodilator therapy, to examine whether
compliance (Cdyn)).7 In males who are intubated and
improvements occurred.
receiving mechanical ventilation, compliance can range
from 40 to 50 mL/cm H2O and at times, based on lung
pathology such as ARDS, can reach as high as 100 mL/
cm H2O.2 Females who are intubated and receive
mechanical ventilation have lung compliances ranging
from 35 to 45 mL/cm H2O and, as in males, can have Airway resistance in the intubated patient can
lung compliance as high as 100 mL/cm H2O.2 vary for a variety of reasons, such as the diameter of
To calculate the static compliance of a patient the artificial airway, airway secretions, bronchospasm,
receiving mechanical ventilation, the respiratory pulmonary edema, chronic obstructive pulmonary
therapist has to obtain a static lung hold, that is, cause disease, surfactant deficiency, and any other pathology
a plateau hold a state of no flow at the end of inspira- that creates a high pressure environment in the
tion before exhalation begins. The static lung hold lungs.2,7 To decrease airway resistance, the clinician
(measured as plateaus pressure) can then be inserted needs to correct the problem causing the restriction
into the equation of lung compliance in the lungs.
Vt
Cst _______________ 8
(Pplateau PEEP)
AIRWAY RESISTANCE CASE STUDY 25-1

Airway resistance, also known as transairway pressure, is
the difference between the pressures at the mouth and A 35–year-old male is intubated in the intensive
at the alveoli.7 Airway resistance informs the respiratory care unit for septic shock and respiratory failure.
therapist of the resistance created by the airway when a He is intubated with an 8.0-mm endotracheal
volume of gas is delivered through the patient’s tube, and mechanical ventilation is initiated.
conducting airway systems. Normal airway resistance The current ventilator settings are: assist control
of a nonintubated patient varies from 0.6 to 2.4 cm with a corrected tidal volume of 600 mL, a
H2O/L/sec if the patient has a spontaneous flow rate PEEP of 5 cm H2O, set respiratory rate of
of 0.5 L/sec.2 An artificial airway increases airway 12 breaths per minute, a flow rate of 60 L/min
resistance; thus an intubated patient may have airway (1 L/sec), and an FIO2 of 40%. On these ventila-
resistance from 6 cm H2O/L/sec and higher based on tor settings, he is reaching a peak inspiratory
artificial airway diameter.2 Mechanically ventilated pressure of 40 cm H2O and a plateau pressure
patients should have airway resistance trended to of 35 cm H2O.
ascertain any changes when the patient receives
bronchodilator therapy, has an artificial airway suc- Questions
tioned, or undergoes any other procedure that may 1. What is the static compliance for this
improve airflow.8 Airway resistance (Raw) equals the ventilated patient?
peak airway pressure in centimeters of water pressure
(cm H2O, (PIP)) subtracted from the plateau pressure 2. What is the dynamic compliance for this
in centimeters of water pressure (cm H2O, Pplateau) ventilated patient?
divided by flow rate in liters per second (L/sec).8 3. What is the calculated airway resistance on
these current ventilator settings?
(PIP Pplateau)
Raw ______________8
flow
of increased airway resistance increases the time

CASE STUDY 25-2 constant by a proportional ratio of 1:1; therefore if
airway resistance increases by 3, the lungs will take
A 60-year-old female has been intubated for three times longer to inflate.
chronic obstructive pulmonary disease exacerba- Changes in lung compliance, on the other hand,
tion (COPD exacerbation) and placed on mechan- affect time constants in a contrasting manner. As
ical ventilation in the intensive care unit. She is compliance decreases, the time constant likewise
placed on assist control ventilation with a tidal decreases. With a decrease in compliance and time
volume of 450 mL, a PEEP of 8 cm H2O, a set constant, the lung unit loses the potential for reaching
respiratory rate of 20 breaths per minute, a flow its total filling capacity. This concept is important in
rate of 40 L/min (0.67 L/sec), and a FIO2 of the newborn with surfactant deficiency, because lung
80%. On these ventilator settings she has a peak compliance is decreased in relation to surfactant
inspiratory pressure of 35 cm H2O and a plateau deficiency. The lung cannot fully inflate and ventilate
pressure of 28 cm H2O. effectively. To assist the newborn child with surfactant
deficiency, it is necessary to provide surfactant therapy
Questions to increase the lung compliance to assist in fully
1. What is the static lung compliance for this ventilating the child.9
ventilated patient? Time constants are an important factor in mechan-
2. What is the dynamic lung compliance for this ical ventilation; they assist the respiratory therapist in
patient? selecting the initial inspiratory time and expiratory
time to suit the patient’s clinical condition. The normal
3. What is the calculated airway resistance for time constant varies from 0.42 to 0.7 seconds in adults
this ventilated patient? and from 0.25 to 0.75 seconds in infants. Delivering
the fully set tidal volume to the patient should take
approximately three time constants. If inspiratory time
is too short, the lung units do not have enough time to
open; conversely, if the inspiratory time is too long,
TIME CONSTANTS inadequate exchange of gas may occur, which can result
in increased carbon dioxide levels.
Lung compliance and airway resistance change con- Likewise, expiratory time needs to be set to meet
stantly during respiration, and, as a result, lung units the patient’s pulmonary condition. If expiratory time is
open and close at different intervals. Lung units with too short, air trapping and autogenic PEEP can occur.
high areas of airway resistance or areas of decreased Expiration can take more than five time units to
compliance require a longer time to inflate. The provide the adequate removal of gas. The respiratory
constant related to the amount of time it takes to therapist should routinely examine time constants in
inflate a lung unit is the time constant (t), which relation to the patient’s condition. As compliance and
indicates the amount of time required to fill a lung unit airway resistance change, time constants are affected
to approximately 60% of its total filling capacity. One and ventilator adjustments need to be made.
time constant is equal to compliance of the lung unit
multiplied by the airway resistance of the lung unit:
t C Raw7
Complications from Mechanical
In a healthy individual:
Ventilation
• One time constant should fill approximately
Mechanical ventilation is utilized for individuals who
60% of a lung unit.2,9
have impairments of the pulmonary, thoracic, neuro-
• Two time constants should fill approximately
logical, and/or cardiac systems. The goal of mechanical
87% of a lung unit.
ventilation is to correct the underlying pathological
• Three time constants should fill approximately
condition while preventing further injury from being
on mechanical ventilation. Invasive or noninvasive
• Four time constants should fill approximately
mechanical ventilation is physiologically abnormal.
98% of a lung unit.
Individuals who receive positive pressure ventilation
• Five time constants should fill approximately
are at risk from ventilator-induced injuries that relate
to the volume, the pressure, and the physiological
As airway resistance increases, it takes longer for reactions that occur as a response to a change in
the lung unit to inflate during ventilation. The amount homeostasis.
TABLE 25-1 Oxygen and PEEP titration

Best Practice strategies
Complications of Mechanical Lower PEEP/ Higher FIO2
Ventilation FIO2 PEEP
0.3 5
The main objective for mechanical ventilation
is to correct the associated problems that lead 0.4 5
to the need for mechanical ventilation and to 0.4 8
minimize the potential physiological effects to 0.5 8
the cardiac, renal, neurological, and associated
0.5 10
body systems. The respiratory therapist needs to
be aware of the associated complications with 0.6 10
mechanical ventilation in order to reduce the 0.7 10
risk of complications. 0.7 12
0.7 14
0.8 14
VOLUTRAUMA 0.9 14
Volutrauma is a condition that occurs when too much 0.9 16
tidal volume is delivered to the lungs. This large 0.9 18
amount of tidal volume has the potential to cause an 1.0 18–24
overdistension of the lungs that results in lung injury.
Overdistension can result in the stretching of the
alveolar spaces, which can lead to an inflammatory Higher PEEP/ Lower FIO2
mediator release that further injures the lungs.2,10 In FIO2 PEEP
May 2000, the National Institute of Health and the 0.3 5
National Heart Lung Blood Institute published a large
0.3 8
study that examined adult patients with acute respira-
tory distress syndrome and the optimal strategies for 0.3 10
preventing injury that may occur as a result of ventila- 0.3 12
tion. The results of the study demonstrated that 0.3 14
patients with acute lung injury or ARDS had an
0.4 14
improved chance of survival with the use of tidal
volumes ranging from 4 to 8 mL/kg ideal body weight 0.4 16
when compared to the traditional 10–15 mL/kg of 0.5 16
body weight.11 0.5 18
The low–tidal-volume-ventilation strategy also 0.5–0.8 20
utilizes a titration of inspired oxygen and positive
end-expiratory pressure to ensure that the patient 0.8 22
receives adequate alveolar distending pressure when 0.9 22
the lungs are in a low lung compliance state 1.0 22
(Table 25-1).11 The goal of oxygenation is to have a 1.0 24
PaO2 of 55–80 mmHg or SpO2 of 8895%.11 The
Source: Adapted from Ventilation with lower tidal volume as compared
minimal positive end expiratory pressure is 5 cm H2O to traditional tidal volume for acute lung injury and the acute respiratory
with a maximum level of 24 cmH2O.11 There are two distress syndrome. N Engl J Med. 2000;18:342:1301–1308.
strategy limbs in the oxygen and PEEP titrations:
The low–tidal-volume strategy concluded early
• One limb utilizes a lower PEEP level and higher
because of the significantly higher survival rate among
FIO2.11
patients who received a lower tidal volume than the
• The second limb utilizes a higher PEEP level
traditional tidal volumes.11 The strategy has been
with a lower FIO2.11
effective in decreasing the mortality of patients with
Either limb has been found acceptable in the treatment acute lung injury and acute respiratory distress
of alveolar stabilization and oxygenation for a patient syndrome, but currently no clinical data support the
who has acute lung injury or acute respiratory distress use of the low–tidal-volume-ventilation strategy for
syndrome.11 all patients who receive mechanical ventilation.
and hemodynamic statuses can result. These

Best Practice changes can lead to hypotension and tissue
hypoxia as a direct result of limited blood flow
Mechanical Ventilation perfusion in tissues.
• Positive pressure ventilation can be attributed
Strategies to a decrease in cardiac output. Cardiac output
Mechanical ventilation is a lifesaving procedure decreases because heightened intrathoracic
and should be utilized to assist patients in the pressure limits the amount of blood returning to
recovery from pulmonary-related illnesses. While the heart, decreasing venous return to the right
providing medical therapy that is in the best heart.2,10 During the expiratory phase of ventila-
interest of the patient, the respiratory therapist tion, venous return increases in a response to the
must refer to the most current medical literature decreasing of intrathoracic pressure.2,10
on treatment guidelines. Current medical litera- • Positive pressure ventilation can also be
ture suggests the use of a low–tidal-volume- attributed to an increase in pulmonary vascular
ventilation strategy to treat adult patients with resistance, which rises in response to an increase
the diagnosis of acute respiratory distress syn- in alveolar pressure that occurs when positive
drome and acute lung injury. Target tidal volumes end-expiratory pressure is present during
for an adult patient with ARDS or acute lung mechanical ventilation. As a result of the
injury, based on the low tidal volume study should increase in pulmonary vascular resistance,
range from 4 to 8 mL/kg ideal body weight.11 cardiac output and left ventricular filling pres-
sure both drop. In response to an increase in
right ventricular afterload, the effect can be right
ventricular hypertrophy, which can cause discord
BAROTRAUMA with left ventricular function.2,10
Barotrauma results from a high level of positive • Patients who receive positive pressure ventilation
pressure, causing air to escape from the alveolar through high-frequency ventilation can be at
areas.2,10 Barotrauma results in airleak syndromes such greater risk for hemodynamic compromise due
as pneumothorax or pulmonary interstitial emphy- to the high levels of mean airway pressure that is
sema, as well as free air in the thoracic cavity. When present in the lungs.12,13,14 High-frequency
plateau pressures rise above the level of 30 cm H2O, ventilation can cause overdistension of the lungs,
lung injury occurs as a result of high airway pressures. which can lead to further decreases in venous
To prevent barotraumas, the clinician should attempt return and, in turn, to increases in pulmonary
to decrease plateau pressures to a level of 30 cm H2O. vascular resistance. Thus cardiac output is further
Ventilator parameters should be adjusted according to reduced.12
the specific patient condition in order to decrease the To minimize the cardiovascular effects of mechani-
plateau pressures. Plateau pressures can be lowered by: cal ventilation, the respiratory therapist must ventilate
• Decreasing the tidal volume. the patient with the lowest possible mean airway
• Decreasing the positive end-expiratory pressure. pressure, positive end-expiratory pressure, and tidal
• Suctioning the patient if the high pressure is a volumes in order to prevent compression of the
result of secretions. vascular structures in the thoracic cavity.12 Some
• Providing bronchodilators if bronchospasm is patients may require the assistance of fluid resuscita-
present. tion and cardiac medication support to improve
• Manipulating the inspiratory time. (Any manip- hemodynamic status. Medical management should
ulation should be specific to the patient’s be made on a case-by-case basis and meet the medical
condition.) needs of the patient.
Renal dysfunction can also result from positive
pressure ventilation in a variety of ways.
DISRUPTION OF PHYSIOLOGICAL FUNCTIONS
• When intrathoracic pressure increases and
Mechanical ventilation can disrupt the normal
cardiac output is decreased, less perfusion is
physiological functions of the body. Positive pressure
available to the kidneys.2,10
ventilation can cause discord among the cardiac,
• There is a release of antidiuretic hormones from
pulmonary, neurological, and renal systems, to
the pituitary glands in response to the change in
name a few. For example:
intrathoracic pressure.2,10
• When a positive pressure environment is intro- • An imbalance of pH, PaCO2, and PaO2 can lead
duced to the thoracic system, changes in cardiac to renal dysfunction.2,10
To prevent edema and third spacing, the therapist has

to closely monitor the fluid status of the patient Best Practice
receiving mechanical ventilation.
Patients with closed head injuries are at risk for Managing Oxygenation
complications:
Other important considerations for managing
• One risk is of decreased cerebral perfusion in oxygenation relate to the titration of positive
response to the hemodynamic changes during end-expiratory pressure and inspired oxygen. To
mechanical ventilation.2,10 Positive end-expiratory assist in alleviating any ill effects of high oxygen
pressure and high mean airway pressures, in concentrations, the practitioner should consider
conjunction with decreased venous return can using positive end-expiratory pressure at the low-
impede the blood flow to the brain.2,10 High est possible oxygen concentration to increase the
levels of positive end-expiratory pressure and surface area for gas exchange.
high mean airway pressures should be avoided,
when possible, to allow adequate perfusion to
the brain.
• With the patient who has a closed head injury,
controversy surrounds the use of hyperventila- Summary
tion, which may cause compromise to the
uninjured areas of the brain. The patient with a Mechanically ventilated patients are at risk for a
closed head injury should be ventilated to number of complications associated with the physi-
prevent any further injury to the brain as well as ological effects of positive pressure ventilation. To
to meet the ventilatory needs of the patient. effectively provide positive pressure ventilation while
alleviating the potential hazards of mechanical ventila-
Hyperoxia-related injuries occur when patients are tion, the respiratory therapist needs to understand the
exposed to high levels of oxygen ( 60% FIO2) for physiological changes that result from mechanical
prolonged periods of time.2,10 Side effects of high ventilation. Early recognition of the potential effects
oxygen levels are: enables the therapist to prevent further complications.
• Retrolental fibroplasia.
• Mucociliary dyskinesis.
• Oxidative stress lung injury.
• Pulmonary tissue injury.2,10
Study Questions
If patient conditions permit, the oxygen concentration REVIEW QUESTIONS
should be lowered to a level that prevents lung injury. 1. How do transairway, transpulmonary, and trans-
One way to do this is to increase the positive end- thoracic pressure interact during the process of
expiratory pressure to allow more time for the gas respiration?
exchange to take place. Oxygen should be set at an 2. Name the two types of lung compliances.
appropriate level to meet the needs of the patient. It is
currently not known what exposure time to oxygen 3. Describe airway resistance and ways of improving
causes lung injury. In neonatal patients during post- high airway resistance.
birth resuscitation, using low levels of oxygen to 4. Discuss time constants and the importance they
prevent oxidation injury is acceptable, but the optimal play with mechanical ventilation.
level has not yet been determined.15 5. What is the difference between volutrauma and
barotrauma?
OTHER CONSIDERATIONS 6. List some of the complications associated with
mechanical ventilation.
Other considerations related to mechanically ventilated
patients are:
• Prevention of ventilator associated pneumonias. MULTIPLE-CHOICE QUESTIONS
• Maintaining adequate nutritional status. 1. What is the normal static lung compliance of a
• Preventing injuries associated with the artificial nonmechanically ventilated patient?
airway. a. 40–60 mL/cm H2O
• Assisting the patient in communication needs. b. 30–40 mL/cm H2O
• Taking care of the psychological well-being of c. 20–30 mL/cm H2O
the long-term mechanically ventilated patient. d. 10–20 mL/cm H2O
2. How many time constants are required to fill 60% References

of a lung region?
a. three 1. Jardins T. Cardiopulmonary Anatomy & Physiology.
b. five 5th ed. Clifton Park: Delmar Cengage Learning;
c. two 2007.
d. one 2. Pilbeam S. Mechanical Ventilation—Physiological
and Clinical Applications. 4th ed. St. Louis: Mosby;
3. Which pressure gradient describes the difference
2006.
between the alveolar pressure and body surface
3. Ward JPT, Ward J, Leach RM, Wiener CM. The
pressure?
Respiratory System at a Glance. 2nd ed. Chichester:
a. transairway pressure
Blackwell Publishing; 2006.
b. transthoracic pressure
4. dos Santos CC, Slutsky AS. Overview of high-
c. transpulmonary pressure
frequency ventilation modes, clinical rationale,
4. What complications may occur if too large a tidal and gas transport mechanisms. Respir Care Clin
volume and high ventilator pressures are consis- N Am. 2001;7:4.
tently delivered to a patient on mechanical 5. Mildner R, Cox P. The preclinical history of
ventilation? high-frequency ventilation. Respir Care Clin N
a. volutrauma Am. 2001;7:4.
b. barotrauma 6. Hess D, Mason S, Branson R. High frequency
c. pneumothorax ventilation, Respir Care Clin N Am. 2001;7:4.
d. all of the above 7. West JB. Respiratory Physiology: The Essentials.
5. Cardiac output decreases as a result of which of the 8th ed. New York: Lippincott Williams &
following factors during mechanical ventilation? Wilkins; 2008,
a. increased intrathoracic pressure 8. Chang DW. Respiratory Care Calculations, 2nd ed.:
b. decreased venous return to right heart Clifton Park Delmar Cengage Learning.; 1998.
c. high mean airway pressures 9. Goldsmith JP, Karotkin EH. Assisted Ventilation
d. all of the above of the Neonate. 4th ed. Philadelphia: Saunders;
6. What is the static compliance for a patient with a 2003.
tidal volume of 500 mL, a respiratory rate of 10, 10. Hess DR, Kacmarek RM. Essentials of Mechanical
positive end-expiratory pressure of 5 cm H2O, Ventilation. 2nd ed. New York: McGraw-Hill;
a flow of 50 Lpm, and an FIO2 set at 30%? The 2002.
patient’s peak airway pressure is 30 cm H2O 11. Ventilation with lower tidal volumes as compared
with a plateau pressure of 20 cm H2O. with traditional tidal volumes for acute lung injury
a. 50 mL/cm H2O and the acute respiratory distress syndrome. N Engl
b. 33.3 mL/ cm H2O J Med. 2000;342,18:1301–1308.
c. 15.8 mL/cm H2O 12. Cotton M, Clark RH. The science of neonatal
d. 25.5 mL/cm H2O high-frequency ventilation. Respir Care Clin N Am.
2001;7:4.
CRITICAL-THINKING QUESTIONS 13. Priebe GP, Arnold JH. High-frequency oscillatory
ventilation in pediatric patients. Respir Care Clin N
1. How can time constants be useful in the initial Am. 2001;7:4.
phases of ventilation? 14. Mehta S, MacDonald R. Implementing and trou-
2. What pulmonary changes occur to a newborn child bleshooting high-frequency oscillatory ventilation
who has respiratory distress and who receives in adults in the intensive care unit, Respir Care Clin
surfactant therapy? N Am. 2001;7:4.
3. How can early extubation or noninvasive ventila- 15. Kattwinkel J. Textbook of Neonatal Resuscitation. 5th
tion curtail the ill effects associated with mechani- ed. Elk Grove Village, IL: American Academy of
cal ventilation? Pediatrics; 2006.
CHAPTER 26
Initiation, Monitoring, and Discontinuing

Mechanical Ventilation
Bethene L. Gregg
OBJECTIVES
• Describe the essential events of initiating mechanical ventilation.
• Interpret changes in peak, plateau, and mean airway pressures
• Identify changes in scalar and/or loop waveforms indicating a leak, air trapping, or patient-ventilator
dyssynchrony.
• Describe PEEP and its application in contrast to auto-PEEP.
• Discuss the hazards and complications of mechanical ventilation including ventilator-associated pneumonia.
• Describe the purpose of ventilator checks in preventing potential complications.
• State the appropriate actions to take in correcting respiratory acidosis, alkalosis, or ventilator dyssynchrony.
• State how changes in the ventilator controls affect volume delivery and mean airway pressure.
• Explain the appropriate course of action when multiple alarms are activated and the patient’s condition has
suddenly deteriorated.
• Discuss methods of weaning, and list two important considerations for extubation.
CHAPTER OUTLINE
Indications for Mechanical Ventilation Ventilator Management
Initiation of Mechanical Ventilation Mechanical Ventilation in Oxygenation Failure
Initial Ventilator Settings Mechanical Ventilation in Chronic
Summary of Initiating Mechanical Ventilation Airflow Obstruction
Mechanical Ventilation in Neuromuscular Disease
Patient Monitoring
Independent Lung Ventilation
Ventilator Check
Waveforms Ventilator Discontinuance
Work of Breathing Short-Term Ventilation Discontinuance
Humidification of Mechanical Ventilation Long-Term Ventilation Discontinuance
Complications of Mechanical Ventilation
698
CHAPTER 26 ■ Initiation, Monitoring, and Discontinuing Mechanical Ventilation 699
KEY TERMS
alveolar recruitment baseline pressure peak pressure
barotrauma mean airway pressure plateau pressure
C
ontinuous mechanical ventilation typically The respiratory therapist (RT) understands why
refers to positive pressure ventilation, in mechanical ventilation alone does not improve arterial
which the patient-ventilator interface is an oxygen tensions in oxygenation failure. Oxygenation
artificial airway, usually an endotracheal or failure is due to pulmonary shunting, in which pulmo-
tracheostomy tube. This chapter focuses on the initia- nary capillary blood passes by collapsed, flooded, or
tion, monitoring/management, and discontinuation of underinflated alveoli.3 Alveoli may also collapse at the
mechanical ventilation in adults. end of a tidal breath and contribute to shunt. The
distribution of ventilation dictates that inspiratory gas
goes to the areas of the lung that are the most easily
Indications for Mechanical expanded (compliant) and that have the least airway
resistance. A tidal breath may not inflate the affected
Ventilation areas at all and therefore does little to reduce shunt and
Initiate mechanical ventilation in cases of: improve oxygenation.
The volume of the lung as a whole must increase;
• Apnea.
specifically, the functional residual capacity (FRC) must
• Acute ventilatory failure.
increase. The increase in FRC is typically accomplished
• Oxygenation failure.
by applying positive end-expiratory pressure (PEEP). PEEP
• Impending ventilatory failure.
holds pressure in the lung and increases the end-tidal
Any condition that impairs the physiologic pathway of lung volume. Because the principles governing the
breathing may lead to apnea or acute ventilatory failure, distribution of ventilation for this added lung volume
which is the failure of the thorax to pump air. Depres- still apply, PEEP may not reexpand a localized area of
sion of the respiratory centers in the brain, spinal cord atelectasis. However, if collapsed, flooded, or underin-
injury, neuromuscular dysfunction, and diaphragmatic flated alveoli are more diffuse throughout the lung,
fatigue can all impair the movement of the thorax. The PEEP may open collapsed alveoli and prevent the
inability of the thorax to move air reduces alveolar end-tidal collapse of others when it is applied early in
ventilation and results in alveolar hypoventilation and the course of acute lung injury or respiratory insuffi-
respiratory acidosis. Hypoxemia is secondary to ciency. The reopening of collapsed alveoli is called
hypercarbia. Mechanical ventilation delivers 14–16 alveolar recruitment.
tidal volumes per minute that restores adequate A critical care ventilator is not needed to apply
alveolar ventilation and corrects the arterial blood PEEP; less complicated devices can provide it. However,
gases by lowering the PaCO2 to normal values. A all critical care ventilators are capable of providing PEEP.
normalized PaCO2 raises the PaO2 and the pH. When applied to patients who are breathing in a
On the other hand, oxygenation failure is the failure spontaneous mode of ventilation or who are indepen-
of the lungs to provide gas exchange. A ventilator dent of a mechanical ventilator, PEEP is referred to as
provides the bulk movement of gas into the lungs: It continuous positive airway pressure (CPAP). Treating cases
does not bring about gas exchange. An extracorporeal of oxygenation failure with CPAP only can present a
membrane oxygenator (ECMO) allows the exchange of problem. If CPAP is applied too late, the expiratory
O2 and CO2 in the blood but does not provide ventila- work of breathing at the elevated pressure may become
tion. Oxygenation failure produces severe hypoxemia excessive and cause respiratory muscle fatigue. Once
that is refractory to oxygen therapy; that is, the PaO2 fatigue occurs, mechanical ventilation becomes neces-
does not increase by at least 10 mm Hg with each sary. For this reason, a patient in oxygenation failure is
increase of 0.20 in FIO2 .1 Hypoxemia stimulates the often intubated to protect the airway and to provide
peripheral chemoreceptors, in turn increasing alveolar mechanical ventilation. In some cases, however, early
ventilation.2 The result is alveolar hyperventilation and intervention with mask CPAP may increase FRC,
respiratory alkalosis. Since ventilation is not impaired improve oxygenation, and avoid intubation.
per se, mechanical ventilation is less effective in To identify impending ventilatory failure,
oxygenation failure, which may progress to acute physiologic function is often measured to determine
respiratory distress syndrome (ARDS). the adequacy of a patient’s capacity to maintain
spontaneous breathing. Variables such as vital capacity, • Set a flow trigger of 2 Lpm.
negative inspiratory pressure, and maximum voluntary • Set 5 cm H2O PEEP.
ventilation are typically measured in addition to • Connect the ventilator in volume control mode
arterial blood gases (ABG). There are critical thresholds to the patient and:
or limits beyond which physiologic function becomes • Check that the patient’s chest expands (that
incompatible with sustained spontaneous breathing. the ventilator delivered a breath).
These values are as follows: • Reduce tidal volume if the high pressure
• Partial pressure of oxygen in arterial blood alarm is activated; check that the plateau
(PaO2) 50 mm Hg pressure is less than or equal to 30 cm
H2O in VC.
• Frequency (f ) 35 bpm
• Check the flow/time waveform that the
• Tidal Volume (VT) 5 mL/kg
expiratory flow returns to baseline; that is,
• Negative inspiratory force or pressure (NIF, NIP)
there’s no air trapping.
20 cm H2O
• Check for signs of patient-ventilator
• Vital Capacity (VC) 10 mL/kg
asynchrony; that is, adjust the peak flow
In general, indicators such as inadequate arterial blood to meet the patient’s inspiratory
gases, coupled with the signs and symptoms of acute demand.
respiratory distress, identify the patient who requires • Perform a ventilator check.
intubation and mechanical ventilation. The notable
exception is the patient with chronic airflow obstruction A ventilator should be on standby, ready for use, and
(CAO). A trial of medical treatment, including oxygen it should have had proper preventative maintenance
therapy and bronchodilators, is indicated in this case by qualified staff. Attach a ventilator circuit and
before intubation and mechanical ventilation. Also, the connect an appropriate humidification system.
use of noninvasive ventilation has gained support in Connect the ventilator to a power and gas source.
emergent situations such as exacerbation of CAO. Before the ventilator is connected to the patient, its
Noninvasive ventilation is discussed in more detail in operation must be verified and the patient values
Chapter 28. entered on the control panel. Most ventilators require
the selection of the type of humidification system,
either a heated wet humidifier or a heat and moisture
Initiation of Mechanical exchanger (HME), during the initial ventilator start-up
Ventilation when the patient’s weight is entered. The initial
start-up is also when flow and oxygen sensors are
Use the following guidelines to initiate mechanical calibrated and when the neonatal, pediatric, or adult
ventilation: patient range is selected. During this time, the patient
• Verify ventilator function, select the humidifier is being ventilated with a manual resuscitator or trans-
type, and connect the humidifier, calibrate the port ventilator.
sensors, set the high airway pressure alarm limit Ventilators vary in their operation verification
on 40 cm H2O for volume control (VC) or on procedures. These programmed self-tests may take
35 cm H2O for volume-targeted pressure control several minutes and result in ventilator failure if
(VTPC). Also for VTPC, set the high tidal volume performed too quickly. Some of the current ventilators
alarm limit equal to 10 mL/kg. have a short leak test, and it should be used. This test
• Set a tidal volume (VT) of 8 mL/kg of predicted creates a pressure hold that checks for leaks, exhalation
body weight (PBW) at a rate of 15 breaths per valve function, and tubing compliance factor. Failure to
minute (bpm). If the plateau pressure is greater perform the manufacturer’s recommended perfor-
than 30 cm H2O when the ventilator is con- mance check may cause the ventilator to malfunction
nected to the patient (low compliance), use 6 during patient use.
mL/kg of PBW VT and a rate of 20 bpm. If the
plateau pressure is still greater than 30 cm H2O,
drop the tidal volume to 4 mL/kg of PBW
(minimum tidal volume) and increase the rate
Best Practice
to 30 bpm (maximum 35 bpm).
• Set a peak flow of 50 Lpm or a flow in milliliters Checking Ventilator Function
per minute equal to VT mL bpm (I E) Always verify the proper functioning of the venti-
• Set the primary disconnect alarm, the high tidal lator according to the manufacturer’s recommen-
volume alarm limit, and the apnea ventilation dations before connecting the unit to the patient.
parameters, if available.
For older ventilators or for those without a short Respiratory therapists must know which ventilators
self-test, check for leaks by observing that the ventilator automatically perform self-tests when first powered on
holds pressure during an inspiratory pause with the and which tests the operator may initiate. Some tests
patient wye occluded. are not to be performed at the bedside. For example,
most ventilators, with the exception of the Puritan
• Set a long pause time and a small tidal in Bennett (PB) 840, may be powered on, and then the
volume control. patient wye can be aseptically blocked. The PB 840
• Adjust the high airway pressure alarm to must not have the patient wye blocked when it is
maximum. powered on. If the patient wye is inadvertently blocked
• The patient wye is aseptically occluded, and a when the PB 840 is powered on, the ventilator switches
breath is manually initiated. to a second microprocessor in the breath delivery unit
• Observe the airway pressure monitor to check that and provides safety ventilation. The ventilator needs to
the ventilator holds pressure during the pause. be shut off and restarted.
A falling pressure during the pause indicates a leak. All
connections should be rechecked and an inspiratory pause
repeated until the system holds pressure. The high-pressure INITIAL VENTILATOR SETTINGS
alarm, pause time, and tidal volume must be readjusted After verifying ventilator operation, adjust the control
when setting the control panel for the patient. settings based on the patient’s ideal or predicted body
For older ventilators, the pause pressure generated weight. Predicted body weight (PBW) may be estimated
during the leak test may be used to calculate the circuit as:
compliance or tubing compliance factor.
Men (in kilograms) 50 2.3 per inch over 5 feet
• Divide the tidal volume by the pause pressure to
calculate the tubing compliance factor. Women (in kilograms) 45.5 2.3 per inch over 5 feet
• Use this factor to calculate the volume that is Men (in pounds) 110 5 per inch over 5 feet
compressed in the circuit during a volume- Women (in pounds) 100 5 per inch over 5 feet
controlled inspiration and that is therefore not
delivered to the patient. The current recommended initial settings are VT 8 mL/
• After the ventilator is connected to the patient, kg of the patient’s ideal body weight and 15 breaths
multiply the pressure during a pause (minus any per minute (bpm). Before the first delivered breath,
PEEP) by the tubing compliance factor to find the high airway pressure alarm should be set on
the compressible volume loss to the circuit. 40 cm H2O. This setting allows a quick check on
• Subtract the compressible volume from the the patient’s compliance with the first volume-
exhaled tidal volume to calculate the tidal controlled breath.
volume that the patient actually receives.
Most current critical care ventilators automatically
calculate tubing compliance during the performance
verification test. Best Practice
A common but not as safe verification practice is to:
• Check that the ventilator is in the proper mode
High Airway Pressure Alarm
to deliver a breath. Check that the high airway pressure alarm is set
• Block the patient wye, on 40 cm H2O before connecting the unit to the
• Manually trigger a breath to observe that pres- patient.
sure builds up during inspiration and activates
the high airway pressure alarm.
Although this practice serves several functions, it does
not always detect a leak or a malfunctioning exhalation Age-Specific Competency
valve. It does:
• Verify that gas is actually exiting the ventilator Pediatric Settings
and that the high pressure alarm functions.
Ventilator settings vary for infants and children.
• Check the patient disconnect alarm if the patient
For example, airway pressure alarms should be
wye is then opened.
less than 30 cm H2O for infants.
This procedure is not recommended, however.
For example, if the patient weighs 70 kg and the set Inspiratory/expiratory ratios (I/Es) of 1:3 or 1:4 are
tidal volume is 560 mL, the high-pressure alarm is usually an adequate starting point. Calculate the peak
activated if the patient’s compliance is severely reduced flow setting in milliliters per minute as:
to around 20 mL/cm H2O, assuming approximately
VT(mL) bpm (I E)
10 cm H2O from airway resistance.
For example, 560 mL 15 4 33,600 mL per
• Should the high-pressure alarm activate with the minute or 33.6 Lpm; therefore, set 34 Lpm for the peak
first delivered breath or if the target tidal volume flow for an I/E ratio of 1:3 if the tidal volume is 560
is not delivered, adjust the tidal volume to 6 mL/ mL and the frequency setting is 15 bpm.
kg and increase the bpm to 20. Check that the The peak flow calculated with this formula is lower
plateau pressure is less than 25, and add 5 cm than what is generally used and appropriate as long as
H2O PEEP. the patient is not triggering every breath. Typically, a
• If the plateau pressure is over 25 cm H2O, drop starting peak flow of 50 Lpm is used initially and
the tidal volume to 4 mL/kg before adding 5 cm adjusted after the ventilator has been connected to the
H2O of PEEP. patient. If the pressure fails to increase immediately
• If the plateau pressure is over 30 cm H2O with during a patient inspiration, the peak flow is not high
the addition of PEEP at a tidal volume of 4 mL/ enough and must be increased.
kg, change the mode to airway pressure release Use a descending ramp flow waveform in volume
ventilation (APRV). Set high pressure on 30 cm control, if available, because a ramp waveform
H2O and low pressure on 0 cm H2O. Set a high provides the highest mean airway pressure at the
time of 4 seconds and a low time of 0.5 seconds. lowest peak pressure. Increasing mean airway
(The management of APRV and the application pressure improves oxygenation as long as cardiac
of PEEP for patients with ARDS are discussed in output does not decrease. The change in flow wave-
more detail later in this chapter.) form from a rectangular to a descending ramp
increases the inspiratory time and produces a larger
The patient must be adequately sedated when
I/E ratio (closer to 1:1); so verify that there is ade-
small tidal volumes (4–6 mL/kg) are delivered in
quate expiratory time after changing to a ramp flow
volume control or the result of either volume-targeted
waveform in VC mode.
pressure control or pressure-controlled (PC) ventilator
There is no documented advantage to initiating
breaths. If the patient increases inspiratory effort in an
ventilation in PC mode over volume control mode if
attempt to take larger breaths, the increased effort may
the patient is apneic, provided the precautions just
generate more negative swings of intrathoracic pressure
discussed are followed. No studies document an
that could exacerbate pulmonary edema. Lung protec-
advantage to VTPC over PC or VC. 5 Initiating volume
tive strategies favor the use of VTPC or PC breaths to
control is more efficient, provided the high airway
reduce the work of breathing from increased patient
pressure alarm is appropriately set, and provides
demand for flow, provided the pressure does not
better control of lung-protective tidal volumes. 6 To
exceed 30 cm H2O. 4 Since most ventilators in VTPC
initiate ventilation in pressure control, ideally the
mode do not allow the pressure to come within 5 cm
respiratory therapist needs to be able to adjust the
H2O of the high airway pressure alarm, the high
level of pressure control rapidly with the turn of
pressure alarm should be set on 35 cm H2O. Because
a knob.
both VTPC and PC breaths are time cycled, the inspira-
A tidal volume of 8 mL/kg and a set rate of
tory time must be set appropriately, usually 1.0 second
15 bpm is still desirable. However, in PC and in
for adults. Inspiratory time may be readjusted after
VTPC, the tidal volume is a function of the pressure
connecting the ventilator to the patient and observing
level, the patient’s pulmonary compliance, and the
flow/time waveforms.
patient’s airway resistance. If the patient’s compliance
When the tidal volume and beats per minute have
is not known, a level of 15 cm H2O of PC is an
been determined in volume control, the flow rate and
appropriate starting point, provided a high tidal
flow pattern need to be set. Both peak flow rate and
volume limit alarm is available and set to a volume
flow pattern determine the length of inspiration, or
equal to 10 mL/kg.7
inspiratory time. The inspiratory flow must be high
enough to meet the patient’s inspiratory demand and • In VTPC modes, the ventilator initially delivers a
to limit the length of inspiration in order to allow volume-controlled breath for the purpose of
adequate time for exhalation. Expiratory time is a calculating the patient’s compliance and resis-
function of the beats-per-minute control. At any tance. Then the ventilator automatically adjusts
given inspiratory time, increasing the number of the PC level until the target tidal volume is
breaths per minute lower the time allowed for exhalation. achieved.
TABLE 26-1 Adaptive pressure control modes

Dräger Evita 4 and XL AutoFlow®
Engström Carestation Pressure controlled, 1s 1.3
volume guaranteed
Hamilton Galileo Adaptive pressure
ventilation
Maquet 300, 300A, Pressure-regulated
Servoi volume control
Puritan Bennett 840 Volume control plus
Newport E500 Volume-targeted
pressure control
Viasys/Pulmonetics Pressure-regulated
PalmTop volume control A B
Viasys Avea Pressure-regulated
FIGURE 26-1 (A) The arrow indicates flow above baseline
volume control
at the end of inspiratory time. (B) The longer inspiratory
time shows flow returning to the baseline.
• In PC, the respiratory therapist needs to adjust control (minus PEEP). The compliance is then used to
the PC level until the target tidal volume is determine the level of pressure control (x) for any
achieved. The inspiratory pressure level should desired tidal volume.
not exceed 30 cm H2O. 500 mL 30 mL 500 x 17 cm H O of PC
_________
x H2O 30 2
The names of volume-targeted pressure control modes,
also called adaptive pressure control5 modes, for If the compliance is 30ml/cm H2O and the desired
various ventilators are listed in Table 26-1. tidal volume is 500ml, the pressure required is 500ml/
The inspiratory time should be fixed in pressure 30 ml/cm2O 17 cm H2O.
control, rather than by fixing the I/E ratio. Fixing the In VTPC, the ventilator automatically adjusts or
inspiratory time may help prevent excessively large adapts the level of pressure control between breaths to
swings in tidal volume in the event of a change in beats maintain the target tidal volume because pressure is the
per minute. For example, if the I/E ratio is fixed and variable controlled by the ventilator during inspiration.
then the set frequency is decreased from 20 to 15 bpm, The control variable may also be switched within a
the increase in inspiratory time could deliver exces- breath. Within-breath changes are typically changes from
sively large tidal volumes. Fixing the I/E ratio is more pressure control to volume control during the same
appropriate when providing inverse ratio ventilation breath. Pressure augmentation on the Bear and volume-
(discussed later in the chapter). assured pressure support (VAPS) on the Bird 8400STi
An inspiratory time of 1.0 second may be used and Tbird essentially provide volume-supported breaths
initially in PC or VTPC and then adjusted according to (that may be time triggered) as long as the target tidal
the flow waveform. Flow waveforms are monitored to volume is delivered before the inspiratory flow falls to
maximize volume delivery for any level of pressure the peak flow setting. In this case, there is no change in
control. In Figure 26-1A, the inspiratory time ends before control variable (Figure 26-2A).
flow has returned to baseline. Increasing the inspiratory However, if inspiratory flow falls to the set peak flow
time to 1.3 seconds increases the volume delivered, as level before the tidal volume has been delivered, the
shown in Figure 26-1B, where the flow returns to control switches to flow (volume control), and gas
baseline before inspiration ends. Any further increase in delivery continues at the peak flow rate setting to
tidal volume requires an increase in the level of pressure complete volume delivery (Figure 26-2B). When the
control. The inspiratory time may need to be adjusted in control switches to flow, airway pressure increases over
VTPC as well. The ventilator automatically adjusts the the set inspiratory pressure limit. Ventilation then
level of pressure in VTPC, but not the inspiratory time. resumes in volume support (that may be time triggered)
Because flow has returned to baseline in Figure with the next breath. The patient can also receive a larger
26-1B, there is a period of no flow at end-inspiration. tidal volume than the target setting (Figure 26-2C).
To estimate the patient’s compliance under this condi- Pressure-limited ventilation on the Dräger
tion, divide the tidal volume by the level of pressure Evita4 and EvitaXL is one of the few modes that has a
Pressure work of breathing through an endotracheal tube for

support/control the spontaneously breathing patient. Automatic tube
level compensation (ATC) (Dräger XL) or tube compensation
(TC) (PB 840) automatically applies a level of pressure
support that is proportional to the resistance across
the endotracheal or tracheostomy tube during inspira-
Set peak
flow (Lpm) tion. The pressure level depends on the calculated
Time value for tracheal pressure. Tracheal pressure is calcu-
lated as the proximal airway pressure minus the
A B C product of the known resistance of the tube, multi-
plied by the squared flow. The flow is measured
FIGURE 26-2 Pressure augmentation (Bear 1000, Bear
instantaneously throughout inspiration. ATC can also
Medical, Riverside, California) and volume-assured pres-
sure support (Bird 8400ST, Bird Corp., Palm Springs, decrease the patient’s expiratory work of breathing by
California) work the same way: (A) A target tidal volume reducing the PEEP as needed to partially compensate
is delivered; no switch in control variable. (B) The flow for resistance of the endotracheal tube during exhala-
falls to the peak flow setting before the target volume is tion.10 The expiratory compensation feature may be
delivered; control variable switches to volume control. turned off.
(C) A greater patient inspiratory effort allows a larger tidal A variation on A/C or SIMV mode is Adaptive
volume than the target volume. Support Ventilation (ASV), available on the Galileo
Gold (Hamilton Medical, Reno, Nevada) that pro-
vides VTPC time-triggered mandatory breaths or
within-breath change from volume to pressure control. volume support for patient-triggered spontaneous
A pressure-limited breath starts in volume control but breaths. ASV automatically selects the ventilator
switches to pressure control if the airway pressure values for respiratory rate, inspiratory time, I/E ratio,
reaches the set maximum pressure (Pmax). Inspiration and pressure limit on the basis of the patient’s
at Pmax continues until the set tidal volume is deliv- required minute volume. The clinician inputs the
ered.8 If the tidal volume is delivered before inspiratory patient’s body weight, and the minute volume is
time ends, inspiratory flow falls to zero, and an inspira- determined as 100 mL/min/kg. The percentage of the
tory pause ensues for the remaining inspiratory time. minute volume to be supplied can be adjusted from
For patients with relatively normal compliance, 10% to 350%.11 The ventilator delivers test breaths to
either assist-control (A/C) or synchronized intermittent calculate compliance, resistance, and intrinsic or
mandatory ventilation (SIMV) mode may be used auto-PEEP (PEEPi). It then automatically adjusts the
initially as long as full ventilatory support is provided. frequency and tidal volume to minimize the elastic
SIMV has several advantages over A/C mode. SIMV and resistive loads according to the minimal work of
prevents excessive triggering of machine breaths that breathing equation described by Otis and associates
could lead to hyperventilation and respiratory alkalosis, in 1950. The ventilator algorithm for ASV is designed
air-trapping, or patient-ventilator dyssynchrony. When to prevent apnea, volutrauma (injury to the lung
SIMV is used, set to the pressure support for any parenchyma from alveolar overexpansion and shear
spontaneous breaths taken in between mandatory stress), PEEPi, or rapid shallow breathing. The flow
(machine) breaths to minimize the patient’s work of cycle variable for VS breaths can be adjusted from
breathing. An initial pressure support level of 5 cm H2O 10% to 40% of the initial peak flow.11
is usually sufficient to overcome most of the resistance For patients with severely reduced compliance,
from the circuit and an endotracheal tube with an inner bilevel ventilation may be initiated. Essentially, bilevel
diameter of 8.0–8.5 mm. The level of pressure support ventilation allows a high and low CPAP setting. The
should be reevaluated after the patient is connected. patient can breathe spontaneously with or without
A variation of pressure support, volume-targeted pressure support at two different pressure levels
pressure support or volume support, is also available (Figure 26-3). The difference between bilevel ventila-
on some ventilators. Both pressure support and volume tion and PC with PEEP is that, on bilevel, the patient is
support are considered spontaneous breathing modes able to exhale during the high-pressure period. Exhala-
because the patient must initiate the breath and tion is possible at the higher pressure level because the
determine when the flow-cycled breath ends. On some exhalation valve is active or floating and allows exhala-
ventilators. the flow cycle variable for terminating tion without terminating the inspiratory phase.12
pressure or volume supported breaths is adjustable.2 During a PC inspiration, the exhalation valve is closed,
In addition to pressure support, several ventilators preventing exhalation because PC is time cycled.
have another option to reduce the resistive inspiratory Table 26-2 summarizes bilevel modes.
• The qualifications and experience of the respira-

Pressure tory care staff.
• The restraints placed on the RCP by the medical
staff’s ventilator knowledge or lack thereof.
All modes have advantages and disadvantages that
must be considered in light of the clinical situation.14
Flow
All modes include a patient trigger setting. The
patient may initiate a breath by creating a drop in
pressure or a drop in flow. A flow trigger setting of
FIGURE 26-3 Bilevel ventilation allows spontaneous
breathing at two levels of pressure. Pressure-supported 2–3 Lpm for adults (1–2 Lpm for infants) is preferable
breaths are also an option in bilevel (not shown). to a pressure trigger for critical care ventilators, except
in the case of an unavoidable leak in the system. A leak
equal to or greater than the flow trigger mimics a
patient’s inspiratory effort and initiates breaths. A
Theoretically, less sedation is required with bilevel
baseline or bias flow is available automatically on
ventilation because the patient is free to initiate breaths
most current ventilators with a flow trigger. The flow
at any time during the high or lower levels of pressure.
trigger is usually not more than half of the baseline
In bilevel ventilation, the patient’s actual inspiratory
flow. The ventilator begins baseline flow delivery
time is not limited by the ventilator. The ventilator’s
through the circuit when at least half the patient’s
control of time simply determines how much time is
exhalation has occurred. The Babylog 8000plus (Dräger,
allowed at the high CPAP level (TH) versus the time
Telford, Pennsylvania) is an infant ventilator with a
allowed at the lower pressure level (TL). APRV typically
flow trigger that allows different expiratory and inspira-
refers to a minimal TH of 4–6 seconds for adults
tory flow rate settings. Activating VIVE (variable inspira-
(2–3 seconds for neonates) and a low CPAP time of
tory variable expiratory) allows the user to independently
0.2–0.8 seconds for adults (0.2–0.4 seconds for
set the expiratory baseline flow rate. A lower baseline
neonates) for an TH/TL ratio of 8:1 or more.13 Ideally,
expiratory flow reduces the infant’s expiratory work of
the low pressure time is set according to the peak
breathing.
expiratory flow. The low pressure time is set to end-
In addition to a flow or pressure trigger, a patient
expiratory time at 50–75% of the peak expiratory flow
can now initiate a breath from the change in electri-
observed from a flow-time waveform or flow-volume
cal activity of the diaphragm. Neurally adjusted
loop. Carbon dioxide elimination is facilitated by a
ventilatory assist (NAVA) applies pressure in propor-
greater difference between the high and low CPAP
tion to the strength of a diaphragmatic contraction.
levels and by more frequent cycles, or releases, from the
Inspiration is also terminated or cycled by a decrease
high to the low pressure levels. Typical APRV pressure
in the electrical activity of the diaphragm.15 NAVA on
settings are 30 cm H2O for the high pressure and 0 cm
the Maquet Servoi was approved by the FDA in 2007
H2O for the low pressure. Sixty divided by the sum of
and requires a specially designed nasogastric (NG)
TH plus TL equals the number of releases per minute.
tube. The NG tube is embedded with microelec-
For example, a TH of 4.5 seconds and a TL of 0.5
trodes and has a cable that transmits the signal to
seconds produces 12 releases per minute.
the Servoi . NAVA improves patient-ventilator syn-
Whichever mode is used in an intensive care unit
chronicity by reducing the number of missed breaths,
depends on:
that is, breaths that the patient attempts to initiate
• The needs of the patient. but that the ventilator fails to allow. NAVA also
• The type of ventilator available. has the potential to reduce the patient’s work of
TABLE 26-2 Bilevel modes

Bilevel 840 (Puritan Bennett, Pleasanton, California)
Bivent Servoi (Maquet, Bridgewater, New Jersey)
Bilevel airway pressure ventilation Engström Carestation (GE Healthcare, Chalfont St. Giles, UK)
Airway pressure release ventilation (APRV) Evita XL (Dräger, Telford, Pennsylvania)
Galileo Gold (Hamilton Medical, Reno, Nevada)
Viasys Avea (Cardinal Health, Dublin, Ohio)
breathing by ending a breath when the neural signal • In volume control with rectangular flow wave-
diminishes.16 forms, calculate airway resistance as (peak
Before connecting the patient to the ventilator, set pressure minus plateau pressure) over peak flow
the primary disconnect alarm if one is available. The in liters per second (Lps).
disconnect alarm is usually the low inspiratory pressure • Ensure that the patient appears comfortable on
alarm or low tidal or minute volume alarm. After the ventilator and is not triggering breaths at a
connecting to patient, the low inspiratory pressure rate over 25/min.
alarm should be set on 10 cm H2O and readjusted to • Observe the flow-time waveform and check that
5–10 cm H2O below the peak pressure. Many ventila- the expiratory flow returns to baseline before the
tors set the low inspiratory pressure alarm automati- start of the next inspiration to verify the absence
cally. The low minute volume alarm should be set of air trapping.
appropriately less than the set minute volume, usually • Observe the pressure-time waveform for
20% less. If using VTPC, set the high tidal volume limit an immediate increase in pressure during
alarm to 10 mL/kg of the patient’s PBW. Any ventilator inspiration.
with a volume-targeted pressure control or support • Check the volume-time waveform to verify that
mode should have a high tidal volume limit alarm. If the expiratory limb returns to baseline, indicat-
oxygenation status is unknown, an FIO2 of 1.0 (100%) ing that there are no leaks in the system.
oxygen should be used initially and the low FIO2 alarm • Note the pulse oximetry saturations and the
set on 95%. A quick check and adjustment of all other FIO2.
alarms completes the process. If the ventilator has • After 15 minutes, obtain an arterial blood gas
apnea ventilation, set the apnea ventilation controls. (ABG). After drawing the ABG, suction the
Several ventilators allow only parameter adjustment of patient and measure cuff inflation pressure. An
apnea ventilation when the selected mode permits appropriate suction catheter size in French
spontaneous breathing. A spontaneous breath by equals half the endotracheal tube inner diameter
definition must be triggered and cycled by the patient.8–9 times 3. Cuff inflation pressure should be
Finally, connect the ventilator circuit to the patient. 20–30 cm H2O to seal the airway and to prevent
secretions immediately above the inflated cuff
• Immediately upon connection, observe that the
from inadvertently passing down around the cuff
patient receives a ventilator breath and that chest
into the lower airway.18
expansion occurs.
• Airway stability is also important. An endotra-
• Breath sounds should be clear, equal, and
cheal tube that is not properly secured is a
bilateral.
problem waiting to happen.
• Set a level of 5 cm H2O PEEP for an adult.
• A manual resuscitator connected to oxygen
• Adjust alarm settings.
with an appropriately sized mask should be
• Complete a ventilator check.
kept available at the bedside under aseptic
• Record the endotracheal tube insertion depth in
conditions.19
centimeters at the teeth. The endotracheal tube
should be inserted to a depth of approximately An initial PEEP/CPAP setting of 5 cm H2O for
23 cm at the incisors in men, 21 cm in adults, 2–3 cm H2O for infants, helps in maintaining
women.1,17 FRC and counteracts the loss of end-expiratory lung
• Note the peak inspiratory pressure and the volume that results from placement of the endotra-
plateau pressure during a pause. cheal tube through the glottis. In cases of ARDS, the
• Calculate the tidal volume, corrected for level of PEEP should coincide with the pressure that
compressible volume loss as appropriate. maintains alveolar recruitment. Some practitioners
• Calculate the patient’s effective compliance as believe this pressure is represented by the lower
exhaled tidal volume over (plateau – PEEP). inflection point of the patient’s pressure-volume
Best Practice
Best Practice
Verify Chest Expansion
Disconnect Alarm Always verify chest expansion from a ventilator
Know the primary patient disconnect alarm and breath when the patient is first connected to the
what conditions activate preprogrammed alarms. ventilator and listen for bilateral breath sounds.

The respiratory therapist is ready to connect the The ventilator is connected to a conscious and
patient to the ventilator and sets the controls for alert patient. The respiratory therapist notices
volume control: A/C. The high pressure alarm that the airway pressure hesitates around zero
limit is on 40 cm H2O. Immediately after the before rapidly increasing at the end of inspira-
patient is connected, the high pressure limit tion. The patient looks agitated and uncomfort-
alarm activates. able. The RT is in volume control with a rectan-
gular flow waveform.
Question
1. The patient is not triggering breaths or biting Question
on the tube. What should you do first? 1. What is most likely the problem?
relaxation curve. Other practitioners advocate an • Check the flow/time waveform that expiratory
optimal PEEP level that maximizes alveolar recruit- flow returns to baseline; that is, there’s no air
ment. The end-expiratory pressure is set above the trapping.
point where significant alveolar destabilization • Check for signs of patient-ventilator asynchrony
occurs, usually determined during decremental if the patient is triggering breaths.
deflation from an alveolar recruitment maneuver.20,21 • Are the patient’s inspiratory efforts
When pressure-volume curves are not measured, failing to initiate inspiration? Check the
increase PEEP as high as possible without exceeding trigger setting and the presence of intrinsic
a plateau pressure of 28–30 cm H2O to improve PEEP.
oxygenation without overdistension and to keep tidal • Does the inspiratory pressure fail to rise
volume equal to 6 mL/kg of predicted body weight.22 immediately? Is the peak flow adequate to
Overdistension is measured as a decrease in effective meet patient’s inspiratory demand (in VC)?
compliance. • Is the patient working to exhale? Shorten the
inspiratory time, reduce or eliminate the pause
time.
SUMMARY OF INITIATING MECHANICAL • Is there air trapping? Shorten the inspiratory
VENTILATION time, increase the peak flow, reduce the
• Verify ventilator function, connect humidifica- number of machine breaths by changing to
tion system, calibrate sensors. SIMV mode.
• Set patient parameters: • Perform a ventilator check
• VT 8 ml/kg at a rate of 15 bpm
• Peak flow of 50 Lpm or a flow in mL equal to
VT bpm (I E) Patient Monitoring
• Flow trigger of 2 Lpm
After mechanical ventilation has been established, the
• PEEP of 5 cm H2O
patient’s ventilation, oxygenation, circulation, and
• Set alarms:
perfusion are assessed to determine the appropriate-
• Primary disconnect
ness of the ventilator settings and to prevent complica-
• High airway pressure alarm: 40 cm H2O for
tions. Arterial blood gases are drawn soon after
VC; 35 cm H2O for VTPC
initiating ventilation and then after changes in the
• High tidal volume limit
patient’s condition or ventilator settings. In general,
• Apnea ventilation, if available
change one ventilator parameter at a time in order to
• Connect the ventilator to the patient and:
assess its effect and wait at least 15 minutes after
• Check that the patient’s chest expands (that
interrupting ventilation or after endotracheal suction-
the ventilator delivers a breath).
ing to obtain a blood gas. Although pulse oximetry
• Reduce tidal volume if the high pressure alarm is
can monitor oxyhemoglobin saturation, it cannot
activated for VC or the volume is not constant
measure arterial PCO2 or pH. The PaCO2 is the best
alert given for VTPC. Check that the plateau pres-
assessment of alveolar ventilation. Pulse oximetry is
sure is less than or equal to 30 cm H2O in VC.
Possibly increase frequency to maintain V E.
useful for trending and detecting hypoxemia, but it
does not warn of hyperoxic conditions. The arterial VENTILATOR CHECK

PO2 blood gas is a better assessment of oxygenation Every hour for the first day and then every two hours
when the FIO2 is considered. The PaO2/FIO2 (P/F) thereafter, a ventilator check sheet is filled out with the
ratio, which should be greater than 300, can also be ventilator settings and patient values. It can be done by
used to predict a lower FIO2 when the PaO2 is greater hand or electronically by a data capture system. The
than 100 mm Hg. respiratory therapist has to remember how the patient
Mean airway pressure provides a measure of the values are determined, especially if a data capture
overall effect of the ventilator settings on oxygenation. system is used. Valuable patient information can be
Oxygenation improves when the mean airway pres- missed if the captured data are not scrutinized for error.
sure increases, unless cardiac output is compromised. For example:
If a higher mean airway pressure decreases venous
return to the right atrium, the cardiac output • I/E ratios are displayed for mandatory or
decreases, especially in a seriously ill patient whose ventilator-defined breaths only, not for
compensatory mechanisms for maintaining blood spontaneous breathing.
pressure are already compromised. A decrease in • Exhaled tidal volumes may be from either
cardiac output and therefore of lung increases alveolar mandatory or spontaneous breaths, depending
deadspace and decreases the expired PCO2 and the on the mode of ventilation.
volume of expired CO2 in mL/min.23 Capnography— • The displayed respiratory rate usually includes
the graphic display of expired CO2 over time or per both mandatory and spontaneous breaths.
volume during a respiratory cycle—may be used to • A peak inspiratory pressure is displayed in most
monitor lung perfusion to optimize oxygenation modes, but a plateau pressure may require the
when setting PEEP. Increasing PEEP is usually the best volume control mode and a set pause time.
method of increasing mean airway pressure. Monitor- Check the displayed or captured lung compli-
ing the fraction of expired CO2 and CO2 volume ance value by dividing the mandatory exhaled
allows the calculation of deadspace and alveolar tidal volume by the plateau minus PEEP
ventilation and, with the temporary addition of a pressure.
rebreathing circuit, cardiac output.24 Ventilator • Recording the difference between peak and
settings may then be adjusted to minimize deadspace plateau pressure as a measure of airway resis-
and maximize alveolar ventilation. tance is appropriate only when the inspiratory
The shape of the capnogram also provides infor- flow is constant (i.e., a volume control mode
mation. A continually rising CO2 pattern in place of a with a rectangular flow waveform).
relatively flat plateau shape indicates that a significant • If the ventilator does not display auto-PEEP, the
proportion of lung units are emptying slowly due to clinician can initiate an end-expiratory pause to
their long time constants. Observing the capnogram for measure its presence. Prior observance that the
a dip in the exhaled CO2 tracing, sometimes referred to expiratory limb of the flow-time waveform fails
as the curare cleft, indicates a patient’s inspiratory to return to baseline indicates the presence of air
attempt and alerts the clinician to the patient’s waning trapping and therefore the need to initiate an
level of sedation. Capnography does not eliminate the expiratory hold to measure auto-PEEP.
need for arterial blood gases because the (a-ET)PCO2 Check that the alarms are set appropriately. Critical
gradient must be measured to accurately interpret care ventilators have extensive alarm systems that
expired PCO2. monitor flow, pressure, exhaled volume, and time.
Life-threatening situations are usually detected by more
than one audiovisual alarm. Alarm conditions are
usually based on the monitored patient parameters,
CASE STUDY 26-3 such as exhaled volume or airway pressure.
Apnea and ventilator disconnection are two of the
The respiratory therapist has just received a most life-threatening situations that alarms are
blood gas back on a ventilator patient. The designed to detect. In most modes currently available,
patient is on 100% oxygen with the arterial P O2 the ventilator is able to detect whether a breath has
of 210 mm Hg. been taken. Flow and pressure sensors measure changes
in inspiratory flow and pressure as well as the length of
Question time when flow or pressure changes are absent. If no
1. What oxygen concentration can be safely inspiration has been detected within a certain period of
used avoid complications of oxygen toxicity? time, usually called the apnea interval, the ventilator
activates an apnea alarm. When the apnea alarm is
activated, some ventilators automatically switch to an

apnea ventilation mode that delivers a preset tidal Best Practice
volume at a preset rate.
Apnea ventilation is usually available for spontane- The Patient First
ous modes, but not all ventilators have apnea ventila-
In the event of a ventilator alarm, the first action
tion. For example:
should be to look at the patient to verify that the
• Pressure support mode on the Servo 300 patient is still connected to the ventilator.
(Maquet, Bridgewater, New Jersey) has an
apnea alarm but does not switch to apnea
ventilation.
• Automode on the Servo 300A and Servoi auto- ventilators. It is crucial that alarm volumes are set
matically switches from pressure support to loud enough to be detected by care givers.
pressure control mode at the set rate if apnea Regardless of which alarm is activated:
occurs. • The number 1 rule when an alarm occurs is to
• The Automode feature automatically switches look at the patient! Make sure the patient is still
back to the spontaneous mode when a patient- connected to the ventilator.
triggered breath is detected on the Servoi. • The second rule is to ensure adequate ventilation
• The Servo 300A requires two consecutive patient- and oxygenation for the patient in the event of a
triggered breaths before switching. ventilator problem, by disconnecting the patient
• If the patient is in volume support mode and from the ventilator and initiating manual
experiences apnea, the Servo 300A and Servoi ventilation. Do not spend minutes searching the
automatically switch to either PRVC or VC, ventilator for the problem while the patient is
depending on which mode is set. inadequately ventilated. Guarantee adequate
Ventilator disconnect alarms usually sense low ventilation while troubleshooting the ventilator
inspiratory pressure. Low inspiratory pressure alarms may system.
be adjusted by the clinician, or they are automatically
determined by the ventilator manufacturer. A low WAVEFORMS
inspiratory pressure alarm activates if the pressure The assessment of breathing involves not only auscul-
during inspiration does not go above the alarm setting. tating breath sounds but also evaluating the quality of
Low exhaled tidal volume or minute volume alarms the breath.
also detect a ventilator disconnection but usually
require a drop in the running breath average exhaled • Is the ventilator responding to the patient’s
volume; so they require a longer period of time before inspiratory effort fast enough?
activation. Adjustable low inspiratory pressure alarms • Is the patient getting enough flow during
are typically set at 10 cm H2O below the peak inspira- inspiration?
tory pressure. • Does breathing appear to be labored?
High airway pressure alarms activate when the • Is the patient fighting the pattern of breathing set
peak airway pressure equals the high pressure alarm by the machine?
setting. Inspiration is usually terminated when the One of the ways to evaluate the quality of breath-
high pressure alarm is activated. Low inspiratory ing is to observe the patient’s waveforms. The graphic
pressure or low exhaled tidal volumes are monitored representation of pressure, flow, and volume over time
to detect a leak in the system or a disconnection of can provide information about the quality of ventilator
the patient from the ventilator. Ventilator error or breaths that is not as easily recognized otherwise.
inoperative alarms are also common on critical care Ventilator settings can be tailored to the patient’s
demand. Volume–over-pressure curves may be used to
determine optimal PEEP levels and to estimate the
Best Practice imposed work of breathing.
Figure 26-4A is an example of a volume-controlled
breath in which the peak flow setting is too low to
Understanding Alarms meet the patient’s inspiratory demand. This situation
Respiratory care practitioners must know what may lead to dyssynchrony between the timing of the
conditions activate the various alarms for their inspiratory flow delivered by the ventilator and the
ventilators. initiation of inspiration by the patient. Eventually,
this results in the patient trying to exhale while the
who meet the criteria for ARDS. With this approach,

the level of PEEP should be 2 cm H2O more than the
pressure at the inflection point. However, not all
Pressure patients with ARDS have a lower inflection point,
particularly during the later phase of ARDS.
VC Figure 26-5 also shows the second point of change
in compliance (point B) that occurs when the lungs
Flow become overinflated. The point or pressure at which
the compliance decreases is called the upper inflection or
deflection point on an inflation static pressure-volume
A B
curve. It represents the plateau pressure that should not
be exceeded. Overinflation creates a pressure spike on a
FIGURE 26-4 (A) Flow is not adequate to meet the dynamic P/V curve.
patient’s inspiratory demand. (B) A higher peak flow Few studies have compared the inflection point
rate allows a steady rise in pressure. In VC, a higher measured with a dynamic pressure-volume waveform
peak flow shortens the time of inspiration. with that obtained by the static method. Lu and cowork-
ers found that resistive properties are reduced when a
flow rate of 9 Lpm is used to measure a dynamic P/V
ventilator is still delivering flow. The increase in airway curve.25 The P/V 2 tool on the Galileo Gold (Hamilton
pressure may activate the high-pressure alarm, ending Medical, Reno, Nevada) uses a low peak flow to generate
inspiration. The set tidal volume is not delivered, dynamic inflation and deflation pressure-volume curves.
contributing to the patient’s sensation of air hunger A time cursor can then be scrolled along the curves to
and the desire to trigger breaths more frequently. display respiratory system compliance at any given point,
Inadequate inspiratory flow is the most common which is particularly useful in identifying the greatest
reason for a patient to fight the ventilator in volume change in compliance on the deflation curve (Figure
control. Figure 26-4B shows the effect of an increase in 26-6). The upper inflection pressure on the deflation curve
the peak flow. As the patient’s inspiratory flow demand after a recruitment maneuver has been suggested as the
is met, the entire tidal volume is delivered, the patient’s optimal PEEP setting to maintain recruited alveoli.20,21
anxiety subsides, and the respiratory rate decreases. Waveforms can help detect a problem as well. A leak
Pressure-volume (P/V) curves performed under in the system is easily observed on a volume-time
static conditions may identify two points where the waveform. The ascending portion represents the inspira-
patient’s compliance changes on the inflation curve, tory volume, and the descending leg is the expiratory
especially in the early phase of ARDS. As shown in volume. If the exhaled volume is less than the inspira-
Figure 26-5A, the first point (point A) represents an tory volume, the descending leg does not return to
improvement in compliance represented by an increase
in the slope of the curve. Some clinicians believe that
this point, called the lower inflection point, occurs when
adequate alveolar recruitment has occurred. Numerous Vol
Deflation
studies have reported that the lower inflection point
generally falls between 10 and 15 cm H2O in patients A
B
Vol Inflation
Pressure
Pressure
FIGURE 26-5 Static pressure-volume curve measured with FIGURE 26-6 A dynamic pressure volume curve measured
the patient sedated and paralyzed. (A) The lower inflexion during a recruitment maneuver: Point A is the maximal
point. (B) The upper inflexion point. curvature on the deflation limb.
Volume I E I E
A B
FIGURE 26-7. (A) A leak has reduced the exhaled volume
returning to the ventilator. (B) A volume-time waveform
showing an inspiratory pause.
A B
baseline (Figure 26-7A). A leak also causes a difference
FIGURE 26-9 (A) Arrows indicate air trapping. An end-
in the ventilator’s patient data displays between the
expiratory pause is needed to measure the actual auto-
inspiratory or set volume and the patient’s exhaled tidal
PEEP; however, patient-triggered breaths make this inac-
volume. If a pause is used, it creates a flattop on the curate. (B) The patient has been sedated, and expiratory
volume-time waveform, as shown in Figure 26-7B. flow shows no evidence of air trapping.
The presence of an air leak may cause the ventilator
to self-trigger if a flow trigger is used. The leak causes a
drop in flow similar to a patient’s inspiratory effort. A
flow trigger should not be used in this case. A leak in the that is greater than baseline pressure is auto-PEEP.
system may also prevent inspiration from ending in a Applied PEEP or CPAP should equal the level of
flow-cycled mode. In pressure support, inspiration ends auto-PEEP to maintain a given pressure trigger. For
when the flow rate falls to 25% of the highest flow that example, a pressure trigger set on 2 when 5 cm H2O
occurred during the inspiration or to some preset level of auto-PEEP is present requires the patient to actually
such as 5 Lpm, depending on the ventilator. A few exert an inspiratory effort of 7 cm H2O. The problem
ventilators have the option of adjusting the flow-cycle in compensating for auto-PEEP, however, is that it
threshold for pressure-supported breaths. The liter flow of varies with the time allowed for exhalation. Higher
the leak may be observed in a flow-time waveform. The patient-triggered respiratory rates increase the level of
flow- cycle threshold could then be adjusted to a higher auto-PEEP by decreasing the time left for exhalation.
flow rate than the leak to end-inspiration (Figure 26-8). Any compensation by increasing the applied PEEP may
A flow-time waveform detects the presence of be overkill if the patient’s respiratory rate slows down.
airtrapping by showing that the expiratory flow does If waveforms are not available on the ventilator, a
not return to baseline by the time the next breath starts comparison of ventilator settings with the patient’s
(Figure 26-9). When this is observed, produce an exhaled values can provide clues. For example, an air
end-expiratory pause to measure the end-expiratory leak in the ventilator circuit, either around the patient’s
pressure. Any end-expiratory pressure during a pause endotracheal tube or out through chest tubes, results in
a loss of exhaled volume, lowers peak airway pressures,
and possibly leads to the loss of end-expiratory pres-
sure. If the patient is in a flow-trigger setting, the air
leak may trigger ventilator breaths in rapid succession,
as discussed previously. The loss of volume and
CASE STUDY 26-4

A patient’s flow-time waveforms appear to

indicate air trapping. The patient is somewhat
agitated and not in synchrony with the ventilator.
The respiratory therapist knows that auto-PEEP
A B often leads to patient-ventilator dyssynchrony.
FIGURE 26-8 (A) Inspiration is prolonged owing to a leak in
the system. (B) The flow-cycle level has been increased Question
to a flow rate greater than the leak. Inspiration ends 1. What should the RT do?
appropriately.
decreases inspiratory muscle strength and the maximal

Best Practice inspiratory pressure. Patients with respiratory muscle
weakness may find even small increases in the pressure
Inadequate Ventilation or effort needed to breathe (increased demand) to be
intolerable. The presence of auto-PEEP creates such a
Whenever adequate ventilation of the patient is
situation. The patient must generate enough inspira-
in question, remove the patient from the ventila-
tory muscle effort to overcome the elevated alveolar
tor and ventilate with a manual resuscitator.
pressure before the pressure at the mouth can drop
below the ambient pressure level to create a pressure
gradient for gas flow.
Diseases or disorders that increase airway resistance
pressure may activate alarms. Whenever adequate (increased inelastic or resistive force) or that decrease
ventilation of the patient is in question, remove the compliance (increased elastic force) of the lungs or
patient from the ventilator and ventilate with a manual chest wall increase the intrinsic work of breathing.
resuscitator. Equipment added to the patient that increases WOB is
extrinsic or imposed work. The endotracheal tube, the
demand flow valve, the ventilator circuit, and the
WORK OF BREATHING humidifier may all be sources of resistance to gas flow
Work of breathing (WOB) is the respiratory muscle that the patient must overcome to take in a breath from
energy or force used to move a tidal volume of air. the ventilator. In addition, the expiratory WOB may
Work is defined in physics as the force times distance. increase if exhalation valves or PEEP valves create
In fluid systems, however, breathing work is measured resistance that makes the patient work harder to exhale.
in terms of pressure times volume (e.g., inspiratory
pressure tidal volume displaced). The units of WOB
are kilogram-meters (kg·m) or joules, with 0.1 kg·m HUMIDIFICATION OF MECHANICAL VENTILATION
equal to 1 joule. WOB is usually expressed as either Gas delivered by a ventilator must be monitored for
joules per liter of ventilation or joules per minute. adequate humidity. Ensuring adequate humidity levels
Work per liter of ventilation (j/L) is a better indication of requires an appropriate humidifier with adequate water
the patient’s breathing capacity when the patient has levels and monitoring of the inspiratory gas tempera-
pulmonary disease.26 Normal WOB in healthy indi- ture at the patient wye. Temperatures should be
viduals is 0.3–0.8 j/L. In patients with CAO, breathing maintained between 31o and 35oC.27 As long as the
workloads over 1.3 j/L are associated with ventilator humidifier is functioning properly, the appropriate
dependence. Patients with marginal ventilatory inspiratory gas temperature reflects the delivery of an
reserves do not tolerate spontaneous breathing even if adequate absolute humidity level when using a ventila-
the workload is only moderately increased. The WOB tor circuit without heated wires. There are two excep-
is excessive any time the demand placed on the tions to letting the inspiratory gas temperature guide
respiratory muscles exceeds their capacity or ability to proper humidity delivery: use of heat and moisture
function. exchangers/hygroscopic condenser humidifiers (HME/
Lung disease that leads to expiratory flow limita- HCH) and heated wire ventilator circuits.
tion causes air trapping and lung hyperinflation. When using heat and moisture exchangers or hygro-
Hyperinflation shortens the inspiratory muscles, scopic condenser humidifiers (HMEs or HCHs):
thereby reducing their capacity to contract farther and
generate force. The reduction in contractile force • Measuring inspiratory airway temperatures is not
useful.
• It is, however, important to monitor secretions,
minute ventilation, and differences between
inhaled and exhaled tidal volumes. Thick,
Best Practice copious secretions are a contraindication for
HME/HCH methods of humidification, as are
Breathing Workloads minute volumes over 10 Lpm and a 30% loss in
Breathing workloads over 1.3 j/L may be exces- volume during exhalation.
sive for patients with CAO and compromise their • High minute volumes exceed the capacity of
ability to breathe spontaneously, particularly most HME/HCHs to provide a minimum of 70%
through an ETT. Recognize and limit the factors relative humidity at body temperature. When the
that may increase the work of breathing. exhaled tidal volume is less than 70% of the
inspiratory tidal volume, an inadequate amount
of exhaled moisture is available for the next circulation from a decrease in cardiac output or from a
inspiration. redistribution of blood flow through major organs. If
• HME/HCHs should not be used in the presence the mean positive airway pressure transmitted across
of large air leaks through chest tubes or air leaks the lung to structures in the thorax is high enough, it
around the artificial airway. HME/HCHs should decreases venous return and therefore cardiac output. A
be removed or bypassed when delivering aerosol drop in cardiac output causes a decrease in blood
therapy.28 pressure because the normal compensatory mecha-
nisms responsible for maintaining blood pressure are
With the use of heated-wire ventilator circuits comes
often compromised in the critically ill patient. The
the added responsibility of monitoring the relative
decrease in blood pressure reduces or redistributes
humidity (RH). The purpose of heated-wire circuits is
perfusion of the brain, heart, lungs, kidneys, liver, and
to prevent cooling of the gas in the tubing as it travels
gut, leading to multiple organ dysfunction. Therefore,
from the heated wet humidifier to the patient connec-
all attempts to improve oxygenation by increasing
tion. Expiratory limb heated wires serve the same
mean airway pressure must be closely monitored for
purpose for exhaled gas from the patient to the exhala-
possible hemodynamic repercussions. A reduction in
tion valve. Maintaining temperature prevents the gas
cardiac output offsets any gain from an increase in
from cooling, which would produce condensation in
arterial oxygen tension, thereby reducing oxygenation.
the tubing, or rainout. With some brands of heated-wire
For example, an increase in PEEP is generally the
circuits, the circuit temperature can be higher than the
best method for increasing mean airway pressure, but
humidifier temperature to the point of lowering the
there is a limit to the amount of PEEP that can improve
delivered relative humidity. In infant ventilation, the
oxygenation. Excessive PEEP increases the volume of the
respiratory therapist has to ensure an adequate RH by
more compliant alveoli. As an alveolus overexpands, its
noting the presence of beads of moisture at the patient
pulmonary capillary is stretched; the stretching increases
wye or at the ventilator circuit connection to the
alveolar-capillary permeability and reduces the lumen of
patient’s endotracheal or tracheostomy tube.29 Failure
the capillary. An increase in alveolar-capillary permeabil-
to monitor the RH leads to inspissated secretions,
ity leads to interstitial pulmonary edema, which reduces
mucus plugging, and arterial hypoxemia.
the compliance of the alveoli. Stretched and narrowed
pulmonary capillaries from overinflated alveoli, in
COMPLICATIONS OF MECHANICAL VENTILATION combination with vasoconstricted capillaries of hypox-
emic collapsed alveoli, increase pulmonary vascular
The underlying purpose of monitoring is to ensure
resistance (PVR). An increase in PVR decreases the blood
patient safety and comfort by anticipating the potential
pressure gradient for venous return to the heart. A
problems of any ventilator patient’s situation. Recogniz-
reduction in blood returning to the heart reduces cardiac
ing the onset of anticipated problems provides time to
output. Increased alveolar pressure that adversely affects
intervene and possibly prevent the complications from
cardiac output and reduces oxygen delivery does not
becoming life-threatening. Potential problems of
improve oxygenation, despite an increase in PaO2.
mechanical ventilation may be classified as patient,
Oxygen delivery is the cardiac output multiplied times
patient-ventilator interface, and ventilator complications.
the oxygen content of the arterial blood. The small
increase in oxygen content from an increase in PaO2
Patient Complications. Patient complications are
does not increase oxygen delivery enough to counterbal-
associated with the delivery of positive pressure. The
ance even a small reduction in cardiac output. The
most common patient complication with the delivery
challenge in providing mechanical ventilation with
of positive pressure ventilation is an alteration in blood
PEEP is therefore to increase alveolar pressure and
volume effectively without causing alveolar overinflation
or compromising the circulatory system.
A reduction in systemic circulation alters perfusion
Best Practice and impairs the function of the brain, lungs, kidneys,
liver, and gut.
Humidification • The brain and kidneys are especially sensitive to
When heated wire circuits are used: alterations in perfusion. Inadequate cerebral
• Ensure that the patient receives adequate perfusion causes disorientation, confusion, and
humidity to prevent inspissated secretions, loss of consciousness.
mucus plugging, and arterial hypoxemia. • A drop in cardiac output redistributes perfusion
• Check for beads of moisture at the patient wye. of the kidney and causes a decrease in urine
output.
• Reduced perfusion of the lung increases alveolar Society guidelines recommend a so-called VAP Bundle
deadspace and decreases expired CO2. to prevent VAPs:
• Mucosal ischemia of the gut reduces absorption
• Keep the head of the patient’s bed elevated
of nutrients and increases the gut’s susceptibility
between 30º and 45º.
to infection and bleeding.
• Use closed suction systems.
• An elevation of venous blood pressure, resulting
• Create frequent “sedation vacations” to evaluate
from positive pressure, impairs venous drainage
the continued need for mechanical ventilation.
of the brain and may lead to an increase in
• Use aseptic technique with an emphasis on
intracranial pressure.
alcohol-based hand rubs.
• Elevated venous pressure impairs liver function.
• Give routine oral care, including nonabsorbable
antibiotics.
Patient-Ventilator Interface Complications. Complica-
Continuous aspiration of subglottic secretions
tions associated with the patient-ventilator interface relate
(CASS) from above the cuff requires a specially
to the use of endotracheal or tracheostomy tubes. Ventila-
designed endotracheal tube (Hi-Lo Evac tube, TYCO
tor disconnection from the artificial airway and pulmo-
Healthcare/Mallinckrodt, St Louis, Missouri, distrib-
nary infection are two such important complications.
uted by Nellcor Puritan Bennett, Pleasanton, Califor-
• The incidence of accidental ventilator disconnection nia). ATS recommends CASS, if available.33 The ATS also
is reduced when the patient is immediately recommends that “endotracheal tube cuff pressure
observed at the time of any ventilator alarm or should be maintained at greater than 20 cm H2O.”
monitor problem. Ventilator disconnection may
also allow the collapse of alveoli and small Ventilator Complications. Complications related to
airways in patients with ARDS. the ventilator are inadequate humidification leading to
• The endotracheal or tracheostomy tube provides mucus plugging and airway obstruction, ventilator
a direct route of transmission of infectious agents malfunction, operator error, and ventilator-induced
to the lower airway. Despite controversies lung injury (VILI).
concerning the frequency of ventilator circuit Inadequate humidification may be avoided by
changes, essential measures of infection control following the AARC clinical practice guidelines for
are aseptic technique during endotracheal tube humidification during mechanical ventilation. An
suctioning or when the patient-ventilator system appropriate airway temperature of inspired gas, humid-
is interrupted, the proper disinfection of ventila- ifier, and percentage relative humidity when using
tor circuit components, and making appropriate heated wire circuits prevents desiccation of airway
ventilator circuit changes.30 secretions. An adequate percentage relative humidity
greater than 70% when using heated wire circuits may
Part of the controversy in establishing definitive
be monitored by the presence of beads of moisture at
guidelines for ventilator circuit changes involves the
the patient-ventilator connection.29 Heat and moisture
difficulty in diagnosing ventilator-associated pneumonia
exchangers (HMEs) can also be monitored by observ-
(VAP), generally defined as pneumonia that develops
ing beads of moisture at the patient connection.37
48–72 hours after intubation.31–33 Diagnosis is difficult
Adherence to the preventive maintenance schedule
in patients with respiratory failure, especially those
published by the ventilator manufacturer aids in
with ARDS who have bilateral diffuse infiltrates on
preventing ventilator malfunction. In many cases,
chest radiographs.34 In a recent multicenter study, VAP
ventilator malfunction is actually operator error.
was diagnosed in 36.5% of the patients with ARDS
Ventilator changes made by health care personnel
compared to 23% in ventilator patients without
inadequately trained in ventilator application—
ARDS.35 Sixty-five percent of the episodes of VAP
operator error—are more often the cause of problems in
occurred after the fifth day of mechanical ventilation.
There was no difference in mortality rate (58%) in
ARDS patients with or without VAP. The survivors with
VAP were on mechanical ventilation twice as long as
the survivors without VAP.
Best Practice
Several risk factors for VAP were analyzed, but
frequency of ventilator circuit change was not reported. Humidification
Currently, routine ventilator circuit changes are not To prevent complications associated with
recommended more often than once a week or when inadequate humidity, monitor the patient-circuit
the circuit is visibly soiled or malfunctioning.36 The connection for beads of moisture.
Centers for Disease Control and the American Thoracic

Proper Training Protective Lung Strategies
Only individuals with extensive training in the Protective lung strategies of ventilation use tidal
function and operation of critical care ventilators volumes of 4–6 mL/kg and PEEP levels that pro-
should make changes in ventilator settings. duce plateau pressures 30 cm H2O.
Respiratory care practitioners are the only
hospital personnel so qualified.
tidal volume and the level of PEEP excessively increase

end-inspiratory lung volume, mechanical ventilation
ventilation than mechanical failure of the ventilator should be applied in a manner that protects the lung.
itself. Improper use of ventilator modes may force the Low tidal volumes should be used in conjunction with
patient to assume more of the work of breathing than PEEP since low tidal volumes alone are associated with
the patient can provide. Patient-ventilator dyssyn- atelectasis.46
chrony from inadequate peak flow in VC, excessively Barotrauma is another type of ventilator-associated
long inspiratory times, and inappropriate rise time % lung injury that is more closely related to regional lung
or slope settings for pressure breaths all increase the distention than to absolute airway pressure. Excessive
patient’s work of breathing.38 transpulmonary pressure (alveolar minus pleural
Ventilator-induced lung injury (VILI) in ARDS occurs pressure) can allow air to enter the interstitial tissue
when regions of the lung are overinflated or strained and dissect along the bronchovesicular sheath to the
(volutrauma) and from the shear stress associated with mediastinum to cause:
repeated opening and closing of terminal airways
• Pneumomediastinum.
(atelectrauma).39,40 Approximately one-third of the lung
• Pneumothorax.
is open in ARDS with collapsed, noncompliant alveoli
• Pneumopericardium.
adjacent to open compliant alveoli.41 Applying tidal
• Subcutaneous emphysema.
volumes over 9 mL/kg of predicted body weight to
• Pulmonary interstitial emphysema.46
patients with ARDS overexpands the compliant alveoli
and creates tissue strain as they attempt to pull away
from their less compliant neighbors.42
Shear stress is also generated by the repetitive Ventilator Management
opening and end-tidal collapse of small airways. These Ideally, (therapist-driven) ventilator management
mechanisms combine to cause diffuse alveolar damage protocols are initiated from the moment the patient is
marked by increased epithelial and endothelial perme- placed on mechanical ventilation. Management
ability, interstitial pulmonary edema, and alveolar priorities are determined by the reason for ventilatory
flooding.43–44 Alveolar damage triggers the inflammatory support. In general, the pulmonary functions of
response, which aggravates the alveolar-capillary injury patients requiring mechanical ventilation fall into one
(biotrauma).39 There is evidence to suggest that micro- of three categories: restrictive, obstructive, or relatively
organisms present in the alveoli may enter the systemic normal. Potential problems associated with the
circulation via the damaged pulmonary capillaries and application of positive pressure in each condition
cause multiple organ dysfunction syndrome (MODS).41 should be anticipated and monitored accordingly.
The landmark ARDSnet clinical trial45 found
approximately 25% fewer deaths among patients
receiving 6 mL/kg tidal volumes as compared to those MECHANICAL VENTILATION
receiving 12 mL/kg volumes. The study protocol IN OXYGENATION FAILURE
required that tidal volumes be adjusted to keep plateau The therapeutic objectives for patients with ARDS are
pressures between 25 and 30 cm H2O in the interven- to promote alveolar recruitment and to prevent alveo-
tion group. This study was the first to provide conclu- lar overinflation. The standard method of opening
sive evidence that small tidal volumes of 6 mL/kg alveoli is to increase alveolar pressure and then provide
improve mortality for patients with ARDS. The impor- PEEP to maintain alveolar expansion. Atelectatic lung
tance of plateau pressures 30 cm H2O is less clear requires approximately 30–40 cm H2O over 7–8
since the control group had mean plateau pressures seconds to reopen.47 There is evidence to support the
33 cm H2O. The two groups also had similar levels of use of small tidal volumes, but less support for setting
PEEP (10 cm H2O). Since volutrauma occurs when PEEP levels 2 cm H2O above the lower inflection
point.48 The level of PEEP may need to be even higher

to prevent alveolar derecruitment, particularly when Best Practice
chest wall compliance is reduced from an increased
intra-abdominal pressure, often associated with the PEEP Settings
extrapulmonary type of ARDS.49 It is also recognized
Set PEEP at a high enough pressure (20 cm
that limiting inspiratory plateau pressure to less than
H2O) after recruitment maneuvers to keep the
30 cm H2O may not prevent alveolar overinflation.50
lung open. Titrate PEEP down to determine the
Therefore, the problem becomes one of how to reex-
derecruitment point. After repeating recruitment
pand the lung without overdistension.
maneuver, set PEEP at the level immediately
before derecruitment occurred.
Recruitment Maneuvers. At this time, there is no
optimal method for performing alveolar recruitment
maneuvers (RMs).51 Ventilators that provide so-called
sighs in the form of higher PEEP levels for two con-
secutive ventilator breaths may not apply the pressure lung ventilation strategy.58 The FIO2 should be 0.45
for a long enough period of time. Giving two consecu- before attempting to decrease the PEEP. Interruptions
tive sighs per minute by increasing the PEEP from 9 to in ventilation require repeated RMs.59
16 cm H2O in volume-controlled ventilation did not Measurement of functional residual capacity
improve oxygenation over volume-controlled ventila- (FRC), such as end-expiratory lung volume (EELV),
tion at a constant level of 16 cm H2O PEEP.52 Lim and could track improvements in lung volume following
coworkers found that high pressure control and PEEP recruitment maneuvers and/or the application of PEEP.
levels (45/16 cm H2O for 2 minutes at an I/E ratio of The gas module on the Engström Carestation ventilator
1:2) were equivalent to a 40-second sustained maneu- (Datex-Ohmeda, Inc. of GE Healthcare) allows a
ver of 45 cm H2O CPAP in three different porcine mod- simplified measurement of the patient’s FRC at the
els of acute lung injury.53 Patients with pulmonary bedside. The FRC measurement uses a modified
ARDS or late-stage extrapulmonary ARDS typically do multiple-breath nitrogen washout/washin technique
not respond favorably to any type of alveolar recruit- that requires inspiratory and expiratory analyses of
ment maneuver. oxygen and carbon dioxide and a change in FIO2 of just
In patients with ARDS Amato et al. (1998) used a 10%. Chiumello and colleagues found that the EELV
recruitment maneuver (RM) of 35-40 cm H2O CPAP measured by the modified nitrogen washout/washin
for 30–40 seconds before initiating protective ventila- technique of the Engström Carestation correlated well
tion.54,55 The same pressure range has been applied with the EELV measured via computed tomography
successfully for 20 seconds.56 Kacmarek and colleagues scanning.60 Two 20-breath measurements are required
recommend a more conservative approach of 30 cm for a single FRC procedure. The FRC measurement may
H2O CPAP for 30–40 seconds. The maneuver needs to take up to 10 minutes to achieve the required steady-
produce a passive inflation, which usually requires state condition. The FRC INview™ function also allows
sedation of the patient. The patient should also be the scheduling of a series of FRC procedures at speci-
preoxygenated with an FIO2 of 1.0 for 5–10 minutes. If fied intervals. The PEEP INview™ function automati-
oxygenation does not improve after the first recruit- cally measures FRC at incremental levels of PEEP. The
ment period but the patient tolerated the procedure, clinician sets the number of steps to be made between
repeat the RM in 15–20 minutes at a CPAP of the start and stop PEEP levels. Each PEEP level is held
35–40 cm H2O. A third maneuver at 40 cm H2O may for 5 minutes, and the FRC-at-PEEP values are plotted
be required to produce a positive response in some on a graph and displayed numerically.61 FRC measure-
patients. A PaO2/FIO2 ratio 300 indicates effective ments may aid in quantifying recruited lung volume
recruitment. To maintain recruited lung after the and lung overinflation.
maneuver, set a PEEP of 20 cm H2O and reduce the
FIO2 until the SpO2 is around 92%.57 The benefit from Prone Ventilation. The mechanical ventilation of
the recruitment maneuver is lost if a low level of PEEP ARDS patients in the prone position improves oxygen-
is then set and adjusted up. The PEEP of 20 cm H2O ation in roughly 50–75% of cases. The improvement in
can then be reduced by 2 cm H20 every 30 minutes oxygenation persists after returning to the supine
until desaturation occurs.57 The PEEP level before position. The prone position theoretically creates a
desaturation is the level that prevents derecruitment. more uniform distribution of ventilation that enhances
Set PEEP at that level after repeating RMs to reopen the the expansion of dorsal lung units that were previously
lung. The practice of using low tidal volumes of 6 mL/ compressed by the weight of edematous ventral lung
kg and setting the PEEP as just described after a units.62 Pelosi and coworkers found that changes in
recruitment maneuver has been referred to as the open oxygenation from prone positioning were associated
with a reduction in chest wall compliance but not improves oxygenation in ARDS by vasodilating the
related to elevations in end-expiratory lung volume or capillaries adjacent to well ventilated alveoli. Increased
improvement in lung compliance.63 Regional changes blood flow to ventilated alveoli reduces perfusion to
in ventilation/perfusion ratios were given as the only poorly ventilated alveoli. The vasodilator response to
explanation for improved oxygenation. Prone position- iNO occurs in 5–15 minutes. Once inhaled, it is
ing can be expected to improve oxygenation only in rapidly inactivated by binding to hemoglobin to form
patients who have severe inflammatory pulmonary methemoglobin. At doses of iNO below 20 ppm,
edema, and to date no study has been properly methemoglobin levels are generally less than 3%.
designed to determine the impact of prone positioning The administration of iNO requires special equip-
on survival in this specific population.64 ment. Since gaseous NO reacts with oxygen to form
nitrogen dioxide (NO2), a toxic gas, iNO is stored in
Inverse Ratio Ventilation. When inspiratory time nitrogen and bled into the ventilator circuit. Scavenger
exceeds expiratory time, the I/E ratio is inverse. Length- systems and NO2 analyzers must ensure that the level
ening the time of inspiration increases mean airway of NO2 is kept to less than 2 ppm. In the form admin-
pressure and improves oxygenation up to the point of istered to patients, iNO is also potentially toxic as a free
hemodynamic compromise. Inverse ratio ventilation radical when it reacts with other free radicals such as
(IRV) may be instituted in either pressure-control or superoxide. In combination, NO and superoxide form
volume-control ventilation. If VC is used, a ramp flow peroxynitrate (ONNO), an oxidizing compound
waveform is preferred. In either case, limiting the thought to cause acute lung injury.67
inspiratory or plateau pressure results in lower tidal Despite numerous studies of the effects of iNO,
volumes. Because low tidal volumes and prolonged there have been no large randomized clinical trials
inspiratory times are uncomfortable, the patient needs demonstrating its efficacy in reducing morbidity or
to be sedated and paralyzed. Tidal volumes of less than mortality in patients with ARDS.68 Only one study has
5 mL/kg require RMs and appropriate PEEP levels to demonstrated that it improves oxygenation after the
prevent atelectasis. The respiratory rate can be increased first day. Inhaled nitric oxide administration should be
to maintain minute ventilation, but this reduces the considered experimental.
time available for exhalation. Incomplete emptying of
the lung causes air trapping. Air trapping creates High-Frequency Oscillation Ventillation. In 2001, the
auto-PEEP that raises mean airway pressure, but that Food and Drug Administration approved the Sensor-
pressure favors overdistension of the more compliant Medics 3100B high-frequency oscillatory ventilator
lung units. Yanos and coworkers found that auto-PEEP (Yorba Linda, California) for use in patients whose
from IRV increased mean airway pressure but was less actual body weight is more than 35 kg. High-frequency
beneficial for improving gas exchange.65 Certainly oscillatory ventilation (HFOV) has been used for decades
APRV is preferable to IRV in most cases and has the to treat respiratory distress syndrome in neonatal and
added benefit of greater patient comfort with less pediatric patients, successfully preventing ventilator-
sedation by allowing spontaneous breathing. Sponta- induced lung injury.
neous breathing in APRV eliminates the inverse ratio Theoretically, the very small tidal volumes pro-
component of IRV while achieving a comparable duced with HFOV protect the lungs, and the relatively
increase in mean airway pressure. high mean airway pressures facilitate alveolar recruit-
ment and maintenance of restored end-expiratory lung
Permissive Hypercapnia. If the increase in respiratory volume to improve oxygenation. However, the actual
rate is not enough to maintain minute ventilation in guidelines for HFOV application to adults favor
IRV, PaCO2 rises. As long as this change occurs gradu- amplitude and frequency settings that produce larger
ally and the pH is 7.25 or higher, the effects of hyper- tidal volumes to maximize CO2 clearance.69 The
capnia are not serious.66 However, increased PaCO2 and recommended starting amplitudes (ΔP) of 20 PaCO2
the associated decrease in pH cause cerebral vasodila- (~ 60 cm H2O) and low frequencies (5–6 Hertz)
tion. The increase in cerebral blood flow and in produce larger tidal volumes with greater potential for
intracranial pressure is detrimental if cerebral edema is lung injury. Proponents of HFOV recommend higher
a concern. amplitudes of 90 cm H20 at the highest possible
frequency (well over 6 Hz) to reduce tidal volumes and
Inhaled Nitric Oxide. Endogenous nitric oxide (NO), protect the lungs.69 The problem then becomes the
first identified in 1987, is synthesized by vascular relatively high mean airway pressures that may be
endothelial cells, able to diffuse rapidly across cell required to improve oxygenation.70 A mean airway
membranes, and relaxes vascular smooth muscle. Nitric pressure of 45 cm H2O is not expected to offer much
oxide administered as an inhaled agent (iNO) is a protection against volutrauma and is more likely to
potent and selective pulmonary vasodilator. It compromise circulation. There is no evidence to date
that HFOV improves patient outcomes when compared breathing. Patients with a limited ventilatory reserve
to low tidal volume strategies.71 have little tolerance for excessive workloads. After a
period of respiratory muscle rest for ventilatory failure
due to respiratory muscle fatigue, the mode must allow
MECHANICAL VENTILATION IN CHRONIC the use of the patient’s respiratory muscles without
AIRFLOW OBSTRUCTION (CAO) imposing an excessive load. In the past, SIMV with
Ventilation of a patient with CAO requires a very pressure support and CPAP were thought to provide a
different approach than for patients with ARDS. The way to balance the work of breathing between the
concerns are less about oxygenation and more about patient and the ventilator. Limiting the number of
ventilation, the work of breathing, and reducing machine breaths in SIMV theoretically reduces the risk
auto-PEEP from hyperinflation.72 In many cases of CAO of air trapping. Now we know the patient’s work of
exacerbation, noninvasive positive pressure ventilation breathing may vary little between machine and sup-
provides effective treatment and reduces the need for ported breaths. There is evidence to suggest that
intubation. Obstructive airway disease requires atten- patients do not reduce their work of breathing with
tion to the appropriateness of the minute ventilation, pressure support immediately but rather that they
maintaining airway patency, and allowing adequate allow pressure support to increase the efficiency of
expiratory time to reduce hyperinflation. The least breathing.76
amount of ventilation should be provided while Pressure support increases breathing efficiency if
ensuring that flow rates meet the patient’s inspiratory patient-ventilator dyssynchrony from delays in trigger-
demand. Higher inspiratory flow rates allow a longer ing (initiating) and cycling (terminating) breaths is
time for expiration and reduce auto- or intrinsic PEEP.73 avoided. Trigger delays are reduced by correcting the
Also, low levels of applied PEEP/CPAP may be required auto-PEEP from dynamic hyperinflation. Cycle delays
to unload the respiratory muscles in the presence of may contribute to dynamic hyperinflation and should
auto-PEEP.74 Sedation may be required to prevent be minimized by increasing the Inspiratory Cycle-off
patient-ventilator dyssynchrony and auto-PEEP because % or Esen % setting to achieve a higher cycle flow rate.
patient-triggered respiratory rates over 15 bpm may be The cycle flow rate should be high enough to termi-
sufficient to increase air trapping. Minute ventilation nate a pressure-supported breath immediately before
should be titrated to the pH, not to PaCO2.75 the patient attempts to exhale. An active expiratory
These patients may experience dyspnea even when effort toward the end of a pressure-supported, or
the PaO2 is adequate. A possible explanation is that the pressure-controlled, inspiration creates a spike in
hyperinflated condition of the thorax places the pressure. as indicated by the arrow in Figure 26-10.73
respiratory muscles at a mechanical disadvantage. The To end the breath before the spike occurs, either
force generated by the inspiratory muscles is dispropor-
tionately large for the minimal change in muscle length
(i.e., inspiratory volume that is achieved). This imbal- 2
ance is sensed by proprioreceptors in the lung and
Flow (L/sec)
contributes to the sensation of dyspnea. High respira-

tory rates, causing inadequate expiratory time, increase
auto-PEEP and hyperinflation. The challenge is to
provide adequate ventilation at inspiratory flow rates
high enough to meet the patient’s inspiratory demand
and allow adequate time for exhalation. −2
The mode of ventilation for patients with CAO
must also be considered in terms of their work of 40
Paw (cm H2O)
Best Practice
−10
The CAO Patient
Because of the high expiratory airway resistance 0 3 6
in patients with CAO, the time allowed for exha- Time (sec)
lation generally needs to be three to four times FIGURE 26-10 Arrow points to airway pressure spike toward
longer than the length of time for inspiration. the end of a pressure-supported inspiration, indicating
the patient’s attempt to exhale.
increase the cycle flow rate for pressure support, or aim is to avoid the inflation of one lung while the
decrease the inspiratory time for pressure control. other is in exhalation. A see-saw ventilatory pattern
Terminating the breath before the pressure spike would be counterproductive.
relieves cycle delays, decreases the inspiratory period,
increases the time available for exhalation, and thereby
reduces dynamic hyperinflation. Ventilator Discontinuance
Mechanical ventilation with a helium-oxygen
The transition from ventilator-supported breathing
mixtures (heliox) may be indicated for some patients
through an artificial airway to breathing without the
with refractory asthma to reduce airway resistance and
need of either the ventilator or the artificial airway is
PaCO2s.77 The Viasys Avea™ (Cardinal Health, Dublin,
generally referred to as ventilator discontinuance. The
Ohio) simplifies Heliox delivery by allowing an 80/20
process can be rapid or require weeks, months, or even
heliox gas input connection in place of the medical air.
years. After the indication for mechanical ventilation
The special connector that flows heliox signals the
has greatly improved or resolved, patients who do not
ventilator to automatically correct all delivered and
tolerate a period of spontaneous breathing need to be
displayed volumes. Increasing the oxygen percentage
weaned from the ventilator. In the past, weaning was
on the ventilator to 30% delivers a 70/30 heliox mix.
the process of gradually reducing support provided by
The benefits from breathing the lower density Heliox
the ventilator until the patient could maintain sponta-
are lost with mixtures less than 60/40. Heliox has been
neous breathing on minimal support. Clinical studies
documented to:
have failed to demonstrate that a gradual withdrawal of
• Increase ventilation. ventilator support through a periodic reduction in the
• Reduce peak pressures. SIMV rate is superior to other weaning methods.
• Increase peak expiratory flows.78
SHORT-TERM VENTILATION DISCONTINUANCE

MECHANICAL VENTILATION IN Most patients do not require weaning postoperatively.
NEUROMUSCULAR DISEASE They are extubated when the effects of the anesthesia
Patients with neuromuscular disease requiring mechan- have dissipated, the patient’s condition has stabilized,
ical ventilation have relatively normal lung compliance. and the gag reflex is functional. Because the protective
Neuromuscular disease results in respiratory muscle reflexes of the upper airway return in an ascending
weakness that reduces the patient’s capacity to take order, the presence of the gag reflex means that the
deep breaths and cough effectively. Ventilator manage- laryngeal and tracheal protective reflexes are also
ment for these patients should include larger tidal functional. Readiness for extubation requires assess-
volumes, higher inspiratory flow rates, and aggressive ment of the patient’s ability to provide and protect a
management of secretions. Oxygenation is usually not patent upper airway as well as to maintain adequate
a problem for this group, so low PEEP levels are gas exchange during spontaneous breathing. These
adequate.75 Noninvasive ventilation plays a more needs should be assessed separately.
important role in neuromuscular disease. Factors affecting airway patency and protection are
related to the patient’s medical condition, airway
anatomy, and neurologic function. Abnormalities may
INDEPENDENT LUNG VENTILATION compromise the patient’s ability to clear secretions,
Independent lung ventilation is indicated when the increase the risk of pulmonary aspiration, or may
pulmonary problem is primarily unilateral. Large heighten the potential of airway obstruction. A negative
bronchopleural fistulas or air leaks are typically an inspiratory pressure or force (NIF) of 20 cm H2O is
indication that oxygenation and ventilation should be correlated with a vital capacity of 15 mL/kg, a mini-
maintained by the uninvolved lung. A double-lumen mally acceptable volume for an effective cough in
endotracheal tube isolates each lung and allows subjects with relatively normal pulmonary function.
independent ventilation. Each lung has its own ventila- However, in a study of healthy volunteers who were
tor, and the ventilatory pattern may be different given muscle relaxants, an NIF of 25 cm H2O was
between the two. The injured lung may be on CPAP or associated with adequate minute ventilation, even
high-frequency ventilation while the functional lung is though the muscles that protect the airway were still
ventilated more conventionally. When two ventilators nonfunctional. The AARC clinical practice guideline for
are used in this situation, one ventilator is designated the removal of an endotracheal tube recommends a
as the primary and the other as the secondary. The negative inspiratory force of greater than 30 cm H2O.79
primary ventilator establishes the timing of the respira- The NIF is the peak negative pressure measured
tory cycle that the secondary ventilator follows. The during a patient’s maximal inspiratory effort and
reflects the strength of the ventilatory muscles. The the need arise. Although rare, laryngeal spasm follow-
negative pressure measured after the first 100 millisec- ing extubation should be treated immediately by the
onds of a patient’s inspiratory effort is the airway application of a constant low pressure via mask and
occlusion pressure (P0.1) and reflects ventilatory muscle bag until muscle relaxants are given and reintubation
strength and central ventilatory drive.80 A high ventila- is performed. Under extreme conditions, the loss of
tory drive is associated with a greater ventilatory airway patency may require cricothyrotomy or transtra-
demand and a greater WOB. A normal P0.1 at rest is 2 cheal catheter ventilation. The extubation of patients
to 4 cm H2O. Values more negative than 4.5 cm H2O at risk of developing airway obstruction should be
have been associated with poorer extubation rates.81 attempted only if personnel skilled in intubation and
However, the accurate interpretation of P0.1 values may ventilatory support are immediately available.
be difficult in the presence of neuromuscular impair- Extubation should be considered when the indica-
ment, respiratory muscle weakness or altered resting tion for mechanical ventilation is no longer present.
end-expiratory lung volume.82 Protocols typically call for frequent screening of the
Patients at risk of developing edema leading to patient to assess oxygenation status, alveolar ventila-
airway obstruction during the postextubation period tion, acid-base balance, sputum production, and
are those who have had either head or neck surgery or mechanics of ventilation. The patient should have a
smoke inhalation injury. The cuff leak test assesses the minimal need for vasopressors or sedatives and an
presence of edema while the tube is still in place. When acceptable nutritional status. The screening criteria that
the patient is able to breathe spontaneously without may be included in an extubation protocol are as
ventilatory support, the cuff on the endotracheal tube follows:
(ETT) is deflated. The ETT is then manually occluded,
• P/F 150
and the patient’s ability to breathe around the tube is
• PEEP 5
evaluated. If the patient is able to breathe around the
• NIF 20
ETT, there is a good chance that extubation will be
• SpO2 90
successful.
• ABGs
Obviously, failure of the cuff leak test does not pro-
• VE 15 L/m
hibit extubation. The test may be sensitive only for
• RR 30
patients with obvious neck or airway involvement.
• VT/RR 105 (better predictive value if patient is
Partial airway obstruction due to glottic edema may
not on PS/CPAP85)
produce stridor that presents within minutes after
• VR 50%
extubation. Rapidly developing stridor indicates a
serious compromise of the airway and the need for Patients with acceptable screening values are given
reintubation. Stridor that occurs after an hour is a trial of spontaneous breathing for 30 minutes on
usually not a serious problem and should respond to 5 cm H2O CPAP, CPAP and pressure support (PS), or
aerosolized racemic epinephrine, which is used for its T-tube. If the patient tolerates the trial of spontaneous
vasoconstrictive properties to reduce mucosal edema. breathing, extubation is in order. Signs that the patient
Engoren used a different version of the cuff leak is not tolerating the trial are:
test in 531 cardiac surgery patients before extubation.83
• Agitation.
The patient was left on the ventilator in assist/control
• Diaphoresis.
mode, and the cuff was deflated. The difference
• Decreased mental status.
between inspiratory and exhaled tidal volumes defined
• Frequency of more than 35 bpm or an increase
the leak. A leak of 110 mL or less was considered a posi-
in frequency of 50%.
tive test. None of the 20 patients with a positive test
• Increase in heart rate or systolic blood pressure
developed stridor. The three patients who did develop
of 20%.
stridor all had leaks of more than 350 mL around the
• Or a drop in oxyhemoglobin saturation to
tube. There was no mention of head or neck reasons to
90%.
suspect stridor in this population, but 4% had prob-
lems not detected by this method.83 In a retrospective If the screening values are unacceptable or if the patient
study by Shin and colleagues, four trauma patients cannot tolerate spontaneous breathing after repeated
(10%) who had a good leak test of more than 10% of trials, the patient is placed on a weaning protocol.
the tidal volume required reintubation.84 None of
the patients with a poor cuff leak test required
reintubation. LONG-TERM VENTILATION DISCONTINUANCE
All extubations should be performed by clinicians Of the variety of modes and strategies used to wean
capable of providing mask and bag ventilation should patients from mechanical ventilation, no single
method has been proven to be superior. In a recent breathing through an endotracheal tube to mimic
systematic review of the literature, Butler and col- postextubation work of breathing.91
leagues suggest that the method in which the mode is Proportional assist ventilation (PAV) was designed to
applied has a greater impact on the duration of unload the respiratory system in a predictable fashion
mechanical ventilation and weaning outcome than the and improve patient comfort. Theoretically, PAV can
mode itself.86 The mode of ventilation during the unload elastic and inelastic (resistive) components of
weaning process must not place excessive demands on the work of breathing by adjusting volume-assist or
the respiratory system of the patient with a marginal flow-assist. Ventilatory support is provided in propor-
respiratory reserve due to preexisting impairment of tion to the patient’s inspiratory effort. Greater inspira-
cardiopulmonary or neurological function. Excessive tory effort on the part of the patient results in higher
demands on the respiratory system may be caused by: inspiratory pressure. The work provided by the ventila-
tor is set as a percentage of support. A few small studies
• High pressure loads due to abnormal mechanics
have favored PAV over PS, but PS remains the primary
of ventilation.
method of improving ventilation during spontaneous
• Increased ventilatory load from elevated minute
breathing trials.92
ventilation.
The sample weaning protocol presented in this
• Or workloads imposed by the ventilator system.
section calls for a 2-hour trial. However, Esteban and
Any method that promotes respiratory muscle fatigue coworkers found no difference in the reintubation rate
prolongs the duration of mechanical ventilation and when the spontaneous breathing trial was reduced
extends the weaning process. from 120 to 30 minutes.93 Longer trials may offer more
There is valid evidence to support that weaning reassurance for the weaning team than benefits for the
protocols implemented by respiratory therapists and patient. In a recent study by Mokhlesi and coworkers,
nurses reduce the duration of mechanical ventilation 13% of 122 patients who were extubated following a
and that the protocols should include a daily screening successful 2-hour spontaneous breathing trial had to be
of the patient’s respiratory function.87,88 The screening reintubated within 48 hours.94 The patients who
values are similar to those for the extubation protocol required reintubation had, during their spontaneous
criteria: breathing trials:
• P/F 150 • Significantly more secretions.
• PEEP 7.5 • A Glasgow Coma Scale score of 10 or less.
• NIF 20 • PaCO2s of 44 mm Hg or more.
• Small or moderate amount of sputum
There is some evidence that automated weaning
• VE 20 Lpm
approaches may shorten weaning time to a spontane-
• RR 30 bpm
ous breathing trial or to extubation.
• Minimal vasopressors and sedative agents
• Acceptable nutritional status • Automode, available on the Servo 300A and
Servoi, automatically switches the patient to a
If the patient meets the criteria, a trial of spontane-
spontaneous breathing mode with the patient’s
ous breathing is indicated. Most clinicians favor
first triggered breath in an assist/control mode
pressure-supported breathing trials over T-piece
(300A requires two consecutively triggered
breathing to eliminate the work of breathing imposed
breaths).
by the endotracheal tube. However, in a recent study by
• Should the patient become apneic for the
Mehta and associates, there was no significant differ-
interval set by the Trigger Timeout limit, Auto-
ence in the work of breathing (j/L) during 5 cm H2O of
mode returns the patient to the assist/control
PS, 5 cm H2O of CPAP, or T-piece breathing trials.89
mode. An indicator illuminates when the patient
Tidal volumes on both pressure support and CPAP
is breathing in the spontaneous mode.
overestimated postextubation tidal volumes, but tidal
• The clinician can track the respiratory rates, tidal
volumes on T-piece did not. The work of breathing for
volumes, and time periods of the patient’s
any of the three trial methods was significantly less
spontaneous breathing in the trends display to
than the work of breathing measured at 15 and 60
decide whether the patient should be screened
minutes postextubation.89 Ishaaya and colleagues also
for extubation.
reported an increased work of breathing after extuba-
tion in their patients that was not due to tracheal or Hendrix and coworkers found that Automode on the
laryngeal factors. They speculated that upper airway 300A reduced the time to extubation by 2 hours, when
narrowing may have been due to pharyngeal soft tissue compared to their standard extubation protocol of
edema.90 Straus and coworkers found the work of assist/control to SIMV to CPAP, in a small group of
20 postoperative coronary artery bypass graft (CABG) under Medical History. Selecting Yes for neurological
patients. The study was underpowered, however, and the disorder increases the higher-frequency limit to
difference of 2 hours was not significant (p 0.069).95 34 bpm for body weights of 36 kg and over. Selecting
Petter and coworkers compared Adaptive Support the COPD setting sets the high etCO2 limit to 65 mm
Ventilation to SIMV in a slightly larger patient group Hg. Ventilator alarms for etCO2, high frequency, and
(n 34) and found no difference between the two tidal volume need to be set according to the selected
methods in time to extubation or in time in the inten- Medical History limits, because activation of a ventila-
sive care unit (ICU). However, there were fewer manipu- tor alarm interrupts SmartCare. Once interrupted, the
lations of the ventilator controls and fewer alarms in unit needs to be manually restarted.
the ASV group. Gruber and colleagues found that ASV Ventilation classified as not in the normal range for
resulted in shorter mechanical ventilation time and less that patient prompts an increase or decrease in pressure
time to extubation, when compared to PRVC and support by 2 or 4 mbar (1 mbar 1.02 1 cm H2O),
Automode, for 48 postoperative CABG patients.96 depending on which parameter limit is violated. If
In a 2006 study, Lellouche and coworkers com- SmartCare changes the level of pressure support,
pared frequent screenings for spontaneous breathing reclassification of ventilation takes 5 minutes. If there is
trials (SBTs) to a closed-loop knowledge-based system no change in the level of pressure support, SmartCare
for driving pressure support (SmartCare, EvitaXL, analyzes ventilation every 2 minutes. The goal is to
Dräger, Telford, Pennsylvania) in 144 ICU patients on obtain a target level of pressure support that indicates
mechanical ventilation for at least 24 hours.97 They the patient may be discontinued from the ventilator.
found that SmartCare significantly reduced the time to The target PS is 5–12 cm H2O, depending on the type of
extubation, the time of mechanical ventilation, and the airway and type of humidifier. For example, the target
length of ICU stay. pressure support for ventilator discontinuance is 12 cm
SmartCare automatically adjusts the level of H2O for the patient with an endotracheal tube and an
pressure support to keep the patient’s frequency, tidal HME humidifier. The SC program conducts a spontane-
volume, and end-tidal CO2 values within a specific ous breathing test when the target PS has been
range, or so-called comfort zone. Three comfort zones obtained, providing the PEEP is 5 cm H2O or less. If the
are defined according to the patient’s actual body test is successful, a message is displayed indicating that
weight: 15–35 kg, 36–55 kg, and 55 kg. Each body the patient may be discontinued from the ventilator.
weight range has predetermined criteria for acceptable
tidal volume, frequency, and etCO2
SmartCare compares the patient’s initial frequency, Summary
tidal volume, and etCO2 to the acceptable criteria and The initiation and management of a patient on
assigns the patient’s ventilation to one of eight categories: mechanical ventilation require a thorough understand-
ing of the function of various ventilator modes and
• Normal
how changes in the patient’s compliance and resistance
• Insufficient
affect gas delivery. Respiratory therapists need to be
• Hypoventilation
able to determine the primary control variable during
• Central hypoventilation
the inspiratory phase to make sense of the ventilator
• Tachypnea
manufacturer’s mode terminology. For example, it’s
• Severe tachypnea
important to clarify what is actually meant by the term
• Hyperventilation
“spontaneous breathing” when it is used to describe
• Unexplained hyperventilation
any given mode. Knowledge of how a specific ventilator
Each category is defined by frequency, tidal volume, breath is triggered, limited, and cycled, coupled with
and etCO2 criteria. For patients weighing over 55 kg, basic cardiopulmonary physiology, provides the
normal ventilation is defined as a spontaneous fre- foundation for appropriate patient application,
quency between 15 and 30 breaths per minute, a tidal management, and subsequent discontinuation of
volume over 300 mL, and an etCO2 below 55 mm Hg. mechanical ventilation.
Insufficient ventilation is classified as an acceptable
frequency, but the etCO2 is too high or the tidal volume REVIEW QUESTIONS
is too low. Hypoventilation, on the other hand, is
considered to be an acceptable tidal volume but the 1. Describe the classification system for mechanical
etCO2 is too high and the frequency is too low. The ventilators using the following terms: trigger,
remaining categories are similarly delineated.98 control, cycle, and limit.
The initial setup screen for SmartCare allows the 2. State the advantages and disadvantages of the
user to select Neurological Disorder, COPD, or both following modes: VC or PC CMV, VC or PC SIMV,
MMV, PS, VS, PRVC (AutoFlow, VC), Automode, c. Inspiration is volume cycled.
Proportional Assist Ventilation, Adaptive Support d. Inspiration is flow cycled.
Ventilation, and CPAP. 5. Which one of the following statements describes
3. Discuss the advantages and disadvantages of the AutoFlow mode on the Evita XL ventilator?
the different waveforms, and interpret the a. Inspiratory flow is constant (rectangular
peak, plateau, and mean airway pressures in waveform).
each type. b. Pressure is constant (rectangular waveform).
4. Describe PEEP and its application in contrast to c. Inspiration is volume cycled.
auto-PEEP. d. Inspiration is flow cycled.
5. Discuss the hazards and complications of 6. (Peak – Plateau)/peak flow estimates airway
mechanical ventilation. resistance only for which flow pattern in VC?
a. rectangular
6. Describe the purpose of ventilator checks in
b. descending ramp
preventing potential complications.
c. decelerating
7. State the appropriate actions to take in correcting d. sine
respiratory acidosis, alkalosis, or ventilator
7. Which term does not create essentially two levels
dyssynchrony.
of CPAP?
8. State how changes in the ventilator controls affect a. APRV
volume delivery and mean airway pressure. b. bilevel
9. Explain the special considerations in the initiation c. bivent
and management of mechanical ventilation in d. AutoFlow
given patient cases. 8. What is a patient-triggered breath in Adaptive
10. Discuss methods of weaning and list two impor- Support Ventilation?
tant considerations for extubation. a. pressure support
b. volume support
c. PRVC
MULTIPLE-CHOICE QUESTIONS d. PC-CMV
1. Which of the following creates a greater difference 9. All of the following modes provide volume
between the peak and plateau pressures with a targeted pressure controlled breaths except:
constant flow mandatory breath? a. AutoFlow.
a. pneumothorax b. PRVC.
b. atelectasis c. VC.
c. pleural effusion d. ATC.
d. bronchospasm 10. Which one of the following ventilator conditions
2. Which of the following increases the plateau may increase the work of breathing for the
pressure with a constant flow mandatory breath? patient?
a. atelectasis a. Inspiratory flow is too low in volume control
b. bronchospasm mode.
c. increased peak flow rate b. The pressure trigger level is set on 8 cm H2O.
d. both b and c c. Inspiration is prolonged in pressure support.
3. In a pressure support or pressure control mode of d. All of the above are correct.
ventilation, the inspiratory flow to the patient is
the highest at: CRITICAL-THINKING QUESTIONS
a. the beginning of inspiration.
b. midinspiration. 1. How would respiratory therapists determine the
c. end-inspiration. ventilator’s response to a change in the patient’s
d. none of the above. compliance and resistance for a new mode that
they have never worked with before?
4. Which one of the following statements describes
the pressure-regulated volume control (PRVC) 2. Under what circumstances can one estimate the
mode on the Servoi ventilator? patient’s lung compliance in a pressure-controlled
a. Inspiratory flow is constant (rectangular mode?
waveform). 3. In volume control mode with a rectangular flow
b. Pressure is constant (rectangular waveform). waveform, the difference between peak and plateau
pressure reflects the patient’s airway resistance. tube compensation. Inten Care Med. 1997;23:
Why is this difference in pressure not reflective of 545–552.
the patient’s airway resistance in volume control 11. Hamilton-Medical-AG. Adaptive Support Ventila-
with a descending ramp flow waveform? tion: user’s guide. Switzerland; 2006.
4. In the management of a ventilator on a patient 12. Jiao G.-Y, Newhart JW. Bench study on active
with chronic airflow obstruction, what are impor- exhalation valve performance. Respir Care.
tant considerations? 2008;53,12:1697–1702.
13. Habashi NM. Other approaches to open-lung
5. In the management of a ventilator on a patient
ventilation: airway pressure release ventilation.
with acute respiratory distress syndrome, what are
Critical Care Medicine. Supp. 2005;33,3:S228–S240.
important considerations?
14. Branson RD, Johannigman JA. What is the evi-
6. What should always be considered in pressure dence base for the newer ventilation modes? Respir
support mode when adding nebulizer treatments Care. 2004;49,7:742–760.
or when there is a leak in the system? 15. Sinderby C, et al. Inspiratory muscle unloading by
neurally adjusted ventilatory assist during maximal
inspiratory efforts in healthy subjects. Chest.
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CHAPTER 27
Mechanics and Modes of Mechanical

Ventilation
Tina Wellman
OBJECTIVES
• Identify the benefits of using real-time ventilator graphics to manage patient-ventilator interactions.
• Utilize ventilator graphics to differentiate pressure and volume control ventilation.
• Utilize ventilator graphics to differentiate modes of ventilation.
• Explain the effect of clinically significant changes in airway resistance and lung compliance on ventilator
graphics.
• Identify common clinical problems using ventilator graphics.
CHAPTER OUTLINE
Waveforms Ventilator Modes
Interaction of Pressure, Volume, Interpretation of Ventilator Graphics
and Flow over Time Step 1: Determine the Type of Ventilation
The I/E Ratio Step 2: Determine the Mode of Ventilation
Types of Ventilation Loops
Volume Ventilation Pressure-Volume Loops
Pressure Ventilation Flow-Volume Loops
KEY TERMS
airway resistance (Raw) inspiratory rise time pressure ventilation
autocycling intrinsic PEEP pressure-volume loop
auto-PEEP mean airway pressure (MAP) scalar
flow-volume loop peak inspiratory pressure static compliance
I/E ratio plateau pressure (Pplateau) volume ventilation
inspiratory cycle off positive end expiratory pressure
inspiratory pause (PEEP)
728
CHAPTER 27 ■ Mechanics and Modes of Mechanical Ventilation 729
R
espiratory therapists working in intensive on the horizontal, or x, axis and the variable being
care units (ICUs) today are fortunate to be measured on the y axis. A few typical shapes or wave-
using ventilators with graphic displays that forms are seen in scalars during mechanical ventilation
are capable of presenting a variety of (Figure 27-1).4,5
waveforms. In fact, purchasing a modern ICU
• Square—The square scalar waveform is
ventilator without graphic displays would be difficult
generated by a constant flow rate throughout
because all manufacturers and end users recognize
inspiration. The waveform can also be
the need for this monitoring tool. Many currently
referred to as a rectangular or constant flow
available ventilators are designed with graphic
rate wave.
displays that also serve as the user interface. This
• Decelerating—The decelerating waveform is
design allows for the graphics to be monitored
generated by flow that begins at peak and
continuously while at the patient bedside. Some of
decreases in a linear manner until the end of
these ventilators are included in this chapter as
inspiration. This waveform is also known as a
examples, including the Draeger Evita XL, VIASYS
descending waveform.
Avea, Puritan Bennett 840, and the Maquet Servoi.
• Accelerating—The accelerating waveform is
The reason continuous monitoring of graphics has
generated by flow that begins with a low level
become so important is that the graphics provide an
and then increases throughout inspiration. This
immediate display of the patient-ventilator interac-
waveform has also been called an ascending
tion on which clinicians have come to rely.1 Much
waveform.
like pulmonary function testing, a clinician can learn
• Sinusoidal—The sinusoidal waveform is gener-
and use pattern recognition to detect and evaluate a
ated by flow that increases to a peak and then
patient’s normal and abnormal breathing patterns
decreases. At times only half of this curve may
while on the ventilator.2
be present.
Ventilator graphics (waveforms) provide important
• Decay—The exponential decay waveform is
data in real time at the bedside. They can help in:
generated by flow that begins at peak and
• Forming a clinical diagnosis. decreases.
• Providing information about the patients’ • Rise—The exponential rise waveform is
pulmonary mechanics and patient-ventilator generated by flow that begins at a low level
interaction. and then increases gradually throughout
• Determining the appropriateness of the ventila- inspiration.
tor settings, including triggering, synchrony,
and flow.
• Troubleshooting. Interaction of Pressure, Volume,
• Trending patient progress.
• Quickly recognizing patient changes.2,3
and Flow over Time
The interaction of the three measured variables of
Mastering ventilator waveform interpretation is pressure, volume, and flow over time is what the
a skill that takes time and commitment. This skill, ventilator uses to calculate and draw the waveforms.
however, is a-proficiency that can help a clinician The interaction includes a number of components of
recognize many problematic clinical situations mechanical ventilation in order to create the waveform
and ultimately improve the care provided to the displays:
patient.4
• Tidal volume (Vt) delivered depends on the flow
rate used and the inspiratory time allowed: flow
rate (Lpm) ⫻ inspiratory time (s) ⫽ tidal
Waveforms volume (mL).3
Three primary variables are assessed with waveforms: • The lungs inflate as the result of a pressure
pressure, volume, and flow. These specific waveforms gradient. If the pressure on the outside of the
are commonly referred to as scalar. The term scalar lungs (the ventilator circuit) is higher than the
means that the waveform is related to either pressure, pressure inside the lungs, the lungs inflate. The
volume, or flow and is plotted against time. They are larger the gradient is, the higher the generated
always represented as pressure versus time, volume flow rates are and the faster the lungs inflate. The
versus time, or flow versus time. Time is always plotted flow is measured as the volume change per unit
Pressure
Pressure
Square Decelerating
(A) Time
(B) Time
Pressure
Pressure
Accelerating Sinusoidal
(D) Time
(C) Time
Pressure
Pressure
Decay Rise
(F) Time
(E) Time
FIGURE 27-1 (A) A square scalar waveform. (B) A decelerating waveform. (C) An accelerating waveform. (D) A sinusoidal
waveform. (E) An exponential decay waveform. (F) An exponential rise waveform.
of time: tidal volume ⫼ inspiratory time ⫽ flow laminar or turbulent, on the dimensions of the
rate (in volume control modes only).4 airway, and on the viscosity of the gas. If the
• The amount of pressure required to inflate the airway diameter is large with low resistance, the
lungs depends on the lung compliance. Compli- greater the flow is that can move through the
ance is the distensibility of an elastic structure, airways. If the airway diameter is narrow
such as the lung, and is defined as the change in (constricted), the greater the resistance is, and
volume of the structure produced by a change in therefore the lower the flow rate is that can move
pressure across that structure. If the lungs are through the airways.3 The resistance through the
healthy and inflate easily (compliant), not much airways can greatly affect the pressures, whether
pressure is needed. If the lungs are very stiff set or created on the ventilator, and cause
(low compliance), however, a large amount of specific variations in the waveforms.
pressure may be needed to inflate the lungs. • Another important factor in looking at waveforms
• Airway resistance, another factor related to is total cycle time (Figure 27-2). The total cycle time
pressure in mechanical ventilation, is the (TCT) is the total respiratory cycle, that is, the time
opposition to flow caused by the forces of required for both inspiration (Ti) and expiration
friction. It is defined as the ratio of driving (Te) and the events that occur during that time.6
pressure to the rate of air flow. Resistance to flow
in the airways depends on whether the flow is TCT ⫽ Ti ⫹ Te
Minute Respiratory Rate TCT In Figure 27-3A, the ventilator is set for a

respiratory rate (RR) of 8 breaths per minute with
60 sec 60 1
an inspiratory time of 1 second. The TCT in this case
60 sec 30 2 is 7.5 seconds (60 seconds ⫼ 8 RR ⫽ 7.5 TCT). The
60 sec 20 3 I/E ratio is 1:6.5. The yellow line on the graph is
showing the period of time between breaths. If the
60 sec 15 4
inspiratory time remains constant while the ventilator
60 sec 12 5
respiratory rate is changed, the expiratory time and
60 sec 10 6 I/E ratio must change.
60 sec 6 10 In Figure 27-3B, the ventilator is set with a respira-
If the Ti is set the Te must change. tory rate of 15 breaths per minute and a 1-second
inspiratory time. The yellow line in this example is
FIGURE 27-2 Total cycle time.
tracing the period of time between breaths. There is
much less time between breaths than seen in Fig-
ure 27-3A with a respiratory rate of 8 breaths per
THE I/E RATIO minute. With the set rate of 15 breaths per minute
The I/E ratio is simply a proportion of the inspiratory and a 1-second inspiratory time, the I/E ratio is
and expiratory time in a respiratory cycle.6 To figure 1:3 and the TCT is only 4 seconds.
out the I/E ratio, refer to the TCT in Figure 27-2 (TCT ⫽ In Figure 27-3C, the ventilator is set with a
Ti ⫹ Te). The TCT cycle time must be divided between respiratory rate of 20 breaths per minute and a 1-
the two portions. A normal I/E ratio is 1:2 or 1:3 (Ti second inspiratory time. The yellow line is tracing the
to Te), giving the patient more time for exhalation than period of time between breaths, which is even shorter.
inhalation. If the ratio is changed to be 2:1 or 3:1, it is The TCT in this example is only 3 seconds with an I/E
called an inverse ratio. This is done at times to improve ratio of 1:2. The higher the respiratory rate gets with
oxygenation in a sick patient but is not considered the same inspiratory time, the less time the patient
normal.3 has to exhale.
(A)
FIGURE 27-3 If the inspiratory time remains constant while the ventilator respira-
tory rate is changed, the expiratory time and I/E ratio must change. (A) I/E of
1:6.5, (B) I/E of 1:3, (C) I/E of 1:2. (continues)
(B)
(C)
FIGURE 27-3 (continued)
Types of Ventilation VOLUME VENTILATION

In volume ventilation, there are many active param-
There are only two fundamental types of mechanical
eters on the ventilator. However, a few operator-set
ventilation. The patient is ventilated either with
parameters affect the ventilator waveforms in predict-
pressure or with volume ventilation. Understanding
able ways:
these principles makes understanding ventilator
waveforms very easy. All the modes of ventilation • Tidal volume (Vt)
on any ventilator fall under one of these two categories. • Inspiratory time (Ti)
Pressure
Pressure
Constant Flow Decelerating Flow

FIGURE 27-4 Typical volume ventilator breath. FIGURE 27-5 Typical pressure-ventilated breath.
Courtesy of Maquet Inc. Courtesy of Maquet Inc.
• Respiratory rate inspiration on positive pressure ventilation.4 Set

• Rise time times—inspiratory time (Ti), rise time, respiratory
• Flow rate rate, and PEEP—give the patient a variable tidal
• Positive end-expiratory pressure (PEEP), volume and a decelerating inspiratory flow rate.
the positive pressure at the end of exhalation Figure 27-5 shows a typical pressure ventilated
during spontaneous breathing or mechanical breath. The breath begins at peak flow and decreases
ventilation4 in a linear fashion until the end of inspiration.
Exhalation occurs passively at the end of the inspira-
These settings generate an accelerating inspiratory
tory time. The constant pressure in the ventilator
pressure.
circuit is depicted in the Figure 27-5 as a square
Figure 27-4 shows a typical volume ventilator
wave. During inspiration, pressure continuously
breath. The breath begins at a low flow and quickly
increases in the periphery of the lung. This results
increases to the set amount, where it is maintained at
in a continuous diminishing of the pressure gradient
that constant rate until the end of the inspiratory
across the lung until there is none. Without a
phase (green line). Then exhalation occurs. This
pressure gradient, there can be no flow into the
figure shows that, with a constant flow rate in
lung. Inspiration ends when the preset inspiratory
volume ventilation, the pressure tracing generated
time (TI) is reached, as shown in the figure as a
is accelerating.
decelerating flow rate.5
This outcome is due to the anatomy of the lung.
The square inspiratory pressure waveform that is
When a constant flow rate is applied to the lung, the
produced during a pressure-ventilated breath not only
pressure generated increases as it travels to the
limits airway pressure, but also gives constant pressure
smaller airways. The resistance is higher in the small
throughout the inspiratory phase. Because of the initial
airways than in the larger airways. The increase in
high peak flow at the beginning of the breath, the preset
resistance generates higher pressures, which in turn
pressure is achieved quickly and remains at this level
cause the pressure tracing associated with volume-
until the set inspiratory time is achieved. In pressure
ventilated breaths to accelerate. Volume ventilation
ventilation, the inspiratory flow and the TI are indepen-
breaths guarantee the set tidal volume delivery
dent of one another. The RCP sets the inspiratory time
regardless of changes in the lung characteristic such
according to the patient’s particular needs, and the
as compliance and resistance. This can be an asset if
decelerating inspiratory flow pattern provides a more
control of PaCO2 is needed by guaranteeing a set
even distribution of air to the alveoli regardless of
minute ventilation (Ve). Minute ventilation is the
compliance.7
product of respiratory rate and tidal volume:
Ve ⫽ RR ⫻ Vt.
Ventilator Modes
PRESSURE VENTILATION Ventilator modes correlate to either pressure or volume.
In pressure ventilation, a few set parameters affect Within the two categories (pressure and volume) are
the waveform. There is a set/constant peak inspiratory four modes: controlled modes, assist-controlled modes,
pressure or ventilating pressure (Peak). Peak inspiratory support modes, and combination modes. Understand-
pressure is the highest pressure achieved during ing the type of mode being used is important in
optimizing synchrony. Knowing the type of mode helps Interpretation of Ventilator

in identifying normal versus abnormal breathing
patterns displayed on the graphics. Graphics
• Controlled modes. In controlled modes, the Figure 27-6 is a representative graphics display of
ventilator starts the breath, controls the volume ventilation for the VIASYS Avea ventilator.
inspiratory gas delivery, and ends inspiration • The top waveform represents the pressure scalar
with no input from the patient.6 With each waveform. The measured pressure is shown in
breath is a guaranteed delivery of either a preset cm H2O.
pressure or tidal volume that is controlled by • The middle waveform represents the flow scalar. The
the ventilator. measured flow is shown in liters per min (Lpm).
• Assist-controlled mode. Assist-controlled modes are • The bottom waveform represents volume scalar
identical to controlled modes except that the and the measured volume is shown in
patient is able to trigger the ventilator by exert- milliliters (mL).
ing respiratory muscles.
• Support modes. In support modes, where the These are the three main waveforms that are monitored
patient is breathing spontaneously, the patient on all ventilators in the ICU. When interpreting
initiates the breath and controls the depth of the ventilator graphics, follow a set of steps.
breath and the flow rate at which the breath is
delivered.3 STEP 1: DETERMINE THE TYPE OF VENTILATION
• Combination mode. The combination modes First, identify what type of ventilation the patient is on:
include both types of breaths (control and pressure or volume. To decipher a volume mode from a
support). It is primarily used to provide pressure mode, look at the flow scalar first, then the
partial mechanical support. The patient can pressure scalar.
take some spontaneous breaths but may
also receive some mandatory or control Volume Ventilation. Recall that the flow scalar for a
breaths as well. volume breath should be square or constant flow. The
Table 27-1 provides examples of common modali- flow rate may vary in a predictable fashion if a flow
ties that may be seen on modern ventilators. pattern is “set” on the ventilator controls. This is shown
in Figure 27-6. The pressure increases at a constant rate
due to the constant, or square, flow pattern. The
pressure increases as the volume being delivered
TABLE 27-1 Categories pressure and inflates the lung. This is what a typical pressure
volume with designated ventilator modes scalar waveform looks like in volume ventilation.
Category Mode
Pressure Ventilation. In Figure 27-7, the top scalar on
Volume Category this ventilator is the pressure scalar, and it is displaying a
Volume control (VC) Controlled mode square, or constant, pressure pattern. The bottom scalar
Synchronized intermittent Combination mode is the flow scalar, which has a decelerating flow pattern.
mandatory ventilation This pattern is consistent with pressure ventilation.
(VC-SIMV)
Pressure Category STEP 2: DETERMINE THE MODE OF VENTILATION
Pressure control (PC) Controlled mode After determining the type of ventilation, ascertain
whether the mode is a controlled, assist-controlled,
Pressure support (PSV) Assist-control or support support, or a combination. To do this, first look at the
mode breaths to see whether they all look exactly alike.
PC-SIMV Combination mode
• Are they the same size?
Volume support Assist-control or support • Are they the same shape?
mode • Do they come at a regular and marchable
Pressure-regulated volume Controlled mode frequency?
control (PRVC)
If these questions can be answered positively, the
SIMV-PRVC Combination mode mode is most likely controlled or assist-controlled.
Airway pressure release Combination mode
• In both controlled and assist-controlled modes,
ventilation (APRV)
the inspiratory time, or flow rate, is set by
FIGURE 27-6 Typical waveforms in a volume ventilation.

the operator of the ventilator. In that case, • In combination modes, some breaths are exactly
each breath has exactly the same inspiratory the same while others are varied.
time.
If the inspiratory times and the “shape” of inspira-
• In spontaneous modes, the inspiratory time is
tion are consistent from breath to breath, then the
controlled by the patient and therefore has some
breaths are identical. To understand the concept of
variability.
B being delivered to the patient. If the patient had

C triggered a breath, a negative deflection would appear
just prior to the mechanical breath in either the
pressure or flow scalar depending on the ventilator
setup with regard to trigger sensitivity. The negative
A deflection indicates a patient-initiated breath. Once the
Constant Flow breath has been started, it is generally shaped by the set
D parameters. If the flow rate, and/or volume, are not set
appropriately patient/ventilator dysynchrony is likely
to result.
In Figure 27-9B, the first arrow on the flow scalar
FIGURE 27-8 Parts of the breath on a waveform: (A) The represents the beginning of exhalation, where inspira-
beginning of inspiration. (B) Inspiration, or inspiratory tion ends and exhalation begins. The second arrow
time. (C) The end of inspiration and the beginning of represents the end of exhalation. When the patient is
exhalation. (D) The end of exhalation. finished exhaling, the breath comes all the way back
to baseline between breaths. This is what a normal
breath looks like upon complete exhalation. If the
waveform does not return to baseline between the
shaping inspiration, the respiratory therapist must be
breaths, it is abnormal and results in auto-PEEP, or
able to distinguish the parts of the breath on the
intrinsic PEEP. Auto-PEEP is abnormal and is
waveform. In Figure 27-8:
usually undetected above the atmospheric pressure
• (A) is the beginning of inspiration. Inspiration can remaining in the alveoli at the end of exhalation due
be initiated by the ventilator or by the patient, to dynamic air trapping.3 Auto-PEEP, or air trapping,
depending on the mode of ventilation. If the may result from:
patient has triggered the breath, there is a negative
• Inadequate expiratory time.
deflection just prior to the mechanical breath.
• Too high a respiratory rate.
• (B) represents inspiration or inspiratory time. This
• Long inspiratory times.
period of time is set by the clinician on the
• Prolonged exhalation due to bronchoconstric-
ventilator in controlled and assist-controlled
tion, dynamic airway collapse, small endotra-
modes. During inspiration of a volume breath,
cheal tubes, and clogged expiratory filters, or
the flow is constant [that is, the flow pattern is
similar disorders.4,8
predictable (a set parameter)], and the pressure
develops at a rate that depends on the character- In Figure 27-9C, the first two arrows on the pressure
istics of the lung and the ventilator settings. scalar represent the patient’s set PEEP. The waveform
• (C) represents the end of inspiration and the remains above zero cm H2O (blue arrow). For this
beginning of exhalation. Exhalation is passive and patient, the operator has set a therapeutic PEEP level.
commences upon the ventilator’s opening of the The third arrow represents the peak pressure being
expiratory valve. generated. Notice it occurs at the end of inspiration
• (D) is the end of exhalation. In a normal breath, when the patient’s lungs are the most inflated.
exhalation should return to baseline before the Figure 27-9D provides a closer look at the volume
next breath begins. The characteristics of the scalar. The waveform is divided into two unequal
lung, as well as parts of the ventilator circuit pieces: The first half is inspiration, and the second
(such as smaller endotracheal tubes and clogged half is exhalation. This is an example of a normal
expiratory filters) can slow patient exhalation. volume scalar. Volume scalar waveforms generally
look the same regardless of the mode or type of
ventilation. In a normal breathing pattern, the
Volume Ventilation. Figure 27-9A shows a volume- tracing in a volume scalar should come to baseline
control mode that is not being assisted by the patient.
between breaths.
On the flow scalar (middle) waveform, the first arrow
The volume scalar may appear differently in two
represents the beginning of inspiration. The second
instances.
arrow represents the inspiratory time for this breath.
Based on the inspiratory time for all three breaths on • One is in the face of a leak in the system, either
the graph, the breaths appear to be identical. This is a in the ventilator circuit, around the cuff of the
volume control mode, and no assisted breaths are artificial airway, or in the ventilator itself.
(A) (B)
(C) (D)
(E)
FIGURE 27-9 (A) A volume-control mode that is not being assisted by the patient. (B) A normal breath with complete
exhalation. (C) PEEP setting. (D) A normal volume scalar. (E) A change in setting showing inspiratory pause and
inspiratory rise time.
Courtesy of Maquet Inc.
• The other is if the patient is forcibly exhaling When setting rise time, the therapist must remember
instead of allowing the normal passive exhalation. that patient effort and work of breathing are known to
If a patient is forcibly exhaling, the waveform be affected by the ventilator’s ability to meet the
appears steeper due to the speed of the volume patient’s peak inspiratory demand. If the inspiratory
changing, and the area between breaths might flow does not meet the demand, then patient-ventilator
dip below the baseline. dyssynchrony results. In Figure 27-9E, it is apparent
that a substantial rise time is set. In the first breath of
Inspiratory Pause and Inspiratory Rise Time In Fig- the flow scalar (green), the white line represents how
ure 27-9E, this is still volume ventilation, but a couple the breath would look without rise time—a very sharp
of settings have been changed. and square breath. In the second breath, the arrow
marks the very sloped and gradual climb to the set
• All the breaths look identical, but an inspiratory
constant flow rate. This is what a volume breath with a
pause has been set. An inspiratory pause is just
significant amount of rise time looks like.
an extension of the inspiratory time where the
In Figure 27-10, an inspiratory pause has been set
exhalation valve of the ventilator remains closed.
to lengthen the inspiratory time. (An inspiratory pause
Inspiration continues until the pause has ended
is added is to improve patient oxygenation.4) The
and then exhalation begins.4 Inspiratory pause
arrows on all three scalar waveforms point out the
results in plateaus on all the scalars.
same characteristic. During an inspiratory pause,
• A second new setting affects inspiratory rise
there is no additional flow from the ventilator into
time. Rise time is a setting on a ventilator that
the patient’s lungs. This is a static maneuver.
allows a clinician to control the rate at which the
ventilator disperses the initial gas burst from the • So the flow scalar shows a drop in flow that is
ventilator. In volume ventilation, the gas nor- held at zero until exhalation begins.
mally comes out of the ventilator very quickly • The pressure scalar also shows a decrease in
and rises to the set constant flow rate, where it pressure from the peak pressure to the plateau
remains until exhalation. The clinician can slow pressure. The plateau pressure (Pplateau) is the
down the initial gas burst using rise time. An pressure measured in the patient’s circuit of a
appropriately set rise time should result in ventilator during an inspiratory hold maneuver,
greater patient comfort and a more laminar in addition to the added pressure to overcome
flow, decreasing resistance. the elastic component of the lungs (static
FIGURE 27-10 An inspiratory pause set to lengthen the inspiratory time.

FIGURE 27-11 A calculation for compliance uses data from exhaled tidal volume
divided by the plateau pressure minus the PEEP.
compliance) during breath delivery.6 Differences • The frictional force associated with ventilation
between peak pressure and plateau pressure are due to the anatomical structure of conduit
the result of resistance to inspiratory flow. airways.
• Finally, the tip of the volume scalar has flattened • The resistance to gas flow through the airways.
out from its traditional triangular top. During • The viscous resistance of the lungs and the
the inspiratory pause, when no additional flow is adjacent tissues and organs as the lungs expand
entering the patient, no additional volume is and contract.4
added.
In Figure 27-12, the two arrows are pointing to
Static Compliance Compliance is equal to a volume the peak and plateau pressures. In trending airway
change divided by a pressure change.4 Static compli- resistance on a ventilator, these are the two param-
ance is a compliance measurement done under eters to monitor. If the plateau pressure remains
conditions of no gas flow, and it can be trended over constant, there is a directly related increase in the
time using waveforms. Most modern ICU ventilators airway resistance with every increase in the peak
allow for an inspiratory pause to be set briefly in order pressure. This is a dynamic measurement. Table 27-2
to gain data, or it can be added to every mandatory demonstrates the relationship between compliance
breath to improve oxygenation. In Figure 27-11 the two and resistance.
arrows are pointing out the plateau pressure and the As another example of determining compliance
PEEP. The ventilator uses a formula to calculate the change versus resistance change, see Figure 27-13. The
compliance using exhaled tidal volume divided by the pressure scalar makes it apparent that this is volume
plateau pressure minus the PEEP. Over time this data ventilation with an inspiratory pause set on each
can be used as a trend to see whether the patient’s breath. A line drawn across the captured plateau
lungs are becoming more or less compliant. The greater pressures makes clear that these plateau pressures have
the difference is between plateau pressure and PEEP, remained the same. The peak pressures, however, show
the lower the compliance of the patient will be. a significant reduction in pressure from the first breath
to the second. This pattern is consistent with a decrease
Airway Resistance Using the same trending technique, in Raw. This type of reduction in Raw could come
airway resistance (Raw) can also be monitored. from suctioning the patient or administering a
Resistance is: bronchodilator.
FIGURE 27-12 With every increase in the peak pressure, there is a directly related
increase in the airway resistance if the plateau pressure remains constant.
TABLE 27-2 Compliance and resistance however, it is typically used with the addition of
pressure support ventilation (PSV), which is a pressure
Peak Plateau type of ventilation. PSV is a patient-triggered,
pressure pressure Indicates pressure-limited, flow-cycled mode of ventilator
Increases Remains the same Increased RAW support that allows the patient control of the
respiratory frequency, inspiratory time, and
Decreases Remains the same Decreased RAW inspiratory flow rate.9
Figure 27-15 shows an example of a VC-SIMV with
Remains the Increases Decreased
PSV. The third and seventh breaths, shown with arrows
same compliance
on the flow scalar, are clearly volume-type breaths with
Remains the Decreases Increased a set pause. However, the rest of the breaths look
same compliance considerably different. The patient initiated these
breaths. Because they are pressure support breaths,
Increases Increases Decreased they have a decelerating flow pattern, and they are
compliance and controlled by the patient throughout the entire cycle.
increased RAW This is a combination mode designed to be used for
Decreases Decreases Increased weaning.
compliance and
decreased RAW Pressure Control Ventilation. As noted, pressure
breaths look different from volume breaths.
Figure 27-14 presents a change in airway resistance. Figure 27-16 shows a breath under pressure
The horizontal green line drawn over the pause of each type ventilation.
breath shows that the plateau pressure has remained
the same while the peak pressure has decreased. This • (A) is the beginning of inspiration. Inspiration
pattern indicates a decrease in Raw. can be initiated by the ventilator or the patient
depending on the mode of ventilation. If the
Synchronized Intermittent Mandatory Ventilation. patient has triggered the breath, a negative
Synchronized intermittent mandatory ventilation deflection appears just prior to the mechanical
(VC-SIMV) is another type of volume ventilation; breath.
FIGURE 27-13 A significant reduction in pressure from the first breath to the

second is consistent with a decrease in Raw.
FIGURE 27-14 The plateau pressure has remained the same while the peak
pressures mean has decreased, indicating a decrease in Raw.
• (B) represents inspiration or inspiratory time. commences upon ventilator’s opening the
This period of time is set by the clinician expiratory valve.
on the ventilator. During the inspiratory • (D) is the end of exhalation. In a normal breath,
portion of a pressure-controlled breath, exhalation should return to baseline before the
the pressure is constant and the flow rate next breath begins. Characteristics of the lung
decelerates. can slow patient exhalation, as well as parts of
• (C) is the end of inspiration and the beginning the ventilator circuit, such as smaller endotra-
of exhalation. Exhalation is passive and cheal tubes and clogged expiratory filters.
FIGURE 27-15 The third and seventh breaths, shown with arrows on the flow
scalar, are volume-type breaths with a set pause; the remaining are pressure
support breaths with a decelerating flow pattern, controlled by the patient
throughout the entire inspiratory cycle.
Courtesy of Draeger Medical
Pressure Pressure support

C
Proximol Airway Pressure (cmH2O)
20 overshoot Delayed
B
termination
D
C 2
A B
15
2 Pressure support Premature
Decelerating Flow undershoot because termination
D of inadequate flow
10
A Patient trigger
FIGURE 27-16 Pressure ventilation: (A) The begin- 5
ning of inspiration. (B) Inspiration or inspiratory
time. (C) The end of inspiration and the begin-
ning of exhalation. (D) The end of exhalation.
Time
The most important facet of pressure support ventila- FIGURE 27-17 Pressure support breath: (A) The normal
tion is the delivery of flow and responding pressures. triggering of a spontaneous pressure support breath.
Figure 27-17 presents the components that make up a (B) The rapid increase in pressure to the set pressure level.
pressure support: (C) The set inspiratory pressure level. (D) Inspiration
terminates when the inspiratory flow decreases to the
• (A) represents the normal triggering of a sponta-
specific threshold of the system, allowing the pressure
neous pressure support breath. to drop back to baseline.
• (B) represents the rapid increase in pressure to the
set pressure level (C). The tapered dotted line
• (C) represents the set inspiratory pressure level.
represents a scenario where the flow may be
• In (D), inspiration terminates when the inspira-
inadequate to meet the inspiratory demand of
tory flow decreases to the specific threshold of
the patient. The patient may outstrip the avail-
the system, allowing the pressure to drop back to
able flow. The pressure overshoot can occur as a
baseline. Delayed termination can happen when
result of the quickly increasing pressure colliding
a dysynchronous patient attempts to end the
with a small ETT or an obstructed airway. This
breath early.
pressure overshoot can also occur if the flow
exceeds the patient’s demand usually for a Figure 27-18 presents the parts of the waveforms
brief period before the pressure settles again to in pressure ventilation. In Figure 27-18A, the arrows
the set level. on both breaths of the flow scalar (bottom waveform)

indicate the beginnings of inspiration of these step in interpreting waveforms. To determine the mode,
pressure type breaths. The inspiratory time is set by examine the inspiratory time of all the breaths.
the clinician on the ventilator in controlled modes
of ventilation. • Are they the same length?
Determining whether the mode is controlled, • Do the breaths appear to be the same size and
assist-controlled, support, or combination is the second shape?
FIGURE 27-19 On each breath in the flow scalar, the arrow points to the beginning
of inspiration for the following breath. The exhalation of each of these breaths is
cut short by the patient’s next breath, causing the patient to generate significant
auto-PEEP over time.
If the answer is yes to these questions, as in the case of not return to baseline. On each breath in the flow
Figure 27-18B, the mode is controlled. In both support scalar, the arrow points to the beginning of inspiration
modes and combination modes, there would be some for the following breath. The exhalation of each of
variability in the inspiratory times, sizes, and shapes of these breaths is cut short by the patient’s next breath,
the breaths. causing the patient to generate significant auto-PEEP
The first arrow on the first breath of the flow scalar over time.
of Figure 27-18C represents the beginning of exhalation. Looking at the end of exhalation observe that in
The second arrow represents the end of exhalation. the best scenario the patient’s breath should return to
Notice that when this patient is finished exhaling, the baseline between breaths. Now examine the beginning
breath returns to baseline between breaths. This is an of inspiration again and see how rise time can affect a
example of a normal breath with complete exhalation. pressure type breath.
If the tracing does not return to baseline, the patient Earlier in this chapter, Figure 27-9D illustrated the
did not completely exhale, indicating auto-PEEP. effects of rise time on the waveform of volume type
In Figure 27-18D, the red arrow represents the ventilation. Rise time has a similar effect graphically in
space between breaths. This space is very important. For pressure type ventilation, but it can be slightly more
the patient to be able to completely exhale, the breath difficult to see. Figure 27-20A presents an example of
must return to the baseline for a period of time before pressure type ventilation. In looking at the flow scalar it
the next breath begins. If this does not occur the patient is observed that by comparing the ventilator waveform
generates auto-PEEP. The management of this space to the drawn in line that there is a slight difference.
between breaths and ensuring that the breath returns to Typically, with decelerating waveforms in pressure type
baseline is done by the precise control of the I/E ratio. ventilation, the flow starts at peak and then decreases
The Figure 27-19 graphic is from the VIASYS Avea in a linear manner. There is a slight delay in this
ventilator. The screen is set up with the pressure scalar graphic in reaching peak flow. This is rise time, and it
on top, the flow scalar in the middle, and the volume allows the clinician to slow the initial gas flow to meet
scalar on the bottom. This graphic is an example of the needs of the patient. The clinician has a range of
pressure type ventilation where the exhaled breath does choices depending on the ventilator being used. Faster
(A)
(B)
FIGURE 27-20 (A) Comparing the ventilator waveform to the drawn line shows a
slight difference; the delay in reaching peak flow is rise time. (B) This patient
has a set rise time, as illustrated by comparing the drawn line and the actual
waveforms. (C) On the second breath, an arrow points to the end of inspiration.
This same point is also the beginning of exhalation. In this example, the end of
inspiration is exactly correct for this patient. (continues)
rise times allow for more available flow and can In Figure 27-20B, a comparison of the drawn line
decrease the work of breathing for the patient. If the and the actual waveforms shows that this patient has a
rise time slows the flow too much, it can be inadequate set rise time. The delay is much more significant than
for the patient, making the patient flow starved and in the last example in Figure 27-20A. In this scenario,
dyssynchronous. The flow waveform should smoothly the flow takes longer to reach peak. This setting is used
reach peak flow and then gradually decrease.10 mostly for patient comfort and to improve synchrony
(C)
with the ventilator. However, it affects both the ability modes, the patient controls the entire inspiratory cycle.
of the ventilator to meet the patient’s flow demands In combination modes, the Ti, or flow rate, can be set
and the mean airway pressure (MAP),11 which is the only on the mandatory breaths, and often the inspira-
average pressure occurring in the airway during the tory time is set incorrectly. It is a setting or parameter
complete respiratory cycle.6 Although rise time does on the ventilator that should be checked frequently
not change, the set inspiratory time does change the because the requirements may change for a patient
amount of time the peak flow/pressure is applied to several times throughout a day.
the airways. This can affect the MAP by decreasing it Figure 27-21 is an example of pressure ventilation
overall.12 where the inspiratory time is significantly shorter than
We have looked at the end of exhalation and the optimal. On the flow scalar for the first breath, a red
beginning of inspiration so far. It is time to look at the arrow indicates where inspiration has been prema-
end of inspiration. Due to their respective flow wave- turely ended. On the flow scalar for the second breath,
forms, it is much more important to look at the end of a red dotted line represents the plane the tracing
inspiration in pressure type ventilation than it is in should have followed if the Ti had been optimally set.
volume ventilation. In volume ventilation, the square Figure 27-22 also shows the end of inspiration. In
flow waveform gives no graphic indication of an the flow scalar (middle waveform), the arrows show
optimized inspiratory time. In pressure ventilation, that inspiration ends long before the breath reaches
however, there is a decelerating flow waveform. This baseline. The inspiratory time is too short and therefore
waveform is the most similar to a normal, unventilated not optimized for this patient. Optimizing this Ti
breathing pattern (negative pressure), and it can be means that it is increased until the breath tracing
seen graphically if there are optimal settings for the reaches the baseline, thereby increasing the inspiratory
inspiratory time. time and the MAP. Increasing the MAP is a technique
Figure 27-20C shows a pressure type ventilation. In often used to increase the patient’s oxygenation.12
the flow scalar for the second breath, an arrow points Figure 27-23 demonstrates pressure type ventila-
to the end of inspiration. This same point is also the tion. On the flow scalar (middle waveform), the
beginning of exhalation. In this example, the end of inspiratory times are not all the same for the three
inspiration is exactly correct for this patient. It should breaths shown. In the first breath on the flow scalar,
decelerate linearly until it reaches the baseline, after the inspiratory time is set too long; note the arrow. The
which exhalation immediately follows. Inspiratory breath returns to the baseline and continues to follow
time, or flow rate, can be set only in controlled and the baseline for a period of time before allowing the
assist-controlled modes of ventilation. In spontaneous patient to exhale. This is not an optimized inspiratory
FIGURE 27-22 In the flow scalar (middle waveform), the arrows show that inspiration
ends long before the breath reaches baseline. The inspiratory time is too short
and therefore not optimized for this patient.
time. Although it is longer and increases the MAP, it Figure 27-24 is an example of pressure type
can also increase asynchrony between the patient and ventilation with an inappropriately set inspiratory time.
the ventilator. At times, increasing the inspiratory time Notice the second breath on the flow scalar. The
to beyond optimal is a technique used to increase inspiratory portion of the breath returns to the baseline
oxygenation and may be an inverse ratio type of and then follows the baseline for an extended period of
ventilation. This is not considered a normal time. The inspiratory portion of this breath should
inspiratory time. have ended sooner. In response to this extended
FIGURE 27-23 On the flow scalar (middle waveform), the inspiratory times are not
all the same for the three breaths shown; the arrow indicates a inspiratory time
that is set too long.
FIGURE 27-24 This is an example of asynchrony due to inappropriately set

inspiratory time.
inspiratory time, the patient begins to experience some attempting to exhale against the closed expiratory
asynchrony. Line up the pressure scalar (top waveform) valve, which is closed due to the set inspiratory time.
with the point on the flow scalar where the inspiratory This is an example of asynchrony due to an inappropri-
time should have ended (dotted vertical line), and ately set inspiratory time. Learning to set an appropri-
note the corresponding increase in pressure directly ate inspiratory time is one of the most beneficial
following. This pressure increase is due to the patient aspects of mastering waveform analysis.
FIGURE 27-25 An example of an extended inspiratory time.

Figure 27-25 (from the Draeger Evita XL) presents are not only significantly different inspiratory times,
another example of an extended inspiratory time. The but also large volume and pressure differences between
top scalar of this ventilator is pressure versus time. breaths. However, some of the breaths seem to follow a
The middle scalar is flow versus time, and the bottom pattern and have similarity. The waveform begins with
scalar is volume versus time. The first breath on the flow a mandatory pressure control breath, and then the next
scalar (the red line) is the portion of the inspiratory breath is a pressure support, patient-initiated breath.
time where no additional flow is being added. The This pattern continues throughout the example. This is
patient however, is unable to exhale due to the set Ti. a combination mode pressure control synchronized
The second breath in the flow scalar (the red dotted intermittent mandatory ventilation (PC-SIMV).
line) is the path that a more optimally set inspiratory The next step is to determine whether the manda-
time would follow. On the volume scalar, the typical tory breaths are optimized. Look closely at the
triangular shape is not present. The top of the triangle inspiratory time of the mandatory breaths. The tops
is flattened out, signaling that a long inspiratory time of the waveforms (note the arrows) appear to be
or a pause is set. somewhat flattened. Unless an inspiratory hold is
clinically desired, the inspiratory time may be too
Combination Mode Pressure Ventilation. Figure 27-26 long. This conclusion is confirmed by the slightly
presents another type of pressure ventilation. It is a flattened tops of the volume tracings. When the
combination mode, more specifically PC-SIMV with control and support pressures are set close to each
PSV. Again, follow the steps of interpretation to other, differentiating mandatory pressure control
determine the type of ventilation. breaths from pressure support spontaneous breaths
Is it pressure or volume ventilation? The flow scalar in the combination mode can be difficult—especially
is a decelerating flow waveform, which is generally when the patient is initiating some or all of the
indicative of pressure ventilation. In this case, every mandatory breaths.
breath is a pressure type breath.
Is this is a controlled, support, or combination Pressure Support Ventilation. Figure 27-27 depicts
mode? Examine the inspiratory time, size, and shape of pressure support ventilation (PSV). In this pressure
the breath. Are they all the same? In this example, not type of ventilation, the waveform is characterized by a
all the breath waveforms are identical. This must be decelerating flow pattern. This is not a controlled
either a support or combination mode, in which case mode. All breaths are initiated by the patient and may
some variability in inspiratory times is expected. There vary considerably in terms of their inspiratory times,
FIGURE 27-26 An example of a combination mode, more specifically PC-SIMV

with PSV.
FIGURE 27-27 A pressure support ventilation.

volumes, and shapes. To differentiate between a tidal volume can vary greatly depending on patient
combination mode and a support mode, look at the effort and lung physiology.
volume and pressure delivered. The amount of pressure Note that the patient has triggered each breath. The
displayed on the pressure scalar remains consistent ventilator used to generate the waveform in Figure 27-27
while there is a wide range of delivered volume. In this notifies the clinician of patient triggering by turning the
mode, the clinician sets an inspiratory pressure, but the flow scalar from green to pink upon initiation of the
FIGURE 27-28 A pressure control ventilation in which the patient is attempting to

trigger some of the pressure controlled breaths.
breath. PSV is patient triggered and pressure limited. is found, clinicians can try to improve synchrony by
The ventilator can be initiated by either a pressure or making ventilator changes.
a flow trigger. Figure 27-28 depicts pressure control ventilation.
The patient is attempting to trigger some of the pres-
• For the patient effort to be detected in pressure
sure controlled breaths. This patient has a significant
triggering, the patient must be able to decrease
amount of auto-PEEP (note the white arrows in the
the airway pressure from the end-expiratory level
flow scalar). As a result, the patient is having difficulty
to the predetermined negative pressure set on
triggering the ventilator (Servoi), which has a flow
the ventilator (pressure sensitivity).
trigger set as a parameter. The clinician is made aware
• Flow triggering is similar. The patient effort is
of that because the flow scalar on some of the breaths
detected by a flow change in the ventilator circuit
has turned from green to pink, indicating patient
beyond a predetermined parameter level set on
triggering. If the ventilator were set for pressure trigger-
the ventilator (flow sensitivity).
ing, this color change would be taking place in the
Triggering plays a large role in patient-ventilator pressure scalar when the patient initiated the breath.
synchrony. In addition to using a flow or pressure On the pressure scalar, the patient’s trigger attempts are
trigger, a patient can initiate a breath from the change both successful and failed at times.
in electrical activity of the diaphragm. Neurally adjusted
ventilatory assist (NAVA) applies pressure in proportion • In the first two breaths of the pressure graph,
to the strength of a diaphragmatic contraction. Inspira- the patient did not attempt to take a breath; the
tion is also terminated or cycled by a decrease in the breaths were mandatory breaths from the
electrical activity of the diaphragm.13 ventilator. There is no observable negative
Auto-PEEP can have a negative impact on trigger- deflection just prior to the mechanical breath,
ing. Patients must exert enough effort to first overcome which would indicate patient triggering. The
the auto-PEEP before they can change flow or pressure corresponding flow scalar for these two breaths
enough to trigger the ventilator. The amount of effort it did not turn pink, indicating no patient effort.
takes to overcome the auto-PEEP can be much greater • In the third breath on the pressure scalar, a blue
than the effort needed to trigger the ventilator.14,15 arrow points to a decrease in pressure that
In patients who are experiencing auto-PEEP, look reached baseline. This is a successful trigger by
for failed trigger attempts graphically. If this condition the patient. The effort was sufficient to decrease
the pressure enough to trigger the ventilator, patient. Leaks are common in mechanical ventilation.
even though the patient had to overcome the Depending on its cause and size, the leak can be rather
auto-PEEP. For the corresponding breath on the problematic in mechanical ventilation. In dealing with
flow scalar, the tracing changed from green to a leak, the first step is to identify the source and try to
pink, indicating a successful patient trigger. correct it. In some cases, the clinician is unable to
• In the fourth breath on the pressure scalar, a red completely correct the leak.
arrow points to a decrease in pressure that does Figure 27-30 demonstrates a pressure support
not reach baseline. This is a failed trigger waveform with a leak. In the first breath on the flow
attempt. The patient was unable to generate scalar, the yellow arrow indicates a normal PSV breath.
enough effort to overcome the auto-PEEP and The inspiratory portion of the breath is a normal
trigger the ventilator. In the corresponding decelerating waveform that comes all the way to the
breath in the flow scalar, there is no color baseline before the patient exhales. The second and the
change, indicating no registered effort by third breaths in the flow scalar, red arrows, show an
the patient. abnormal waveform. On both breaths, the inspiratory
portions begin to come toward the baseline, but,
Dyssynchrony caused from failed trigger attempts instead of going into exhalation, the tracing starts
can be very fatiguing for the patient. Clinicians can to travel upward again. The point at which the
adjust the sensitivity parameters to promote patient flow tracing turns upward and continues on is due
synchrony, but this can be a difficult task. A setting not to the leak.
sensitive enough can make the patient use considerable This pattern is echoed in the volume tracing. In the
muscle effort, whereas a setting that is too sensitive can first breath, the blue arrow shows a normal breath. The
cause autocycling3,10,14 (autotriggering), which occurs second and third breaths, however, do not have the
when the ventilator triggers a breath without a patient characteristic shape expected with a pressure support
effort.4 Autocycling can result from patient movement, breath (a triangle tipped to the right.) The white arrows
a leak in the system, water in the ventilator circuit, or point to the portion of the tracing that shows the leak.
cardiogenic occilations.10,13 Another common form of The tracing is showing that the volume delivered is not
trigger asynchrony is double triggering or breath returning to the baseline. Instead of the lungs filling
stacking. Double triggering happens when a patient has and the patient ending inspiration, thereby signaling
a continued inspiratory effort that causes a change in the ventilator to end inspiration, the volume continues
pressure or flow below the predetermined level that to be delivered and is lost to the leak.
triggers a second breath prior to the set time frame.10 The ventilator, of course, cannot tell the difference
Figure 27-29 is an example of autocycling due to a between an excessively long inspiration and a leak. If
leak in the system. The ventilator is cycling one breath the leak is large, it can cause dyssynchrony at times
after another without any delay or effort from the because the patient is unable to end inspiration. In
FIGURE 27-29 Autocycling due to a leak in the system.

Courtesy of Maquet. Inc.
FIGURE 27-30 A pressure support waveform with a leak.

support modes, ventilators have a built-in time clinician to decide when inspiration should end based
threshold for inspiration that tells them to stop on graphics in pressure support. In controlled modes,
inspiration for safety purposes. (In support modes, the the inspiratory time is already the limit; there is no
patient is in control of the entire breath cycle.) If a leak need for a further parameter control. Inspiratory
occurs in a support mode, the patient may not be able cycle off allows the clinician to end inspiration before
to control inspiration due to inadequate respiratory the leak.
muscle strength. Some ventilators also have a param- Figure 27-31 is another example of a leak. The
eter, called inspiratory cycle off, that allows the dotted yellow line shows where the leak is occurring.
FIGURE 27-31 A leak: The dotted yellow line shows where the leak is occurring.
FIGURE 27-32 A pressure support ventilation with a leak.

Figure 27-32 demonstrates a pressure support same leak. The drawn line through the breath shows
ventilation with a leak. The first breath in the flow the path the breath should have followed without the
scalar is a normal breath. The second breath is showing leak. This is also the path the breath will take once the
a leak. The yellow arrow points to where the leak is breath has been cycled off.
beginning and where the breath should be cycled off Figure 27-33 is a pressure support with the addi-
by the clinician, using the parameter inspiratory cycle tional setting page of the Servoi ventilator open. This
off. The third breath in the flow scalar also shows the patient had a leak that was treated by setting inspiratory
FIGURE 27-33 A pressure support with the additional setting page of the
Servoi ventilator open.
FIGURE 27-34 A pressure support breath being cycled off at 10% of

peak flow.
cycle off. In the first breath on the flow scalar, two the inspiratory cycle off is set. The inspiratory flow off
white arrows point out 100% of peak flow and base- allows the patient to begin exhalation, thereby improv-
line, or 0%, of peak flow. The goal of setting the ing synchrony. Figure 27-34 demonstrates a pressure
inspiratory cycle off is to set the terminal flow level support breath cycled off at 10% of peak flow.
higher than the leak in order to stop the extended Figure 27-35 shows a pressure support breath with
inspiratory time. The second breath of the flow scalar a leak. The breath is being cycled off at 60% using the
has a yellow arrow pointing to the 20% point, where inspiratory cycle off parameter. This is a large leak.
FIGURE 27-35 A pressure support breath with a leak.

FIGURE 27-36 A pressure support breath that has been cycled off at 60%
due to a large leak.
When patients have large leaks like this one, the inspiratory and expiratory phases that are connected
clinician must be aware that the patient is losing a lot but not related to time. The easiest way to interpret
of tidal volume. Every effort should be made to deter- loops is to become familiar with what the normal
mine where the leak is and, to the extent possible, loops look like for both types.
eliminate it.
Figure 27-36 shows a pressure support breath that
has been cycled off at 60% due to a large leak. The red PRESSURE-VOLUME LOOPS
shaded area approximates the volume being lost by Figure 27-38 demonstrates a normal pressure-volume
cycling this breath off so early in the inspiratory phase. loop in mechanical ventilation that traces changes
This volume would also be lost to some degree should in pressures and corresponding changes in volume.
the leak remain uncorrected. In addition, the patient Normal pressure-volume loops should sit at a
would have considerable dyssynchrony, and perhaps 45° angle within the two axes, the vertical axis being
discomfort, if such a large leak were left untreated. The volume and the horizontal being pressure. This loop
amount of loss to the leak can be calculated as follows: is often referred to as football shaped, but in reality it
rarely has equal or symmetrical halves for inspiration
leak percentage ⫽
and expiration. In this example, the upper half is
inspiratory volume ⫺ expiratory volume
____________________________________ expiration, and the lower half is inspiration.
⫻ 100
inspiratory volume Inspiration begins from the FRC level and termi-
nates when the preset parameter (volume or pressure)
is achieved. The tracing continues during expiration
Loops and returns to FRC at end of exhalation. Peak inspira-
Clinicians can use loops much as they use scalar tory pressure and delivered tidal volume are readily
waveforms. The patterns are recognizable and can aid obtained from the pressure-volume loop.16 The pattern
in diagnosing and trending changes in the patient’s is drawn counterclockwise with each breath. The points
lung characteristics. Two types of loops are discussed marked with 1 and 2 indicate the inflections during
here: a pressure-volume loop and a flow-volume loop inspiration (point 1) and exhalation (point 2) of this
(Figure 27-37). Both types of loops are made up of breath.
Constant Flow Decelerating Flow

FIGURE 27-37 Examples of loops.
E I
FIGURE 27-38 A normal pressure-volume loop in mechanical ventilation that traces

changes in pressures and corresponding changes in volume.
Historically, these inflection points have been can be used as a reference for overdistension
thought to represent the onset of recruitment of the (Figure 27-42). The idea is that the best compliance
alveoli during inspiration and the derecruitment of for a patient is between the two inflection points
alveoli during exhalation. More recently it has been and that ventilating the patient using pressures
found that recruitment can occur throughout infla- within the zone limited by the upper and lower
tion at a wide range of pressures.17 It is also thought inspiratory inflection points may prevent damage
that an upper inflection point during inspiration to the lung tissue.17,18
FIGURE 27-39 A volume-pressure loop with normal compliance.

FIGURE 27-40 A volume-pressure loop with very poor compliance, or

stiff lungs.
Using the pressure-volume loop to assess lung Figure 27-40 demonstrates a volume-pressure loop
compliance changes can be done relatively quickly and with very poor compliance, or stiff lungs. The typical
easily. Normally, the slope of the loop is 45º and is an result of stiff lungs is for the loop to shift to the right. If
indication of the patient’s lung compliance. The slope the patient had overly compliant lungs, the loop can
of the loop can change greatly as compliance increases tip from normal in the opposite direction (left) as
or decreases. well.16
Figure 27-39 demonstrtates a volume-pressure Airway resistance can also be detected using
loop with normal compliance. The loop is sitting at a pressure-volume loops. During pressure-regulated
45º angle and is football-shaped. modes of ventilation, the increased airway resistance
FIGURE 27-41 The pressure-volume loop is widened, FIGURE 27-42 A volume pressure loop that is showing
showing increased airway resistance. overdistension.
Courtesy of Maquet Inc. Courtesy of Maquet Inc.
causes flow rates to slow down and pressure to increase. beyond the plateau. This phenomenon is often referred
The slower flow rate causes the change in volume to be to as beaking because the graph shape resembles a
less in relation to the change in pressure, a phenomena bird’s beak.4,16
called hysteresis.16 In Figure 27-41, the pressure-volume Figure 27-43 represents the work of breathing in a
loop is widened due to increased airway resistance. positive pressure breath. The red area represents the
Higher pressures are reached with a comparatively work associated with overcoming the elastic resistance
small change in volume, and the controlled pressure of the lungs during inspiration. The crossed-hatched
remains constant until the end of inspiration. Inspira- area represents the work associated with overcoming
tory time may have to be increased in order to deliver airway resistance during exhalation.4,16 The sum of add-
the desired volume. ing both pieces of a breath together is the total amount
Figure 27-42 is a volume pressure loop that is of work associated with that breath. The work of
showing overdistension. The ventilator is continuing to breathing can be performed by the ventilator, by the
add pressure to the patient’s lungs without gaining patient, or by both.
significant added volume. The lungs are overdistended Figure 27-44 provides an example of a leak. The
and cannot accept any more gas volume. The cross- area denoted by the red marker (volume leaked)
hatched area graphically depicts the overdistension. indicates that the inspiratory and expiratory tidal
Increasing the pressure has no further volume benefit volumes are not equal.
FIGURE 27-43 The work of breathing in a positive pressure breath.

FIGURE 27-44 An example of a leak.

FLOW-VOLUME LOOPS on the patient’s tidal breathing. In addition, a mechan-

Figure 27-45 shows a normal flow-volume loop (FVL) ically ventilated patient is also breathing through an
of a mechanically ventilated breath. The shape of the ETT or tracheostomy, which creates far more airway
loop can look differently depending on the mode set resistance than a nonventilated patient has. This is why
on the ventilator and pressure-volume ventilation. the traditional ranges used for the classification of
Although this loop may look familiar—similar to mild, moderate, and severe obstruction in pulmonary
pulmonary function testing—the orientations of function testing do not correlate with mechanically
inspiration and expiration may be different depending ventilated patients’ loops.
on the equipment being used. Figure 27-46 demonstrates an abnormal FVL. In
There are other differences. In pulmonary function this example, the top half is representing inspiration
testing, the patient is breathing spontaneously and is while the bottom half is exhalation. The loop exhibits
asked to give a maximal inspiratory and expiratory flow limitation throughout both inspiration and exha-
effort (FVC) when creating an FVL. A ventilated patient lation, but the limitation is more prominent on
is unable to do this maneuver and generally exhales exhalation. The normal pattern for the expiratory flow
passively. In mechanical ventilation, the loop is based is linear, showing that the lung is reacting the same
FIGURE 27-45 A normal flow-volume loop (FVL) of a mechanically ventilated breath.

FIGURE 27-46 An abnormal FVL.

throughout (homogenous lung), during exhalation. to the exhaled gases being compressed in the patient’s
When lung disease is present, as in this example, there ventilator circuit. Arrow 2 points to air trapping, or
is a less linear tracing throughout exhalation, showing auto-PEEP, which is also common in COPD. Notice
that some areas of the lung behave differently than that the expiratory flow does not return to baseline.4,18
others during exhalation. This example is consistent In Figure 27-47, the patient is exhibiting auto-
with a diagnosis of COPD. Arrow 1 in the figure PEEP. Inspiration is beginning before exhalation is
shows a very high flow at the onset of exhalation due complete, as depicted by the arrow.
FIGURE 27-47 The patient is exhibiting auto-PEEP.

FIGURE 27-48 An example of a leak in the system.

Figure 27-48 is an example of a leak in the system. airway secretions and creating a lot of turbulence in the
On this ventilator, the inspiratory portion of the breath breath. In the second FVL, after the patient has been
is red, and the expiratory portion is blue. Notice how suctioned, there is much more laminar flow, which
the expiratory portion does not return to baseline at results in a smoother tracing. The pre- and post-FVL
the end the breath. The area traced in yellow is the lost technique is also used in mechanical ventilation to
volume from the leak. measure response to bronchodilators. The expectation
In Figure 27-49, the flow volume loops show a is to see a bigger loop, representing more volume
pre- and postrepresentation of the effect of suctioning. and improved peak flow following bronchodilator
In the first FVL, there is a lot of irritability in the tracing administration.
of the loop. This is the result of the gas flowing through
FIGURE 27-49 A pre- and postrepresentation of the effect of suctioning.

Summary 2. The scalar functions of the ventilator graphics

relate pressure, flow, and volume to what?
Currently available mechanical ventilators that are a. compliance
designed for use in critical care have ventilator graphic b. each other
displays (or at a minimum options to include ventila- c. time
tor graphics). Ventilator graphics have provided the d. mechanical and patient resistance
respiratory therapist with a clinically significant tool for
3. Resistance to flow in the lung is dependent on:
managing patient-ventilator interactions, monitoring
I. type of flow (turbulent or laminar).
pulmonary mechanics, and detecting clinically signifi-
II. airway diameter.
cant issues with the ventilator system.
III. types and distribution of tissue.
Mastering the interpretation of ventilator graphics
IV. gas viscosity.
can be challenging for the respiratory therapist, but
a. I and II
understanding ventilator graphics is an important
b. II and III
element in the improvement of patient care in critical
c. I, II, and IV
care and other patient care areas.
d. I and III
This chapter provides a fundamental approach to
understanding the information that ventilator graphics 4. TCT ⫽ Ti ⫹ Te:
provide and the analysis of that information. Some of a. only when Raw is low.
the commonly observed abnormal patterns have been b. True.
discussed in this chapter. However, not every clinical c. False.
situation and/or every available ventilator could be d. Only during low-volume ventilation.
included. Respiratory therapists are challenged to 5. If TCT ⫽ 5 seconds and Ti ⫽ 1.5 seconds, what
continue to improve their understanding and utilize does Te ⫽ ?
ventilator graphics as a tool to enhance patient care a. 1.5 seconds
and management of patient-ventilator interactions. b. 2.0 seconds
Follow-up suggested readings are included at the end c. 4.5 seconds
of the chapter, and manufacturers’ representatives and d. 3.5 seconds
Web sites can provide equipment-specific information. 6. In the previous question, what is the respiratory
Experienced colleagues can also be a valuable resource rate (RR)?
by sharing their accumulated knowledge. a. 12/minute
b. 10/minute
Study Questions c. 15/minute
d. Not enough data was given.
REVIEW QUESTIONS
7. In constant flow volume ventilation, the ventilator
1. List the three primary variables that are plotted graphic indicates which scalar form?
against time during mechanical ventilation. a. decelerating
2. Discuss the use of ventilator graphics in monitor- b. sinusoidal
ing changes in compliance. c. square
d. accelerating
3. Discuss the use of ventilator graphics in monitor-
ing changes in airway resistance. 8. During pressure ventilation, the initial flow _____
in a linear fashion to maintain the set pressure.
4. How is patient inspiratory effort observed on a
a. decelerates
ventilator graphic display during mechanical
b. remains constant
ventilation?
c. increases
5. Describe patient-ventilator dyssynchrony. d. varies in a sinusoidal manner
6. What is an inflection point? 9. Failure of the graphic to reach baseline at the end
of expiration may result from:
MULTIPLE-CHOICE QUESTIONS I. a small diameter ET tube.
1. Ventilator graphics can do all of the following except: II. kinked ventilator tubing.
a. provide information on ventilator-patient III. clogged expiratory filter(s).
interaction. IV. patient chewing on ET tube.
b. determine the patient’s clinical diagnosis. a. I, II, III, and IV
c. illustrate the patient-ventilator mechanics. b. II and III
d. present graphic interpretation triggering pres- c. I and III
sure, synchrony, and flow-volume relationships. d. II and IV
10. Failure to meet the patient’s inspiratory demand is 7. Shortall S, Oakes D. Practical uses of pressure
reflected in: control ventilation. Focus Journal for Respiratory Care
a. increased rise time. and Sleep Medicine. 2005;(2):64.
b. ventilator dyssynchrony. 8. Blanch L, Bernabe F, Lucangelo U. Measurement of
c. increased expiratory time (Te). air trapping, intrinsic positive expiratory pressure,
d. increased respiratory rate (RR). and dynamic hyperinflation in mechanically
11. Airway resistance (Raw) can be approximated by ventilated patients. Respir Care. 2005;50:110.
which formula? 9. Branson RD. Enhanced capabilities of current
a. plateau pressure (Pplat) – peak ICU ventilators: do they really benefit patients.
pressure (Ppeak) Respir Care. 1991;36:362.
b. Vt – Ppeak 10. Nilsestuen JO, Hargett KD. Using ventilator
c. peak flow (Fpeak) ⫼ Ppeak graphics to identify patient-ventilator asynchrony.
d. Ppeak – Pplat Respir Care. 2005;50:202.
11. Chatmongkolchart S, Williams P, Hess D, Kaczmarek
12. In a pressure-volume curve, the inspiratory portion R. Evaluations of inspiratory rise time and inspira-
of the curve moves: tion termination criteria in new generation
a. upward to the left. mechanical ventilators: a lung model study.
b. downward to the right. Respir Care. 2001;46:666.
c. upward to the right. 12. Holt T. Physics and physiology of ventilator
d. downward to the left. support. In: Scanlan CJ, Wilkins RL, Stoller JK, eds.
Egan’s Fundamentals of Respiratory Care. St. Louis,
CRITICAL-THINKING QUESTIONS MO: Mosby; 1999.
1. Using ventilator graphic displays, differentiate 13. Sinderby C, et al. Inspiratory muscle unloading by
between constant flow and constant pressure neurally adjusted ventilatory assist during maximal
ventilation. inspiratory efforts in healthy subjects. Chest.
2. How might inflection points be used to identify a 2007;131,3:711–717.
“safe” inspiratory pressure? 14. Hess D. Ventilator waveforms and physiology of
3. How might inflection points be used to set PEEP? pressure support ventilation. Respir Care.
4. How might a respiratory therapist use a ventilator 2005;50:166.
graphic display to observe a partially obstructed 15. Sasson CSH, Mahutte CK. What you need to know
endotracheal tube? about the ventilator in weaning. Respir Care.
5. How can ventilator graphics be used to detect 1995;40:249.
auto-PEEP? 16. Waugh JB, Deshpande VM, Harwood RJ. Rapid
6. How can ventilator graphics be used to detect a Interpretation of Ventilator Waveforms. Upper Saddle
leak in the ventilation system? River, NJ: Prentice Hall; 1999.
17. Hess D, Kaczmarek R. Advanced pulmonary
mechanics. In: Hess D, Kaczmarek R, eds. Essentials
References of Mechanical Ventilation. New York: McGraw Hill
1. Lucangelo U, Bernabe F, Blanch L. Respiratory Professional; 2002.
mechanics derived from signals in the ventilator 18. Chatburn RL. Fundamentals of mechanical ventila-
circuit. Respir Care. 2005;50:50. tion: a short course in the theory and application
2. Dhand R. Ventilator graphics and respiratory of mechanical ventilators. Cleveland Heights, OH:
mechanics in the patient with obstructive lung Mandu Press Ltd; 2003.
disease. Respir Care. 2005;50:246.
3. Nilsestuen JO, Hargett BS. Managing the patient-
ventilator system using graphic analysis: an over- Suggested Readings
view and introduction to graphics corner. Respir
Care. 1996;41:1105. Ouellet P. Waveform and Loop Analysis in Mechanical
4. Pilbeam SP, Cairo JM. Mechanical Ventilation: Ventilation. Solna, Sweden: Siemens-Elema; 1997.
Physiologic and Clinical Applications. 4th ed. Rittner F, Doring M. Curves and Loops in Mechanical
St. Louis, MO: Mosby; 2006. Ventilation. Telford, PA: Draeger Medical; 1996.
5. Rau JL. Inspiratory flow patterns: the shape of Waugh J, Deshpande V, Harwood R. Rapid Interpretation
ventilation. Respir Care. 1993;38:132. of Ventilator Waveforms. Upper Saddle River, NJ:
6. Pilbeam SP. Introductions to ventilators. In: Cairo Prentice Hall; 1999.
JM, Pilbeam SP, eds. Mosby’s respiratory care
equipment. St Louis, MO: Mosby; 1999.
CHAPTER 28
Noninvasive Mechanical Ventilation

Bethene L. Gregg
OBJECTIVES
• Describe the advantages of noninvasive positive pressure ventilation (NPPV).
• State which patients in acute respiratory failure may benefit the most from noninvasive positive pressure
ventilation according to the recommendations of the 2001 International Consensus Conferences in Inten-
sive Care Medicine: noninvasive positive pressure ventilation in acute respiratory failure and the 2009
42nd Respiratory Care Journal Conference Noninvasive ventilation in acute care: controversies and emerging
concepts, Parts I and II.
• Identify the advantages and disadvantages of using critical care versus home care positive pressure
ventilators for NPPV.
• Describe the patient interface for NPPV.
• Explain the function of the major settings on the ventilators discussed.
• Describe how pressure support may be cycled for some critical care ventilators.
• Describe a common complication of NPPV delivered via face mask.
• Explain when NPPV should be discontinued.
• List one advantage and one disadvantage of negative pressure ventilators.
CHAPTER OUTLINE
Noninvasive Positive Pressure Ventilation Ventilators Used
Indications for Use Acute Care Continuous Positive Airway Pressure Units
Contraindications Long-Term Use
Application Negative Pressure Ventilation
Initial Ventilator Settings Types
Monitoring Physiologic Effects
Complications Ventilators
Limitations Indications for Use
766
CHAPTER 28 ■ Noninvasive Mechanical Ventilation 767
KEY TERMS
castle port nasal mask shape signal
continuous positive airway negative pressure ventilation spontaneous mode
pressure (CPAP) (NPV) spontaneous or timed (S/T) mode
expiratory positive airway noninvasive positive pressure
pressure (EPAP) ventilation (NPPV)
extrathoracic oronasal mask
inspiratory positive airway pressure support (PS)
pressure (IPAP) rise time percentage
N
oninvasive mechanical ventilation includes bag-mask device, introduced by Chaussier in 1780. In
both positive and negative pressure ventila- 1887, Dr. George Fell applied a bellows ventilator using
tor applications that do not require the a face mask.7 Barach and associates pioneered the
placement of an endotracheal or tracheos- application of continuous positive airway pressure
tomy tube. Short-term noninvasive ventilatory support (CPAP) breathing, which was used as a method of
to treat acute respiratory failure in adults is discussed in delivering oxygen to pilots flying at high altitudes
this chapter. Long-term noninvasive ventilatory support during World War II. In the mid-1940s, V. Ray Bennett
in home care is also discussed briefly. expanded the clinical application of positive pressure
Noninvasive positive pressure ventilation breathing when he engineered a device to deliver
(NPPV) is a treatment for hypercapnic respiratory oxygen under pressure during inspiration via intermit-
failure in which the ventilator-patient interface is tent positive pressure breathing (IPPB).8 IPPB via face
typically a nasal mask or an oronasal mask (a mask mask was used extensively in the 1950s and 1960s to
that covers the nose and mouth). In negative pressure treat patients with acute respiratory failure (ARF).
ventilation (NPV), the ventilator is applied to the The successful use of NPPV was limited by technol-
thorax and abdomen or to the entire body from the ogy. The rubber face mask did not seal properly unless
neck down, and no ventilator apparatus is in contact applied with a great deal of pressure. Skin injury from
with the face. In both types of noninvasive ventilation, the mask was a common complication. Full-face
gas flows through the upper airway and into the lungs. masks, which were opaque, concealed the presence of
The purpose of noninvasive ventilation is to oral secretions or emesis. Aspiration was frequently
provide adequate gas exchange while avoiding the cited as a complication. Leaky IPPB devices used in the
complications associated with endotracheal intubation 1960s and 1970s did not function well. Interest in
and invasive ventilation. For example: NPPV declined in the late 1960s, when volume-cycled
ventilators became available and endotracheal tubes
• The incidence of ventilator-associated pneumo-
were improved.
nia is reduced with NPPV.1,2
After 20 years of use of volume-limited ventilators
• Nourdine and colleagues found that NPPV
and endotracheal tubes, NPPV was reconsidered as a way
reduced the risk of ventilator-associated pneu-
of treating ARF to avoid endotracheal intubation and its
monia and hospital-acquired infection when
associated complications and costs. Pressure support
compared with intubated ventilation, regardless
(PS) and pressure control ventilation available on the
of the severity of illness.2,3
Siemens Servo 900C (Siemens Medical Systems, Inc.,
• Noninvasive ventilation also eliminates the
Danvers, Massachusetts) renewed interest in the applica-
problems associated with an increased work of
tion of pressure ventilation. (In pressure support,
breathing through an endotracheal tube that
exhalation starts when the patient’s airway pressure
may prolong the weaning process.4–6
approaches the inspiratory target pressure, causing a
decrease in inspiratory flow to the patient. When the flow
Noninvasive Positive Pressure drops to the cycle threshold, inspiration ends.) The use of
mask CPAP to treat obstructive sleep apnea prompted the
Ventilation design of better masks and CPAP devices. Noninvasive
Noninvasive positive pressure ventilation (NPPV) dates positive pressure ventilation found increased use in
to the first reports of mouth-to-mouth resuscitation. home care to support ventilator-dependent individuals.
Successful use of it in the mid-1700s led to the first In the 1980s, there were numerous clinical studies in the
use of pressure support applied by face mask or nasal In one study, patients treated successfully with
mask to treat ARF. NPPV had a higher level of consciousness (LOC)
During the 1990s, the efficacy of NPPV in treating initially and improved LOC, PaCO2, and pH values after
ARF was well established, particularly for patients 1 hour.12 Results from numerous clinical studies indicate
with acute exacerbation of COPD. In 1996 the that intubation can be avoided in 50–75% of patients in
American Association for Respiratory Care (AARC), acute ventilatory failure supported with NPPV. Postextu-
the American Respiratory Care Foundation, and the bation application of NPPV also has been successful in
Respiratory Care Journal convened the Consensus avoiding reintubation, especially in COPD patients with
Conference on Noninvasive Positive Pressure Ventila- hypercapnic respiratory insufficiency.13,14 For patients
tion (AARC Consensus Conference) to clarify termi- with neuromuscular disease, NPPV has been effective
nology and describe the appropriate application of when swallowing was not severely impaired and assisted
NPPV in various clinical settings.9 Then, in 1997, the cough flows were greater than 160 Lpm.15 There is also
federal government effectively curtailed the use of substantial evidence that CPAP and NPPV improve
long-term NPPV in the United States through the physiologic variables and reduce the intubation rate for
Balanced Budget Act (BBA), which redefined which patients with acute cardiogenic pulmonary edema.16,17
health care costs are covered by Medicare (discussed However, there is little evidence that NPPV is superior to
later in this chapter). CPAP in terms of intubation rate or mortality for these
patients.18 There is enough evidence to recommend a
trial of NPPV in immunocompromised patients with
INDICATIONS FOR USE IN ACUTE CARE ARF and bilateral pulmonary infiltrates.11
In cases of acute respiratory failure, NPPV provides Evidence does not support the use of NPPV when
adequate gas exchange and decreased respiratory refractory hypoxemia is the primary cause of respiratory
muscle work without the need for an endotracheal tube failure, as in acute respiratory distress syndrome
or when intubation is undesirable. When applied (ARDS).11 There is also inadequate evidence to support
properly, NPPV of patients with acute exacerbation of the routine use of NPPV for patients with community-
COPD reduces mortality and length of intensive care acquired pneumonia, asthma, or blunt chest trauma.19,20
stay.10 NPPV also reduces the intubation rate in patients
with more severe COPD exacerbations.11 The successful CONTRAINDICATIONS
application of NPPV requires the patient to be able to
clear secretions effectively. Absolute contraindications for NPPV are listed in
A trial of NPPV is indicated for patients with Table 28-1. Noninvasive ventilation is contraindicated
COPD when they fail to respond to standard medical for respiratory arrest and circulatory collapse. Signs of
care. According to the AARC Consensus Conference, imminent respiratory arrest include altered level of
NPPV is indicated when at least two of the following consciousness, the presence of respiratory muscle
criteria are present: fatigue, obvious exhaustion, quiet chest. diaphoresis,
and hemodynamic instability (systolic BP 90 mm Hg).
• Respiratory distress with moderate to severe Such patients require endotracheal intubation.21
dyspnea, use of accessory muscles, and abdomi- Relative contraindications that may lead to unsuc-
nal paradox cessful NPPV are also listed in Table 28-1. Additional
• pH 7.35 with PaCO2 45 mm Hg factors that reduce the chance of successful NPPV are
• A respiratory rate 25 bpm excessive secretions and a high acute physiologic and
TABLE 28-1 Absolute and relative contraindications for noninvasive

positive pressure ventilation
Absolute Contraindications Relative Contraindications
Facial burns, facial or skull trauma Altered level of consciousness
Hemodynamic instability ARDS
Need for airway protection—vomiting, etc. Excessive secretions
Respiratory arrest (need for immediate intubation) Extreme anxiety
Uncooperative patient Massive obesity
Source: From Bach JR. Consensus statement: noninvasive positive pressure ventilation. Paper presented at the Consensus Conference IV: Noninvasive Positive
Pressure Ventilation. Vail, Colorado; 1997
chronic health evaluation (APACHE) score.9 The • The patient interface for short-term NPPV is a
APACHE score, comprised of physiologic variables, is nasal mask (Figure 28-1) or an oronasal mask
used to estimate the probability of hospital mortality (Figure 28-2), held in place by head straps.
for adult ICU admissions. Oronasal masks specifically designed for NPPV
are more effective than face masks used with
manual resuscitators.
APPLICATION • Full-face masks (Figure 28-3) are also an
The application of NPPV requires a ventilator, an option.
appropriate circuit, and a patient interface. • The helmet (Figure 28-4) is an option.22,23
(C)
FIGURE 28-1 Nasal masks: Text not available due to copyright restrictions Text not available due to copyright restrictions
(C) FlexiFit 405 Nasal Mask (Used withTMpermission Fisher and Paykel).
(E) Comfort Gel (Courtesy of Philips Respironics). (F) Comfort Curve (Courtesy of Philips
Respironics). (G) Comfort Fusion (Courtesy of Philips Respironics). (H) Comfort Lite 2 (Courtesy of Philips
Respironics). (I) Simplicity (Courtesy of Philips Respironics). (continues)
(E) (F) (G)
(H) (I)
• Nasal pillows (Figure 28-5), a lip seal, or a is flow or time triggered, pressure limited, and flow
mouthpiece (Figure 28-6) are more commonly or timed cycled. IPAP and EPAP are modes on the
used for nocturnal or long-term NPPV. BiPAP and Vision ventilatory support devices (Philips
Respironics Inc., Murrysville, Pennsylvania). Home
The wide variety of patient interfaces currently avail- care ventilators may be indicated if the patient requires
able increase the likelihood of achieving effective higher pressures or volume control ventilation.25
NPPV.24 Critical care ventilators are also commonly used to
Ventilators specifically designed for NPPV provide deliver short-term NPPV in the emergency department
inspiratory positive airway pressure (IPAP) and or intensive care unit, and they usually work best with
expiratory positive airway pressure (EPAP). IPAP oronasal masks.
(C)
(D) (E)
FIGURE 28-2 Oronasal masks: Text not available due to copyright restrictions
Text not available due to copyright restrictions (C) Disposable 6500 Tri-Glide (Courtesy of Hans Rudolph, Inc).
(D) FormaTM Full Face Mask (Fisher and Paykel). (E) ComfortFull (Courtesy of Philips Respironics).
Fitting the Mask. Successful NPPV depends on the provided there is no excessive leak at the mouth or
selection of the proper interface as much as it does on partial obstruction of the nasopharynx. A chinstrap
the appropriate ventilator settings.26 If the mask is too may keep the mouth closed sufficiently. Nasal polyps
uncomfortable, the patient does not tolerate NPPV. or a deviated septum may increase upper airway
Masks that are sized and positioned well do not need resistance and patient discomfort with nasal masks.
to be strapped on too tightly for patient comfort.10 The The goal is to get patients accustomed to wearing a
clinician should be able to slide two fingers under the mask that is blowing air into their nose or face while
straps of the head harness for an appropriate fit. Overly they are deciding on the proper mask size. For exam-
tight masks are likely to cause skin abrasions. Nasal ple, using ventilator settings of 8 cm H2O of IPAP and
masks may be better tolerated than full-face masks, 0 cm H2O of EPAP, hold the mask in place to assess
Best Practice
Mask Fit
To prevent leaks, having the nasal mask a little
too small is better than having one that is
too large.
Reducing Patient Anxiety
The indications for NPPV use are based on
clinical studies of elderly patients with chronic
lung disease. Chronic dyspnea and past experi-
ences with face masks may predispose some
patients to feel extremely anxious when masks
FIGURE 28-3 Full-face masks: FitLife Total Face Mask. are applied. Reassurance and encouragement
Courtesy of Philips Respironics are key factors that influence patient tolerance
of mask ventilation.
the fit.27 The top of a mask should fit halfway down the
bridge of the nose to prevent excessive leaks or damage
to the eyes. Nasal masks should be large enough to
barely clear the sides of the nose. Figure 28-7 shows the
use of a nasal mask gauge to size Philips Respironics
nasal masks. Mask-size cutouts are also included as part
of the mask packaging. In Figure 28-7 the medium-
wide size barely clears the sides of the nose at (A) but
may extend too high up the bridge of the nose (B). In
this example, if a medium-wide mask is used, the leak
at the top of the mask might be excessive. A nasal mask
that is too small is better than one that is too large. A
variety of mask styles should be available to increase
the likelihood of finding a mask that seals properly. A
synthetic covering, such as Duoderm (Bristol-Myers
Squibb, New York, New York), may be applied over the
bridge of the nose to prevent skin damage.
INITIAL VENTILATOR SETTINGS

Initial ventilator settings depend on whether volume or
pressure ventilation is used and on the type of ventila-
tor. With ventilators specifically designed for NPPV that
provide pressure support with positive end-expiratory
pressure (PEEP), inspiratory pressures are increased as
needed to achieve a respiratory frequency of less than
25 bpm and a tidal volume of 6–7 mL/kg body weight.
FIGURE 28-4 StarMed Castar R helmet. Inspiratory pressures over 20 cm H2O may be required
Courtesy of STARMED SpA but result in a greater leak.6,28

(D)
(E) (F)
FIGURE 28-5 Nasal pillows: Text not available due to copyright restrictions
Text not available due to copyright restrictions (D) OpusTM 360 Nasal Pillows Mask (Courtesy of
Fisher and Paykel). (E) OptiLife (Courtesy of Philips Respironics). (F) ComfortLite 2 (Courtesy of Philips
Respironics).
in reducing air trapping, which may be considerable in

COPD patients. However, higher EPAP pressures may
create more of a leak around the mask.
Most devices designed specifically for NPPV are
blower driven; so if supplemental oxygen is required, it
must be added. Oxygen is added to a mask port or
placed in-line between the exhalation port and the
mask. The delivered oxygen concentration vary with
the oxygen liter flow, the pressure gradient, and the
EPAP level.29 In addition, when oxygen is added to the
ventilator outlet, oxygen concentrations may be higher
FIGURE 28-6 Oral interfaces: Oracle Oral Mask. at the outlet than at the mask port.30 However, oxygen
Fisher and Paykel added to the ventilator outlet is close to the blower
intake and constitutes a fire hazard. Oxygen should be
added as described in the ventilator’s operation
manual. The BiPAP Vision (Philips Respironics) can
deliver set oxygen concentrations when connected to a
50-psig oxygen source.
NPPV should not be given continuously. Most
patients respond within 1–2 hours, but some may take
up to 20 hours. After the patient has been stabilized,
NPPV should be interrupted and the mask should be
removed for rest periods of 10–15 minutes.9 If NPPV is
initiated in the emergency department and the patient
stabilizes, consider transporting the patient to the ICU
on oxygen alone. Reestablish NPPV and reduce the

time of ventilation as tolerated with the same amount
of rest time. One of the advantages of NPPV is that the
patient knows it can be interrupted periodically.
Aerosol therapy may be given in-line with various
FIGURE 28-7 A nasal mask gauge may be used to deter- pressure support units. The BiPAP manual recommends
mine the proper size of a nasal mask. In this example,
the medium-wide size barely clears the sides of the nose
at (A) but may extend up too high on the bridge of the
nose (B).
Best Practice
Inspiratory Airway Pressure
Expiratory pressures are generally 4–8 cm H2O. Airway pressures greater than 20 cm H2O may be
The risk of rebreathing at EPAP levels is reduced at least required but may create a greater leak. If higher
4 cm H2O. Although some rebreathing occurs, it may pressures are needed, check that the mask is the
not be as clinically important, given the flow delivery appropriate size.
systems of current ventilators designed for NPPV.
Rebreathing may be more of a problem with oronasal
masks. Check that the exhalation port in the circuit is
not blocked. In most cases, the circuit must be specified
by the ventilator manufacturer.
When pressure support and CPAP are being
Best Practice
compared with bilevel ventilation, pressure support
corresponds to the difference in pressure between IPAP Expiratory Pressure
and EPAP, or the pressure gradient. To increase the tidal An EPAP pressure of at least 4 cm H2O reduces
ventilation, increase the pressure gradient by increasing the amount of rebreathing. Higher tidal volumes
the IPAP pressure. An increase in the EPAP level may require a higher level of EPAP to reduce
without the same adjustment in IPAP reduces the rebreathing. Do not block the exhalation port,
pressure gradient and, as a consequence, reduces the and direct it away from the patient’s face.
tidal volume. Expiratory pressures of 4–8 cm H2O help
adding the nebulizer between the mask and exhalation of patient comfort falls to the nursing staff. All person-
port.31 There should be a main-flow bacteria filter at nel involved in providing NPPV must be trained in the
the ventilator outlet. A mouthpiece is recommended in goals, techniques, complications, and patient comfort
place of the mask for the duration of the treatment. An aspects of NPPV.
adapter for a metered-dose inhaler can also be added
to the circuit. If the patient is stable, NPPV may be
interrupted for the treatment. COMPLICATIONS
Many of the problems encountered with NPPV are
related to improper mask fit. A mask strapped on too
MONITORING tightly for prolonged periods damages the skin.
Noninvasive ventilatory support requires attentive Conjunctivitis may occur if the mask rides too high on
monitoring of the patient’s initial response and the bridge of the nose or is loose and slips out of
comfort. position.33 Excessive leaking leads to patient-ventilator
dyssynchrony and inadequate tidal volumes.34 Progres-
• Assess clinical signs of the patient’s work of
sive hypercapnia is a reason to terminate NPPV and
breathing for improvement: reduced use of
intubate. Masks that reduce most complications if they
accessory muscles, respiratory rate 25 bpm,
are fitted properly are available. For example, the
and reduced distress.
Profile mask by Philips Respironics has a gel cushion
• Patient-ventilator asynchrony may be difficult to
that conforms to the contours of the face.
detect with a ventilator that does not display
The second most common problem associated
pressure, flow, and volume waveforms.
with NPPV is patient intolerance. Several types of
• Titrate inspiratory pressures or volumes accord-
patient interfaces should be available to increase the
ing to arterial blood gases.
likelihood of finding one that the patient can tolerate.
• The estimated tidal volumes displayed on
The sensation of relatively high flow rates applied
pressure support devices may be more than
200 mL less than actual volumes but are useful
for trending purposes.32
• After establishing adequate ventilation, titrate
oxygen flow rate to achieve pulse oximeter
Best Practice
saturations over 90%.
Personnel
Patients require continued coaching and reassur-
ance during NPPV. If respiratory care staffing dictates All personnel involved in providing NPPV must
only periodic checks after initial stabilization, the task be trained in the goals, techniques, complica-
tions, and patient comfort aspects of NPPV. Key
personnel should be included in the training
program and in establishing a protocol for the
Best Practice initiation and management of NPPV.
Pressure Gradient
The pressure gradient between IPAP and EPAP
determines the tidal volume. If EPAP is increased, Spotlight
increase the IPAP by the same amount. On
The Profile Lite
The Profile Lite nasal mask (Philips Respironics
Best Practice Inc.) has a gel cushion that can be formed to fit
the contour of the patient’s face. The mask is
submerged in boiling water for 4 minutes and
Oxygen Hazard then cooled in cold water for 10 seconds. The
Oxygen added to the ventilator outlet is close mask is then attached to the spacer and head-
to the blower intake and is a fire hazard. Add gear, and it is worn for 5 minutes to allow time
oxygen as described in the ventilator’s operation for the gel cushion to conform to the face. The
manual to either a mask port or placed in-line mask retains its shape when removed and can be
between the exhalation port and the mask. reshaped by repeating the process.
nasally may be too uncomfortable. Ventilators that

allow the adjustment of the initial flow rate with a rise CASE STUDY 28-1
time percentage control may increase comfort. Nasal
or oral dryness may also contribute to discomfort and I. O., a 64-year-old man with COPD, is treated
can be alleviated by adding a heated passover-type in the emergency department for respiratory
humidifier. distress. His initial blood gas values are pH
7.30, PaCO2 63 mm Hg, PaO2 52 mm Hg, SpO2
86%, and HCO3– 29 mEq/L. He receives
LIMITATIONS standard medical care, including inhaled
Rebreathing of carbon dioxide (CO2) has been bronchodilators, oxygen, antibiotics, systemic
reported to increase frequency, minute volume, and the corticosteroids, intravenous aminophylline, and
work of breathing by 50%.35 Use of a nonrebreathing diuretics. After 20 minutes on 2-Lpm oxygen via
exhalation valve increases the time required for flow to nasal cannula, his blood gas values are pH 7.29,
reach peak value and increases resistance during PaCO2 67 mm Hg, PaO2 56 mm Hg, and SpO2
exhalation.36 Increased resistance also decreases tidal 88%. His respiratory rate has dropped from 34
volume. Ferguson and Gilmartin (1995) found that the to 31 bpm.
Sanders NRV-2 nonrebreather valve or the Plateau
Exhalation Valve, both from Philips Respironics, with Questions
the BiPAP prevented exhaled CO2 from entering the 1. Why is this patient a candidate for a trial of
ventilator circuit when compared to the fixed-resistance NPPV?
exhalation port of the Whisper-Swivel. They found 2. What initial settings would be used on the
that, with the Whisper-Swivel, an EPAP level of 8 cm BiPAP S/T?
H2O was needed to prevent rebreathing when an IPAP 3. How is the tidal volume adjusted after the
of 20 cm H2O provided tidal volumes of approximately patient accepts the mask and it is strapped
1200 mL. Eight cm H2O of EPAP provided enough flow in place?
to flush the exhaled volume out the exhalation port
(Figure 28-8).37 High EPAP may increase the leak 4. Where should oxygen be added and
around the mask to an unacceptable level. Some how much?
ventilatory support devices are not compatible with a
nonrebreathing exhalation valve. The additional flow
required to maintain expiratory pressures favors the use
of at least 4 cm H2O EPAP to reduce rebreathing.
FIGURE 28-8 The flow rate required to maintain EPAP (A) is equal to or greater than the patient’s exhaled flow
rate (B), CO2 is flushed from the circuit through the exhalation port (C).
Modified from the Vision Clinic Manual. Courtesy of Philips Respironics Inc., Pittsburgh, Pa.
The primary disadvantage of critical care ventilators

CASE STUDY 28-2 in the past was that few were designed to function in
the presence of a leak. Several critical care ventilators
M. C., a patient treated in the emergency depart- now have a mask or noninvasive option. For most
ment for acute exacerbation of COPD, is now in critical care ventilators, a pressure-supported inspira-
stable condition on nasal mask NPPV. She is tion ends when the flow falls to a specific threshold,
going to be transferred to the respiratory inten- usually 5 Lpm or 25% of the peak flow achieved during
sive care unit (RICU). inspiration.
In NPPV a leak at the mask may exceed the flow
Questions cycle threshold of pressure-supported breaths and
1. How should the patient be transferred to prolong inspiration. Prolonged inspirations unrespon-
the RICU? sive to the patient’s breathing pattern promote asyn-
2. What are now important factors for this chrony and reduce patient tolerance of NPPV. Several
patient on NPPV? critical care ventilators have an adjustable flow cycle
threshold for pressure-supported breaths. The expira-
tory sensitivity percentage (Esens %) on the Puritan
Bennett 840 (Nellcor Puritan Bennett LLC) and the
inspiratory cycle off on the Servoi (Maquet, Bridge-
Best Practice water, New Jersey) allows the clinician to adjust the
terminal flow rate to a value greater than the leak
Setting the bpm Rate for flow rate.
Pressure-Supported Breaths For ventilators lacking an expiratory sensitivity
adjustment, the pressure control mode may be used
For Servo 300A ventilators that limit the time of with a set inspiratory time of less than 1 second. The
a pressure-supported breath to 80% of the total inspiratory time should be adjusted to match the
cycle time (TCT), use the following formula to patient’s breathing pattern. In addition, some critical
determine the breaths per minute rate to set: care ventilators, such as the Servo 300A, limit the
Desired TI/0.8 TCT duration of a pressure-supported breath to 80% of the
60/tct bpm setting total cycle time. The total cycle time is the period of
For example, start with a desired inspiratory time time equal to 60 over the set breaths per minute. The
of 1.2 seconds. The formula becomes 1.2 0.8 breaths per minute control can be adjusted to time-
1.5 and 60 1.5 40 bpm. The rate should cycle a pressure-supported breath in synchrony with
be set on 40 bpm to time cycle pressure- the patient’s breathing pattern.
supported breaths after 1.2 seconds. Time cycle Home care ventilators are traditionally volume
a pressure-supported breath if the leak is too controlled. Larger tidal volumes can generally compen-
much and the inspiratory cycle off threshold sate for the leak with NPPV. Slow responding pressure
cannot be adjusted high enough. triggers on these ventilators make them better suited for
patients with neuromuscular disease who tolerate
time-triggered inspirations. The fixed inspiratory flow
pattern delivered by most home care ventilators may not
VENTILATORS USED meet the inspiratory flow required by patients in acute
Critical care and home care ventilators have been used respiratory failure who have a high respiratory rate.
to provide NPPV, in either pressure control or volume Patient-triggered breaths should be monitored
control mode. Some ventilators are designed specifi- closely because the presence of a leak affects the
cally for NPPV that provide pressure support or pres-
sure control and PEEP.
Advantages of critical care ventilators are:
Best Practice
• The delivery of a precise oxygen concentration.
• Greater flexibility in modifying the breathing
pattern. Mask Leaks
• Graphic display of waveforms. Mask ventilation in volume control may require
• More accurate monitors. larger tidal volumes to compensate for the leak.
• Extensive alarm systems. The leak may also compromise the patient’s
• An exhalation valve to prevent rebreathing of ability to trigger breaths.
expired CO2.
ventilator’s sensitivity to the patient’s inspiratory

efforts. Pressure-triggered breaths are more difficult to
initiate. The use of a flow trigger may result in autotrig-
gering. In either case, ventilator-patient asynchrony
may increase the patient’s work of breathing and
reduce patient tolerance of mask ventilation.
Pressure ventilation, sometimes referred to as bilevel
ventilation in NPPV, usually means providing pressure
support or pressure control and PEEP. BiLevel (a trade-
mark mode for the Puritan Bennett 840) is basically two
levels of CPAP called High PEEP and Low PEEP. An
active exhalation valve in BiLevel allows spontaneous
breathing at either level of pressure. Spontaneous
breaths are also pressure supported. The breathing time
allowed at each pressure level is adjustable, and the
changeover from one level of pressure to the other is
synchronized with the patient’s inspiratory effort. FIGURE 28-9 Pressure-time and flow-time waveforms as
In general, most pressure ventilators designed the rise time percentage is increased: The peak flow
specifically for NPPV are similar in design. decreases as the rise time percentage increases. The
front edge of the pressure-time waveform rounds off as
• They are electrically powered, blower driven, more inspiratory time is taken to reach the pressure limit.
microprocessor controlled, flow triggered,
pressure limited, and flow cycled.
• Internal components consist of a blower, flow
sensor, pressure-regulating valve, and pressure intentional leak out of the exhalation port during the
transducer. initial setup and performance check. When the baseline
• Controls allow the selection of the mode, the leak is established, additional leak at the mask can be
inspiratory and expiratory pressures, breaths per recognized and compensated for by adjusting flow to
minute, and inspiratory time percentage. maintain the preset pressure limits. Many ventilator
• Some ventilators include a rise time percentage circuits do not include a standard exhalation valve.
control that allows a gradual increase to the set Exhalation is a function of the size of the leak in the
pressure limit, thereby reducing the initial blast circuit’s exhalation port at the patient interface. As
of flow. Pressure and flow waveforms in Fig- noted, rebreathing is possible and could prevent
ure 28-9 illustrate the effect of increasing rise adequate alveolar ventilation if EPAP levels of 4 cm
time percentages. Reducing the initial blast of H2O are used. Long inspiratory times, low inspiratory
flow increases patient comfort but may also pressures, or large tidal volumes tend to increase the
reduce the tidal volume for any given level of level of CO2 rebreathing. In these cases, Philips Respi-
pressure support or control. Rise time percentage ronics recommends the use of the Plateau Exhalation
is available for both pressure support and Valve instead of the Whisper Swivel to reduce the level
pressure control breaths on most ventilators. of CO2 rebreathing for their ventilators. Both the
Whisper Swivel II and the Plateau Exhalation Valve are
Most units use continuous flow from the blower to reusable; the castle port comes with the disposable
control inspiratory and expiratory pressures. The circuit. All BiPAP circuits must have one of these three
ventilator’s microprocessor measures the known or types of exhalation devices.
BiPAP. The BiPAP S/T-D (Philips Respironics) has

IPAP, EPAP, spontaneous mode, spontaneous or
Best Practice timed (S/T) mode, and timed modes. When either the
IPAP or EPAP mode is selected, the patient is receiving
CPAP. In spontaneous mode, the IPAP setting should
Increasing Rise Time be set higher than the EPAP pressure level or PEEP. The
Increasing the rise time percentage may make initiation of inspiration depends on the patient’s
inspiration more comfortable but could reduce respiratory effort. The patient triggers inspiration when
tidal volume. A long rise time may lead to the flow sensor measures an increase in flow of 40 mL
patient-ventilator dyssynchrony. per second over the leak flow for 30 ms. The minimum
IPAP time is 180 ms. After 180 ms have elapsed, the
unit flow cycles when the inspiratory flow equals the

leak flow.31 Best Practice
In S/T mode, a breaths-per-minute rate may be set
to ensure time-triggered breaths in addition to setting Inspiratory Flow
the IPAP and EPAP pressure levels. The patient is still
Inspirations are flow triggered and flow cycled
able to trigger inspiration. In timed mode, the addition
when using the BiPAP ventilator in the spontane-
of the inspiratory time percentage control is added to
ous mode. To flow-trigger a breath, the patient’s
determine the length of time that the IPAP pressure is
inspiratory effort must increase the flow by
applied. The patient’s respiratory efforts cannot influ-
40 mL per second over the leak flow for 30 ms.
ence a changeover in the inspiratory or expiratory
The unit flow cycles when the inspiratory flow
phase in the timed mode.
equals the leak flow after 180 ms have elapsed.
The monitor on the detachable control panel
allows selection of IPAP, EPAP, estimated tidal volume
(VT in milliliters), or estimated leak (Lpm) for the LED
display. A similar control panel is located under the
• Set the IPAP at 8 cm H2O and the EPAP at 5 cm
back cover of the unit. In the estimated VT position, the
H2O and wait for 5 seconds.
display flashes when the tidal volume is inaccurate
• The Vest (estimated leak) display should be
because the estimated leak has changed by 15 Lpm.
20 Lpm or less.
• A display of “000” indicates that there has not
Also check the APM by creating each of the alarm
been a change in flow for 20 seconds.
conditions and checking for alarm activation.
• When less than 1.0 cm H2O is sensed by the
pressure transducer, “OFL” is displayed in any of
BiPAP Vision. Philips Respironics also makes the
the selected positions.
BiPAP Vision with CPAP and S/T modes.
The battery-powered airway pressure monitor (APM) In the S/T mode, a rate of 4–40 bpm may be set for
should be turned on whenever the unit is on. The time-triggered inspirations. In clinical practice, a set rate of
Inadvertent Off alarm activates if the APM is not turned 10 bpm is appropriate for most adults because the patient
on and the airway pressure is over 5 cm H2O. There are should trigger inspiration. The inspiratory time control
also adjustable high- and low-airway-pressure alarms. determines the duration of inspiration or cycle time for
timed-triggered, pressure control breaths. The patient
• The low-airway-pressure alarm activates if the
triggers and cycles inspiration as long as the respiratory
airway pressure does not exceed the alarm setting
rate is greater than the breaths per minute control setting.
within the adjustable delay time.
The user interface is as follows:
• The audible low-pressure-alarm can be silenced
for either 20 or 60 seconds. The silence time is • A liquid crystal control panel displays wave-
set by a switch located inside the device. forms, patient settings, FIO2, and alarm values.
• A Replace Battery alarm warns when the batteries • Four hard keys change the main screen to display
to the APM need replacing. monitoring, parameters, mode, or alarms values.
• The monitoring screen displays the current
To check the operation of the BiPAP before use:
operating mode, parameters, and waveforms for
• Connect the circuit without the mask attached. pressure, flow, and volume.
• Completely block the tubing outlet without • The main screen automatically returns to the mon-
blocking the exhalation port. itoring view if no key is pressed for 3 minutes.
Best Practice
Reducing CO2 Rebreathing Best Practice
Long inspiratory times, low inspiratory pres-
sures, or large tidal volumes tend to increase the
Verifying BiPAP Performance
level of CO2 rebreathing. In these cases, Philips The performance verification of the BiPAP is a
Respironics recommends the use of the Plateau check of the estimated leak. Block the circuit
Exhalation Valve instead of the Whisper Swivel outlet, and set the IPAP on 8 cm H2O and the
to reduce the level of CO2 rebreathing for its EPAP on 5 cm H2O. The estimated leak dis-
ventilators. played should be 20 Lpm or less.
• Ventilator settings are adjusted by pressing the PREESURE

parameter hard key.
IPAP
• The parameter screen displays the selected
settings by pressing the soft key next to the
displayed variable. The selected value can then
be adjusted by turning a knob. Each click of the
EPAP
knob changes the value by 1, regardless of the
variable.
• The same process applies for changing the mode FLOW
and alarm values. Cycle to EPAP
The BiPAP Vision can respond to changes in Crossover Point
unintentional leaks at the patient interface by auto-
Shape Signal
matically adjusting its trigger and cycle criteria.
Unintentional leaks are recognized as a change in the
expiratory flow rate at 5 seconds or as the difference Estimated
between inspiratory and expiratory tidal volumes. In Patient Flow
either case, the baseline flow rate previously allowed
for the intentional leak through the exhalation port is
reset to include the flow from the unintentional leak.
Intentional leak may also be manually reset by press-
ing Learn Base Flow. Learn Base (baseline) Flow
should be pressed whenever gas flow from an external Trigger to IPAP
Crossover Point
source is added to the circuit, for example, to power an
inline medication nebulizer.
FIGURE 28-10 Inspiration is triggered and cycled when the
The trigger on the BiPAP Vision is either a 6-mL actual flow pattern crosses the delayed flow pattern.
volume trigger or a shape signal. The shape signal is Courtesy of Philips Respironics
described as a graphic representation of the patient’s
actual flow pattern that is delayed by 300 ms and
reduced by 15 Lpm (Figure 28-10). When the patient’s The performance verification of the Vision includes
actual flow signal crosses the shape signal: a check of the battery-powered Ventilator Inoperative
alarm, exhalation port test, mode function, and alarms.
• Inspiration begins. (The shape signal is
When the Vision is powered on, a 60-second self-test is
sensitive to changing ventilatory patterns and
initiated. The setup screen then displays the soft key to
circuit leaks.)
run the exhalation port test. With the circuit connected
• The shape signal can also cycle spontaneous
and the circuit outlet occluded, start the test. The
breaths.
exhalation port test allows the unit to measure the leak
Inspiration ends when the patient’s: at the exhalation port over the complete pressure range.
This intentional leak information is stored in memory
• Inspiratory flow falls to 75% of the peak flow
and used in leak calculations and in estimating the
achieved during inspiration (spontaneous
displayed tidal volume. If the exhalation port test is
expiratory threshold).
performed, the Patient’s Leak % is displayed next to the
• Inspiratory time exceeds 3 seconds.
minute ventilation. If the circuit is connected to the
• Or the flow toward the end of inspiration
patient without running the exhalation port test, the
suddenly increases (flow reversal).
Total Leak % is displayed. After the leak test is com-
A rise time control can be set at either 0.05, 0.1, plete, press the monitoring hard key to begin operation
0.2, or 0.4 second. Increasing the rise time lengthens with the last settings used before the unit was turned
the time required to reach the pressure limit and off. Verify mode, control, and alarm function before
reduces the blast of gas flow that the patient experi- applying the flow to the patient.38
ences at the start of inspiration.
The oxygen module on the Vision adds oxygen to BiPAP-AVAPS39. Philips Respironics recently intro-
the air from the blower, allowing set oxygen concentra- duced the BiPAP-AVAPS (Figure 28-11). Activation
tions up to 100%. The delivered oxygen concentration of the average volume-assured pressure-support
is within 3% of the set percentage in concentrations (AVAPS) feature provides volume-targeted pressure-
of 30% or less, and it should be within ±10% of the set support/control breaths in all modes except CPAP.
oxygen concentration in concentrations of over 30%. The modes are CPAP, spontaneous (PS/CPAP),
Spotlight
On
Shape Signal
The BiPAP Vision maintains trigger sensitivity
despite changes in the patient’s ventilatory
pattern and circuit leaks by using a shape signal.
A shape signal is a duplication of the patient’s
actual flow pattern, delayed by 300 ms and
reduced by 15 Lpm. Inspiration begins or ends
whenever the actual flow pattern crosses the
shape signal.
Best Practice
FIGURE 28-11 BiPAP ® AVAPS TM
BiPAP Vision Performance Test Courtesy of Philips Respironics, Murrysville, Pennsylvania
Run the exhalation port test (EPT) as the per-

formance check for the BiPAP Vision. The EPT spontaneous/timed, timed and pressure control. All
establishes the leak at the exhalation port over breaths in the CPAP and spontaneous modes are
the entire pressure range. This intentional leak patient triggered and cycled by the Digital Auto-Trak
information is stored in memory and used to system previously described for the Vision. Breaths are
track leaks and to estimate displayed tidal vol- time triggered in S/T mode if the patient fails to initiate
umes during ventilation. a breath within the set total cycle time window that
equals 60/bpm. Machine-triggered breaths are time
cycled. The patient’s inspiratory efforts do not trigger a
breath in the Timed mode, in which all breaths are
CASE STUDY 28-3 time triggered and cycled. In pressure control mode,
breaths may be patient or machine triggered, but all
J. R., a patient treated in the emergency depart- breaths are time cycled.
ment with NPPV, has received nasal mask ventila- When the unit is first connected to power with the
tion with the BiPAP S/T-D for 2 hours. Ventilator side pressure button off:
settings for the last 30 minutes in S/T mode are
• The screen lights up and begins to scroll through
IPAP 20 cm H2O, EPAP 5 cm H2O, respiratory
self-test, software version, blower hours, and
rate 10 bpm, and total respiratory rate 17 bpm.
standby screens. The standby screen displays the
The patient’s PaCO2 has remained elevated but
enable features: patient, apnea, light, and
consistently between 65 and 69 cm H2O since
whether Encore SmartCard is inserted. The
admission. The SpO2 has been between 90% and
Encore SmartCard records compliance data,
92% with oxygen added at 8 Lpm.
short-term and long-term ventilation trends, and
The respiratory therapist notices that J. has
ventilation statistics.
lost consciousness and his blood pressure has
• Setup is displayed in the upper right corner if the
started to fall. He is no longer triggering inspira-
unit is in Provider mode, which allows access to
tion. SpO2 has dropped to 85%.
settings that are not available to the patient.
Questions • The numbers on the standby screen indicate the
hours of use at pressure.
1. What action is now indicated?
• Pressing the pressure button displays the moni-
2. What ventilator settings would be appropriate? toring screen.
3. Why would not the appropriate action have • The monitoring screen displays the mode and
been to maintain NPPV and change the actual pressure Activation of FLEX or AVAPS will
mode on the BiPAP to timed mode with an allow a Bi-FLEX reduction of the IPAP at end-
inspiration time of 25%? inspiration and drops the EPAP during active
exhalation to improve patient comfort. Bi-FLEX
settings are 0–3, with setting 3 creating the

greatest reduction in EPAP (to zero pressure).
• The measured parameters of leak, respiratory
rate, minute ventilation, and exhaled tidal
volume may be viewed by pressing the small
circular Scroll button located above the Reset Image not available due to copyright restrictions
button.
In the User mode:
• Settings for the humidifier, Bi-FLEX, rise time,
ramp start, and LED backlight may be viewed
and changed.
• Holding the Heat button down in the standby or
monitoring screen displays the humidifier setting
screen. The humidifier is on if “HEAT” appears
on the screen.
• The Bi-FLEX setting appears only in the sponta- PB AchievaPS. The AchievaPS (Covidien Puritan
neous mode and only if the IPAP is set on 20 cm Bennett, Boulder, Colorado) is a portable ventilator
H2O or less. intended for use with adult and pediatric patients in
• Rise time can be changed if the mode is not the subacute and home care settings (Figure 28-12).
CPAP and if the Bi-FLEX setting is zero. The ventilator is piston driven and microprocessor
• The ramp start may be adjusted from 4 cm H2O controlled, with download capabilities to a computer
to the EPAP pressure setting. or modem. The AchievaPS provides both volume-
• Backlighting of the control buttons may be limited and pressure-limited A/C, volume-limited
turned on or off. SIMV with pressure support, and a spontaneous mode
of pressure support with CPAP. There is no backup
When the AVAPS feature is activated:
ventilation in the spontaneous mode. Pressure-limited
• The provider sets the target tidal volume, the ventilation is activated in A/C mode by setting an inspi-
IPAPmax at 25–30 cm H2O, the IPAPmin at ratory pressure level. In volume-limited A/C, tidal
EPAP 4 cm H2O, and EPAP. The unit automat- volumes can be adjusted from 50 to 2200 mL at
ically adjusts IPAP to provide the target tidal frequencies of 1–80 bpm. The AchievaPS has an
volume. internal PEEP valve and an internal oxygen blender.
• The unit must be in the Provider mode to A fully charged internal battery lasts approximately
activate AVAPS or change AVAPS settings. To 1 hour during high load operation and 4 hours under
access the Provider mode when the unit is in the minimal load.
User mode, press and hold down the Right and The three buttons along the top of the inside front
Silence buttons simultaneously for 2 seconds. A panel are Standby, Ventilate, and Menu/Esc.
short audible alarm indicates access to the
• Pressing the Start/Enter switch powers the
Provider mode.
ventilator on in Standby mode.
• Use the Heat or Ramp button to select a mode.
• While in Standby mode, an operation verifica-
• When the desired mode is displayed, press the
tion test can be initiated through the Menu/Esc
Right user button to activate AVAPS.
key.
• Use the Heat or Ramp button to display a 1 to
• After setting the controls, initiate ventilation by
activate AVAPS or a 0 to deactivate it.
pressing Ventilate. Indicators light, and a nonad-
• With AVAPS activated, press the Right user
justable audible alarm sounds.
button to set the parameters: target volume,
• Allow three ventilator breaths to check the low
IPAPmax, IPAPmin, EPAP, bpm, inspiratory time,
inspiratory alarm function. The circuit must be
ramp length in seconds, ramp start pressure, rise
disconnected from the patient to set the low
time, apnea interval, patient disconnect alarm in
pressure alarm. The pressure trigger setting
seconds, low minute ventilation alarm, and low
flashes in the display for verification.
tidal volume alarm.
• Flow trigger settings are continuously displayed
• Use the Heat button to increase or the Ramp
under the sensitivity. Breaths are flow or pressure
button to decrease the value for each setting.
triggered, depending on which trigger condition
Inspiratory time and bpm settings are not available in occurs first. Pressure triggering is recommended
spontaneous mode. when using PEEP.40
and its use in the home care setting for obstructive

Spotlight sleep apnea are discussed elsewhere in this text. Both
On NPPV and CPAP devices share common patient
interfaces, as well as the problem of providing
Humidified CPAP adequate humidification. An unheated passover
The HC200 Series Humidified CPAP System humidifier can be added to most CPAP systems.
supplies a built-in heated humidifier with the Certain heated humidifiers may also be used in the
CPAP system. A warm-up mode gradually increases home care setting.
the pressure to allow the patient to fall asleep.
HC200 Series Humidified CPAP System. The HC200
Series Humidified CPAP System (Fisher & Paykel,
Auckland, New Zealand) is a CPAP device with a
CONTINUOUS POSITIVE AIRWAY built-in heated humidification system. The humidity
PRESSURE UNITS system of the HC200 ensures adequate humidification
The devices just described for NPPV can also deliver overnight. Set pressure varies at 3–18 cm H2O. The
CPAP. However, if the patient requires only nocturnal warm-up mode allows a gradual increase in airflow and
CPAP, a less expensive CPAP unit is indicated. CPAP pressure as the heater plate reaches the set temperature,
Restrictive Thoracic/Neuromuscular Disease (page 1)
Medical documentation of progressive No

neuromuscular disease or severe Deny Coverage
thoracic deformity?
Thoracic
Yes Deformity
No
No
≥ ≤ MIP <60 cmH2O
Neuro
Or
No No FVC <50%
Yes Yes
Yes
Go to page 2
COPD is significant to pulmonary limitation?
Yes COPD
No
Coverage for 3
Discontinue
months EO470 or
EO471
No
See
EO470 or EO471 desired for continued use Continued
past 3 months* Yes Coverage
page 5
*EO471 will not be covered for OSA

FIGURE 28-13 Medicare flowchart of coverage criteria for NPPV. (continues)
Reprinted with permission from Hill KF. NPPRA revisited. American Association of Respiratory Care Home Care
Bulletin. 2000:1–3
Severe COPD (page 2)
Medical documentation
No
Yes
No Deny coverage
No
Yes
Go to
page 4
OSA
Yes
No
OSA & treatment with CPAP have been OSA is present & CPAP is an
considered and ruled out indicated form of therapy
No
Yes
EO470 See EO470

EO471 use desired coverage for
coverage allowed
for 3 months severe COPD
page 6
See
No Yes continued
Discontinue EO470 desired for continued coverage coverage
page 5
FIGURE 28-13 (continues)
which is adjustable by the user. The unit can also be has been ineffective. Medicare policy refers to the
switched from warm-up mode to the full set pressure bilevel units specifically designed for NPPV as respira-
in the Test mode. The power supply can use either 110 tory assist devices (RAD) to provide noninvasive
or 240 V for international travel. positive pressure respiratory assist (NPPRA). The
complicated Medicare coverage criteria for RAD are
shown in Figure 28-13.41
Long-Term Use The Medicare criteria were based in part on the
Medicare coverage of long-term NPPV for patients with recommendations from the 1998 Consensus Confer-
COPD is essentially limited to patients without ence on indications for nasal NPPV, convened by the
obstructive sleep apnea, as documented by a multi- National Association for Medical Direction of Respira-
channel sleep study, or to cases where nocturnal CPAP tory Care (NAMDRC). The conference was held at the
Central Sleep Apnea (page 3)
Medical documentation with diagnosis

of Central Sleep Apnea following
an attended Polysomnogram
No
Yes
No OSA present &

OSA excluded as primary CPAP indicated
cause of hypoventilation if YES go to Deny coverage
No page 4–OSA
Yes
No
CPAP ruled out as effective therapy
No
Yes
SaO2 88% for 5 minutes or more

continous while breathing oxygen at 2 L/m
or patients usual FIO2, whichever is more No
Yes
Documentation of significant improvement

of hypoventilation with use of EO470 or
EO471 device. While breathing usual FIO2
Yes
See
Coverage for 3 continued
months for EO470 coverage
or EO471 page 5
request of the Centers for Medicaid & Medicare incorporated a backup rate control.42 To provide their
Services (CMMS), which pays for the services and patients with quality respiratory care services in the
equipment provided to Medicare beneficiaries. Reim- home that were otherwise not covered under Medicare,
bursement for NPPV devices that did not have a some physicians prescribed NPPV devices with backup
backup rate control was approximately $240 per rates. CMMS saw the rapid increase in the use of nasal
month for up to 15 months in 1998. These devices NPPV with mechanical ventilators as an abuse of the
were not categorized as mechanical ventilators. The system. Rather than recognizing that respiratory care
NPPV device was classified as a mechanical ventilator services are an important element in quality home care
with reimbursement of approximately $550 per and worthy of reimbursement, CMMS simply changed
month for as long as the device was being used if it the rules of reimbursement for NPPV. The guidelines
Obstructive Sleep Apnea (OSA) (page 4)
Facility-based attended polysomnogram No

with diagnosis of OSA (30 apnic episodes Deny coverage
per night minimum)
Yes
Deny coverage
No
CPAP tried and proven therapy as EO470 & pay
as CPAP (EO601)
Yes
EO470
coverage for 3
months*
Continued Continued Coverage (page 5)

coverage Between 61 and 90 days from initiation of RAD therapy
desired
See Physician seen for evaluation of

continued compliance and benefit?
coverage
page 5 No
Yes
Documentation of progress of
relevant symptoms? No
Deny coutinued
Yes
coverage
No
Documentation of device usage
for 4 or more hours per 24 hour period?
No
Yes
Patient beneficiary statement

completed and signed?
Yes
Continued coverage

Timed RAD Coverage for COPD (EO471) (page 6)

IF EO471 is desired for the patient the following
criteria must be met for medicare coverage
Must have had 61 days of compliant

EO470 usage. 4 hours minimum per 24
hour period
No
Yes
EO470
≤ ≤
No
EO470
Deny coverage
Yes of EO471 device
No
Physician documentation of compliant
usage of EO470 & patient is
NOT benefiting
No
Yes No
Medicare benificiary statement completed

and signed by patient, no sooner than
61 days after EO470 device initiated
Yes
≤
EO470
Yes
Coverage of EO471
allowed
from the conference proceedings are listed in Negative Pressure Ventilation

Table 28-2. There are some discrepancies between the
conference guidelines and the Medicare flowcharts. Negative pressure ventilators date back to the 1800s,
Medicare coverage changed again in 2006 when when inventors in the United States and Europe were
certain RADs that had been classified as durable independently developing similar devices. J. Dalziel
medical equipment (DME) requiring frequent servic- described the first tank ventilator in 1832.43 In 1928, P.
ing were reclassified as capped rental DME items. The Drinker and L. Shaw produced the first practical model
covered rental payment drops after 3 months, and of the tank ventilator, dubbed the iron lung. J. H.
the patient takes over ownership of the device after Emerson Co. (Cambridge, Massachusetts) modified the
13 months. design and made the iron lung commercially available.
TABLE 28-2 NAMDRC guidelines for nasal NPPV for restrictive thoracic disorders, COPD,
and nocturnal hypoventilation
Nocturnal Hypoventilation
Restrictive Thoracic from Other Than COPD or
COPD Disorders Neuromuscular Disease
Disease History, physical exam, and History, physical exam, and History, physical exam, and
diagnostic tests diagnostic tests; optimal polysomnogram for diagnosis of
Optimal management and management of underlying OSA; CPAP trial unless previous
management of underlying disease; sleep study if indicated trial unsuccessful
disorders; sleep study if Includes sequelae of polio
indicated spinal cord injury, neuropathics,
Includes chronic bronchitis, myopathics, and dystrophics,
emphysema, bronchiectasis, amyotrophic lateral sclerosis,
and cystic fibrosis chest wall deformities, and
kyphoscoliosis
Indications Symptoms: fatigue, dyspnea, Symptoms: fatigue, dyspnea, Polysomnography (PSG) criteria
for use morning headache, etc. morning headache, etc. of OSA not responsive to CPAP
One of the following: One of the following: PSG criteria for mixed sleep
• PaCO2 55 mm Hg • PaCO2 45 mm Hg apnea not responsive to CPAP
• PaCO2 50–54 mm Hg and • Nocturnal desaturation 88% Central sleep apnea
nocturnal desaturation (SpO2) for 5 continuous minutes Other forms of nocturnal
88% for 5 continuous • For progressive neuromuscular hypoventilation
minutes on 2 Lpm O2 disease, maximal inspiratory
• PaCO2 50–54 mm Hg and pressure 60 cm
hospitalization related to • H2O or FVC 50% predicted
recurrent (2 in 12 months)
episodes of hypercapnic
respiratory failure
Source: Goldberg A, Legar P, Hill N, et al. Clinical indications for noninvasive positive pressure ventilation in chronic respiratory failure due to restrictive lung
disease, COPD, and nocturnal hypoventilation—a consensus conference report. Chest. 1999;116: 521–534. Reprinted with permission
For the next 20 years. the iron lung was used exten- with neuromuscular disease and COPD. Positive
sively to provide both acute and long-term ventilatory pressure ventilators still outnumber negative pressure
support. The polio epidemics of the 1930s and 1940s units used in the home. Currently in the United
put hundreds of patients with respiratory muscle States, approximately 50 individuals are using the
paralysis in iron lungs.44
During a particularly severe polio outbreak in
Denmark in 1952, the iron lung supply was quickly Best Practice
depleted, and over 2000 cases of respiratory failure were
managed with manual positive pressure ventilation. Negative Pressure Ventilation
The success of positive pressure ventilation in Denmark
sparked a fervor of research and development of positive Support
pressure ventilators. The advance of the Salk polio Negative pressure can support ventilation in four
vaccine in 1955, however, marked a dramatic decline in ways: during inspiration, continuously, continu-
new cases of respiratory muscle paralysis from polio. ously with additional pressure during inspiration,
Intubation and positive pressure ventilation were and as negative pressure during inspiration with
widely accepted as best practice by the mid-1960s. In positive pressure applied during exhalation. Con-
the 1980s, the nocturnal use of negative pressure tinuous negative pressure can provide the same
ventilation gained attention as a way to improve increase in lung volume as CPAP.
daytime oxygen and carbon dioxide levels for patients
Emerson iron lung. However, several pulmonary The Pulmo-Wrap and cuirass may have less of an effect
rehabilitation centers in Europe predominantly use on cardiac output because the applied negative pres-
negative pressure ventilators. Recent studies report the sure is less effective in expanding the lungs compared
use of tank ventilators for patients with acute respira- with tank ventilators.
tory failure.9,43,45–47
VENTILATORS
TYPES These devices apply subambient pressure to the body
Negative pressure ventilation can be applied during surface. As the chest wall moves outward, alveolar
inspiration to provide adequate tidal volumes: pressure drops below ambient pressure, creating a
pressure gradient for gas flow into the lungs. When the
• Intermittent negative pressure ventilation (INPV)
negative extrathoracic pressure is released, the elastic
to continuously increase lung volume during
recoil of the lungs increases alveolar pressure, reversing
spontaneous breathing
the pressure gradient for exhalation. Tank ventilators
• Continuous negative extrathoracic pressure
apply subambient pressure to the entire body from the
(CNEP) for the same increase in lung volume as
neck down. Chest shells like the cuirass or Pulmo-Wrap
CPAP
fit over the thorax and abdomen or only over the
• Intermittent negative pressure, superimposed on
thorax.52 There is no need for an artificial airway in
continuous negative pressure breathing
either case, but the natural upper airway must be patent.
• A negative pressure during inspiration and
Negative pressure devices use a vacuum pump to
positive pressure during exhalation
generate negative pressure. The peak negative inspira-
tory pressure control determines the tidal volume. A
PHYSIOLOGIC EFFECTS square or rectangular negative pressure waveform
produces a greater tidal volume than does a sine
A tank ventilator can provide adequate alveolar ventila- waveform. Most devices have inspiratory and expiratory
tion for a patient with little or no spontaneous inspira- time controls or an inspiratory time and rate setting.
tory effort. Negative pressure ventilation has been used Most can provide CNEP. Some units can be flow
to treat hypercapnic respiratory failure in patients with triggered via a nasal sensor. Tank ventilators are the
COPD. In a study that compared positive pressure most efficient, followed by the Pulmo-Wrap and then
ventilation with negative pressure ventilation in the chest cuirass. Less efficient ventilators require
26 pairs of patients with COPD, there was no signifi- higher negative pressures to achieve tidal volumes
cant difference in mortality, complications, or the similar to those from a tank ventilator.53 Peak negative
median number of days in the hospital.48 The duration pressure is adjusted on the basis of tidal volumes
of mechanical ventilation in the group ventilated with measured at the mouth by a handheld respirometer.
negative pressure was significantly shorter.
There is some evidence that NPV can effectively rest
the respiratory muscles in patients with COPD. In two INDICATIONS FOR USE
studies, respiratory muscle strength increased, and Negative pressure ventilation may be an option for
PaCO2 decreased after a week in which either a tank or patients who are able to maintain a patent upper
Pulmo-Wrap device was used for 6 hours continuously airway but who are unable to tolerate NPPV or for
or for 8 hours intermittently each day.49,50 In another patients who find tracheostomies undesirable. There is
report, the electromyographic activity of the respiratory inadequate evidence to support the use of negative
muscles of patients with COPD decreased dramatically pressure ventilation for patients with acute exacerba-
during NPV when compared with spontaneous tion of COPD.9
breathing.51
A major concern with NPV is its effect on the
upper airway. NPV may decrease the caliber of the
upper airway at the glottic or subglottic level. When Best Practice
NPV is applied during sleep, normally coordinated
respiratory activity between the pharyngeal, laryngeal, Adjusting Peak Negative
and inspiratory muscles may be abolished and result in
upper airway obstruction. Negative pressure ventilation Pressure
may also cause lower esophageal dysfunction and During NPV, the peak negative pressure is
increase the risk of regurgitation and aspiration. adjusted on the basis of tidal volumes measured
Tank ventilators also have the same adverse effects at the mouth by a handheld respirometer.
on hemodynamics as do positive pressure ventilators.
3. What are the advantages and disadvantages of

CASE STUDY 28-4 using critical care versus home care positive
pressure ventilators for NPPV?
A therapist working in the Unita di Terapia 4. What are the various types of patient interfaces
Intensiva Respiratoria in a hospital in Firenze, used in noninvasive positive pressure ventilation?
Italy, was called to the emergency room. G. S., 5. What are the primary settings on the BiPAP S/T-D
who has a chest wall deformity, was admitted for ventilator?
acute ventilatory failure. The physician ordered 6. What is an alternative method of cycling pressure
negative pressure ventilation for Mr. S., and he support for some critical care ventilators?
was is placed in a Porta-Lung tank ventilator. 7. What is a common complication of NPPV
delivered via face mask?
Questions 8. Under what circumstances should NPPV be
1. What control determines the tidal volume? discontinued?
2. What negative pressure setting should be 9. What is one advantage and one disadvantage of
used initially? negative pressure ventilators?
3. How is the tidal volume monitored?
4. How should the breaths per minute and I/E
ratio be adjusted? 1. Which of the following is not associated with NPPV?
a. head straps
b. endotracheal tube
c. nasal mask
Although NPV has been used successfully over the d. nasal pillows
years to support patients in respiratory failure from a
2. Which of the following are complications of NPPV?
variety of etiologies, no randomized controlled trials
I. aspiration
have demonstrated its superiority over positive pressure
II. vocal cord paralysis
ventilation. There are enough concerns about airway
III. eye irritation or conjunctivitis
integrity during NPV to restrict its use to selected
IV. skin abrasions on the nose
patients.
a. I, II, III, and IV
b. I and IV only
Summary c. II only
Although noninvasive ventilation is not new, the d. I, III, and IV only
technology associated with noninvasive positive 3. Which of the following have occurred for patients
pressure ventilation (NPPV) ventilation has improved with acute respiratory failure due to exacerbation
since the 1990s. In the acute care setting, NPPV may be of COPD who have been treated with NPPV?
an alternative to intubation and invasive ventilation in I. decreased mortality
75% of the patients with acute exacerbation of COPD. II. decreased duration of mechanical ventilation
Long-term NPPV is an option for select patients with III. reduced incidence of ventilator-associated
COPD who meet Medicare’s coverage criteria. The use pneumonia
of negative pressure ventilation in the same patient IV. decreased need for endotracheal intubation
population is not currently supported by the results of a. I, II, III, and IV
clinical trials but may be useful in patients unable to b. I and IV only
tolerate mask ventilation. Finally, CPAP or NPPV c. III and IV only
application represents the current standard of care in d. IV only
cases of acute cardiogenic pulmonary edema. 4. Which of the following are contraindications
(absolute or relative) for the use of NPPV in
Study Questions patients with acute respiratory failure due to
exacerbation of COPD?
REVIEW QUESTIONS I. respiratory arrest
1. What are the advantages of noninvasive positive II. excessive secretions
pressure ventilation? III. increased PaCO2 level
2. According to the recommendations of the AARC IV. severe claustrophobia
Conference on Noninvasive Positive Pressure Venti- a. I, II, III, and IV
lation, which patients in acute respiratory failure b. IV only
may benefit the most from noninvasive positive c. I, II, and IV
pressure ventilation? d. I only
5. Which pressure support ventilator allows the user to 4. Girault, C., et al. Noninvasive ventilation as a
set an oxygen concentration? systematic extubation and weaning technique in
a. BiPAP S/T-D acute-on-chronic respiratory failure: a prospective,
b. BiPAP AVAPS randomized controlled study. Am J Respir Crit Care
c. BiPAP Vision Med. 1999;160,1:86–92.
d. none of the above 5. Nava S, et al. Noninvasive mechanical ventilation
6. Which of the following alters the oxygen concen- in the weaning of patients with respiratory failure
tration delivered when supplemental oxygen is due to chronic obstructive pulmonary disease. A
added to the circuit? randomized, controlled trial. Ann Intern Med.
I. a change in the pressure gradient (IPAP – EPAP) 1998;128,9:721–728.
II. an increase in IPAP alone 6. Kallet RH, Diaz JV. The physiologic effects of
III. an increase in EPAP alone noninvasive ventilation. Respir Care.
IV. a change in the percentage inspiratory time 2009;54,1:102–115.
a. I, II, III, and IV 7. Pierson DJ. Noninvasive positive pressure ventila-
b. I and III only tion: history and terminology. In: Consensus
c. II and IV only Conference IV: Noninvasive Positive Pressure Ventila-
d. I only tion. Vail, Colorado: Daedalus Enterprises, Inc.;
1997.
7. Which one of the following types of negative
8. Mushin W, et al. Historical Background to Automatic
pressure ventilation has the same effect as CPAP?
Ventilation. 3rd ed. A.V.o.t. Lungs. St. Louis, MO:
a. negative pressure during inspiration only
Blackwell Mosby; 1980.
b. negative pressure during inspiration and
9. Bach JR. Consensus statement: noninvasive
positive pressure during exhalation
positive pressure ventilation. In: Consensus
c. continuous negative extrathoracic pressure with
Conference IV: Noninvasive Positive Pressure
a greater negative pressure superimposed
Ventilation. Vail, Colorado: Daedalus Enterprises,
during inspiration
Inc.; 1997.
d. continuous negative extrathoracic pressure
10. Brochard L. Noninvasive ventilation in acute
respiratory failure. Respir Care. 1996;41,5:
456–446.
CRITICAL-THINKING QUESTIONS 11. Keenan SP, Mehta S. Noninvasive ventilation for
patients presenting with acute respiratory failure:
1. What is one way to determine the IPAP level for a the randomized controlled trials. Respir Care. 2009;
patient in acute or chronic respiratory failure? 54,1:116–126.
2. Why is it important to check the pressure support 12. Anton A, et al. Predicting the result of noninvasive
ventilators by occluding the circuit? ventilation in severe acute exacerbations of patients
3. Why would 4 cm H2O EPAP probably be appropri- with chronic airflow limitation. Chest. 2000;117,3:
ate for most patients? 828–833.
13. Hilbert G, et al. Noninvasive pressure support
4. Under what circumstance would negative pressure ventilation in COPD patients with postextubation
ventilation be inappropriate? hypercapnic respiratory insufficiency. Eur Respir J.
1998;11,6:1349–1353.
14. Ferrer M, et al. Early noninvasive ventilation averts
extubation failure in patients at risk: a randomized
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SECTION V
Levels of Care Delivery

CHAPTER 29
Neonatal and Pediatric Respiratory Care

John Salyer and Robert DiBlasi
OBJECTIVES
• List the common neonatal respiratory disorders.
• List common pediatric respiratory disorders.
• List the effects of prematurity on the neonatal lung.
• Describe fetal blood flow and the transition to adult circulatory pathways.
• Describe the components of a respiratory assessment of neonatal and pediatric patients.
• List the key steps and techniques related to the resuscitation of a newborn.
• Describe the factors that influence the performance of pulse oximeters in infants and children.
• Describe the appropriate device selection for oxygen delivery and aerosolized medication delivery to a
pediatric patient.
• Describe the basics of CPAP administration in infants and children
CHAPTER OUTLINE
The Practice of Neonatal and Pediatric Retinopathy of Prematurity
Respiratory Care Respiratory Distress Syndrome
Epidemiology Air Leak Syndrome
Common Neonatal Respiratory Diseases Congenital Diaphragmatic Hernia
and Conditions Common Pediatric Respiratory Diseases
Transition from Intra-uterine to and Conditions
Postnatal Circulation Asthma
Newborn Resuscitation Bronchiolitis
Apgar Scoring Acute Respiratory Distress Syndrome
Prematurity
Respiratory Assessment in the Neonatal
Neutral Thermal Environment, Insensible Water and Pediatric Patient
Loss, and Minimal Stimulation
(continues)
797
798 SECTION V ■ Levels of Care Delivery
(continued)
Technology of Pediatric and Neonatal High-Frequency Ventilators

Respiratory Therapy Continuous Positive Airway Pressure
Manual Resuscitators Nasal CPAP Systems
Monitoring Oxygen Delivery
Pulse Oximetry Aerosol Delivery
Conventional Ventilators
KEY TERMS
conduction evaporation neonatal
convection meconium pediatric
diaphragmatic hernia
S
ome of the most widely used technological More specifically, “neonatal” typically refers to the
advances in the treatment of respiratory failure period from birth through the first four weeks of life,
were first developed in neonatal and pediatric and “pediatric” refers to the period from 1 month to
practice and then introduced into adult 18 years of age. However, most pediatric hospitals
populations. These include continuous positive airway admit a small number of patients over 18 years of age,
pressure, intermittent mandatory ventilation, high- some as old as 23 years. These are typically patients
frequency ventilation, inhaled nitric oxide therapy, and with a chronic disease who have been managed all
extra corporeal membrane oxygenation.1,2 The clinician their lives by pediatric subspecialists.
who is considering practicing in units and hospitals Many misconceptions surround the care of neo-
specializing in the treatment of neonatal and pediatric nates and pediatric patients. It is important to dispel
patients will enter an environment with a history of these myths about the care of these populations in
innovation and research and one in which new tech- order to learn how to properly care for them.
nologies are continuously being developed.
• Misconception: Neonatal and pediatric practice is
Through the steady accumulation of a solid base of
harder or more demanding than respiratory care for
scientific evidence, improvements in the quantity and
adult populations.
quality of training, as well as the introduction of new
Truth: These respective practice environments
technologies, remarkable improvements in outcomes
are simply different. So, to practice effectively
have been accomplished over the last four decades.3
in most neonatal and pediatric populations,
Respiratory therapists have played a vital role in this
the respiratory therapist needs different
steady progress.4
preparation, training, and experience than
respiratory therapists who treat adult
populations.
The Practice of Neonatal and • Misconception: Pediatric patients are small adults,
Pediatric Respiratory Care and neonates are smaller pediatric patients.
Truth: Nothing could be further from the truth.
The terms “neonatal” and “pediatric” are used through-
For example, a premature neonate is indeed very
out this chapter because, functionally, these are fairly
small but also has tissues and organ systems in
distinct populations of patients (although there is
various stages of development. Depending on
some overlap).
the patient’s gestational age at birth, some organ
• Neonatal is from the Greek neos for “new” and systems can be very underdeveloped, particularly
the Latin natus for “born.” Thus, the term the lungs in babies born under 35 weeks of
“newborn” is often substituted for neonatal. gestation. In general, the airways form early in
• Pediatric is from the Greek pais for “child” and gestational life (by about 17 weeks) and grow by
iatreia for “treatment.” enlargement. At the same time, the alveoli
CHAPTER 29 ■ Neonatal and Pediatric Respiratory Care 799
TABLE 29-1 Distinctions between the adult and the neonatal and pediatric
respiratory tract
1. Prior to 28 weeks of gestation the premature lung has no real alveoli. Instead the airways end in saccules, which
are larger, and thicker walled than true alveoli. Some gas exchange can probably occur in these units.
2. Elastin and collagen (important connective tissues that lend stability to lung structures) are nearly absent during
late gestation and at birth. This may be why it is relatively easy to rupture the air spaces of the premature lung
(air leak).
3. The development of airways, the vasculature and alveoli are adversely affected by chronic hypoxia.
4. The young lung lacks elastic recoil; as a result, airways are less well supported, leading to greater airway closure
and the development of patchy atelectasis frequently observed in the child under school age.
5. Airway walls of young lungs may be thicker. This, combined with reduced elastic recoil, favors greater airway
narrowing for any degree of smooth muscle contraction.
6. The chest wall is relatively more compliant in the young child and stiffens with increasing age. As a result, the
infant can develop paradoxical respiration. Diaphragmatic movement during inspiration, and the resulting negative
intra-thoracic pressure can produce inward displacement of the rib cage, contributing to increased work of breathing
for a given level of ventilation. Chest wall-abdominal paradox may be normal in the premature infant during REM
sleep but not in the older child or adult.
7. Infants and children from large families or those who attend day care have frequent respiratory tract infections.
It may be that the profuse secretions are aspirated and with a shorter path length to peripheral airways, the
epithelium lining these structures becomes infected. Because of complex structural differences with adults,
the effects of any degree of airway smooth muscle contraction will be exaggerated and contribute to the
uneven ventilation and perfusion and modest hypoxemia observed in so many children with respiratory tract
infections.
8. The rate of mucociliary clearance is less in infants than adults.
9. The infants’ airway has a higher ratio of mucus glands than adults.
Source: Wohl, M. E. B. Developmental physiology of the respiratory system. In: Chernick, V.C., Boat, T.F., Wilmott, R.W., Bush, A., eds. Kendig’s Disorders of
the Respiratory Tract in Children. 7th ed. Philadelphia. Saunders Elsevier, 2006: 23–28.
develop late in gestational life and early simulations helps the clinician be a better neonatal and
childhood and grow by forming new structures. pediatric RT. These credentials are becoming increas-
At term, the healthy newborn has approximately ingly recognized and indeed required to get and keep
150 million alveoli, although this number is employment in some pediatric hospitals.
highly variable. Apparently, new alveolar struc-
tures are added throughout the first few years
of life (for a total of about 274–790 million5), Epidemiology
and further lung growth takes place by enlarge- In 1862, a paper was submitted to the British National
ment of the existing structure.6 Other important Social Science Association entitled, “Excessive Infant-
distinctions between the neonatal/pediatric Mortality: How Can It Be Stayed?” The author, M. A.
and adult respiratory system are listed in Baines, reported the following:
Table 29-1. See Wohl’s excellent summary of
Of the deaths in England in 1859, no less than
developmental physiology of the respiratory
184,264—two in every five of the deaths of the
system.7
year—were of children under five years of age; and
Preparation to become a neonatal and pediatric above half of these—105,629—had scarcely seen
respiratory therapist (RT) includes all of the customary the light, and never saw one return of their birth-
classroom and clinical education for any RT. But RTs can day. . . . from 43 to 45 infant deaths take place in
undertake some additional training and credentialing that every 100 births—45 percent! Almost half of the
better prepares them for neonatal and pediatric practice children who are born, die—perish miserably!
(Table 29-2). Having the credential is not nearly as And this is far from representing the whole mass
valuable as obtaining the credential. The value is in the of pain and suffering, which it is the calamity of
journey. The work done to pass these examinations and children to endure.
TABLE 29-2 Preparations for becoming a neonatal and pediatric respiratory therapist
Credential Issued by Comments
Neonatal Pediatric National Board for This advanced practice credential is well respected in the
Specialist (NPS) Respiratory Care neonatal and pediatric community. It is obtained by passing a
written test.
Neonatal Resuscitation American Academy This training program is a combination of didactic training
Program (NRP) of Pediatrics and laboratory simulation that focuses on the resuscitation
of newborns. This is essential training for anyone who will be
attending deliveries or transporting neonates.
S.T.A.B.L.E.* The S.T.A.B.L.E.® Specialized training in postresuscitation/pre-transport
Program stabilization care of sick infants.
Pediatric Advanced Life American Academy The pediatric equivalent of Advanced Cardiac Life Support
Support (PALS) of Pediatrics for adult patients (ACLS). Anyone who will be attending code
blues or working in a pediatric intensive care unit should have
PALS.
*McCraine-Taylor, R., Price-Douglas, W. The S.T.A.B.L.E.® Program: Post-Resuscitation/Pre-transport Stabilization, Care of Sick Infants. J Perinat Neonat Nurs,
2008:22(2):159–165.
Worldwide infant mortality at one year of life is In utero, the fetal requirements for oxygen and
now about 8 per 1000 live births. Baines reports 45 nutrients are supplied by the oxygenated blood
infant deaths per 100 live births, or 450 per 1000 live flowing from the placenta to the fetus through the
births. When we malign the problems and dislocations umbilical vein. Figure 29-1 illustrates the fetal circula-
of modern life, we might do well to remember that we tory pathways. Carbon dioxide is removed from the
live in an unprecedented time in human history. fetal blood when it flows back out to the placenta via
More than 500,000 babies (one in eight) are born the umbilical arteries. Fetal cardiac and pulmonary
prematurely each year in the United States.8 Most of blood flows are different because the fetus needs little
these infants are cared for in neonatal intensive care blood flow through the lungs. In utero, the resistance
units, of which there are about 700 nationally, com- to blood flow in the lungs is higher than resistance to
prising 16,000 beds.9 Approximately 337 hospitals in blood flow in the rest of the fetus. This causes the
the United States have dedicated pediatric critical care majority output of the right ventricle to shunt past the
beds, and about one-half of all U.S. hospitals admit lung directly to the left or somatic side of the cardiac
pediatric patients, but they do not have specialized circulation.
pediatric beds or units.10 U.S. hospitals receive about There are three major sites of shunting: the foramen
30 million emergency visits from the population under ovale, the patent ductus arteriosus, and the ductus
18 years of age, which is about one-fourth of all venosus.
patients cared for in emergency departments.11
• The foramen ovale is a flaplike opening between
the right and left atria, allowing blood flow only
Common Neonatal Respiratory from the right to the left side of the heart under
normal conditions.
Diseases and Conditions • The ductus arteriosus is a connection between the
TRANSITION FROM INTRA-UTERINE ascending aorta and the pulmonary artery.
TO POST NATAL CIRCULATION • The ductus venosus connects the umbilical vein
directly to the inferior vena cava, allowing most
Normally, blood flow through the fetal heart and lungs
blood to bypass the liver.
is different when in the uterus than in the neonatal
after delivery. During the delivery and in the immediate Normal fetal PaO2 is 25–35 mm Hg. This is possible
postnatal period, the newborn must transition from because the fetus is in a nearly motionless state and in
having gas exchange supported mostly by the mother’s a neutral thermal environment; it needs less oxygen to
cardiac output to completely independent breathing maintain body temperature and muscle activity. Also, a
and adult patterns of blood flow. Failure to make a fetus has predominantly fetal hemoglobin. This variant
rapid transition can result in life-threatening condi- of adult hemoglobin has a higher affinity for oxygen at
tions, such as persistent pulmonary hypertension of lower PaO2s. This fetal hemoglobin is normally replaced
the newborn. by adult hemoglobin shortly after birth.
After the clamping of the umbilical vessels, the • Blood pressure in the right (or pulmonary) side
low-resistance circulatory system of the placenta is of the heart decreases relative to the blood
removed from the fetal circulation. pressure in the left or somatic side of the heart.
• The pressure in the aorta increases and becomes
• As the lungs inflate and gas exchange occurs, greater than the pressure in the pulmonary
an increase in PaO2 causes dilation of the artery. This decreases the amount of right-to-left
pulmonary arterial bed, resulting in a reduction shunting through the ductus arteriosus and
in pulmonary vascular resistance (PVR). foramen ovale.
Aortic arch
Superior vena cava Ductus

arteriosus
Pulmonary
Right atrium veins
Non-inflated
lung
Left atrium
Foramen ovale
(open)
Left ventricle
Ductus venosus
Right ventricle
Aorta
Liver
Key to oxygen
Inferior saturation of blood
Umbilical vein vena cava
High
Umbilical cord
Medium
Portal Low
vein
Umbilical
arteries Internal iliac
artery
ta
cen
Pla To legs
Urinary
bladder
FIGURE 29-1 Fetal circulatory pathways and transition to extra-uterine circulatory pathways. (continues)
Aortic arch
Superior vena cava Ligamentum arteriosum

(formerly ductus arteriosus)
Pulmonary
Right atrium veins
Inflated
lung
Left atrium
Foramen ovale
(closed)
Left ventricle
Ligamentum
venosum (formerly Right ventricle
Aorta
ductus venosus) Liver
Key to oxygen
Inferior saturation of blood
vena cava
High
Low
Ligamentum teres
Portal
(formerly umbilical vein) vein
Medical umbilical Internal iliac

ligaments artery
(formerly umbilical artery)
To legs
Urinary
bladder
• Closure of the ductus arteriosus usually occurs The ductus arteriosus may not close completely in
within the first 24 hours to 2 weeks of life, except some term infants (e.g., in meconium aspiration).
in the premature infant, in whom musculature These patients may experience very high PVR, and
of the ductus arteriosus may not be well devel- blood then flows from right to left through the ductus
oped and its ability to constrict is limited. The arteriosus from the pulmonary circulation to the
PVR is lower than the systemic vascular resis- systemic circulation, bypassing the lungs. Because the
tance (SVR), and blood flows into the lungs foramen ovale flap allows blood to flow only from
from the systemic circulation (left to right). right to left, it closes when the pressures in the LA
become greater than those in the RA. If the foramen staining. If thick meconium is present, the
ovale lacks a flap-like structure or has a defective clinician who delivers the infant should
one, the opening begins to function as an atrial septal suction the upper airway when the head is
defect (ASD). delivered, prior to delivery of the rest of the
infant’s body. After delivery of the rest of
the body, the infant is intubated and
NEWBORN RESUSCITATION immediately suctioned—if possible, before
Proper care and resuscitation of the newborn begin in initiating the first breath by the infant. If
the delivery suite and are essential to the transition to the meconium staining is mild, it is usually
extra-uterine life. RTs who attend deliveries can greatly necessary only to thoroughly suction the
enhance their preparation by getting the NRP creden- upper airway.
tial, which focuses on the resuscitation of newborns.
Table 29-3 describes the basic equipment and steps of There is considerable debate about how to use
newborn resuscitation; Table 29-4 is a guide to select- oxygen (O2) in the resuscitation of newborns. For
ing the appropriate endotracheal tube size based on most of the modern history of resuscitation of
birth weight. newborns, 100% O2 was used during the immediate
Two circumstances are important during the postdelivery resuscitation. But evidence has steadily
resuscitation of newborns: diaphragmatic hernia grown that O2 use has toxic effects in newborns,
and the presence of meconium in the amniotic particularly low-birth-weight infants (discussed late
fluid. in this chapter in “Retinopathy of Prematurity”).
Recent findings suggest that even a brief O2 expo-
• In newborns presenting with a diaphragmatic sure during resuscitation is potentially more toxic
hernia, consider the following: than had been previously thought. There are even
Avoid positive pressure ventilation with a suggestions that resuscitation of the newborn with
mask; this can force air into the stomach. The room air is better than using O2. Stola and colleagues
stomach and or small intestines may be report:
extruding into the chest through the defect in
the diaphragm. If air is forced into the bowel, Clinical studies have shown that delivery room
the portion of the bowel in the chest cavity can resuscitation with 100% oxygen when compared
expand and compress other structures in the with room air is associated with a lower 5-min
chest, including the heart, lungs, and great Apgar score, a prolonged time to first cry and
vessels. If positive pressure ventilation is breath, increased neonatal mortality, increased
needed (which is likely in diaphragmatic oxidative stress that persisted for at least
hernia), the patient should be intubated as 4 weeks after birth in one study, increased
soon after delivery as possible to avoid disten- myocardial and kidney injury and also with
sion of the bowel. a higher risk for childhood leukemia and
• A newborn might have meconium in the cancer. These studies were largely undertaken
amniotic fluid at delivery: Meconium is a thick, in underdeveloped countries and primarily
dark, viscous fluid that is a waste product of the involved term babies.12
fetal bowel and that normally occurs in trace
amounts in the amniotic fluid. It is nearly These findings and others have led to the wide-
sterile but can be chemically irritating to the spread practice of using air-oxygen blenders with
lung. When the infant is stressed during labor resuscitators during delivery. Finer13 summarizes the
and delivery, the bowel can evacuate in utero current state of knowledge and recommends:
and the amniotic fluid can contain varying
amounts of meconium, which can then be Until the results of further studies are available,
aspirated into the infant’s upper airway. If it is, a reasonable approach to resuscitation would
it can cause obstruction of the airways and include initial resuscitation with 30–40% oxygen
chemical irritation of the airways and lung for very preterm infants using targeted SPO2
tissue (meconium aspiration syndrome). This values and blended oxygen during the first
syndrome, in its severe forms, can be life- 10 minutes. For ongoing management of preterm
threatening. During labor, the amniotic infants, SPO2 targets of 85–93% seem to be most
fluid is examined and tested for meconium appropriate . . .
TABLE 29-3 Guide to newborn resuscitation

1) Deliveries that should be considered high risk: 6) Manual Ventilation (if necessary)
a) Thick meconium after maternal membranes a) Indications for manual ventilation
ruptured i) Apnea
b) Fetal distress ii) Heart rate less than 100 breaths
c) “Crash” C-section per min
d) Premature birth b) Manual ventilation with a mask
e) Prenatally diagnosed congenital anomalies, i) Self-inflating bags are preferred because
such as but not limited to: of ease of use and more consistent tidal
i) Congenital diaphragmatic hernia volume and PEEP delivery.
ii) Congenital heart disease ii) Careful attention required to ensure good
mask fit and patent airway.
iii) Abdominal wall defects
iii) Rate ⫽ 40–60 breaths per min
iv) Neural tube defects
iv) Ventilating pressures
2) Equipment to be gathered:
(1) A pressure manometer should
a) Self-inflating bag with reservoir attached to
be used
100% oxygen source
(2) Initial breath after delivery
b) Appropriate size mask
c) Bulb syringe (a) Normal delivery ⫽ 15–20 cmH2O
d) Wall suction (b) Diseased Lungs ⫽ 20–40 cmH2O

e) Warmer bed and blankets 7) Chest Compressions:
f) Intubation equipment a) Indications: If after approximately 30 s of
positive pressure ventilation with 100% FI02
g) Meconium aspirator
the heart rate is below 60 breaths per min
3) Initial step: warm and dry infant or between 60–80 breaths per min and not
a) Place infant under radiant heat warmer bed increasing
and dry infant vigorously. This helps prevent b) Technique:
cold stress and provides stimulation to assist
i) Use two fingers placed one finger’s breadth
the infant with transition.
below nipple line
4) Initiate ABC’s
ii) 1/2 to 3/4 inch compression depth
a) Airway: position head in neutral position and accompanied by ventilations,
suction the nares first, then the mouth.
(1) Frequency of compressions ⫽ 90/min
b) Breathing: assisted ventilation with a manual
(2) Ratio of compressions to breaths
resuscitator if necessary. See below.
is 3:1
c) Circulation: assess heart rate by:
8) Intubation:
i) Auscultating an apical pulse,
a) Indications:
ii) Palpate an umbilical or brachial pulse.
i) If heart rate does not increase to ⬎ 100
5) Evaluate infant for: beats per min within 5 min
a) Color: ii) Apnea
i) Peripheral cyanosis (acrocyanosis) is iii) Inability to adequately oxygenate
normal and typically does not require
b) See Table 29-4 for guide to selecting
supplemental oxygen.
endotracheal tubes.
ii) If centrally cyanotic give infant
supplemental oxygen.
b) Signs of Respiratory distress:
i) Increased work of breathing
ii) Nasal flaring
iii) Grunting
iv) Tachypnea
TABLE 29-4 Guidelines for selection of

Spotlight
endotracheal tube and associated size On
suction catheter for intubation of
newborns Dr. Virginia Apgar
Birth Weight ETT Size Suction Catheter Size Dr. Virginia Apgar has been described as the
⬍1000 g 2.5 mm 5–6 French suction catheter founder of neonatology. She was an anesthesiolo-
gist who specialized in pediatrics. She carried
1000–2000 g 3.0 mm 6 French suction catheter
resuscitation equipment with her everywhere she
2000–3000 g 3.5 mm 8 French suction catheter went. She explained, “Nobody, but nobody, is
⬎3000 g 4.0 mm 8 French suction catheter going to stop breathing on me!”
Best Practice APGAR SCORING

Clinical scoring systems now abound in the hospital.
Avoid Unnecessary There are asthma scores, bronchiolitis scores, coma
Complexity scores, and trauma scores. All these scores help in
bringing a degree of sorely needed standardization
Sometimes clinicians are fooled into thinking to the way clinicians evaluate patients. A pioneer in
they are giving newborns supplemental oxygen this field in the early 1950s, Dr. Virginia Apgar
when they are not. This is because the attach- created a simple yet reliable and effective method of
ment of the resuscitator to a blender is set on assessing the cardio respiratory status of infants at
room air. Sometimes this happens because the delivery and to assess the effectiveness of resuscita-
blender is not mounted clearly within the line of tion efforts.14
site of the bedside clinicians. Apgar scores are typically assessed at 1 and 5
minutes after delivery by the respiratory therapist,
nurse, or doctor participating in the resuscitation. The
scoring is done by evaluating the patient for five signs;
heart rate, color, respiratory effort, muscle tone, and
Note: The addition of blenders to the delivery
reflex irritability, which is related to how the infant
room enhances the potential for mishaps associated
reacts to stimuli. An ordinal score of 0, 1, or 2 is
with clinicians’ ventilating the patient with an
assigned to each of these categories and then totaled.
“unintended” FIO2.1
Table 29-5 lists the details of the Apgar score.
1 We know of multiple episodes of care where clinicians were manually
resuscitating infants with what they thought was 100% oxygen, only to PREMATURITY
discover that the blender was not set on 100%. Sometimes the visual
Infants are considered premature if they are born under
environment is very complex, and blenders can be mounted in places
at the bedside that cannot readily seen by the clinicians. 37 weeks, or the estimated gestational age (EGA). The
TABLE 29-5 Apgar Infant Scoring System

Score
Sign 0 1 2
Heart rate Absent Under 100 beats per min Over 100 beats per min
Respiratory effort Absent Slow (irregular) Good crying
Muscle tone Limp Some flexion of extremities Active motion
Reflex irritability No response Grimace Cough or sneeze
Color Blue, pale Pink body, blue extremities All pink
1. A score of 8–10 is excellent, 4–7 is guarded, 0–3 is critical. This lets you know how the baby is doing and if he/she is going to need extra assistance.
2. Reflex irritability is the newborn response to stimulation. This is often assessed as the response of the child to bulb suctioning of the nose.
gestational age is estimated because the exact date of of prematurity is rare. Figure 29-1 shows the survival in
conception is often not known. Infants of the same EGA different birth weight groupings. With increasing
can have different levels of maturity depending on their prematurity, there is also an increased risk of temporary
exposure to factors and conditions that can accelerate or permanent morbidities and complications that can
or slow their maturation process. For most of human cause physical and/or neurodevelopment disabilities.
history, premature babies had little chance of survival. Respiratory therapists play an important role in helping
The earliest infants to have survived are in the 23–24- to prevent or minimize these risks. Table 29-6 lists some
week gestational age range, although survival at this level common complications.
TABLE 29-6 Morbidities and complications of premature birth

Intraventricular IVH of the newborn is bleeding into the fluid-filled areas (ventricles) surrounded by
hemorrhage (IVH)1 the brain. The condition is most often seen in premature babies. Infants born before
30 weeks of pregnancy are at highest risk for such bleeding. The smaller and more pre-
mature the infant, the higher the risk for IVH. This is because blood vessels in the brain
of premature infants are not yet fully developed and are extremely fragile. IVH is more
common in premature babies who have had physical stress, such as respiratory distress
syndrome, pneumothorax, or high blood pressure. IVH falls into four groups, called
grades. The higher the grade, the more severe the bleeding. Grades 1 and 2 involve a
small amount of bleeding and do not usually cause long-term problems. Grades 3 and
4 involve more severe bleeding, which presses on or leaks into brain tissue. Blood clots
can form and block the flow of cerebrospinal fluid, leading to increased fluid in the brain
(hydrocephalus).
Periventricular PVL is caused by a lack of oxygen or blood flow to the periventricular area of the
leukomalacia (PVL)2 brain, which results in the death or loss of brain tissue. The periventricular area—the
area around the spaces in the brain called ventricles—contains nerve fibers that carry
messages from the brain to the body’s muscles. Although babies with PVL generally
have no outward signs or symptoms of the disorder, they are at risk for motor disorders,
delayed mental development, coordination problems, and vision and hearing impair-
ments. PVL can lead to cerebral palsy. The disorder is diagnosed by ultrasound of
the head.
Extremes in circulating PaCO2 levels have been implicated as contributing to the devel-
opment of cerebrovascular injury in neonates.3 Besides the obvious effects of hyper- or
hypocarbia on pH, extremes also affect cerebral blood flow. Thus, sudden large swings
are to be avoided. These can occur when a new mode of ventilation is introduced, such
as high frequency oscillatory ventilation. The clinician is cautioned to take care not to
over ventilate the patient as well as under ventilate.
Bronchopulmonary BPD is a structural malformation. It is an arrest of lung maturation, with or without
dysplasia (BPD)4 ventilator induced lung injury (VILI). Other features are a halt in alveolarization, abnor-
mal capillary bed development, presence of antioxidants, and lack of surfactant.5 BPD
is characterized by the need for supplemental oxygen at 36 weeks of postmenstrual age.
It affects nearly one third of surviving infants born at less than 1000 grams, but also
occurs in infants born weighing over 1250 grams or more than 30 weeks gestational age.
The etiology of BPD is multifactorial. Lung immaturity, oxygen therapy, and mechanical
ventilation have major roles. Meconium aspiration, pneumonia, and in-utero cytokine
release also are implicated.
Retinopathy of Retinopathy of prematurity (ROP) is a potentially blinding eye disorder that primarily
prematurity (ROP)5,6 affects premature infants born weighing ⬍1250 grams or ⬍ 31 weeks of gestation.
The disorder is caused by giving infants too much oxygen. The smaller a baby is at birth,
the more likely that baby is to develop ROP. We now know that restricting PaO2 or SaO2
levels helps reduce the risk of ROP, although the optimal range of oxygenation levels to
achieve this remains controversial. Until better information is developed, typical target
ranges are PaO2 50–90 mm Hg or SaO2 88–93%
(continues)
TABLE 29-6 Morbidities and complications of premature birth (continued)

Hydrocephalus7 The term hydrocephalus is derived from the Greek words “hydro” meaning water and
“cephalus” meaning head. As the name implies, it is a condition in which the primary
characteristic is excessive accumulation of cerebrospinal fluid in the brain that is caused
by IVH. The excessive accumulation results in an abnormal widening of spaces in the
brain called ventricles. This widening creates potentially harmful pressure on the tissues
of the brain. Hydrocephalus can permanently damage the brain, causing problems with
physical and mental development. If untreated, it is usually fatal. With treatment,
many people lead normal lives with few limitations. Treatment usually involves surgery
to insert a shunt that drains the excess cerebrospinal fluid from the brain to the
peritoneum.
Necrotizing enter colitis NEC occurs when the lining of the intestinal wall dies and the tissue falls off. NEC is the
(NEC)8 most common gastrointestinal emergency in the neonatal intensive care unit and can
be life threatening. It affects approximately 6% to 10% of very low birth weight (VLBW)
infants and a case fatality rate as high as 20% to 40%.5 The etiology of NEC is not
clearly established but appears to be multifactorial, involving enteral feeding, vascular
or perfusion-related gastrointestinal compromise, and bacterial invasion. Those with a
higher risk for this condition include:
• Premature infants
• Infants who are fed concentrated formulas
• Infants in a nursery where an outbreak has occurred
• Infants who have received blood exchange transfusions
Treatment includes surgical excision of necrotic bowel segments.
1 National Institute of Health. http://www.nlm.nih.gov/medlineplus/ency/article/007301.htm. Accessed May 23, 2009.
2 National Institute of Health. http://www.nlm.nih.gov/medlineplus/ency/article/007232.htm. Accessed May 23, 2009.
3 McCrea HJ, Ment LR. The diagnosis, management, and postnatal prevention of intraventricular hemorrhage in the preterm neonate. Clin Perinatol.
2008;35(4):777–92.
4 Ikagami AM. Mechanism initiating lung injury in the preterm infant. In: Goldsmith JP, Karotkin EH. Editors. Assisted Ventilation of the Neonate. Philadelphia,
PA: Saunders: 2003:347.

5 National Eye Institute. http://www.nei.nih.gov/health/rop/. Accessed May 25, 2009.
6 Askie LM, Henderson-Smart DJ, Ko H. Restricted versus liberal oxygen exposure for preventing morbidity and mortality in preterm or low birth weight
infants. Cochrane Database Syst Rev. 2009 Jan 21;(1):CD001077.

7 National Institute of Neurological Disorders and Stroke. http://www.ninds.nih.gov/disorders/hydrocephalus/detail_hydrocephalus.htm. Accessed
May 25, 2009.

8 Meinzen-Derr J, Morrow AL, Hornung RW, Donovan EF, Dietrich KN, Succop PA. Epidemiology of necrotizing enterocolitis temporal clustering in two
neonatology practices. J Pediatr. 2009 May;154(5):656–61.
Preventing premature delivery has been under • Drug use.

investigation for decades, but premature birthrates have • Abnormal uterine morphology.
actually been increasing. Since 1981 there has been a • The inability of the cervix to stay closed during
31% increase in the premature birthrate in the United pregnancy (also known as cervical incompetence).
States, with the rate now at approximately 12%.15 This
has been attributed to the increase in the number of Factors involving the pregnancy include:
multiple births related to the use of fertility drugs. There • Abnormal or decreased function of the placenta.
are persistent ethnic differences in premature birth rates, • Low lying position of the placenta, called
with African American infants having twice the prema- placenta previa.
ture birth rate of Caucasian or Hispanic infants.16 • Early detachment from the uterus, called placental
Maternal factors that can lead to premature birth abruption.
include: • Premature rupture of the amniotic sac
• High blood pressure of pregnancy, also known (membranes).
as pre-eclampsia or toxemia of pregnancy. • Abnormally low or high amounts of amniotic
• Infections of the fetal/placental tissues, vagina, fluid (oligohydramnios and polyhydramnios,
or urinary tract. respectively).
NEUTRAL THERMAL ENVIRONMENT, INSENSIBLE placed under radiant warmers or in incubators, which
WATER LOSS, AND MINIMAL STIMULATION limit heat loss by providing a neutral thermal environ-
Low-birth-weight infants are fragile and delicate. ment around the patient.
They do not tolerate excessive handling well. They are
very sensitive to changes in ambient temperature. Insensible Water Loss. Evaporation on the newborn’s
They have very little physiologic reserve; when skin also causes insensible water loss. In very low-
stressed, they can have a profound response, which birth-weight infants, this effect can be so pronounced
usually manifests itself in hypoxemia and/or brady- that it can become very difficult to maintain fluid
cardia. Newborns and particularly premature infants balance in the patient, particularly because water loss
are at risk of severe physiologic insult if careful cannot be directly measured. Thus some low-birth-
attention is not paid to maintaining their body weight infants are placed in environments to limit water
temperature. loss, such as hoods that go over the whole infant into
which heated humidified ambient gas is circulated and
Neutral Thermal Environment. Unlike adults, incubators into which heated humidified gas is circu-
premature infants have poor mechanisms for self- lated. Very low-birth-weight infants are also sometimes
regulation of body temperature. The ratio of body ensconced in a small framework that is covered with
surface area to body mass increases with decreasing plastic wrap (the same found in kitchens) to provide a
birth weight. This makes the newborn more prone moisture barrier.
to heat loss, which occurs by means of three
mechanisms in newborns: convection, conduction, Minimal Stimulation. It is now well-known that the
and evaporation. intensive care environment can be injurious to the
• Convection is the principle by which heat is neurodevelopment and physical growth of low-birth-
transferred from food in a refrigerator or weight infants.17,18 The principal culprit is the often
freezer. As cool air is circulated around the nonstop visual and auditory stimulation in the ICU
food, heat is transferred from the warmer food environment. These stimulations, when added to the
to the cooler air. So a newborn can lose heat unavoidable noxious stimulation of manipulating the
if air circulating around it is lower than body patient, taking blood samples, inserting catheters,
temperature. bathing, weighing, suctioning, and many other
• Conduction occurs when the newborn’s skin interventions, can create an environment where
comes in direct contact with objects that are there is little chance for quiet or sleep. However,
lower than body temperature. when environmental factors are modified, care is
• Finally, evaporation is a natural cooling mecha- coordinated, and interventions are developed to
nism by which sweat and other liquids on the minimize the number and duration of these kinds of
surface of the skin transition from liquid to the stimulations, improvements have been considerable,
vapor phase, absorbing heat as they do. including:19
Complications and consequences of neonatal • Requiring less ventilator support.

hypothermia are: • Less supplemental oxygen.
• Earlier discharge.
• Increased rate of basal metabolism. which leads to • Lower intraventricular hemorrhage rates.
higher glucose consumption and hypoglycemia. • Improved weight gain.
• Peripheral vasoconstriction and the resulting
decreased peripheral perfusion, tissue ischemia, A list of methods for ensuring minimal stimulation
and possibly metabolic acidosis. can include:
• Vascular changes in the lungs resulting in
• Providing for long periods of reduced lighting.
decreased ventilation, increased demand
• Minimizing loud talking at the bedside and
for oxygen, and worsening of respiratory
throughout the unit.
distress.
• Frequent drainage of ventilator tubing if
• Acidosis and hypoxia, predisposing to pulmo-
excessive water accumulates, causing
nary hemorrhage, and disseminated intravascu-
bubbling.
lar coagulation.
• Minimizing alarm volumes, including various
• Effects on liver function, resulting in hyperbiliru-
monitors and ventilator alarms. Alarms that are
binemia.
hooked to a remote system allow the volume in
Thus newborns must be quickly dried at birth and patient rooms to be kept low, while having the
swaddled in blankets. Premature newborns are soon alarms higher in the rest of the unit.
• Using care to quietly open/close isolette blind from ROP. In milder cases, the disease improves
portholes and doors. and leaves no permanent damage. About 90 percent of
• Utilizing isolette covers on all isolettes. all infants with ROP are in the milder category and do
• Avoiding use of the isolette roof as a shelf or not need treatment.
writing table. The causes of ROP are multifactorial, and
• Removing the bedside phone or turning the ring oxygenation derangement alone does not explain the
to its lowest level. pathology. But oxygen therapy plays a major role,
• Transitioning the infant from the warming table and the RT treating the low-birth-weight/premature
to the isolette as soon as possible. infant has an important role in keeping blood
• Utilizing continuous monitoring to assess vital oxygen levels within a “safe” range to reduce the risk
signs rather than the laying on of hands. of ROP. Generally accepted treatment guidelines
• Posting a “minimal handling” sign on the include keeping PAO2 in the range of 50–90 mm Hg
patient’s bed to notify team members of the or SPO2 in the 88–94%.
protocol.
• Careful coordination of care between respiratory
therapy, nursing, and medicine. This requires the
RT and RN to collaborate and plan their respec- RESPIRATORY DISTRESS SYNDROME
tive interventions so as to minimize the number One of the most common conditions in the NICU is
of times the infant is disturbed. neonatal respiratory distress syndrome (RDS), which is
also known as idiopathic respiratory distress syndrome
or hyaline membrane disease. This condition is primar-
RETINOPATHY OF PREMATURITY ily caused by an insufficient amount of pulmonary
surfactant and immature cell and vascular development
One of the most common causes of vision loss in
in the newborn lung. Pulmonary surfactant is a soapy,
childhood is retinopathy of prematurity (ROP).20 This
slippery, protective phospholipid substance that lines
disorder occurs mostly in newborns weighing ⬍1250 g
the alveolar and terminal airways and helps to reduce
and/or ⬍31 weeks of gestation. The risk of developing
surface tension at the air/fluid interface. Type II pneu-
ROP is inversely related to birth weight and gestational
mocytes produce surfactant, but they develop late in
age. ROP results from the abnormal growth and spread
gestation. Thus, the more premature the lung is, the
of blood vessels throughout the retina. The fragility of
higher the risk is of RDS. Risk is highest in infants
these abnormal blood vessels can lead to leakage,
⬎28–30 weeks, and RDS is very uncommon in term
which can scar the retina. The scarring can pull the
infants.
retina out of position, and in its most severe form can
With insufficient surfactant, the alveoli and
cause retinal detachment and severe loss of vision or
small airways become unstable and tend to collapse
even blindness.
at the end of exhalation, leading to widespread
First described in 1942, ROP emerged as hospital
atelectasis. This results in loss of functional residual
nurseries began using high levels of oxygen in
capacity, decreased pulmonary compliance, increased
incubators to save the lives of premature infants.
airway resistance, hypoxemia, and hypercarbia. The
During this period, measurement of serum oxygen
resultant respiratory acidosis and hypoxemia can
level was not available, and there was little if any
lead to increased pulmonary vascular resistance
ability to control FIO2. Clinicians were giving oxygen
and increased right-to-left shunting of blood at the
to relieve cyanosis. Consequently, an epidemic of
site of the patent ductus arteriosis and foramen
ROP ensued in the 1940s and 1950s. In 1954,
ovale, thus increasing hypoxemia and acidosis,
scientists determined that the relatively high levels
which can lead to lung injury and thus even less
of oxygen routinely given to premature infants at that
surfactant production.
time were an important risk factor and that reducing
Mortality associated with RDS is approximately
the level of oxygen given to premature babies reduced
10% of cases, but at one time was as high as 100%.21
the incidence of ROP. With newer technology and
The disease affects more than 20,000 infants per year,
methods to monitor the oxygen levels of infants,
with significant differences in incidence and mortality
oxygen use as a risk factor has diminished in
among ethnic groups.
importance.
The infant presenting with RDS may have the
Annually about 14,000–16,000 of these infants are
following signs:
affected by some degree of ROP, with 1100 to 1500
infants developing ROP that is severe enough to • Grunting: Infants make this sound while exhaling
require medical treatment. Approximately 400–600 against a partially closed epiglottis. It has been
infants each year in the United States become legally described as the infant’s attempt to maintain
back-pressure in the lungs and thus create a sort • Rales or crackles on auscultation: Rales, also called
of self-administered PEEP. crackles or crepitations, are the fine, crackling
• Nasal flaring: The dilation of the nares on inspira- noises heard on auscultation. They have been
tion has been described as a sign of air-hunger. described as being similar to the sound of rolling
This is an attempt by the infant to reduce airway human hairs between the fingers held close to
resistance by dilating the nasal opening the ear. The word “rales” comes from the French
• Retracting: The chest walls of newborn infants word râle meaning “rattle.” These sounds are
and children are more compliant than those of caused by the “popping open” of small airways
adults. When the diaphragm contracts, creating and alveoli collapsed by fluid, exudate, or lack
negative intrathoracic pressure, the more of aeration during expiration, all of which are
compliant chest collapses slightly because it typical in the premature surfactant-deprived
lacks rigidity. Retractions can be seen between lung.
the ribs (intercostal) and at the suprasternal
This list of signs describes most infants in respira-
notch (sometimes called tracheal tugging).
tory distress, whether the cause is surfactant deficiency
Typically, the more severe the retractions, the
(as in neonatal respiratory distress syndrome) or other
more severe the respiratory disease.
diseases. The key difference in presentation between
• Head bobbing: This occurs when the sternocleido-
diseases is often the breath sounds, such as wheezing
mastoid muscles (accessory respiratory muscles)
in asthma or rales and wheezing in bronchiolitis.
constrict to overcome poor compliance and high
The treatment of neonatal RDS was revolution-
airway resistance. These muscles also serve to lift
ized with the introduction of artificial surfactant
and rotate the head. Thus when they constrict to
in the 1990s. This treatment can cause rapid and
aide in respiration, they also pull the head up
remarkable improvements in compliance and oxy-
and forward.
genation by reducing alveolar surface tension and
• Tachypnea: Normal respiratory rates in newborns
decreasing atelectasis. Table 29-8 lists the basic
are in the range of 30–60 per minute. Normal
procedural steps and considerations for surfactant
respiratory rates adjusted for increasing age can
administration.22
be found in Table 29-7.
Supplemental oxygen therapy, nasal continuous
• Atelectasis: RDS usually produces a diffuse
positive airway pressure (NCPAP), and mechanical
bilateral atelectasis on X-ray, often referred to as
ventilation are also frequently used to treat RDS.
a ground glass.
NCPAP is used to reduce the atelectasis associated
• Hypoxemia: PaO2 ⬍ 50 mm Hg (arterial), or
with RDS and can frequently help in avoiding intuba-
⬍ 35 mm Hg (capillary), or SaO2 ⬍ 88%.
tion in neonates. More severe cases can require
• Hypercarbia: PaCO2 ⬎ 50 mm Hg (arterial or
intubation and mechanical ventilation. In severe
capillary).
cases, high tidal volumes and ventilating pressures
can be required to maintain acceptable blood gases.
With increasing levels of ventilatory support comes
increasing risk of iatrogenic lung injury. In neonates
TABLE 29-7 Normal respiratory rates in
sleeping and awake pediatric patients
Range Spotlight
Sleeping Awake On
6–12 months 22–31 58–75
1–2 yr 17–23 30–40
Neonatal Blood Gases
2–4 yr 16–25 23–42 Views about what constitutes acceptable ranges
for neonatal blood gases are divergent. PaO2 is
4–6 yr 14–23 19–36
normally lower in the newborn infant, and this
6–8 yr 13–23 15–30 fact is widely understood and accepted. But for
8–10 yr 14–23 15–31 a long time, clinicians attempted to normalize
10–12 yr 13–19 15–28 PaCO2 and pH. Clinicians eventually learned that
this was not necessary and that the increased
12–14 yr 15–18 18–26
tidal volumes and ventilating pressures required
Source: Schellhaese, D. E. Examination and assessment of the pediatric to do so contribute to lung injury in the neonate.
patient. In: Walsh, B.K., Czervinske, M.P., Diblasi, R.M., eds. Perinatal and
Pediatric Respiratory Care. 3rd ed. St. Louis, MO: Saunders Elsevier, 2010: This point is discussed more later in this chapter.
261–272.
TABLE 29-8 Surfactant administration: steps and considerations

Preterm infants • Infants with RDS should receive surfactant as a bolus and handling during administration should
first dose be minimized
• Infants ⬍ 27 weeks gestation should be automatically intubated, immediately after birth and
given prophylactic surfactant in the delivery room or as soon as possible after intubation
• Infants ⬎ 27 weeks and ⬍ 30 weeks gestation should receive prophylactic surfactant as soon as
possible if low exposure to antenatal steroids
• Infants ⬎ 30 weeks gestation should receive surfactant therapy if they have a diagnosis of RDS
Preterm Infants • Infants ⬍ 30 weeks gestation with the diagnosis of RDS should receive a second dose of surfactant
Additional as a bolus 6–12 hr after the first dose if they continue intubated on mechanical ventilation,
Doses: regardless of the inspired oxygen concentration
• Infants ⬎ 30 weeks gestation with the diagnosis of RDS should receive a second dose of surfactant
as a bolus 6–12 hr after the first dose if they continue intubated on mechanical ventilation and
require an FIO2 ⬎ 0.3. If the infant remains intubated with an FIO2 0.21–0.29, one should con-
sider a second dose of surfactant.
• One may consider continued treatment with additional doses of surfactant (total of 4 doses
maximum) for preterm infants with RDS and worsening oxygenation 6–12 hr after the s dose
Dosage • 4mL/kg Survanta every 6 hr times 4, if indicated
Equipment • 10-mL syringe
• Adapter for ETT
• Surfactant vial(s)
• Multi Access Catheter (MAC) of appropriate size
• 19-gauge needle
Preparation • Surfactant should be inspected visually for discoloration. Color should be off-white to light brown
• Swirl vial gently (Do Not shake) if settling occurs
• Should be warmed by standing at room temperature for at least 20 min or warmed in hand at
least 8 min
• Unused, unopened warmed vials may be returned to refrigerator within 8 hr of warming only once
• Using sterile technique, aspirate appropriate dose into syringe
Procedure 1. Patient will be intubated and hand-bagged during administration.
2. Suction prior to administration.
3. Obtain a Trach Care Multi Access Catheter (MAC).
4. Obtain matching Y adapter for endotracheal tube.
5. Attach adapter to endotracheal tube.
6. Determine the measurement where endotracheal tube is cut and add 4.5 cm and note marking
on catheter. This will place catheter at end of endotracheal tube.
7. Attach syringe of medication to end of MAC catheter.
8. Advance catheter until measured mark has been reached.
9. Instill ½ dose slowly; pull out catheter after small amount has been given. Then keep instilling
small amounts until the full ½ dose has been given. Administer drug over a period of 5–20 min.
10. Turn infant 45 degrees to the right after administration of the first ½ dose. Hold in this position
for 30 s.
11. Return infant to midline. Repeat procedure with the second ½ dose.
12. Turn to left 45 degrees and hold for 30 seconds.
13. After completion, return infant to midline. Remove syringe and replace with inline suction.
14. Store remaining surfactant in refrigerator for up to 12 hr after labeling with patient name, date/time.
(continues)
TABLE 29-8 Surfactant administration: steps and considerations (continued)

Monitoring 1. The following should be monitored during and 30 min after dose administration:
a. Heart rate
b. Color
c. Tidal volume
d. Pulse oximetry
2. If HR slows, the infant becomes dusky or agitated, oxygen saturations fall more than 15%,
or surfactant backs up in ETT, dosing should be slowed or halted, and, if necessary, ventilatory
support gently increased until the patient returns to baseline.
3. Special care must be taken to keep tidal volumes in “safe” range during or immediately after
surfactant administration. This is typically in the range of 5–7 mL/Kg (some centers use
6–8 mL/Kg). As compliance improves, tidal volume will increase in pressure limited modes.
The PIP must be quickly weaned to limit the risk of lung injury cause by over-distention.
4. Avoid suctioning for at least one hr (preferably two to four hr) after surfactant administration,
unless clinical deterioration is evident and patient is nonresponsive to other measures.
this often manifests itself in various forms of so-called or subpleural space. One or both lungs may be
air-leak syndrome. involved. If dissection of air is severe and
widespread enough, it can cause the lung to
stiffen, that is, reduce lung compliance, making
AIR LEAK SYNDROME ventilation more difficult. This condition can
Pulmonary air leak syndrome is the leakage and dissection often be a precursor to the development of
of air out of the normal pulmonary airspaces. In this bronchopulmonary dysplasia. If one lung is
context, dissection means that the air leaks into non-air significantly more involved than the other, the
spaces and moves along the perivascular sheaths to other infant can benefit from being placed in the
pulmonary structures. The site of leakage is visually lateral recumbent position with the more
represented in Figure 29-2. The distance the air travels affected lung down. This causes more compres-
and the amount of air leakage contribute to which type sion of the bad lung thereby decreasing air
of air leak is present: pulmonary interstitial emphysema, leakage and perhaps improving ventilation of
pneumomediastinum, pneumopericardium, pneumo- the better (elevated) lung.
peritoneum, and pneumothorax. • Pneumomediastinum is the leakage of air into
connective tissue of the mediastinum. This can
• Pulmonary interstitial emphysema is the leakage of be asymptomatic or, in its severe forms, may
gas into the pulmonary interstitium, lymphatics, compress lung tissue.
A
Vascular
Sheath
Arteriole
Bronchiole
Venule A
A
Alveolus
A = Sites of Air Leak

(A) Normal (B) With Leaks
FIGURE 29-2 Schematic representation of possible sites of air leak in the newborn lung.
This cross sectional view is of the terminal respiratory unit.
• Pneumopericardium is the dissection of air into Ventilation during neonatal resuscitation using
the pericardial sac. If sufficient air leaks into positive pressure ventilation via facemask should be
the sac, it can restrict the movement and refilling avoided with CDH. During positive pressure ventila-
of the heart, a condition called cardiac tion with a mask, gas often enters the stomach under
tamponade. pressure and can cause distension of the stomach or
• Pneumoperitoneum is the dissection of air into the bowel. If parts of the bowel or the stomach are in the
peritoneum and is seen almost exclusively in thoracic cavity and are distended by gas, the distended
extremely severe cases of air leak. organs can press more on lung tissue, making ventila-
• Pneumothorax is leakage and dissection of air tion even more difficult. It ventilatory support is
into the pleural space. If air continues to required at the time of delivery, intubation should be
accumulate, causing significant compression of accomplished immediately.
adjacent lung tissues and vascular structure, it The treatment of diaphragmatic hernia involves
is called a tension pneumothorax. Small mechanical ventilation and cardiovascular support
pneumothoraces may resolve spontaneously, until and after the hernia can be surgically corrected.
but larger pneumothoraces require evacuation Because the lung can be very hypoplastic, lung
of the air in the pleural cavity via chest tube. A volumes are often significantly decreased in these
tension pneumothorax happens almost exclu- infants. Pneumothorax is a typical complication of
sively during positive pressure ventilation. mechanical ventilation in CDH patients, occurring in
During inspiration, the positive pressure forces as many as 25% of cases. The presence of a pneumo-
air out through the site(s) of the leak. It is thorax is a risk factor for death, and thus great efforts
assumed that during exhalation, these leak are taken to avoid lung overdistension. Practice from
sites close so that this pressurized air accumu- center to center varies considerably. Some groups use
lates in the pleural space with each successive early high-frequency oscillatory ventilation to keep
breath. Untreated, the tension pneumothorax tidal volumes very small. Others use conventional
may be immediately life-threatening because it ventilators run at very high rates with shortened
can grow to such a large size that it compresses inspiratory times and low peak inspiratory
lung tissue and vascular structures in the pressures and little or no set PEEP (sometimes
thorax. called gentle-a-tion). The theory is that this approach
minimizes volumetric lung distension. The very high
rates probably create inadvertent PEEP because
CONGENITAL DIAPHRAGMATIC HERNIA expiratory times are too short to allow complete
exhalation. Thus the set PEEP is kept at zero, on
During intra-uterine lung development, a defect or the assumption that the patient is getting
hole can occur in the diaphragm. This is called inadvertent PEEP.
congenital diaphragmatic hernia (CDH). If large enough,
the defect allows the abdominal contents (loops of
bowel or the stomach) to enter the chest cavity. These
abdominal structures can then press on the developing
lung and hinder lung growth. The limitation of lung
growth is called pulmonary hypoplasia. In more severe Spotlight
cases, an entire side of the lung cavity can be occupied On
by bowel and result in the development of only one
functional lung, which may also be hypoplastic. Lung
PEEP
hypoplasia can involve significant reductions in lung Inadvertent PEEP has also been creatively and
volumes and severe diffusion defects that can make it variously called occult PEEP, hidden PEEP, or
very difficult to make the transition to extra-uterine intralung PEEP. A conviction among some is that
life. CDH occurs in 1 of every 3000 to 5000 live PEEP that cannot be measured with a proximal
births.23,24 Mortality from CDH is typically described airway pressure measurement needs to be hunted
in the 40% range25 but has been reported as high as down and stamped out. Of course, during some
68%.26 forms of high-frequency ventilation, intralung
About 90% of the hernias affect the left side of the PEEP is an important therapeutic goal. Intralung
diaphragm, although they can occur on either side or PEEP can be measured by occluding the airway
both sides. The majority of hernias are diagnosed at the end of inspiration and noting whether
prenatally, and so the clinician knows about it at the airway pressure returns to zero or rises slightly
time of delivery. Prenatal diagnosis significantly (a sign of PEEP).
improves the chances for survival.
Common Pediatric Respiratory (particularly at night or early in the morning),

wheezing, breathlessness, and chest tightness.
Diseases and Conditions These episodes are usually associated with wide-
spread but variable airflow obstruction that is often
ASTHMA
reversible either spontaneously or with treatment.
Pediatric asthma is one of the most prevalent diseases
affecting children.27 Childhood asthma has been The principal mechanisms of this airflow obstruc-
increasing, and 14 million children in the United States tion are illustrated in Figure 29-3 and can include any
under the age of 18 have been diagnosed at one time or all of the following:
or another to have had asthma (about 14%).28 There • Mucosal edema. The inner lumen of the airways is
are disparities in asthma prevalence and impact among narrowed as the mucosal lining of the airways
ethnic groups and economic strata. There are approxi- becomes swollen.
mately 335,000 hospitalizations per year in the United • Excessive mucus secretion. The inner lumen of the
States for asthma among children 2–17 years of age.29 airways can become completely or partially
A recent large survey conducted to study the scope obstructed by accumulated mucus, which is
and impact of asthma in the lives of children and their secreted in abnormally large amounts when the
families revealed that: airways are inflamed.
• 54% of children four to 18 years of age with • Bronchoconstriction. The smooth bronchial
asthma missed school (or daycare) in the past muscles that surround the airways respond to
year as a result of their disease. inflammation by constricting and narrowing the
• An estimated 21 million school days are lost per lumen of the airway.
year due to asthma. A prominent clinical feature of asthma is wheez-
• Nearly 9% of children with asthma missed more ing. However, the lack of wheezing on auscultation
than two weeks of school in the past year as a does not indicate an absence of airflow obstruction or
result of their condition. of asthma. In a severe attack, asthmatic children can
• More than a third of parents missed work in the appear to have almost no wheezing on auscultation.
past year as a result of their child’s asthma, and 11% This can be an ominous sign because it can indicate
missed more than a week of work in the past year. not enough air is moving into the lung to create a
• An estimated 5 million workdays are lost per wheeze. Also, the lungs can be significantly inflamed
year for parents of children with asthma. even though no wheezing is heard. Conversely, the
(These data are from a survey of over 41,000 homes presence of wheezing does not always indicate asthma.
conducted by GlaxoSmithKline and published on the Other causes of wheezing in children are:
world wide web at http://www.asthmainamerica.com/
• Infections like bronchitis or bronchiolitis.
children_survey.html. Survey findings were then
• Foreign bodies or lesions in or outside the airway.
extrapolated to the entire population of U.S. children.)
• Congenital or acquired malformations of the
Asthma is an inflammatory disease of the lungs.
airways.
It has been the subject of a great deal of work at the
national level to develop standardized and widely Asthma is typically difficult to diagnose in
accepted definitions, descriptions, and treatment children under 3–5 years old, owing to the inability of
guidelines. Under the auspice of the National Institute these patients to cooperate with airflow measurement
of Health, the National Heart Blood and Lung maneuvers. Thus, some infants and toddlers diag-
Institute created the National Asthma Education nosed with other respiratory disorders like bronchiol-
and Prevention Program. The “Expert Panel Report 3: itis are actually pre-emergent asthmatics. This can
Guidelines for the Diagnosis and Management of lead to the mistaken observation that bronchodilators
Asthma” is one of the products of this work and offers seem to work in bronchiolitis (which has been
an excellent tool for the clinician interested in a thor- disproven). The pre-emergent asthmatics are respond-
ough understanding of the nature and treatment of this ing to bronchodilators (which do work in asthma for
disease.30 In the report, asthma is defined as follows: short-term relief).
The primary treatment for asthma is pharmacologi-
Asthma is a chronic inflammatory disorder of the
cal. The rapid relief of acute symptoms and long-term
airways in which many cells and cellular elements
asthma control are the two mainstays of asthma
play a role: in particular, mast cells, eosinophils,
treatment.
neutrophils. . . . T-lymphocytes, macrophages, and
epithelial cells. In susceptible individuals, this • Short-acting inhaled or oral ß2-agonists, short-
inflammation causes recurrent episodes of coughing course oral or intravenous corticosteroids, and
Submucosal
gland
Constricted
Smooth smooth
bronchial muscle
muscle
Airway
epithelium
Excessive
Mucus mucus
plug
Alveoli production
Hyperinflated
alveoli
(A) Normal (B) Asthmatic
FIGURE 29-3 Illustration of normal versus asthmatic airways and terminal respiratory units.
ipratropium bromide are recommended for carrier gas that is mixed with oxygen. Helium has
quick relief. one-third the density of nitrogen, and theoretically this
• Long-term control involves the use of cromolyn less dense gas mixture is easier to breath because the
sodium, inhaled and oral corticosteroids, patient does not have to work as hard to move the
leukotriene modifiers, long-acting ß2-agonists, same volume of gas through narrowed airways.33
nedocromil sodium, and sustained-release Heliox is administered via simple mask or cannula, or
theophylline. it is used to drive nebulizers or administered through a
• A typical clinical quality measure for the treat- mechanical ventilator. Heliox typically comes from the
ment of pediatric asthmatics in emergency rooms supplier in concentrations of approximately 80%
is the elapsed time from arrival to first dose of helium and 20% oxygen. FIO2 can be increased by
steroids, highlighting the importance of anti- adding more oxygen via bleed-in or with specially
inflammatory drugs in the treatment of asthma. modified blender setups. A rule of thumb is that heliox
• Typically, inpatient treatment involves short-term therapy is of little value if the FIO2 ⬎ 0.40 because the
relief with inhaled albuterol and supportive smaller overall amount of helium does not reduce
measures like hydration and oxygen, until the work of breathing enough to make a difference.
steroids can kick in and reduce lung inflammation. There are a limited number of studies on the utility
For severe asthma attacks, other treatments are of this therapy in children,34,35 and the results are
sometimes used, including intubation and mechanical conflicting. It is not clear that heliox really alters
ventilation, although this approach is becoming rarer outcomes for asthma patients, although for some
as the understanding of how to manage asthma patients it clearly offers immediate, visible relief. The
improves. Intubation should be avoided in asthmatics utilization of heliox varies widely with some hospitals
if possible because the introduction of the endotra- hardly ever using it, while others employ it frequently.36
cheal tube can act as an irritant to an airway that is Heliox can be given to intubated asthmatics via a
already hyper-responsive. To this end, some clinicians mechanical ventilator. Most ventilators are not
have used noninvasive positive pressure ventilation to designed for this, and so the therapist must make
avoid intubation.31,32 special adaptations of the blender-ventilator system to
safely control the amount of heliox the patient receives.
Mixtures of oxygen and helium (heliox) have
Whenever heliox is used, the respiratory therapist
been used as a treatment for asthma in children. This
must remember that the lower density gas makes most
therapy replaces nitrogen with helium as the inert
flow meters and flow measurement devices inaccurate. tract infections in infants and children. About two-
To estimate actual flow rate when using heliox, take the thirds of this bronchiolitis is caused by respiratory
visual reading from a typical flow meter and multiply syncitial virus (RSV), a ubiquitous virus that infects over
times 1.8. Some pediatric neonatal ventilators are 90% of children by age 2. In previously healthy infants,
specifically designed to allow the use of heliox. Their the disease typically has a short course (3–5 days) and
intrinsic measurement and flow control systems are very mild to moderate symptoms. However, in more
programmed in such way to allow for accurate opera- severe cases, hospitalization is required. Bronchiolitis
tion in the presence of heliox. (At the time of writing, causes more than180,000 hospitalizations per year in
three widely used ventilators have the built-in capacity children ⬍ 1 year of age at a cost of almost $2.5 billion
to operate accurately with heliox: Viasys Avea, Hamil- annually.38 The reasons for hospitalization include the
ton G5, and Maquet Servoi.) need for:
The diagnosis of asthma involves physical exami-
• Close observation.
nation, history, and assessment of airflow obstruction.
• Supplemental oxygen therapy.
In children older than 5 years of age, diagnosis can
• Bronchodilator treatments.
typically be achieved using peak flow meters at the
• Frequent nasal suctioning.
bedside or spirometry before and after bronchodilator
• Rehydration.
treatment. In younger children, the measurement of
• Treatment for apnea.
airflow obstruction is more difficult and is typically not
routinely used in the assessment of asthma severity or Uncomplicated bronchiolitis in previously healthy
response to therapy. infants is typically a self-limited illness with few
The respiratory treatment of inpatient asthmatics is interventions that actually substantially alter the course
often now guided by the use of asthma clinical scores. of the disease. However, multiple interventions are
These are typically composite scores constructed by frequently used, including corticosteroids, antibiotics,
assessing or scoring patients on several variables. Their ribavirin, the repeated use of bronchodilators, and
basic design is similar to APGAR scores. Table 29-9 chest physical therapy in the form of postural drainage
shows a typical asthma clinical score that was studied and percussion. However, when these interventions
and shown to have a high agreement between different have been tested in controlled scientific studies
providers scoring the same patient.37 The patient’s designed to measure their impact on outcomes, they
clinical score is used to guide the need for bronchodila- have almost universally failed to demonstrate any
tors, dosage and frequency, and periodicity of reassess- efficacy.39,40 This evidence41,42 (or lack thereof) not-
ment. In many facilities, the respiratory care of withstanding, there continues to be considerable
asthmatics is guided by a standardized protocol. The variation in how bronchiolitics are treated when
respiratory therapist and nurses administer the asthma inpatients. There continues to be widespread use of
clinical score and use it to guide the intensity of bronchodilators in this population in spite of repeated
bronchodilator therapy. studies showing a lack of efficacy. Chest physiotherapy,
antibiotics, and steroids are also prone to overutiliza-
BRONCHIOLITIS tion in this group.
Pediatric bronchiolitis is a disease caused by viral lower
respiratory tract infection. It is characterized by acute
airway inflammation, edema, and necrosis of epithelial Spotlight
cells lining the small airways. Generalized interstitial On
swelling, combined with inhibition of pulmonary
surfactant function, leads to the narrowing of airways. Bronchiolitics
The net result is increased secretion production and Patients admitted to the hospital typically expect
decreased secretion clearance due to the compromise that their conditions can be cured or their
of the mucociliary elevator. Brochoconstriction may be suffering can be minimized. So they expect
present, but generally it is not the principal cause of caregivers to intervene, that is, do something for
airway obstruction, which is usually the airway edema them or to them to help them. This is particularly
and accumulated secretions. This explains the failure of true for parents of pediatric cases. In bronchiol-
bronchodilators to work in most of these patients. itis care, this expectation creates pressure among
Signs and symptoms are typically rhinitis, tachypnea, clinicians to do something to help these sick
wheezing, cough, crackles, use of accessory muscles, children. The authors believe that this pressure
and/or nasal flaring. contributes to the overuse of these ineffective
Each year there is a near pandemic in the United interventions in bronchiolitics.
States (and other countries) of viral lower respiratory
TABLE 29-9 A clinical asthma scoring tool.*

Variable 0 point 1 point 2 points 3 points
Respiratory rate (breaths/min)
⬍2 mo ⱕ60 61–69 ⱖ70
2–12 mos ⱕ50 51–59 ⱖ60
1–2 yr ⱕ40 41–44 ⱖ45
2–3 yr ⱕ34 35–39 ⱖ40
4–5 yr ⱕ30 31–35 ⱖ36
6–12 yr ⱕ26 27–30 ⱖ31
⬎ 12 yr ⱕ23 24–27 ⱖ28
Retractions None Subcostal or intercostal 2 of the following: 3 of the following:
subcostal, intercostal, subcostal, intercostal,
substernal, or substernal, suprasternal,
nasal flaring (infants) supraclavicular, or nasal
flaring or head bobbing
(infants)
Dyspnea
0–2 yr Normal feeding, 1 of the following: 2 of the following: Stops feeding, no
vocalizations, and difficulty feeding, difficulty feeding, vocalizations, or drowsy
activity decreased vocalization, decreased vocalization, or confused
or agitated or agitated
2–4 yr Normal feeding, 1 of the following: 2 of the following: Stops eating or drinking,
vocalizations, and decreased appetite, decreased appetite, stops playing, or drowsy
play increased coughing increased coughing after or confused
after play, hyperactivity play, hyperactivity
ⱖ 5 yr Counts to ⱖ 10 in Counts to 7–9 in one Counts to 4–6 in one Counts to ⱕ 3 in one
one breath breath breath breath
Auscultation Normal breathing; End-expiratory wheeze Expiratory wheeze only Inspiratory and expiratory
(as it relates to no wheezing only (greater than end- wheeze or diminished
wheezing) present expiratory wheeze) breath sounds or both
*Scores range from 0–12. Scores ⬍5 are considered mild, while scores ⬎9 are severe. Respiratory rate should be counted for a full min while patient is awake
In our experience, a small number of infants— bronchodilator treatment is given, then the patient
typically about 20% of presenting bronchiolitics— is rescored. If the scores improved, bronchodilators
with uncomplicated bronchiolitis appear to respond to therapy is continued with frequent reassessment. If
bronchodilators. The conventional wisdom holds that the score does not improve, bronchodilator therapy
these are pre-emergent asthmatics, who appear to is discontinued because it did not seem to help the
be more susceptible to bronchiolitis. Thus, most patient. Figure 29-4 is an algorithm for the manage-
bronchiolitis treatment protocols include a trial of ment of bronchodilators. This algorithm and bronchi-
bronchodilators.43,44 Only if the patient clearly olitis score were developed at Primary Children’s
responds to the drug are the treatments continued. Medical Center in Salt Lake City and were very
Response is assessed using clinical bronchiolitis successful in reducing the unnecessary utilization of
scores, some of which are similar to asthma clinical interventions.46
scores. Table 29-10 shows one such bronchiolitis score.45 An essential part of bronchiolitis care is the use of
Typically infants are scored (assessed), their upper nasal pharyngeal suctioning. This technique is sometimes
airways are cleared, and then they are reassessed. If mistakenly referred to as deep suctioning. Usually,
the scores significantly improve, then further treatment deep suctioning is reserved for when an attempt is
with bronchodilators is deemed unnecessary. If upper made to insert the suction catheter all the way to the
airway clearance does not improve the score, then a epiglottis and even into the trachea. The technique
TABLE 29-10 Bronchiolitis Score

Score Assigned Respiratory Rate Wheezing Retractions
0 ⬍30 no wheezing with good air exchange none
1 31–45 late expiratory with stethoscope only mild
2 46–60 entire expiratory or inspiratory phase with moderate
stethoscope only
3 ⬎60 loud wheezes without stethoscope or no severe
wheezing in the presence of severely
diminished gas exchange
0–1 ⫽ normal; 2–3 ⫽ mild; 4–6 ⫽ moderate; 7–9 ⫽ severe
Y Periodically
Score Suction Score Improve?
Reassess
Albuterol Y Continue
Score Improve?
Tx Albuterol
Discontinue
Albuterol
All Treatments Ordered PRN
FIGURE 29-4 Algorithm for managing bronchodilator use in bronchiolitics.

In this particular protocol, nasal pharyngeal suctioning through both
nares into the hypopharynx was used on all infants with bronchiolitis
prior to giving bronchodilators.
includes the passing of an appropriately sized catheter consequent pulmonary edema. Pediatric ARDS can be
through each nare into the hypopharynx. This clearing caused by aspiration, near-drowning, smoke inhala-
of the upper airway reduces work of breathing and tion, lower respiratory tract infections, trauma, and
often reduces symptom severity and resource multisystem organ failure.49,50
consumption.47,48 Some clinicians have argued that it It has been estimated that there are 190,600 cases
is too traumatic to routinely use nasal pharyngeal of ARDS in all age groups, involving 74,500 deaths and
suctioning on infants, but in our experience, when the
staff are properly trained and experienced, nasal
pharyngeal suctioning was safe and effective. Also,
Best Practice
some clinicians have suggested that olive tip style of
suctioning is sufficient, but we find this technique less Suctioning
effective in clearing the upper airway. In children, passing a catheter through the
nose and blindly entering the trachea is all but
impossible. However, simply passing the catheter
ACUTE RESPIRATORY DISTRESS down into the hypopharynx is usually sufficient
SYNDROME (ARDS) to cause a strong cough reflex in the patient,
Acute respiratory distress syndrome (ARDS) is a condition which in the end is usually a good thing to do in
that results from overwhelming inflammation, patients with secretion problems.
increased alveolar capillary permeability, and
and PaCO2 55–65), lower tidal volumes and alveolar

Spotlight distending pressures (plateau pressures).56 Typically,
On tidal volumes are kept in the 4–6 mL/kg or lowest tidal
volume possible while keeping plateau pressures
Statistical Data ⬍30 cm H2O. PEEP is set according the level of
Statistics can be misleading. The adult data required FIO2. Once the oxygenation improves, aggres-
include all hospital days, whereas the pediatric sive attempts are often made to reduce the FIO2 to
data report only PICU days. This is often the case minimize the risk of toxic effects from exposure to high
in broad studies of disease epidemiology and oxygen levels in the lung. Table 29-11 lists some
impact. Data from different studies are sliced guidelines for setting up and managing the mechanical
up in different ways. ventilatory for a child with ARDS.
Respiratory Assessment in the

Neonatal and Pediatric Patient
3.6 million hospital days per year.51 For pediatric A common duty of the neonatal pediatric RT is to
ARDS,52 there is an estimated 7700 cases, 1400 deaths, evaluate the respiratory status of a child. The two
and 6200 pediatric intensive care days per year. principal parts of this respiratory assessment are a
ARDS is characterized by reduced lung compliance, visual inspection and auscultation. In addition to the
increased airway resistance, refractory hypoxemia, and previously described signs associated with assessing
respiratory acidosis. These factors can cause severe respiratory failure in infants, a special consideration for
respiratory failure, which often results in intubation the respiratory assessment of infants and children is the
and mechanical ventilation. use (or lack of use) of blood gases. For the presenting
In adults, mortality from ARDS has been reported infant or child, blood gas sampling can be very difficult
to be approximately 39%.51 The incidence of mortality because of the technical challenges of doing an arterial
in pediatric ARDS has been reported as 18%.52 stick on an infant or small child. In addition, the lack
ARDS often follows a severe physiologic insult like of patient cooperation can make arterial blood gases
trauma or sepsis and presents with: difficult to get. Finally, parents are understandably
reluctant to see their children subjected to a lot of pain.
• An acute onset.
Consequently, blood gases are usually obtained
• Severe arterial hypoxemia refractory to oxygen
only when significant respiratory distress is evident
therapy alone (PaO2/FIO2 ratio ⱕ 200 mm Hg).
from other signs. When blood gases are needed, venous
• Diffuse bilateral pulmonary infiltrates on chest
and capillary samples are sometimes used to avoid the
radiograph.53
need for percutaneous arterial sampling. Capillary
Some pediatric clinicians prefer the use of the sticks are less painful for children. Venous samples are
SpO2/FIO2 ratio in infants and children as a surrogate usually easier because the patients are getting veni-
marker to diagnose ARDS since arterial blood gas puncture for other laboratory work being done, and
sampling can be challenging in infants and children. In additional blood is drawn for blood gases. In general,
fact, an SpO2/FIO2 ⬍ 275 corresponds well with the venous and capillary blood gases are suitable for
predefined PaO2/FIO2 criteria of ⬍ 200 for ARDS.54 determining the level of ventilation and acid-base
In the last decade, the pediatric community has balance, but they have limited value in determining
adopted the successful application of adult lung- oxygenation status. Pulse oximetry is the tool most
protective ventilation strategies. These strategies have often used for assessing oxygenation. Table 29-12
developed out of the growing understanding that the describes normal blood gas and pulse oximetry ranges
application of mechanical ventilation itself can be in neonates and children.
injurious to the acutely ill lung. This is true for neona- Another important issue in neonatal and pediatric
tal, pediatric, and adult scenarios. It was long held that assessment is the lack of reserve that some sick infants
high airway pressures were the chief cause of ventilator- and children exhibit. An infant or child in respiratory
induced lung injury. Excessive lung volumes, not excessive distress can very quickly worsen, and the pulmonary
airway pressures, are the chief cause of ventilator-induced assessment of these patients is in part dependent on
lung injury (discussed later in this chapter). The basic learning how to determine whether these patients are
premise is that limiting tidal volume is more important on the edge of a sudden deterioration. By way of
than limiting pressures in the prevention of injury.55 example, a PaCO2 of 46 mm Hg might not bother you
Conventional mechanical ventilation is generally at all in most infants, children, or adults. But if this
designed to allow permissive hypercapnea (pH⬎7.20 blood gas comes from a 4-year-old asthmatic who is
TABLE 29-11 Guidelines for pediatric ARDS ventilator management

1) Initial ventilator tidal volume and rate adjustments
a) Calculate predicted body weight (PBW)
Best Practice
i) Male ⫽ 50 ⫹ 2.3 [height (inches) – 60] or 50 ⫹ 0.91 [height (cm) –152.4]
PEEP Guidelines:
ii) Female ⫽ 45.5 ⫹ 2.3 [height (inches) – 60] or 45.5 ⫹ 0.91 [height (cm) –152.4] These include
b) Mode: Volume Assist-Control or PRVC Assist-Control recommendations
i) Set initial tidal volume to 8 ml/kg PBW for a lower or higher
PEEP strategy, which
ii) Reduce tidal volume to 7 mL/kg after 1–2 hr and then to 6 mL/kg PBW after 1–2 hr
remains controversial
iii) Set initial ventilator rate to maintain baseline min ventilation (not ⬎ 35 bpm)
Low High
2) Subsequent tidal volume adjustments FIO2 PEEP PEEP
a) Plateau pressure goal: ⱕ 30 cm H2O 0.3 5 5–14
b) If plateau pressure ⬎ 30 cm H2O, decrease tidal volume by 1 mL/kg PBW steps to 5 0.4 5–8 14–16
or if necessary to 4 mL/kg PBW.
0.5 8–10 16–18
c) If plateau pressure ⬍ 25 cm H2O and tidal volume ⬍ 6 mL/kg, increase tidal volume
0.6 10 20
by 1 mL/kg PBW until plateau pressure at ⬎ 25 cm H2O or tidal volume ⫽ 6 mL/kg.
0.7 10–14 20
d) If breath stacking or severe dyspnea occurs, tidal volume may be increased (not
required) to 7 or 8 mL/kg PBW if plateau pressure remains ⱕ 30 cm H2O. 0.8 14 20–22
3) Arterial oxygenation 0.9 14–18 22
a) Goal: PaO2 55–80 mm Hg or SpO2 88–95% 1.0 18–24 22–24
b) Use the FIO2/PEEP combinations in the table to the right to achieve oxygenation goal.
4) Respiratory Rate (RR) and pH (arterial)
a) pH Goal: 7.30–7.45 (arterial)
b) Acidosis Management:
i) If pH 7.15—7.30: Increase set RR until pH ⬎ 7.30 or PaCO2 ⬍ 25 mm Hg
ii) Maximum Set RR ⫽ 35 bpm
iii) If set RR ⫽ 35 bpm and pH ⬍ 7.30, NaHCO3 may be given (not required)
iv) If pH ⬍ 7.15:
(1) Increase set RR to 35 bpm.
(2) If set RR ⫽ 35 and pH ⬍ 7.15 and NaHCO3 has been considered, tidal
volume may be increased in 1 mL/kg PBW steps until pH ⬎ 7.15 (plateau
pressure target may be exceeded).
c) Alkalosis Management: (pH ⬎ 7.45):
i) Decrease set RR until patient RR ⬎ set RR
ii) Minimum set RR ⫽ 6 bpm
d) I/E ratio
i) Goal: 1:1.0 to 1:3.0
ii) Adjust flow rate and inspiratory flow waveform to achieve goal.
TABLE 29-12 Normal (reference) ranges for blood gases and pulse oximetry
Age Range Neonatal Pediatric
Source Arterial Venous Capillary Arterial Venous
pH 7.35–7.45 7.31–7.41 7.31–7.47 7.35–7.45 7.31–7.41
pCO2 35–45 mm Hg 41–51 mm Hg 29–49 mm Hg 35–45 mm Hg 41–51 mm Hg
pO2 50–90 mm Hg 30–40 mm Hg 33–61 mm Hg 80–100 mm Hg 30–40 mm Hg
SpO2 92–94% NA ⬎95% NA
Source: Capillary values are from Cousineaua, J., Anctilb, S., Carcellerb, A., Gonthierb, M., Delvin, E. E. Neonate capillary blood gas reference values. Clin
Biochem 2005;38(10):905–907.
very tachypnic, has labored breathing, and is wheezing intrinsic measurement errors under the best of condi-
loudly on inspiration and expiration, this is an omi- tions of ⫾5% of the absolute reading. Many are worse.
nous blood gas. Pediatric asthmatics can decompensate Some measurement devices have severe limitations
very rapidly, and it is concerning that this patient is under certain conditions, and some of these limitations
working so hard to maintain such a marginal PaCO2. are more pronounced in neonatal/pediatric popula-
This sign could be a portent of a sudden deterioration, tions. Clinicians must have a deep understanding of
and close monitoring and escalation of care is in order. these limitations to make informed decisions about the
The other key factors in respiratory assessment are: quality of the data they produce. Also, some of the
respiratory therapy technology that is suitable for
• Respiratory rate.
adults has serious limitations in neonates and children.
• Grunting.
• Flaring.
• Retracting. MANUAL RESUSCITATORS
• Level of consciousness.
Today, newborns require resuscitation more frequently
• Level of irritation.
than any other patient population, and one of the
The typical child in respiratory distress presents common features of this resuscitation is the application
tachypnic, agitated, or highly irritable with exaggerated of positive pressure ventilation (PPV) using manual
work of breathing. resuscitators.57 Nearly 10 million newborns per year
require some type of resuscitation worldwide.58 Along
with the resuscitation of newborns in the delivery suite,
Technology of Pediatric and manual resuscitators are widely used in the intensive
Neonatal Respiratory Therapy care unit for PPV during disconnection from the
mechanical ventilator and during intra- and interhospi-
A wide array of technical tools are available to the RT
tal transport. The most commonly used manual
in the pediatric setting. Mastering the application of
resuscitators fall into two categories: flow-inflating bags
these devices is essential to practicing successfully.
and self-inflating bags.
Some RTs have been practicing long enough to have
Flow-inflating bags (FIBs) require a constant
seen this amazing transition to a much more complex
(though adjustable) flow of source gas to operate (SIBs
technological environment. In this long passage, they
can operate without a flow of source gas). Positive
have also noticed that this amazing technical wizardry
end-expiratory pressure (PEEP) is maintained by
can make them lose sight of the patient amid all the
partially occluding excess flow out of the bag through a
monitors, catheters, tubes, masks, and machines. The
small hole or an adjustable flow-resisting valve at the
respiratory technician must avoid the black box preoccupa-
tail of the bag. The thumb is used to partially occlude
tion that occurs when the RT at the bedside becomes
the hole in the bag. Adjusting the flow and maintaining
overly focused on the readings of the various machines
PEEP with this type of resuscitator requires a relatively
and monitors. The first and most important indication
advanced degree of both experience and skill.59 How-
of how well the patient is doing is a physical examina-
ever, many less skilled and trained clinicians end up
tion; this fact can be forgotten in the swirl of bedside
using these bags owing to turnover of staff and the
technology. The technology scenario can be visually
constant flow of newly graduated clinicians into our
very poignant with infants and small children, who can
hospitals.
be dwarfed by the size and number of devices and
With self-inflating bags (SIBs), the elastic recoil of
monitors at the bedside.
the bag draws in the gas, which may be ambient or
Consider the patient on a mechanical ventilator,
supplemental oxygen, depending on the bag’s configu-
extracorporeal life support, various infusions of fluids,
ration. The design allows the bag to operate even with
antibiotics, vasopressors, inotropes, a cardiorespiratory
a loss of source gas. Certain brands of SIBs have valve
monitor, pulse oximetry, and capnography. Some 15 to
mechanisms that allow gas to be directed to the patient
20 different screens may be in the room presenting
during inhalation. If PEEP is desired, typically an
digital data in numeric and or graphical form. Along
add-on spring-loaded variable orifice PEEP valve is
with the obvious opportunity to commit errors of
attached to the exhalation port of the bag.
commission or omission in this visually complex
There is a great deal of so-called conventional
environment, the patient tends to be lost amid the
wisdom about the (alleged) relative merits of both types
clutter.
of resuscitators:
There is also a tendency to not really understand
the limitations of the devices being used. Respiratory • FIBs are made of softer material, allowing the
therapists must understand that all measurements are clinician to feel changes in lung compliance
erroneous. Even the best clinical instruments have better than with an SIB.60,61
• FIBs deliver blow-by O2 more effectively than an However, investigators have reported dangers of
SIB. In this context, blow-by refers to the practice higher-than-desired PIP with the Neopuff if the flow
of holding the resuscitator bag (with or without is not set at the recommended levels.68 In another
a mask) close to the face. report, McHale and colleagues report large variations
• When using an SIB for blow-by O2 delivery, the in tidal volume when members of various clinical
bag must be squeezed to deliver O2 to a sponta- disciplines with varying levels of experience ventilated
neously breathing patient.8 a neonatal mannequin with the Neopuff. Also
• SIBs cannot give as high an FIO2 as FIBs. reported were large variations in mean airway
• SIBs are easier to use, more suitable for inexperi- pressures and tidal volumes that were independent
enced personnel, do not require a compressed of experience. More research needs to be done to
gas source, have a lower incidence of gastric determine whether the Neopuff really offers neonates
inflation, and provide more consistent ventila- an advantage.
tion and PEEP.10–14
Research by the authors and others has disproved MONITORING

most of these assumptions:62–63
Continuous and intermittent monitoring of respiratory
• SIBs produce more consistent tidal volumes than status and/or the performance of respiratory support
FIBs. devices has become a very large part of the duties of
• SIBs produce more consistent PEEP than FIBs. respiratory therapists. RTs should be experts on the
• Clinicians do not feel changes in compliance principles of operation and limitations of every monitoring
more with either style of bag. and treatment device they operate. It is to the benefit of
• SIBs can effectively be used for blow-by oxygen if the sick children they care for to become expert on how
configured properly. these devices really work and on the strengths and
limitations of each. As clinicians, RTs spend a signifi-
During manual ventilation, the importance of cant portion of their time at the bedside interpreting
limiting tidal volume to minimize volutrauma and monitoring data and trying to determine whether to
the maintenance of appropriate levels of PEEP change therapeutic interventions. The way to become
atelectrauma in limiting iatrogenic lung injury64 expert is to thoroughly digest the operating manuals
should not be forgotten. Low-birth-weight infants and a textbook on the topic.
with surfactant-depleted, fluid-filled, underdeveloped
lungs are at particularly higher risk for developing
lung injury and consequent chronic lung disease. PULSE OXIMETRY
Cellular mediators that signal lung inflammation have The pulse oximeter can (under ideal conditions)
been measured in the lungs of premature infants after estimate the level of oxygenation saturation of hemo-
brief manual resuscitation, suggesting that even globin and heart rate. Newer pulse oximeter technology
short-term ventilation can be injurious to the lungs.65 also allows for the noninvasive determination of
Thus, when all factors are considered, SIBs are better various other types of hemoglobin, including carboxy-
for use during the manual ventilation of infants and hemoglobin, methemoglobin, and total hemoglobin.69
small children. A more detailed description of the operation of
New technology may offer advantages over either oximeters is beyond the scope of this chapter but can
FIB or SIB with regard to limiting ventilation variabil- be found elsewhere.70
ity. The Neopuff (Fisher and Paykel, Auckland, New In pediatric and neonatal applications, conditions
Zealand) is a neonatal resuscitator that allows a fixed are often not ideal. The oximeter has difficulty continu-
inspiratory flow rate and pressure-limiting neonatal ously producing reliable and accurate data due to three
resuscitator. The operator controls inspiratory time circumstances: motion artifact, low peripheral perfu-
with a thumb, and the peak inspiratory pressure is sion and elevated levels of dyshemoglobins, explained
controlled via a pressure relief mechanism in the in detail in Table 29-13. All three of these circum-
device. The obvious advantage is that the flow and stances can be prevalent in certain neonatal and
inspiratory pressures are more carefully controlled than pediatric populations. There has been a great debate
during bagging. The apparent result is more consistent about the comparative performance of various brands
ventilating pressures and limited excessive overpres- of oximeters. Conventional wisdom holds that most
sures or high PEEP levels.66 Of course, tidal volume can oximeter brands work sufficiently well on about 80%
still vary considerably, probably as a result of variations of patients they are used on. But on certain patient
in the inspiratory time created by the operator’s thumb types and under certain conditions, performance
and a poor face seal with a mask.67 differences are more notable, particularly in pediatric
TABLE 29-13 Circumstances affecting the reliability of pulse oximeter readings in

neonatal and pediatric applications
Circumstance Affect on Measurement Principle Clinical Impact
Motion artifact When the tissue bed being measured Many brands and models of oximeters (especially older
is distorted by movement, this can versions) simply “drop-out,” or fail to show a reading.
create very small changes in the Other brands freeze the reading. Sometimes a reading
absorption of the light emitted by the is displayed, but the reading can be profoundly
pulse oximeter. inaccurate.1 Infants and toddlers are prone to motion
and thus this can be problematic in this population.
However, some models of oximeters have demonstrated
improved performance during motion artifact.2
Low peripheral The signal processing in most oxim- This also can result in “drop-outs,” freezes, and false
perfusion eters requires the detection of pulsatile alarms. Often you simply cannot get a reading at all.
changes in absorption that occurs as a Children with congenital cardiac disease can be prone
result of systole. During low perfusion to poor peripheral perfusion. Also, cardiac patients who
states it is very hard for the oximeter have had their body cooled down for surgery can be
to detect these pulsatile changes. Also, difficult to monitor in the immediate post-operative
poor peripheral perfusion can lead to period. Again, there are important performance
oxygenation readings of the peripheral differences between oximeter brands under these
blood that is really not representative conditions.3
of systemic oxygenation.
Elevated levels of Hemoglobin exists in a number of Elevated levels of dyshemoglobins causes most pulse
dyshemoglobins variants under normal conditions. oximeters to display a falsely high SPO2. Thus the
Some of these are called clinician can believe that patient’s blood is carrying
“dyshemoglobins” because they are much more oxygen than it really is. There can be
unable to carry oxygen and thus significant hypoxia while the pulse oximeter continues to
are dysfunctional. They include display normal levels of SPO2. Currently only one brand
carboxyhemoglobin and methemoglobin. of pulse oximeter measures more than two wavelengths
The standard two wavelength pulse of light and thus can distinguish these dyshemoglobins.4
oximeters (currently all brands except Carboxyhemoglobin can be present when the patient
one) can distinguish these inhales elevated levels of carbon monoxide, e.g., smoke
dyshemoglobins from oxygenated inhalation or inhaling the exhaust from internal
hemoglobin. combustion engines. There is now a commercially
available pulse oximeter that can measure total
hemoglobin (g/dL) noninvasively.5,6
1 Van de Louw A, Cracco C, Cerf C, Harl A, Duvaldestin P, Lemair F, et al. Accuracy of pulse oximetry in the intensive care unit. Intensive Care Med.
2001:27:1606–1613.
2 R Sahni, A Gupta, K Ohira-Kist, T S Rosen Motion resistant pulse oximetry in neonates. Arch Dis Child Fetal Neonatal Ed 2003;88:F505–F508.
3 Kawagishi T, Kanaya N, Nakayama M, Kurosawa S, MD, Namiki A. A comparison of the failure times of pulse oximeters during blood pressure cuff-induced
hypoperfusion in volunteers. Anesth Analg. 2004;99:793–6.

4 Barker SJ, Curry J, Redford D, Morgan S. Measurement of carboxyhemoglobin and methemoglobin by pulse oximetry: a human volunteer study.
Anesthesiology. 2006;105:892–897.
5 Macknet MR, Norton S, Kimball-Jones P, Applegate R, Martin R, Allard M. Continuous non-invasive measurement of hemoglobin via pulse oximetry.
Anesth Analg. 2007;104:S–117.

6 Macknet MR, Norton S, Kimball-Jones P, Applegate R, Martin R, Allard M. A prospective study to validate continuous non-invasive measurement of
hemoglobin via pulse CO-oximetry.
and neonatal populations who are prone to movement under the challenging conditions of pediatric care.
and poor peripheral perfusion. (Of course, this could change as more peer-reviewed
A dizzying array of claims and counterclaims are scientific literature is published on the latest generation
made about oximeter brands. But a careful review of of oximeter signal processing.) Signal extraction
the scientific literature indicates important perfor- technology (Masimo Inc., Irvine, California) uses a
mance differences among the brands. As of this writing, proprietary combination of filtering and statistical
one technology in particular appears to perform better treatment of the pulse oximeter signal. This device
produces saturation readings that are less prone to injured by the ventilator. These injuries fall into three
dropout and false desaturations.71,72 False alarms basic categories: mechanical injury (lung overdisten-
and false desaturations are a major problem with pulse sion), biochemical injury (oxygen toxicity), and
oximetry, particularly in pediatrics. It is reported in two infection injury (ventilator associated pneumonias).
studies that: At the risk of oversimplification, these can be loosely
categorized as four “schools” of ventilation: pressure-
• 44–63% of all critical care alarms were caused by
limited, volume-targeted, noninvasive, and high-
pulse oximeters.
frequency. These categories are not mutually exclusive;
• 94% of oximeter alarms were considered clini-
they represent a general focus.
cally unimportant.
• 71% were false alarms.73,74 • The pressure-limited focus holds that the best way
At the bedside, RTs spend a lot of time trying to analyze to minimize the risk of overdistension is by
monitoring data and to use it to make care decisions carefully limiting airway pressure.
about patients. • The volume-targeted adherents suggest that the
Typically, the pulse oximeter is used to ensure that careful control of tidal volumes is the best way.
patients have a minimal level of oxygen saturation. • The noninvasive school advocates the avoidance
There are two exceptions: neonatal patients and of intubation whenever possible through the use
patients with certain types of congenital cardiac defects. of various noninvasive ventilation techniques,
In neonatal patients, RTs need to ensure both minimal such as nasal continuous positive airway pres-
and maximal allowable levels of oxygenation to reduce sure, to minimize the risk of lung injury and
the risk of retinopathy of prematurity (as explained infection.
earlier in this chapter). Thus, both upper and lower • Advocates of early intervention with high-
alarm limits are set. Opinions are divergent about the frequency ventilation maintain this is a less risky
best limits to set to reduce the risk. Currently, a typical (in terms of lung injury) technique than conven-
recommendation is 88–93% in neonates.75 This is a tional positive pressure ventilation.
sea-level recommendation, and care must be taken to
There is tremendous variation in the use of these
adjust for hospitals at higher altitudes.
techniques among neonatal and pediatric practice
groups. At this point in time, a consensus has not
yet developed about the best ways to use these
CONVENTIONAL VENTILATORS interventions.
As far as I am concerned the whole area of ventilation of The many claims and counterclaims about the best
infants with respiratory distress syndrome is one of chaos. modes of ventilation include the time-triggered,
Claims and counterclaims about the best and least harmful flow-triggered, pressure-triggered, time-cycled, flow-
method of ventilating the premature infant make me cycled, volume-cycled, and single- and dual-control
light-headed. I can’t wait for the solution or solutions to modes. Yet there has historically been surprisingly little
premature birth, and I look forward to the day when all this evidence that any one mode is any better than others in
gadgetry will come to an end and the neonatologist will be terms of the effect of the ventilation on morbidities
retired. (Gellis SS. 1977 Yearbook of Pediatrics. In Gellis and mortality conference.79
SS, ed. London: YB Medical Publishers; 1978.) In the early 1970s, technology was developed that
Since the time of this famous quote, the gadgetry allowed time-triggered, time-cycled, pressure-limited infant
has not come to an end and indeed has increased and (TCPL) ventilation. This revolutionized neonatal
become more complex. The claims and counterclaims respiratory care and, along with surfactant replacement
have also continued. There are several camps in the therapy, contributed to a 50% reduction in the infant
neonatal community regarding mechanical ventilation, mortality rate in the 20 years that followed.80
and exploring them all in depth is beyond the scope of Improvements in ventilator capabilities now
this chapter. The interested student is cautioned that, provide better ways for neonatal and pediatric patients
in the area of mechanical ventilation, very few claims to synchronize their breathing efforts with those
and counterclaims have ever been thoroughly tested generated by the ventilator using a mode called
and or proven to be efficacious.76 Further details synchronized IMV (SIMV).
about the state of the evidence base for mechanical Another important advance in neonatal and
ventilation of neonates can be found in the writing pediatric ventilators has been the development of the
of Donn.77,78 accurate measurement of airflow and tidal volumes in
The general ventilation goal of sustaining gas very small patients. This is generally accomplished by
exchange that is compatible with life is balanced with using proximal airway sensors that measure airflow at
the goal of minimizing the patient’s chance of being the connection of the ventilator’s circuit and the
patient’s artificial airway. It has been shown that problem. Loss of the airway can be a life-threatening
ventilators that do not measure tidal volume with a event, and much work goes into securing endotracheal
sensor at the proximal airway produce tidal volume tubes. Of the wide range of taping techniques, few have
measurements that are insufficiently accurate for use in actually been tested. One technique that has shown
managing the ventilator in neonates and infants.81,82 particular promise involves the use of modified
Thus, the best neonatal and pediatric ventilators have umbilical clamps to help hold the ETT in place.
proximal airway flow sensors for the accurate determi- This technique has been shown to reduce accidental
nation of inhaled and exhaled tidal volumes. extubations.83
The overall goals for managing pediatrics using
mechanical ventilation are to:
HIGH-FREQUENCY VENTILATORS
• Maintain adequate lung volume and alveolar The U.S. Food and Drug Administration (FDA) defines
ventilation. a high-frequency ventilator (HFV) as a device that
• Support gas exchange. provides respiratory frequencies under 150 breaths/min.
• Improve lung mechanics. High-frequency ventilators can apply high frequencies
• Reduce the work of breathing. (150–900 breaths/min) while using smaller-than-
• Minimize lung injury. normal tidal volumes. High-frequency ventilation has
Pediatric patients receiving mechanical ventilation been applied to patients using a number of devices,
are different from adults on many levels. including high-frequency jet ventilation, high-
frequency low interrupter ventilation, and high-
• Pediatric patients decompensate more quickly frequency oscillatory ventilation.84
than adults and respond to hypoxia by becom- High-frequency oscillatory ventilation is the most
ing bradycardic, whereas adults typically become commonly used modality in neonatal and pediatrics
tachycardic. today. This approach differs from the other modes in
• Airway resistance is greater and compliance is that it uses a rapidly oscillating piston diaphragm. So
lower in infants than in adults. gas is forced into the lung under positive pressure and
• Small endotracheal tubes can kink and become pulled from the lung during exhalation with an equal
occluded with secretions easier than do larger amount of negative pressure. Thus, this mode is said to
ones. have active exhalation.
However, like all mechanically ventilated patients, For reasons that are not entirely understood, gas
pediatrics and adults alike, the clinician must be well exchange and lung recruitment are often enhanced
aware of changes in the lung pathophysiology by when very diseased lungs are switched from conven-
carefully monitoring and assessing the patient’s airway tional to high-frequency ventilation. In some ways, the
and respiratory status. physical principles and mechanisms of gas exchange
Table 29-14 shows some general initial guidelines are similar to those of conventional ventilation (con-
for implementing ventilation in neonatal and pediatric vection and molecular diffusion), but some principles
patients. are believed to be inherently different when using an
The management of the endotracheal tube is also a HFV: asymmetric velocity profiles, pendeluft ventila-
particular challenge among infants and children. The tion, augmented diffusion, bulk alveolar ventilation,
small tubes and the lack of patient cooperation in this and cardiogenic gas mixing.85 It has also been specu-
population make accidental extubations an ongoing lated that the improvements in gas exchange and lung
TABLE 29-14 Initial mechanical ventilator settings

Premature Infant Infant Toddler Small Child Child Adolescent
Frequency (bpm) 40–60 25–40 20–35 20–30 18–25 12–20
VT (mL/Kg) 4–6 5–8 5–8 6–9 7–10 7–10
TI (s) 0.25–0.4 0.3–0.4 0.6–0.7 0.7–0.8 0.8–1.0 1.0–1.2
PEEP (cm H2O) 3–5 5 5 5 5 5
FIO2 Start 0.10 higher than preintubation oxygen requirement
Frequency ⫽ respiratory rate set on ventilator, VT ⫽ tidal volume, TI ⫽ inspiratory time, PEEP ⫽ positive end expiratory pressure, FIO2 ⫽ fraction of inspired
oxygen. Adapted from Walsh, B. K., DiBlasi, R. M. Mechanical ventilation of the neonate and pediatric patient. In Walsh, B. K., Czervinske, M., DiBlasi, R.M.,
edi. Perinatal and Pediatric Respiratory Care, 3rd ed. St. Louis, MO: Elsevier; 2009: 325.
recruitment are related to higher mean airway pressure have failed to find compelling evidence to suggest that
that are obtainable during HFV without the cardiovas- HFOV produces better outcomes than conventional
cular and lung injury consequences of achieving these ventilation.88,89 We look forward to the day when
higher pressures with a conventional ventilator. widely accepted standardized, evidence-based
High-frequency oscillatory ventilation (HFOV) has approaches to mechanical ventilation are in place.
been described simply as CPAP with wiggles and in A probable reason for the divergent findings in the
many ways may be simpler to operate than conven- literature is a lack of established standards for manag-
tional mechanical ventilation. The reason is that this ing HFOV. Table 29-15 lists some basic guidelines for
mode allows the clinician separate controls for manag- the management of HFOV.
ing oxygenation and ventilation. During HFOV, the
primary adjustments for oxygenation are FIO2 and
mean airway pressure, and for ventilation (CO2 CONTINUOUS POSITIVE AIRWAY PRESSURE
removal) it is the amplitude and frequency settings.
The mean airway pressure (MAP) can be compared Continuous positive airway pressure (CPAP) is a form of
to a super CPAP setting that is applied continuously to respiratory support that is used primarily in spontane-
the airway. MAP is adjusted upward in increments of ously breathing patients with lung disease and apnea.
1–2 cm H2O to augment lung volume and improve NCPAP applies a continuous distending pressure to the
oxygenation. Amplitude (power) is typically set to nasal airway during inhalation and exhalation. CPAP
achieve adequate shaking (or wiggling) from the was first described and used in neonates by Gregory
shoulder to the umbilicus in infants and from the and colleagues in 1971.90 In theory, the technique
shoulder to the midthigh in larger pediatrics. Typically, simulates the physiologic effects of grunting in intu-
the clinician increases the amplitude in response to bated newborns. It was speculated that neonates with
hypercarbia and reduces the amplitude in response to respiratory distress grunted to create a slight back-
hypocapnea. Amplitude can be thought of as analo- pressure at the end of exhalation. The back-pressure is
gous to tidal volume, although actual tidal volumes believed to be a form of self-administered CPAP that
during HFOV are not known. prevents widespread alveolar collapse with each breath.
Relatively high amplitudes can be set in pediatrics This collapse is a consequence of insufficient surfactant
without causing lung injury. One reason for this is that production and performance in the premature lung.
high frequencies, combined with the small internal Since CPAP seemed to be self-administered, the
diameter of neonatal and pediatric endotracheal tubes, assumption was that artificially administered CPAP
cause the pressure signal to be significantly attenuated. might be beneficial.
Thus, only a fraction of the pressure swing measured at Infants have been described as being obligatory
the airway is actually transmitted into the lung. nasal breathers, and therefore nasal CPAP is effective in
The hertz setting controls the frequency (set respira- providing a continuous pressure to the lungs. However,
tory rate) by which these pressure oscillations occur. there is considerable debate about the ability of
The frequency is usually set and not adjusted much newborns to breathe through their mouths when their
unless the patient is exhibiting poor ventilation noses are occluded.91 Whether infants are true obligate
responses as a result of adjusting the amplitude. nose breathers or preferential nose breathers is not
Frequency during HFOV is inversely proportionate to clear. While this debate may seem arcane, it is actually
the CO2 level. Unlike conventional ventilation, a lower very important when physiologists attempt to explain
frequency results in a lower PaCO2, and vice versa. whey NCPAP and heated high-flow nasal cannula
Decreasing the frequency permits more time for the appear to work in some neonates.
airway pressures to equilibrate with the lung; thus, The most common indication for NCPAP is for
airway pressure oscillations have more time to premature infants with RDS and apnea; however,
penetrate deeper into the lung. NCPAP has been used successfully in supporting
In pediatrics, high-frequency ventilation has newborn infants with nearly all types of restrictive and
traditionally been used for children failing conven- obstructive lung disorders. In larger patients, NCPAP is
tional ventilation. Concerns about ventilator-induced used in intubated patients as an adjunct for weaning or
lung injury have led many clinicians to favor HFOV to relieve upper airway obstruction using a nasal mask.
over conventional ventilation in pediatric applications NCPAP has many potentially beneficial effects:92
and to move sooner to HFOV. However, practices • Increasing the functional residual capacity
continue to vary widely. This variation is contributed to • Improving gas exchange
by the divergent literature on HFOV use in infants and • Reduced work of breathing.
children. Some studies seem to support early interven- • Reducing airway resistance by holding (or
tion in neonatal and pediatric patients.86,87 However, stenting) the airways open during exhalation
other studies of both neonates and pediatric patients (under certain conditions, as some theorize)
TABLE 29-15 Guidelines for HFOV management

1) Initial HFOV Settings ii) Increasing the amplitude and decreasing
a) Oxygenation the frequency (Hz) increases the delivered
tidal volume and conversely decreasing the
i) The main determinant of oxygenation
amplitude and increasing the frequency
during HFOV is the MAP this is generally
(Hz) decreased the delivered tidal volume
initiated at 5–8 cm H2O above the
and allows PaCO2 to rise.
MAP on conventional ventilation in large
patients and 2 cm H2O in premature iii) The amplitude is usually initiated at a
patients. value where the patient has good visual
chest wall vibration (wiggle). For neonates
ii) Brief hypotension after initiation of HFOV
this “wiggle” should be visible to the
is usually managed with a trial of fluid
mid-abdominal level. For the larger
boluses to improve preload.
pediatric patient this wiggle should be
iii) FIO2 is usually set at 100% on initiation visible to the mid thigh level.
of HFOV, and then tapered using pulse
iv) The initial frequency is set at 6–8 Hz for
oximetry guidance to maintain Sp02 of ⱖ
pediatric patients. This frequency is titrated
88% in pediatric patients, and 88–94%
upward for smaller neonatal patients to the
in neonates.
point where neonates ⬍ 1000 g should
iv) If SpO2 or PaO2 has not improved enough have a frequency of approximately 15 Hz.
to allow weaning of FIO2 %, the MAP is
v) Aggressive action is required for a rapidly
increased by 3–5 cm H2O increments at
rising PaCO2 during initiation of HFOV
30–60 min intervals in hopes of improving
because improvements in PaCO2 do not
lung recruitment. Incremental increases
occur quickly as is noted when changes
are less in neonatal patients.
are made to conventional ventilators.
v) Some patients may slowly improve
vi) An ABG should be obtained 15 to 20 min
oxygenation only after a period of several
after starting HFOV to determine the trend
hr. Vigilance and patience are required
of the PaCO2; subsequent ABGs are
during the early phase of treatment.
generally obtained at 30–60 min intervals
b) Ventilation until stabilization occurs. In neonates,
i) The main determinants of PaCO2 removal where vascular access to arterial blood is
are the pressure amplitude of oscillation limited, transcutaneous carbon-dioxide
(which is controlled by the power setting) should be monitored throughout the period
and the frequency setting (Hz). when the patient is on HFOV.
• Reduced incidence and severity of apneic marginal. However, NCPAP levels greater than 10 cm H2O
episodes in infants by providing improvements are usually reserved for infants with obstructive airway
in oxygenation and nasal airflow stimulation lesions that are prone to collapse (i.e., tracheal malacia).
• Reduced need for surfactant administration, Infants showing signs of excessive end-expiratory lung
endotracheal intubation, and mechanical volume (hyperinflation) warrant lower CPAP levels.
ventilation The monitoring of the patient’s respiratory status
• Avoidance or minimization of the risk factors using blood gases, pulse oximetry, and chest X-rays are
associated with intubation and mechanical essential to the successful management of infants
ventilation, including infection, accidental supported by NCPAP. The frequent monitoring of the
extubation, and ventilator-induced lung injury nasal prong patency, the proper fit of prongs, and the
• Decreased lung injury and promotion of better proper adjustment of the fixation being used to secure
lung growth and development the prongs in place are essential. If done properly, the
• Association with improved survival and reduced amount of bedside care required by infants receiving
incidence and severity of BPD when compared CPAP is similar to or greater than that of a mechani-
with infants managed using mechanical cally ventilated patient.
ventilation as the primary form of respiratory Unfortunately, not all infants can be supported
support using NCPAP alone. Infants failing CPAP typically
present with increased grunting, nasal flaring, retrac-
Infants are supported initially using 4–6 cm H2O of
tions, worsening oxygenation (PaO2 ⬍50 mm Hg on
CPAP. The CPAP level can be increased if oxygenation is
FIO2 ⬎0.60), worsening ventilation (PaCO2 ⬎ TABLE 29-16 Traditional estimated oxygen
65 mm Hg and PH ⬍7.20), and increased episodes of delivery capabilities during pediatric
apnea and bradycardia. Approximately 40–50% of
premature infants supported initially with NCPAP fail
applications
and require intubation and mechanical ventilation Device Flow rate (L/min) FIO2*
for surfactant administration. Nearly 30% of infants Nasal cannula 0.01–6 0.24–0.44
supported with CPAP following extubation require Blow-by oxygen 10 0.3–0.4
reintubation related to poor gas exchange and severe
apneic episodes (stefanescu). Therefore, other types of Oxygen hood 7–15 L/min 0.21–1.0
noninvasive support, including noninvasive positive Simple mask 5–8 0.35–0.55
pressure ventilation, are focused in an area of intense Air-entrainment mask 2–10 0.24–0.50
clinical research. Nonrebreather mask 6–10 L/min 0.6–0.8
Source: Adapted in part. Pilbeam and Cairo text. Walsh and Grenier 2009
NASAL CPAP SYSTEMS Respiratory Care. Walsh and Diblasi. 2002 CPG guidelines for administering
oxygen to children.
The nasal CPAP system consists of a nasal prong or
nasal mask interface, heated humidified gas source,
patient circuit, and a pressure-generating device. CPAP
systems also incorporate pressure-monitoring (manom- based on the patient’s size and oxygen requirement.
eter) and pressure relief mechanisms (Pop-off). CPAP Table 29-16 shows the range of oxygen delivery devices,
is generated using a number of devices, including flow ranges, and the approximate FIO2 levels. Oxygen is
mechanical ventilators, fluidic devices (Infant Flow and typically applied using either a low-flow meter (0.125–
Airlife), and a water-seal column (bubble CPAP). Each 3.0 Lpm) or a standard flow meter to provide 100%
of these devices has its advantages and disadvantages, oxygen through the device. Air-oxygen blenders are
but there is insufficient evidence to support the concept commonly found in NICU settings and provide precise
that one device is better than another for reducing adjustments in FIO2. The delivered FIO2 to the patient
mortality or incidence of BPD. may be very different from what is set on the blender
The complications of NCPAP are similar to those or what is coming from the flow meter. Pulse oximetry
reported using all forms of positive pressure ventilation is an extremely useful clinical tool for monitoring the
(air leak, decreased cardiac output, and so on). The effectiveness of oxygen delivery and weaning.
most prevalent and frequently reported complication The FIO2 can be highly variable using a nasal
with NCPAP is gastric insufflation, which can be cannula. Changes in inspiratory flow, tidal volume and
relieved using an orogastric catheter. Because infants respiratory rate affect the rate of air entrainment, which
are being supported longer with NCPAP, nasal break- can cause fluctuations in FIO2. However, the conven-
down, erosion, and nasal distortion are frequently tional wisdom that only a low FIO2 is possible with
reported. These problems put the infant at a greater risk nasal cannula has been shown to be most probably
for infections. These problems can be lessened by untrue (see Table 29-16). In larger patients, the flow
ensuring proper prong size and fixation and by fre- used to adjust the FIO2 is 0–6 Lpm; however, conven-
quently assessing areas prone to nasal damage. tional wisdom holds that the maximum flow rate
should be limited to 2 Lpm in infants and newborns.
A common practice is the intermittent administra-
OXYGEN DELIVERY tion of oxygen via free-flow or blow-by. This practice
In newborn infants, hypoxemia is indicated when PaO2 has oxygen blown by the face in an uncontrolled and
is ⬍60 mm Hg. The exception to this is the infant with highly variable fashion using a variety of techniques:
a congenital cardiac defect. In certain varieties of these
• A simple oxygen mask held near the face
defects, more profound hypoxia is acceptable and in
• A flow-inflating manual resuscitator with the
some cases even desirable. In older pediatrics, hypox-
patient connection held close to the face
emia is indicated when PaO2⬍80 mm Hg. Patients
• A self-inflating bag equipped with a corrugate
presenting with hypoxia typically manifest with
reservoir tube that is held near the patient’s face
tachypnea, nasal flaring, retractions, tachycardia,
bradycardia, and cyanosis. Prolonged hypoxia can lead This method of oxygen delivery to children is
to severe metabolic acidosis from anaerobic metabo- discouraged because it is highly variable and the
lism. If not treated, persistent hypoxia can also lead to clinician has no idea how much oxygen the patient is
severe neurologic sequela and death. actually receiving. The oxygen requirement of these
Oxygen therapy can be administered using a patients is an important indication of the severity of
number of oxygen delivery devices that are chosen respiratory symptoms.
AEROSOL DELIVERY using technology in their treatment. Some techniques

The selection of devices for delivering inhaled medica- that work well in adult scenarios perform differently in
tions in children has historically not been well these populations, such as oxygen delivery, aerosol
described in the literature. Inertia and tradition have delivery, mechanical ventilation, and airway manage-
contributed to a widespread belief that small-volume ment. Recently, certain practices have been exposed as
and large-volume pneumatic nebulizers are the ineffective or inefficient, including blow-by oxygen
preferred method of delivering inhaled medications or aerosol delivery and the use of pneumatic (jet)
to infants and children. However, a growing body of nebulizers for the delivery of aerosolized medications.
literature has led to an evolving practice. Conventional
wisdom dictated that metered dose inhalers (MDIs) could
not be effectively used in infants and children because Study Questions
of children’s inability to cooperate or even to have
sufficient hand-eye coordination to allow the effective REVIEW QUESTIONS
operation of an MDI.
1. What are the three distinctions between the
The authors’ work has shown that, when used with
respiratory tract of neonatal/pediatric patients and
the appropriately valved holding chamber and mask,
that of adults?
MDIs are very efficient and effective methods of
delivering inhaled medications to children.93 The 2. What are the three sites of cardiac shunting during
authors now use an MDI with a valved holding cham- fetal circulatory pathways?
ber (VHC) to administer nearly 90% of all inhaled 3. What special considerations should be taken when
albuterol to inpatients and have reduced our albuterol resuscitating a newborn with diaphragmatic
delivery costs by 21%. The source of these savings has hernia?
been a reduction in the time required to give an MDI 4. Describe several techniques to ensure minimal
versus a small-volume nebulizer. It has been repeatedly stimulation of premature infants.
shown that using an MDI with a VHC for inhaled
5. Identify four signs of respiratory distress in infants.
medication administration in infants and children
produces outcomes that are equivalent to and 6. Describe the role of nasopharyngeal suctioning in
sometimes better than those produced by using the treatment of bronchiolitis.
small-volume nebulizers.94,95
The authors place no age limitations on the use
of MDI-VHC, using it to give medications to infants,
toddlers, and larger children. An internal panel of 1. The chief cause of ventilator-induced lung injury in
experts arrived at a dosing equivalency: pediatric ARDS is:
a. excessive airway pressures.
• A nebulizer dose of 2.5 mg of albuterol is b. excessive lung volumes.
equivalent to 4 puffs via MDI-VHC. c. malpositioned endotracheal tube.
• A 5-mg nebulizer dose is equivalent to 8 puffs d. inappropriate modes of ventilation.
via MDI.
2. Which of the following statements is true about
The authors have largely eliminated the use of the flow-inflating and self-inflating manual resuscitators?
blow-by technique for aerosol medication delivery in a. Clinicians cannot feel changes in compliance
children. In this widespread practice, the therapist better with flow-inflating bag.
holds the output of a nebulizer near the face, blowing b. Self-inflating resuscitators produce more
toward the nose and mouth. The procedure has been consistent tidal volumes than flow-inflating
largely discredited,96 although it is still probably widely resuscitators.
used.97 c. Flow-inflating resuscitators produce more
variable PEEP than self-inflating resuscitators.
d. Self-inflating bags can be used for blow-by\
oxygen if configured properly.
Summary e. All of the above
Respiratory care of the pediatric patient presents 3. What is a typical recommended range for main-
clinicians with unique challenges. An understanding of taining SPO2 in neonates?
the diseases and pathologies related to infants and a. 88–93%
children are essential to craft effective respiratory care b. ⬎95%
for this population. The size and complexity of some c. 90–98%
pediatric patients present special challenges when d. 92–98%
4. Which of the following is not a potential benefit 10. During mechanical ventilation of pediatric patients
of nasal continuous positive airway pressure for with acute respiratory distress syndrome, what
neonatal patients? level of positive end-expiratory pressure is recom-
a. increasing the functional residual mended if the FIO2 is 0.50 using a high-PEEP
capacity strategy?
b. improving gas exchange a. 18–24 cm H2O
c. reduced work of breathing b. 16–18 cm H2O
d. improved cerebral blood flow c. 10–12 cm H2O
5. Which interventions have been proven to be d. 8–10 cm H2O
efficacious in uncomplicated bronchiolitis in
infants?
a. aerosolized bronchodilators CRITICAL-THINKING QUESTIONS
b. chest physical therapy 1. How are the lungs and airways of adults different
c. inhaled corticosteroids from infants and children?
d. antibiotics
2. Describe the important design and performance
6. Which of the following statements is true? differences between child manual and infant
a. Small-volume nebulizers are typically a better resuscitators and how the differences might affect
way to give bronchodilators to nonintubated the ventilation of infants and children.
infants and children.
3. Describe the mechanisms of airway obstruction in
b. Metered dose inhalers should usually not be
asthma, including the role of inflammation, in this
used in infants and children because of the
disease process.
patients’ inability to coordinate actuation of
the inhaler with inspiration. 4. What is minimal stimulation of neonates, and why
c. Metered dose inhalers with valved holding is it important.
chambers are a more expensive way to give 5. Discuss the role of tidal volume measurement and
inhaled bronchodilators compared to small- targeting in preventing ventilator-induced lung
volume nebulizers. injury in neonates.
d. Metered dose inhalers with spacers/holding
chambers have been shown to be as effective
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Doyle LW, Morley CJ. Neonatal resuscitation 2: 50:149.
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dilator therapy to treat wheezing in children aged 586–591.
CHAPTER 30
Geriatric Applications
Melaine Head Giordano and Helen M. Sorenson
OBJECTIVES
• Describe the changing demographics of the U.S. population.
• Address issues related to the current cost of health care for elders.
• Identify and explain the major components of a comprehensive geriatric assessment.
• Discuss the fundamental elements involved in the functional assessment of older adults.
• Discuss pharmacodynamics and pharmacokinetics in the older adult.
• Identify clinical interventions to promote medication compliance.
• Explain ways to improve communication with older adult patients.
CHAPTER OUTLINE
Demographic Changes in the United States Environmental Assessment
Health Care Venues Socioeconomic Assessment
The Cost of Health Care Cognitive Assessment
Assessment of the Older Patient Assessment of Medication Use
Physical Assessment Communicating with Older Patients
Functional Assessment
KEY TERMS
activities of daily living (ADLs) geriatrics Medicare
adherence iatrogenic ototoxicity
aphasia instrumental activities pharmacodynamics
centenarian of daily living (IADLs) pharmacokinetics
chronic life expectancy polypharmacy
cohort life span
comorbid Medicaid
835
A
t the beginning of the twenty-first century, African Americans, Asian Americans, Pacific Island-
the United States faces many complex ers, and Latinos. Minorities represent about 10% of
challenges associated with the unprec- the older population; by 2020, they will account for
edented increase in the growth of the older more than 15%. By 2050, it is estimated that more
population (defined as age 65 and older). Among than 38% of the older population will be minori-
those challenges is the provision of social services, ties.2 The health care implications of the growing
adequate housing, and financial assistance. Because number of older minorities are immense because
of the increased incidence of health problems, these groups experience a significantly higher
however, one of the most crucial areas in preparing incidence of morbidity and mortality than older
for the growth of this cohort (a group of individuals whites.3 The higher incidence of health problems
having a statistical factor in common in a demo- among minority populations is attributed to risk
graphic study) is the challenge of providing for their factors such as smoking, poor nutrition, limited
health care needs. access to health care services, and inadequate
The dramatic increase in life expectancy, coupled housing.
with technological advances in medicine, will increase Not only is the older population growing in size,
the need for long-term care. The appropriate delivery but they are also living longer. In addition to the
of care for older adults with chronic disease will be minorities, another rapidly growing segment of the
the greatest challenge. (Chronic refers to an illness older population in the United States are people over
that lasts for more than 3 months.) This will require 85. According to the Census 2000 Summary File, in
an enormous amount of health care, social, financial, 2000 over 4.2 million adults were 85 and older, and
familial, and community support. Historically, U.S. an astonishing 337,000 were 95 and older.4 Unfortu-
health care systems were designed around acute care nately, many of the oldest-old (persons over 85) do not
models. As the population ages, this system will soon enjoy good health and may require assistance with
be outdated due to the increased numbers of chroni- basic self-care activities.
cally ill. Health care will increasingly need to be Life expectancy (the number of years that an
provided in alternative care sites such as the home, individual is expected to live, determined by statistics)
assisted-living facilities, nursing homes, congregate in the United States increased from 49 years in 1900 to
housing, outpatient settings, and rehabilitation over 78 years in 2005.5 The increase in life expectancy
hospitals. can probably be attributed to advances in the preven-
One other challenge presented by the so-called tion and treatment of infectious diseases, as well as to
gray explosion is the provision of health care profes- improvements in nutrition, basic health care, educa-
sionals who are educated in geriatrics (a specialized tion, and technology. Women have a longer life
branch of medicine that deals with the diseases of expectancy than men (Table 30-1). The gender dispar-
later life and the provision of health care for older ity is attributed to differences in lifestyle and health
people). Unfortunately, the aging citizens in the behaviors of the two sexes. It probably will diminish in
United States, according to a new report from the the future, as women increasingly adopt lifestyle and
Institute of Medicine (IOM) are relying on a health health behaviors that have traditionally been associated
care workforce that is too small and unprepared to with men.
meet their needs.1 Despite the statistics indicating that health
declines with age, individuals enjoy healthy, produc-
tive lives well into their eighties and nineties, and a
Demographic Changes in the few are still active and healthy beyond their 100th
birthday. In 2006, there were 67,000 centenarians
United States (adults 100 years and older) in the United States,
Demographic changes, owing to the lowered birth and this number has been projected to be 580,000
rates during the Great Depression (1929–1939), have by 2040.6
been gradual. As the baby boomers (individuals born There is a limit, however, to just how old a person
between 1946 and 1964) reach 65, between 2010 and can get. The human life span (the length of time an
2030 (Figure 30-1), there will be a dramatic increase organism or species can be expected to survive) is
(10,000 individuals per day) in the older adult approximately 120 years old. One thing is certain; the
population. aging process is very individual. It is not uncommon
One of the fastest growing segments of the older to observe a 75-year-old who appears to be in her
population are minorities. Identified as members of early sixties or a fifty-year-old who appears to be in
the non-European population: Native Americans, his sixties.
CHAPTER 30 ■ Geriatric Applications 837
Growth of the U.S. 65+ Population,

by Age Group: 1900 to 2050.
90 25%
80
20%
70
60
Number in millions
15%
50
40
10%
30
20
5%
10
0 0
1900 1910 1920 1930 1940 1950 1960 1970 1980 1990 2000 2010 2020 2030 2040 2050
65–74 75–84
85+ %65+
FIGURE 30-1 Growth of the U.S. 65 population by age group: 1900–2050.
Courtesy of National Center for Health Statistics, Hyattsville, Maryland
TABLE 30-1 Life expectancy in selected Health Care Venues

regions, by gender, 2006 Because of the chronic nature of respiratory disease, the
Countries Male Female respiratory therapist encounters older patients in all health
care venues. Today, 60% of acute care patients, 80% of
Australia 79.2 83.9
home care patients, and 90% of nursing home patients are
Belize 65.3 73.6 65 years or older. Advances in medical technology, expedi-
Brazil 68.4 75.1 ent hospital discharges, a demand for cost-efficient health
Canada 78.3 82.9 care services, and the growing number of older adults have
contributed to a phenomenal growth in the home health
Central African Republic 48.3 47.8
care industry (see Chapter 35), along with the utilization of
Denmark 76.2 81.3 subacute and long-term care facilities (Chapter 34) and
Haiti 59 63.4 rehabilitation facilities (Chapters 34 and 36).
Japan 79.2 85.9
United Kingdom 77 81.3 The Cost of Health Care
United States 75.5 80.4 Reimbursement for health care services for the aging
Source: World Health Organization Life Tables for WHO Member States, population comes from three sources: Medicare, Medicaid
2006. WHO Statistical Information System. www.who.int/reseach/en/-cached (see Chapter 1), and private out-of-pocket payments.
Medicare provides health insurance for people Assessment of the Older Patient
age 65 or older, adults under 65 with certain disabili-
ties, and individuals of any age with end-stage-renal One of the most daunting aspects of caring for older
disease (permanent kidney failure requiring dialysis individuals is addressing the multitude of age-related
or a kidney transplant). Medicare has four different issues they face. These may include Alzheimer’s disease
parts: or other memory disorders, chronic illnesses, mobility
difficulties, caregiver dilemmas, complex medication
• Part A. Hospital insurance, also covers skilled issues, sensory deficits, and nutritional inadequacies.
nursing facilities, hospice, and home health care To provide efficient and effective geriatric care, the
under certain conditions. clinician must assess the older person in a systematic
• Part B. Medical insurance, helps cover medically manner. A comprehensive geriatric assessment (CGA),
necessary services like physician’s services and while time-consuming, offers the clinician the best
outpatient care. Some preventative services are tool to systematically evaluate the overall health status
also covered. Part B requires a monthly premium of an older adult. As caregivers for so many elderly
of $115.40 as of 2011. patients, respiratory therapists (RTs) must think
• Part C. Medicare Advantage Plus, combines outside of the pulmonary system and assess older
Parts A, B, and sometimes D (prescription drug patients in a more holistic manner. Because CGAs are
coverage). Medicare Advantage Plans are man- multidisciplinary evaluations in which the multiple
aged by private insurance companies approved health issues of the older adult are uncovered,
by Medicare, which allows for copayments, described, and explained, RTs may reasonably take
coinsurance, and deductibles to vary among their place at the table.
providers. The American Geriatrics Society, in its Compre-
• Part D. Medicare Prescription Drug Coverage, hensive Geriatric Assessment Position Statement
helps cover prescription drugs. This plan was (updated in August 2005), promulgated the CGA as a
developed to help lower prescription drug costs cost-effective intervention that improves quality of
and to protect against higher future costs.7 life, quality of health, and quality of social care.10
Unfortunately, the application of the CGA is not
Medicaid is a federally mandated, state-funded always used in the United States. The assessment itself
health insurance program designed to provide health may be time intensive and impractical in most
care services to the poor and disabled. As of 2002, primary care settings. Adding to the problem is that,
about 41 million people in the United States were on of the 650,000 licensed physicians practicing in this
Medicaid. Low-income parents and children make up country, fewer than 9,000 of them are geriatricians.11
73% of all Medicare recipients, but they account for When viewed as a multidisciplinary task, however,
only 27.5% of all Medicaid expenses. The elderly, and approached as a comprehensive health screening,
disabled, and mentally challenged collectively com- coordinated care plans can be developed that address
prise only 27% of Medicaid recipients, but account individual patient needs.
for 72.5% of all expenditures.8 A comprehensive assessment does not have to
Medicaid is the single largest payer of nursing conform to a single format. CGAs have been effective
home charges in the United States and for many, is in a number of settings: inpatient geriatric evaluation
the last resort when there are no other means of units, inpatient geriatric consultation, ambulatory
paying for long-term care. Medicaid, however, will pay geriatric assessment clinics, and in-home geriatric
for nursing home care only if provided in a facility assessment programs.12 One series of interventions
certified by the government to provide services to that has shown great promise is a combination of:
Medicaid recipients.9
Older adults may qualify for both the Medicare • An initial CGA.
and Medicaid programs. Dual-eligible beneficiaries are • Followed by providing recommendations to the
determined on the basis of financial need. Those who older patient/family members.
typically qualify for dual eligibility are the older-old • And a follow-up home visit to see if the recom-
(85 or older), ethnic minorities, females, and persons mendations are being implemented.
living in rural areas. The ultimate goal is to identify older adults at high risk
The health care financing system is complex and for functional decline and follow-up with programs
confusing for people of any age. For an older person combining rehabilitation and coordinated care. When
with physical and financial limitations, it can be decline is inevitable, the CGA can result in an
impenetrable. Many organizations and agencies can improved quality of life by mobilizing available
help. For a list of some resources for patients and medical, psychological, and social resources. Although
professionals, see Resources at the end of this chapter. this may sound simplistic, there is enough interest in
healthy aging, as well as an adequate supply of very old PHYSICAL ASSESSMENT

adults, to make some iteration of the CGA possible in Physical well-being, or the lack of it (frailty), is a major
every community. issue. Unfortunately, many health care professionals
How does this relate to respiratory therapists? RTs assume that aging is parallel to a disease process and
make up one of the multidisciplinary components of that signs and symptoms of disease are simply a part of
coordinated care planning for older adults. We care for getting old.
older patients with cardiopulmonary disease, both in Any clinician assessing an older person’s physical
the hospital and after discharge; so we need to be health must be familiar with normal age-related
educated about our role in the CGA. physiological changes in order to distinguish them
The following are core elements of a multidiscip- from signs and symptoms of disease processes
linary comprehensive geriatric assessment: (Table 30-2).
• Physical assessment The physical evaluation of an older person takes
• Functional assessment more time. Standard procedures may have to be
• Environmental assessment modified to accommodate the special circumstances
• Socioeconomic assessment of the older adult. Breath sounds are softer, pulses
• Cognitive (mental) assessment and respiration more irregular, body temperature may
• Medication assessment (Meducation) be lower, and the cough reflex may be weaker. Older
patients may find it more difficult to move around in
bed, and getting them in an optimal position for
patient assessment is often time-consuming.
Review the patient’s past medical records before
performing the physical assessment. This reduces the time
CASE STUDY 30-1
Mrs A. is an 86-year-old Latino woman who
has been a widow for 20 years. She lives alone
(in publicly funded housing), and her sources
of income are a small pension and a monthly Best Practice
Social Security check for a total of $540 a
month. Her rent, utilities, and Medicare premi- Health Care Characteristics of
ums average $425 a month. She finances her Older Patients
medical expenditures through Medicare Parts
A and B and has obtained nutritional assistance Chronological age is not a good indicator of
by means of food stamps and Meals on Wheels. physiological age or organ system functioning.
Six months ago, Mrs. A. rated her health as The rate of age changes is distinctively indi-
good, and if it were not for arthritis and dimin- vidualized, and the assessment must reflect the
ished vision, she would have rated her health uniqueness of each person. However, when
as excellent. assessing older persons (especially those over
Last week, Mrs. A. was diagnosed with 75) the practitioner should keep in mind their
congestive heart failure (CHF) and asthma, and health care characteristics and vulnerability.
she was prescribed three new medications at a Older patients tend to:
monthly cost of $80. This new expense is a
• Exhibit greater medical complexity and
challenge for Mrs. A.; the cost of the additional
vulnerability than younger patients.
medications is more than half of her disposable
• Have illnesses with atypical or obscure
income.
presentations.
Questions • Suffer major cognitive, affective, and
functional problems.
1. Would a Managed Medicare program help
• Be especially vulnerable to iatrogenic
Mrs. A.?
diseases or symptoms (induced by
2. How could Mrs. A. get help with the expense examinations or treatments).
of her medication? • Be socially isolated and economically
3. Identify professionals who could assist deprived.
Mrs. A. in meeting her financial and health • Be at high risk for premature or
care needs. inappropriate institutionalization.
TABLE 30-2 Normal age-related physiological changes

System Increase Decrease
Pulmonary Residual volume increases Vital capacity, both slow and forced (32 mm/yr for men;
almost 50% by age 70 25 mm/yr for women)
Functional residual capacity Peak expiratory flow rate
Inspiratory capacity
Forced expiratory flow rate (25–75%)
Forced expiratory volume (32 mm/yr for men; 25 mm/yr
for women)
Diffusing capacity (20% over the course of adult life)
Arterial partial pressure of oxygen, although not as much as
previously thought (Resting PaO2 can be estimated:
PaO2 104 [age 0.42] supine position and PaO2
104 [age 0.27] sitting position.)
Mucocilliary clearance
Elasticity
Cardiovascular Left ventricular wall size Elasticity in the large arteries and aorta
Peripheral vascular resistance Serum albumin
Maximal O2 consumption during exercise (men about 10%
and women about 7.5% with each decade of life)
Renal Renal blood flow (10% with each decade)
Renal mass
Glomerular filtration rate (50% from age 30 to 90)
Total number of glomeruli (30–40% by age 80)
Tubular secretion
Hepatic Liver mass
Blood flow (40–50%)
Enzyme activity
Gastrointestinal pH Acid
Blood flow to stomach (30–40%)
Motility
Absorption
Body Fatty tissue (15–18%) Muscle mass
Skin dryness Body water
Height (2–3 in.)
Elasticity of skin
Vital signs Core temperature (96°–98.6°F; 35.6°–37°C)
spent in asking questions and allows the therapist to Having a family member present (if the patient
focus on key events in the history that need clarification. agrees) during the history portion of the physical
The medical record is a useful tool for identifying high- examination may be helpful because family members
risk health care patterns such as repeated hospitalizations can supply supplemental information. However, ask
or emergency room visits, noncompliance with prescribed assistance of the family member only after giving the
medication regimes, and inadequate support systems. patient sufficient time to respond.
TABLE 30-3 Chronic conditions most

frequently reported by older adults
CASE STUDY 30-2
Percentage (%) of G. A., a 76-year-old male, was admitted to the
Condition Elderly (>65 years old) local community hospital emergency room on
1. Arthritis 50 December 16. He was complaining of loss of
2. Hypertension 36 appetite and malaise. He was extremely con-
fused, and he had fallen twice in the last 2 days.
3. Heart disease 32
Mr. A. was accompanied by his wife. Because of
4. Cataracts 17 his altered mental state, it was difficult to obtain
5. Hearing impairment 16 the necessary medical information from Mr. A.
6. Orthopedic 16 Mrs. A. reported that he had been in relatively
impairments good health until this current episode. She stated
that Mr. A.’s symptoms had come on gradually
7. Sinusitis 15
over the past 3 or 4 days. She stated further that
8. Diabetes 10 her growing concern over her husband’s increas-
ing confusion had caused her to seek hospital
assistance.
Vital signs for Mr. A. are heart rate 110,
Illness in older people is generally characterized as
respiratory rate 30, temperature 98°F, and blood
being chronic. On average, most older adults report
pressure 130/92. His laboratory results and
having one to three chronic diseases (Table 30-3).
chest X-ray were unremarkable.
Arthritis, reported by 50% of older adults, is very
common. The multiplicity of complaints, related to Questions
comorbid (coexisting) disease processes, make it
1. On the basis of his confusion, vital signs,
difficult to discern the true nature of the current
laboratory results, and chest X-ray, what
complaint. It is extremely important for therapists,
might the RT assume is Mr. A.’s problem?
to assess each patient individually without any
preconceived expectations based solely upon the age of 2. What is another possible diagnosis, and
the patient. which of Mr. A.’s presentations indicate
Another complication of geriatric care is that which of the possible diagnoses is correct?
diseases in older adults may have atypical presenta-
tions. For example, the classic signs of pneumonia

Best Practice (fever, chills, cough, dyspnea, and sputum production)
are commonly absent in the older person. Older
Pneumococcal Immunization patients with pneumonia may present with vague
and atypical symptoms such as abdominal pain and
Respiratory therapists should educate older confusion. They are often afebrile, have no elevation of
patients concerning the importance of pneumo- white blood cells, and do not have a cough; their chest
coccal immunization. Each year, pneumococcal X-rays are inconclusive. Unfortunately, other disease
disease accounts for an estimated 500,000 processes such as myocardial infarction, pulmonary
cases of pneumonia and approximately 40,000 embolism, and atelectasis can also present in the same
deaths in adults aged 65 and older. Healthy atypical manner.3
People 2010 had a goal of vaccinating 90% of
adults over the age of 65 with Pneumovax. In
2002, 54% were vaccinated. Current recommen- FUNCTIONAL ASSESSMENT
dations are that every adult over age 65 should Chronic diseases, are not always curable; so the focus
receive a pneumococcal vaccine. Revaccination of care is to restore or maintain the functional status of
is indicated if the first vaccination was before the older patient. The loss of physical, mental, and
the age of 65 and more than 5 years has elapsed social function can result in the inability to perform
since the initial immunization. self-care and seriously impair an older adults’ ability
Source: From MMWR (Morbidity Mortality Weekly Report) April 1, to live independently. The functional assessment is a
2005;54,RR05: 1–11. methodical evaluation of an individual’s ability to
perform tasks that are necessary for independent living,
and it serves as a benchmark to monitor the patient’s TABLE 30-5 Instrumental activities of
functioning over time. A functional assessment should daily living
routinely be performed in all health care environments
and should be well documented in the patient’s Laundry. Inquire as to the ability to do one’s own
records. laundry with machine or by hand.
Some functional decline may not be reversible; Telephone. Determine ability to read numbers, dial
progressive functional loss often accompanies the phone, hear the phone ring, and hear conversation
patients with degenerative joint disease, Parkinson’s over the phone.
disease, dementia, heart failure, and cancer. Other Housekeeping. Inquire if any assistance is needed in
chronic illnesses including exacerbation of COPD or performing housekeeping chores, such as making bed,
cardiovascular disease, although acute infections and cleaning house, washing dishes, and taking out trash.
joint replacements may respond well to rehabilita-
Access to community. Determine access to
tion and a recovery of function.
transportation, such as taking the bus or driving a car
Many instruments and methods are available for
to shop, go to the doctor, and perform other necessary
conducting a functional assessment. Commonly used
functions outside the home.
instruments evaluate activities of daily living (ADLs)
and instrumental activities of daily living (IADLs). Food preparation. Determine ability to plan, prepare,
ADLs are basic self-care activities and can be evaluated and serve adequate meals independently.
following the guidelines described in Table 30-4. The Medication. Determine ability to take medications in
likelihood of institutionalization is extremely high for the right dose at the right time.
persons who have difficulty performing ADLs. Accord- Managing money. Determine ability to plan, budget,
ing to a recent meta-analysis predicting nursing home write checks or money orders, and exchange currency
admission, a person with three or more ADL depen- or coins. Includes ability to count and to open and
dencies, cognitive impairment, and prior nursing post mail.
home use are the strongest predictors of nursing
home admission.13
IADLs are activities that require both physical and
cognitive functioning. To evaluate a person’s IADLs,
follow the guidelines presented in Table 30-5. If alert the therapist to an underlying disease process,
individuals lose the ability to perform IADLs, they an exacerbation of a chronic condition, alterations in
should be assessed to determine the cause. A recent loss cognitive function, or some combination of those.
of functional ability (both ADLs and IADLs) should When identified early, loss of the ability to perform
IADLs should trigger the implementation of appropri-
ate clinical or community interventions that put
off or prevent the onset of deficits and premature
institutionalization.
TABLE 30-4 Activities of daily living The level of function in older adults depends on
Dressing. Inquire if any assistance is needed in their sensory perception (auditory, visual, olfactory,
dressing, including fastening buttons or zippers and and tactile) and dexterity. Any impairment in sensory
tying shoes. perception can be disabling and can affect the older
Grooming. Determine ability to trim nails (feet and person’s health status.
hands), shave, brush teeth, and brush hair.
Vision Assessment. Age-associated changes in the
Bathing. Inquire if any assistance is needed in
eyes can result in impaired vision. Studies vary in the
bathing in tub or shower, such as preparing
magnitude of this problem, but most agree that the
bathwater, getting into or out of tub or shower, and
degree of impaired or lost vision is significant in the
washing all body parts.
older adult population. The most common causes of
Toileting. Determine if help is needed in using the toilet. visual impairment are presbyopia, cataract, glaucoma,
Mobility. Inquire if the client has difficulty diabetic retinopathy, and macular degeneration. Visual
ambulating in the home, such as getting into and out disorders can result in decreased mobility, poor
of bed, lowering to or rising from a chair, walking, orientation, feelings of vulnerability, isolation, poor
climbing stairs, reaching for items in cupboards, and hygiene, the inability to manage medication delivery,
opening doors. and loss of independence. The Snellen Eye Chart is a
Eating. Ask if any help is needed in eating, such as using useful screening tool. Referral to a specialist is recom-
the utensils, cutting food, and putting food in mouth. mended when visual acuity is worse then 20/40 and
the impairment is interfering with daily activities.14
Respiratory therapists who care for elderly patients appear to be the wrong shape or size, or straight lines
can appropriately implement clinical interventions to may appear to be wavy or crooked. Color vision is
compensate for visual deficits that certainly are an asset gradually lost, and ultimately a dark area occupies the
to the patient and the health care team. center of the field of vision, as if the person were
looking through a camera with a spot on the center of
• If the patient wears glasses, make sure they are
the lens. Peripheral vision generally remains intact.
clean and accessible.
• If the loss of vision impairs their ability to
Glaucoma Glaucoma is a group of diseases that can
distinguish MDIs, help patients come up with
lead to damage to the optic nerve and result in blind-
creative solutions to distinguish between their
ness. It is a result of increased pressure in the eye. At
long-acting and rescue inhalers. Some practical
first, glaucoma has no symptoms. Unless the pressure
suggestions: a short length of flex tubing, rubber
at the front of the eye is controlled, however, it can
bands, puff paint, and/or Velcro dots can all be
eventually damage the optic nerve and cause blurred
used to enhance tactile ability. Ideally this
vision, loss of peripheral vision, and the appearance
intervention takes place before the patient leaves
of colored rings around lights. If glaucoma goes
the hospital, allowing therapists to modify
untreated, the remaining forward vision may decrease
misconceptions.
until none is left.
• If the patient’s vision loss makes it difficult for
them to distinguish pills, suggest that they use
Diabetic Retinopathy Diabetic retinopathy is a poten-
a piece of black felt (which provides contrast
tially blinding complication of diabetes that damages
and keeps pills from rolling around) to sort
the retina of the eye. It occurs when diabetes damages
the pills before placing them into a dated pill
the tiny blood vessels in the retina. At first, most people
container. Having a family member double-
do not notice any change in vision. As the disease
check the accuracy of their pills is an excellent
progresses, fragile blood vessels grow along the retina.
idea.
These blood vessels can bleed, clouding vision and
• In the hospital, patients with vision loss are
destroying the retina. In extreme cases, a person is able
adept at moving around their room as long as
to tell only light from dark. Large hemorrhages tend to
the furniture is not moved without their knowl-
happen more than once, often during sleep.
edge. Even moving a wastebasket to a location
more suitable for the therapist may create a
Additional Clinical Interventions for Patients with
stumbling block for the patient.
Visual Disorders
• If written instructions need to be sent home
with the patient, assure that the font is large • Encourage regular eye examinations.
enough (14 font), the font color is black, the • Clean the patient’s glasses.
paper is white (for contrast), and the writing is • Avoid the use of pastel colors; reds, yellows, and
double-spaced. oranges are easier to see than are blues and
greens.
Cataracts Cataracts are the most common cause of • Apply red nail polish or colored tape to identify
poor vision in older adults. A cataract is a clouding of different medication bottles.
the eye’s lens that causes loss of vision. A cataract starts • Use elastic bands to indicate the daily number of
out small, at which point it has little effect on vision doses; each time a pill is taken, a band is removed.
(like looking through a cloudy piece of glass). As the At the end of the day the bands are replaced.
cataract gets bigger and begins to cloud more of the • Make sure that lighting is bright and at a con-
lens, vision becomes increasingly yellowed. The stant level, with glare and reflection eliminated
yellowish tint distorts the eye’s color vision; blues and as much as possible.
greens are particularly hard to see. Cataracts can cause
images to appear hazy and out of focus, and double
vision is possible. The eyes become overly sensitive Best Practice
to light and glare, making night driving difficult.
Age-Related Macular Degeneration Age-related macular Diabetic Retinopathy

degeneration (AMD) affects central vision. It is a com- Diabetic retinopathy is particularly prevalent
mon cause of vision loss among people over 60. among Hispanics, African Americans, and Native
Because only the central vision is affected, people rarely Americans. Diabetic patients in those groups
go blind from the disease. A person with AMD gradu- should be checked frequently.
ally loses the ability to see things clearly. Objects may
• Ensure adequate lighting on stairwells, hallways, Clinical Interventions for Patients with Hearing Loss
and steps and in the bedroom. Use a night-light To help patients with hearing deficits:
if necessary.
• Check to see that the hearing aid is functioning
• Use large-button phones and remote controls.
properly.
• Place textured warning strips or brightly colored
• Face the patient when speaking.
tape at changes in floor level.
• Have the patient put on a stethoscope to amplify
• Paint door frames in colors that contrast with
your voice and speak into the bell.
that of the walls.
• Carry a writing pad to use when clarification is
• Supplement teaching with audiotapes.
needed.
• Organize a list of emergency numbers (in large
• Lower the tone of your voice, and do not shout
bold type), and preprogram the telephone for
at the patient.
emergency numbers.
• Use facial expressions and hand gestures.
Auditory Assessment. Many elders have hearing prob- • Decrease extraneous noise.
lems. They mistake words in a conversation, miss mu- • Encourage the use of visuals (e.g., a flashing
sical notes at a concert, or leave ringing doorbells or light), as well auditory alerts for smoke alarms,
telephones unanswered. Hearing problems can be small security systems, doorbells, and telephones.
(missing certain sounds) or large (total deafness).
Some adults may not admit they have trouble Nutritional Assessment. Because malnutrition and
hearing. Older people who cannot hear well may undernutrition are common in the geriatric popula-
become depressed or withdraw from others to avoid tion, assessment of this problem and intervention are
the frustration or embarrassment of not understanding important considerations. Additionally, the prevalence
what is being said. They may become suspicious of or of malnutrition in ill elderly is cited at up to 60%.15
angry at relatives, friends, or health care providers who A compromised nutritional status delays healing and
“mumble” or “don’t speak up.” It is easy to mistakenly prolongs hospital stays. Therapists may notice some of
identify behaviors caused by hearing deficits as confu- the signs of malnutrition in their patients (Table 30-6).
sion, unresponsiveness, or lack of cooperation. Some For community-dwelling elders, the Nutritional Health
obvious indications, however, that a person is experi- Screen is simple to administer and may help prevent
encing hearing loss are as follows: problems in at-risk older adults. Malnutrition has
serious consequences in older patients, thus nutritional
• Difficulty hearing telephone conversations
assessment, followed by appropriate interventions, may
• Turning up the volume on the television or radio
save a life.
• Difficulty understanding women and children
talking
Dexterity Assessment Older adults commonly have
• Appearing to be straining to understand
arthritis, as well as difficulty bending, kneeling, and
conversations
stooping. Normal aging changes, such as decreased
muscle mass, strength, and joint flexibility, greatly affect
Hearing Loss
the older person’s agility, mobility, and dexterity. Other
• Presbycusis, the most common hearing impair- factors that adversely affect dexterity are medications,
ment in older adults, is a progressive high-fre-
quency hearing loss. This auditory impairment
decreases the ability to hear what others are
saying, thereby hindering communication.
TABLE 30-6 Signs of malnutrition in
• Conductive hearing loss occurs when sound waves
are not properly conducted to the inner ear. elderly patients
Sounds seem to be muffled. Ear wax in the ear An emaciated appearance, 15–20% below ideal body
canal, fluid in the middle ear, abnormal bone weight (IBW)
growth, or a middle ear infection can cause Muscle wasting, loss of subcutaneous fat
this loss.
Poor coordination
• Sensorineural hearing loss occurs when there is
damage to the inner ear or auditory nerve. Muscle weakness, fatigue
Sound waves reach the inner ear but are not Dry, brittle thinning hair, or hair loss
properly converted into a message that the brain Dry skin, poor coloring
can understand. Sounds are distorted. In general,
Dry cracked lips
low-pitched tones are easier to hear than high-
pitched tones. Swollen red tongue
alcohol, medical procedures, disease processes, and lack Interior Evaluation. Assess the kitchen for the
of exercise. Lack of mobility and dexterity can lead to following:
falls. Comprehensive risk assessments for falls can
• Control knobs for the stove toward the front,
include two simple evaluations:
and large control knobs for stove and oven
• The one-leg balance (ability to stand unaided on • The refrigerator temperature set to 40°F or lower
one leg for 5 seconds) to prevent food spoilage
• The get-up-and-go test (rise from a sitting posi- • Nonglare lighting in all work and living areas to
tion, walk 10 feet, return to the chair and sit) help reduce the incidence of cuts, burns, and falls
• Lightweight pots and pans to reduce the occur-
Both are easy to administer. If completion of the
rence of spills and burns
get-up-and-go test takes longer than 16 seconds, the
• Removal of all throw rugs
patient may be at increased risk for falling.
Assess the bedroom for the following items:
ENVIRONMENTAL ASSESSMENT • Fire alarms

• A telephone with large buttons within arm’s
Accessible housing enables older adults to live their
reach of the bed
lives independently. Many homes and commercial
• Night-lights with red bulbs (the aging eye can
environments, however, are full of potential booby
more readily accommodate to red light than to
traps for the older adult. As in exercise, imagine your
white light)
home, a health care facility, or a patient’s home.
• The elimination of heating devices—electric
Picture an older person who is suffering from func-
blankets, portable heaters, and heating pads
tional impairments walking through this environ-
• “No Smoking” signs clearly posted in bedrooms
ment. How many physical barriers must the person
to discourage smoking in bed or near a supple-
overcome? How many hazards must the person
mental oxygen supply
avoid?
A thorough environmental assessment and appro- Assess the bathrooms for presence of safety
priate environmental adaptations promote safety, precautions:
reduce accidents, reduce visits to the emergency room
• Ground circuit interrupters to protect against
and subsequent hospital stays, and improve the quality
accidental shock
of life for the older adult. The most efficient way to
• Hot water heaters set to 120F or below
perform an environmental assessment is to evaluate
• Nonskid bath mats
the exterior access to the house or facility and then
• Grab bars installed around toilets, in dressing
evaluate each room in it. Home care therapists may
areas, and in the bathing area
be the first to note the need for such an evaluation.
Although environmental assessments are outside the
scope of the RT’s practice, therapists can contact social SOCIOECONOMIC ASSESSMENT
workers who can make arrangements for such an
Historically in America in the early 1900s, the problem
evaluation.
of old age was primarily a problem of poverty. Few
organizations had any provisions or safety nets for
Exterior Access Evaluation. Outside things to
older adults at retirement age. In 1910, only 9 of the
look for:
nation’s 56 largest cities (2%) had pension plans for
• Adequate nonglare lighting their teachers, police officers, or firemen.16 Even in
• Handrails on both sides of the steps and extend- 1935, when Social Security was first enacted, little help
ing the full length of the stairs was provided to the indigent or poor. Not until 1965,
• Filling in potholes and irregular surfaces on when Medicare and Medicaid were passed, was major
driveways and sidewalks help provided for adults over age 65. Over the years,
• Appropriate flooring and surfaces: ramps, many revisions of the Social Security Act have made it
reflector tape to indicate level changes, nonskid more equitable and a source of steady income for our
texturing on stairs and surfaces that get wet, elderly citizens. In 2000, Social Security was the major
color (no blues, greens, or pastels) to highlight source of income for older adults, but it was not their
entrances and signage only resource. On average, according to the 2000 Social
• Lightweight doors with lever handles Security Fact Sheet, fewer than 22% of older adults
• Deadbolt locks and wide-angle peepholes cited Social Security as their only income.17
(installed at the appropriate height for the Does poverty still exist among the elderly in
person) America? Will we see patients who cannot afford
on this test using either a 10-point or 18-point clock

Best
Best Practice
Practice drawing scoring system, are also validated screening
instruments and easier to incorporate into clinical
Need
Need for
for Financial
Financial Assistance
Assistance practice.
Communicating with cognitively impaired elders
If
If someone
someone does
does not
not have
have enough
enough money
money to to may be challenging also. Instead of walking away in
buy
buy food and to pay rent, what are are
food and to pay the rent, what the the
oddsodds
frustration, try some of the following interventions for
of the patient purchasing the
of the patient purchasing three newlythree newly pre-
more successful communication:
scribed
prescribedMDIs?
MDIs?Simply asking
Simply the the
asking patient if the
patient
cost
if the cost of medications, housing, or food fi-
of medications, housing, or food causes • Identify yourself by approaching the patient
nancial
causes fistrain
nancialgives the gives
strain patientthethe opportunity
patient the to from the front, calling the patient by name and
communicate the need for financial
opportunity to communicate the need for assistance. limiting distractions.
financial assistance. • Speak slowly and distinctly; choose words
carefully, using short simple sentences. Avoid
vague words and confusing expressions.
• Avoid sudden movements. Use friendly facial
expressions and maintain eye contact.
health care? Unfortunately, the answer to both • Ask one question at a time. Give the patient
questions is yes. A growing concern today is about the time to reply. Repeat information. Turn ques-
rising cost of living and the rising cost of health care tions into answers. Offer a guess if the patient
expenditures. To those on fixed incomes, to those used the wrong word and cannot find the
living below the poverty level, and to the indigent, right one.
medical care may be substandard. Financial insecurity • Give simple directions and simple explanations,
affects an older person’s ability to seek medical offer pictures if available.
assistance, to purchase prescribed drugs, to satisfy • Try a written note when spoken messages seem
minimal nutritional requirements, and to maintain too confusing. Encourage unspoken communi-
adequate housing. Because many aspects of the social cation such as pointing or gesturing.
situation can affect functional ability, therapists • Be patient and supportive. Avoid criticizing or
should inquire about any recent changes that have correcting. Offer comfort and reassurance.
occurred in their patients’ living arrangements,
activities, or financial support. Home care therapists
may be in the best position to do this, but any ASSESSMENT OF MEDICATION USE
therapist assisting a patient with hospital discharge Studies have estimated that 40–70% of older adults do
has an opportunity to intervene. Patients may be not take their medication as prescribed (at the right time
eligible for assistance provided by caregivers, and or in the right amount).19 Adherence to a drug regimen
many patients are still unaware of the resources may be challenging for older adults for a variety of
available to them. As uncomfortable as doing so may reasons. A study conducted on patients two weeks after
be, the respiratory therapist must assess the financial
means of the older patient.
COGNITIVE ASSESSMENT Spotlight

Cognitive impairments can greatly restrict an older On
person’s ability to live independently, manage financial
affairs, adhere to medical regimens, and interact Geriatric Assessment
socially. Typically, older adults experience alterations in The geriatric assessment should be applied at
mental functioning such as a decreased ability to think each encounter with an older patient. The system-
abstractly, decreased short-term memory, reduced atic approach of the geriatric assessment guides
attention span, and alterations in the ability to concen- the clinician through the complex multidisciplinary
trate. Due to the increased incidence of Alzheimer’s nature of illness in older adults and promotes a
disease, impaired cognition, and other dementias in thorough assessment of the older individual.
this population, the yield of screening for cognitive Thinking through the six components of the
impairment increases with age. The Mini-Mental State geriatric assessment enables the clinician to detect
exam, which consists of 30 questions, can be used to and evaluate signs or symptoms that affect the
assess several dimensions of cognitive function.18 The health and well-being of the older patient.
Clock Drawing Test (CDT), as well as the recall of items
hospital discharge to home revealed that 49% of the the systems just listed as well as in the cardiovas-
elderly patients were noncompliant with their drugs, cular, nervous, and endocrine systems. In
either over- or undermedicating themselves.20 An addition, many prescription and over-the-
alarming number of nursing home admissions are due, counter preparations are contraindicated in
at least in part, to the persons’ inability to take medica- patients with respiratory disorders (Table 30-8).
tions correctly. A recent systematic review revealed that, • Adherence to a medication regimen is a
compared to the prevalence of hospital admissions multidimensional phenomenon. The World
associated with an adverse drug reaction (ADR) in Health Organization defines it as the extent to
children of 4.1%, for the elderly the admission rate which a person’s behavior in taking their
was 10.7%. 21 medication corresponds with agreed recom-
Because older adults frequently suffer from comor- mendations from a health care provider.22
bid disease processes, they are likely to have three or Failure to take drugs as recommended is
four physicians independently treating the disease defined as nonadherence.
processes. Each of these physicians prescribes medica-
Factors that contribute to adverse drug reactions and
tions to treat a particular disease process, and often
nonadherence with medication regimes are:
physicians are unaware of the prescribing practices of
the other physician. • Use of nonprescription medications.
• Polypharmacy (the use of multiple medica- • Use of alcohol and caffeine.
tions), age-related physiological changes, and • Nutritional deficits.
comorbid disease processes have a direct effect • Dexterity limitations.
on the pharmacokinetics and pharmacody- • Use of vitamin and herbal preparations.
namics of medication in the older adult. • Sensory impairment.
Polypharmacy may harm the patient or • Alterations in cognitive function.
nullify medication benefits because of drug • Financial difficulties (including lack of insurance).
interactions, and determining which • Impairment of swallowing ability.
medication is causing undesired affects • Health care professionals’ inadequate knowledge
becomes difficult. of geriatric pharmacology.
• Pharmacokinetics is the body’s absorption, • Lack of appropriate patient education.
distribution, hepatic metabolism, and renal Unfortunately, no medication regimen is without risk.
clearance of a drug. Because of age-related All medications, including herbal compounds, have
changes in the renal, hepatic, and gastrointesti- the potential to cause side effects, some minor and
nal systems and in muscle mass and fatty tissue some fatal.
(see Table 30-7), drugs may not have their Educating the patient about medications and
intended effects. Disease states may also affect medication regimens is, without exception, the greatest
pharmacokinetics. factor in improving adherence to medication regimes.
• Pharmacodynamics (a drug’s mechanism of To promote safe and effective pharmacological treat-
action) can be affected by age-related changes in ment of the older patient, the practitioner must ensure
that the patient understands the answers to the follow-
ing questions for each medication prescribed:
TABLE 30-7 Disease states that affect • What is the medicine’s name, and what is it
pharmacokinetics supposed to do?
Malabsorption • How, when, and for how long must it be taken?
• While the patient is taking this medicine, what
Pancreatitis
should be avoided:
Gastric surgery - Certain foods and dietary supplements?
Congestive heart failure - Caffeine, alcohol, and other beverages?
Hepatic or renal insufficiency - Other medicines (prescription or over-the-
counter)?
Congestive heart failure
- Certain activities (such as driving or smoking)?
Thyroid disease • What are the side effects, and what should the
Cancer patient do if they occur?
Volume depletion • Will this medicine affect sleep or activity level?
Chronic renal insufficiency • What should be done if the patient misses a
dose?
TABLE 30-8 Nonasthma medications with increased potential for adverse effects in the
older patient with asthma
Comorbid Conditions for
Medication Which Drug is Prescribed Adverse Effect Comment
Beta-adrenergic Hypertension Worsening asthma Avoid when possible; when
blocking agent Heart disease Bronchospasm must be used, use a highly
beta-selective drug
Tremor Decreased response to
Glaucoma bronchodilator
Decreased response to
epinephrine in
anaphylaxis
Nonsteroidal Arthritis Worsening asthma Not all older patients with
anti-inflammatory Musculoskeletal diseases Bronchospasm asthma have nontolerance of
drugs NSAIDs, but they are best
avoided if possible.
Non-potassium Hypertension Worsening cardiac Additive effect with antiasthma
sparing diuretics Congestive heart failure function or medications that also produce
dysrhythmias due potassium loss (steroids,
to hypokalemia beta-agonist); older patients
also likely to be receiving
drugs (e.g., digitalis) that
increase the likelihood of
hypokalemia
Certain nonsedating Allergic rhinitis Worsening cardiac
antihistamines function or ventricular
(terfenadine and arrhythmias
astemizole)
Cholinergenic Urinary retention Bronchospasm Some over-the-counter asthma
agents Glaucoma Bronchorrhea medications contain ephedrine,
which can aggravate urinary
retention, glaucoma.
ACE inhibitors Heart failure Increased incidence Hypertension
of cough
Source: From National Asthma Education and Prevention Program. Considerations for diagnosing and managing asthma in the elderly. Washington, DC:
National Heart, Lung, and Blood Institute, National Institutes of Health; February 1996. NIH Publication No 96-3662.
When discussing medication adherence with older

Best Practice adults:
• Present the information in a clear and concise
Medication History manner.
The respiratory therapist must record a thorough • Keep it simple; eliminate medical jargon.
and accurate medication history in the patient • Provide information in small segments, and
record and update the record as needed. The reinforce teaching with each patient encounter.
medication history should include all prescription It often is helpful to coordinate medication
and over-the-counter medications. administration times with activities of the day
(e.g., mealtime, bedtime, and awakening).
• Make sure patients understand the teaching by

Best Practice asking them questions to assess their under-
standing of the drug’s actions and side effects.
Medication Education • Give them a sheet of instructions containing the
phone numbers of their physician and pharmacist.
To promote the understanding and retention of
medication education, you must employ clini-
cal interventions that minimize the effects of
sensory, cognitive, and functional impairments. Communicating with
Plan to take extra time when educating the older Older Patients
adult because often repetition and reinforcement
Communication implies two things: a message deliv-
of information are needed.
ered and a message understood. When caring for older
adults, therapists must be cognizant of some potential
barriers to communication.
• Simply telling patients who you are and what
therapy the physician wants you to deliver does
not guarantee that they have processed the
CASE STUDY 30-3 information. Hearing deficits are not uncommon
in older adults, especially older male patients. If
T. W. is a 76-year-old widow who lives alone there is noise in the room—television, radio,
in the home she and her husband purchased equipment humming, noise from the hallway, or
50 years ago. Her medical problems include noise from construction outside the hospital—
COPD, congestive heart failure, arthritis, hyper- patients may not hear the message.
lipidemia, cataracts, and insomnia. She has been • Some drugs can cause ototoxicity, a damaging
hospitalized for the past 6 days because of an effect on the eighth cranial nerve, resulting in
exacerbation of her COPD. She is in stable transient or permanent hearing impairment.
condition, and, except for the fact that she • Patients who are depressed may hear the therapist
fractured her right clavicle 2 nights ago after speak but may disconnect from the message.
slipping on her IV tubing, her stay has been unre- • Poststroke patients who suffer from aphasia
markable. Her physician plans to discharge her may have lost the power of speech and/or
in 2 days. Mrs. W.’s discharge orders include: comprehension of the spoken word. This does
not mean that they did not receive the message,
Continuous home oxygen therapy: 2 Lpm
but rather, because they do not respond,
Albuterol metered-dose inhaler: 2 puffs Q4
therapists may assume that the message was
Corticosteroid metered-dose inhaler:
not delivered.
2 puffs qd
• Dementia, as in Alzheimer’s disease, is always a
Prednisone: 10 mg qd
challenge. The patient may not remember who
Diazepam: 10 mg HS PRN
you are, or your instructions 5 minutes after you
Digoxin: 0.25 mg qd
leave the room.
Cipro: 500 mg BID
• In addition to potential pathology-related lack
Hydrochlorothiazide: 25 mg qd
of communication, the RT has to remember that
Theophylline: 400 mg TID
hearing loss may simply be part of the normal
Home physical therapy twice a week
aging process. As stated by Robinson and
Questions coworkers, “at a time when older patients have
the greatest need to communicate with their
1. What, if any, complications or potential
doctors [and caregivers] life and physiologic
problems do you see with Mrs. W.’s current
changes make it the most difficult.”
prescription medications?
2. Describe how you would educate Mrs. W., The following communication tips are similar to those
and prioritize your teaching. suggested for use with hearing impaired individuals:
3. What environmental concerns do you have • Make a connection physically and emotionally
for Mrs. W.? Which interventions would be with the patient; smiling may remove the fear
beneficial for her? factor or lessen the “white coat” increase in
blood pressure.
• Allow a little extra time to deliver therapy to and competent care. Change can take place only if there
older patients. If therapists appear rushed, is a determined effort to turn the corner and embrace
irritated, or disinterested, communication may geriatric educational initiatives. The older adult patient
not happen at all. population will be available, the time to train is now.
• Avoid distraction if possible, and let the patient
know that your time in the room is their time,
even if it is only 7–10 minutes. Study Questions
• Maintain eye contact and listen to their
responses, comments, or questions. Research REVIEW QUESTIONS
indicates that physicians listen to patients for an 1. What challenges will the gray explosion present to
average of 18 seconds before they interrupt, the health care system?
causing them to miss the message the patient is
2. What population of older adults derives the
trying to deliver.
greatest benefit from a comprehensive geriatric
• Deliver one message at a time, speaking
assessment? Why?
clearly and loudly enough for them to hear
(not shouting) and making sure they can see 3. What is the value of the functional assessment? List
your lips clearly. Multiple instructions given the components of a functional assessment. Who
as you are multitasking is a recipe for can do the assessments?
miscommunication. 4. Medications can be hazardous to the health of an
• When teaching a new technique and using older adult. Why? How can older adults be made
good communication skills, ask the patient more aware of the benefits and hazards of drug
for a return demonstration. If they cannot therapy?
do what you taught them and or if they 5. How can the clinician promote medication
leave out steps, the whole message was not compliance among older adults?
understood.
6. Describe ways that therapists can communicate
Communication is a learned activity, often referred to more effectively with older patients when deliver-
as the art of communication. There is no exact science ing therapy.
to delivering an understandable message. Sometimes
the strategies work; sometimes they are unsuccessful.
Patients respond if the effort is sincere, and, over time, MULTIPLE-CHOICE QUESTIONS
they will understand enough of the basics to participate
in therapeutic endeavors. 1. Which of the following factors is not associated
with hospital readmission for the older population?
a. limitations in ADLs
b. polypharmacy
Summary c. low economic status
d. male gender
In 2002, a document titled “Ten Reasons Why America
is Not Ready for the Coming Age Boom” was published 2. Which statement is true concerning illness in the
by the Alliance for Aging Research. Their statistics are older person?
compelling, their message even more so. Despite a. The assessment of activities of daily living and
increased numbers of older adult patients, physicians instrumental activities of daily living is not a
trained in geriatrics will be woefully lacking. The same reliable indicator of failing health.
goes for allied health professionals; there will be more b. Most older persons who are ill require acute
older patients, but fewer therapists (occupational health care.
therapy, physical therapy, respiratory therapy) will be c. Most older adults have at least one chronic
trained in bedside geriatric care. The approaching and condition, and many have multiple
very real geriatric gap has the potential to overwhelm conditions.
the health care system. d. Most older persons have an average of
It does not have to be that way. The graying of 10 chronic conditions.
America will offer superior job security to those who are 3. One of the fastest growing segments of the U.S.
competent in the skills and knowledge required to care aging population consists of:
for the aging population. The aged patient will chal- a. baby boomers.
lenge the therapist to look beyond the obvious answers. b. the 65–75 age group.
Therapists will need to use all their clinical skills, senses, c. the 75–85 age group.
intuition, reasoning, and common sense to provide safe d. the 85-plus age group.
4. Activities of daily living are: CRITICAL-THINKING QUESTIONS

a. useful in identifying individuals who are at risk
1. What changes in the present health care system are
for institutionalization.
most beneficial to the older patient as well as to
b. fundamental self-care tasks essential to
the economy?
maintaining independence.
c. beneficial in identifying exacerbation of disease 2. How has Medicare Part D impacted older adults on
processes. a variety of medications?
d. physical exercises older patients perform on a
daily basis. ACTIVITIES
5. All of the following interventions help the cogni-
tively impaired retain learning material except: 1. Visit a health care facility and describe the design
a. presenting material slowly. features of the facility. Comment on its best and
b. introducing small amounts of new information. worst design features. How does the physical
c. keeping reading level of written information at environment accommodate and present obstacles
the tenth grade level. to the older patient?
d. repetition. 2. Interview a person over 70 years old. Write a
6. What is pharmcokinetics? summary of the interview, including the subject’s
a. the concurrent use of different medications age, gender, and level of independence. Have them
b. an adverse effect of medication answers the following questions: How has the
c. what the body does with a drug world changed since you were young? What are
d. the inert chemical compounds found in some positive aspects of aging? What are some
medications negative aspects of aging? What do you enjoy now
that you did not enjoy in your younger years?
7. What is an appropriate font size for literature
designed for an older adult with a visual
disorder? References
a. 14 point
b. 10 point 1. Institute of Medicine. Retooling for an aging
c. 16 point America: building the health care workforce.
d. 8 point Washington, DC: National Academies Press;
Available: April 14, 2008. www.iom.edu/CMS
8. What percentage of older adults cite Social Security
2. Yancy CW. The prevention of heart failure in
as their only income?
minority communities and discrepancies in health
a. 22%
care delivery systems. Medical Clinics of North
b. 32%
America. 2004;88,5:1347–1368.
c. 42%
3. U.S. Department of Health and Human Services:
d. 52%
What are health disparities: www.omhrc.gov
9. The geriatric assessment is designed: Content last modified 11/18/2005.
a. to provide a systematic diagnostic tool for the 4. Census 2000 Summary File 1 (SF1). http://factfinder
treatment of acutely ill older adults. .census.gov/servlet/DatasetMainPageServlet?_langen
b. to be multidisciplinary in nature and used by 5. National Center for Health Statistics. U.S. life
all health care professionals in any health care expectancy hits new high of nearly 78 years.
setting. September 2007. www.cdc.gov/nchs
c. for older patients who do not have comorbid 6. U.S. Census Bureau. Facts for features. March 2006.
disease processes. www.census.gov/Press-Release/www/releases/archives/
d. to allow the health care practitioner to facts_for_features_special_editions/ 006537.html
independently assess each component 7. Centers for Medicare& Medicaid Services. Medi-
separately. care and you, 2008. Department of Health and
10. Which of the following is not a characteristic of Human Services CMS Publication #10050;
disease in old age or of an older patient? January 2008.
a. tendency to get angry at people who mumble 8. Feldstein PJ. Health Care Economics. 6th ed. Clifton
b. belief that the medical condition is just a part Park, NY: Delmar Cengage Learning; 2005.
of the aging process 9. Centers for Medicare & Medicaid Services, U.S.
c. atypical presentation of disease states Department of Health and Human Services.
d. having more muscle mass than when Nursing homes: paying for care. March 27, 2008.
younger www.medicare.gov/Nursing/Payment.asp
10. Comprehensive Geriatric Assessment Position Nursing Home Database (information about nursing
Statement. (Special thanks to Dr. Paul Mulhausen.) homes, including results of recent surveys): http://
New York: AGS Public Policy Committee, May 2005. www.medicare.gov/coverage/home.asp
11. Alliance for Aging Research: Executive Summary.
Medical never-never land: ten reasons why America
is not ready for the coming age boom. February VISION INFORMATION AND RESOURCES
2002. www.agingresearch.org American Foundation for the Blind: 1-212-502-7661 or
12. Osterweil D. Comprehensive geriatric assessment: afbinfo@afb.org
lessons in progress. Israel Medical Association Journal American Optometric Association: 1-314-991-4100
(IMAJ). 2003;5:371–374. Lighthouse National Center for Vision and Aging:
13. Gaugler JE, Duval S, Anderson KA, Kane RL. 1-800-334-5497
Predicting nursing home admission in the US: A National Eye Care Project of the Americas of the Ameri-
meta-analysis. BMC Geriatrics. 2007;7:13. can Academy of Ophthalmology (a help line to refer
14. Miller KE, Zylstra RG, Standridge JB. The geriatric callers to local ophthalmologists who will volunteer
patient: a systematic approach to maintaining health. to provide needed medical care): 1-800-222-EYES
American Family Physician. February 15, 2000. National Eye Institute: http://www.nih/gov/
http://www.aafp.org/afp/20000215/1089.html publications
15. Seiler WO. Clinical pictures of malnutrition in ill National Institute on Aging: 1-800-222-2225 or
elderly subjects. Nutrition. 2001;17:496–498. 1-800-222-4225 (text telephone)
16. Fischer DH. Growing Old in America. New York: The National Library Service for the Blind and Visually
Oxford University Press; 1975. Handicapped (provides free medical services to
17. Social Security Administration. Income of the people with vision problems and offers braille
population 55 or older, 2000. Washington, DC: and large-print materials and recorded books):
Government Printing Office, 2002. 1-800-424-8567
18. Wagenaar DB. Communicating with the elderly. Vision Foundation (publishes the Vision Resource List,
Dialogue and Diagnosis. April 2007. www.do-online which includes information on special products and
.org/pdf/pub_dd0407wagenaar.pdf services for people with visual impairments):
19. Salzman C, Kupfer DJ Medication compliance in 1-617-926-4232
the elderly. The Journal of Clinical Psychiatry. Supp.
1.1995;56:18–23.
AUDITORY INFORMATION AND RESOURCES
20. Gray SL, Mahoney JE, Blough DK. Medication
adherence in elderly patients receiving home American Academy of Otolaryngology—Head Neck
health services following hospital discharge. The Surgery, Inc.: 1-703-836-4444 or 1-703-519-1585
Annals of Pharmacotherapy. 2001;35:539–545. (text telephone)
21. Kongkaew C, Noyce PR, Ashcroft DM. Hospital American Speech-Language-Hearing Association:
admissions associated with adverse drug reactions: a 1-800-638-8255 (voice/text telephone)
systematic review of prospective observational studies. National Information Center on Deafness: 1-202-651-
The Annals of Pharmacotherapy. 2008;32,7:1017–1025. 5051 or 1-206-651-5052
22. Sabate E, ed. Adherence to Long-Term Therapies: Evidence National Institute on Aging: 1-800-222-2225 or
for Action. Geneva: World Health Organization; 2003. 1-800-222-4225
National Institute on Deafness and Other Communica-
tion Disorders: 1-800-241-1044 or 1-800-241-1055
Resources Self-Help for Hard of Hearing People, Inc.: 1-301-657-
2248 or 1-301-657-2249 (text telephone)
COMMUNITY AND HEALTH RESOURCES
Centers for Medicare & Medicaid Services, formerly
the Health Care Finance Administration ENVIRONMENTAL RESOURCES
(Medicare and Medicaid information): http:// Abledata: The National Database for Assistive Technol-
www.hcfa.gov/ ogy Information 8455 Colesville Road, Suite 935,
Eldercare Locator (a nationwide directory designed to Silver Spring, MD 20910-3319; 1-800-227-0216 or
help older persons and caregivers locate support 1-301-427-0277(voice/text telephone) http://www
services): Call1-800-677-1116 or contact the local .abledata.com
area agency on aging. American Association for Retired Persons (AARP): The
Medicare Fraud and Abuse: 1-800-HHS-TIPS Do-Able Renewable Home. AARP publication, online
(1-800-447-8477) access: http://www.usc.edu/go/hmap/library/
Medicare Information: 1-800-318-2596 drhome/
CHAPTER 31
Emergency Respiratory Care

Robert R. Fluck Jr.
OBJECTIVES
• Highlight the importance of ABCs in any patient situation.
• Describe manual methods of maintaining airway patency.
• Describe the equipment and techniques for maintaining airway patency.
• Describe the management of the first 10 minutes of an adult cardiac arrest.
• Describe the priorities in the management of cardiac arrest in a child.
• Differentiate priorities between infant and adult resuscitation.
• Describe situations under which airway adjuncts other than an endotracheal tube are used.
CHAPTER OUTLINE
Basic Life Support Fluid Therapy and Drugs
Components of Basic Life Support Resuscitating the Newborn Outside the
Adult Airway Obstruction Delivery Room
Child Airway Obstruction Cardiac Rhythm Disturbances
Infant Airway Obstruction Pediatric Trauma
Advanced Cardiovascular Life Support Neonatal Resuscitation Program
Ventricular Fibrillation (VF), and Pulseless Primary Versus Secondary Apnea
Ventricular Tachycardia (v-tach) Changes in Lungs and Circulation at Birth
Asystole Ventilation
Pulseless Electrical Activity Circulation
Bradycardias Intubation
Tachycardias Drug and Volume Therapy During Resuscitation
Acute Coronary Syndromes (ACS) Emergency Airway Adjuncts
Defibrillation Esophageal Obturator Airway/Esophageal Gastric
Pediatric Advanced Life Support Tube Airway
Broselow Tape Esophageal Tracheal Combitube
Initial Patient Assessment and Prevention Laryngeal Mask Airway
853
KEY TERMS
advanced cardiovascular life support (ACLS) laryngeal mask airway (LMA)
automatic external defibrillator (AED) neonatal resuscitation program (NRP)
basic life support (BLS) pediatric advanced life support (PALS)
esophageal obturator airway (EOA)/esophageal ventricular fibrillation (VF)
gastric tube airway (EGTA) ventricular tachycardia (v-tach)
esophageal tracheal combitube (ETC)
I
n nearly every emergency situation, the respira- confirmed in one step. However, if there is no response, it
tory therapist (RT) is a valuable player. The is next appropriate to call for help. Rarely, if ever, does the
therapist’s expertise lies in the area of maintain- single rescuer complete a resuscitation singlehandedly.
ing the airway, breathing, and circulation—the If the patient is in a bed with the head elevated, the
ABCs of resuscitation. Regardless of the etiology or rescuer has two choices:
circumstances of the emergency, the victim’s airway
• The bed can be quickly lowered to the flat
must be secured, breathing assured, and circulation
position. If the rescuer chooses to leave the
supported. Whether one looks in burn, neurosurgery,
patient on the bed, the head of the bed can be
or orthopedic literature, the first measures are the same:
removed (the head of every hospital bed comes
Take care of ABCs and worry about the injuries later.
off) and then used for a firm surface under the
The proper actions must be taken in the proper order
patient’s back to facilitate compressions.
and in a timely fashion. If the actions are not proper
• The other option is to move the patient to the floor
and timely, the result is almost invariably what is
(if the rescuer has been trained to do so without
euphemistically termed in medicine an unfavorable
sustaining an injury or injuring the patient).
outcome: The patient dies or worse, survives in a
persistent vegetative state. The ability of a respiratory The rescuer should then check for no more than
therapist to assess the patient rapidly and just as 10 seconds for the presence of a pulse. If there is no
rapidly institute the appropriate life-saving or -sustaining
treatment puts the RT at the head of the bed when the
patient is in trouble. The reader should note that the
guidelines for resuscitations are updated every five
Best Practice
years and should therefore stay abreast of these
changes. The techniques specified in this chapter are Defibrillation
recommended as of the time of this writing (2011). The vast majority of adults who suffer cardiac
arrest have ventricular fibrillation (VF) or, less
commonly, ventricular tachycardia (v-tach) as their
Basic Life Support initial rhythm. The only treatment for fibrillation
Basic life support (BLS) encompasses all the actions is defibrillation. Therefore, in contrast to what we
that can be accomplished without adjunctive equip- have all learned, the priority in an adult arrest is
ment. In spite of the fact that it is basic, it is indeed acquiring a monitor to determine the patient’s
vital; advanced treatments become meaningless (and rhythm and then defibrillating that rhythm if doing
ineffective) without well performed BLS. According to so is appropriate. Therefore the action taken first
the American Heart Association, in the adult patient in depends on location and on the available equip-
cardiac arrest, the time to cardiopulmonary resuscita- ment. In a hospital, head for the automatic
tion (CPR) is one of the two determinants of survival external defibrillator (AED), which is at every
after an arrest (ACLS Instructor’s Manual, 2010). nursing station and which all respiratory therapists
have been trained to use. On a medical-surgical
floor in a hospital without an AED, begin BLS un-
COMPONENTS OF BASIC LIFE SUPPORT til the arrival of someone who can use the manual
In performing BLS, the rescuer must first ascertain that the monitor-defibrillator (unless the RT is authorized
patient is indeed in need of resuscitation. The shake and by the hospital to use the manual unit). So it
shout maneuver (shaking the victim’s shoulders vigorously comes down to priorities versus resources: If it is
and shouting, “Are you OK?”) provides both tactile and possible to defibrillate, do so at the earliest time.
audible stimuli to the patient to attempt to elicit a If not, wait until the trained people get there.
response. If the patient is able to speak, the ABCs are
CHAPTER 31 ■ Emergency Respiratory Care 855
pulse, begin chest compressions with a depth of at least 30 compressions and 2 breaths, checking the mouth
2 inches (on an adult) at a rate of 100 per minute. If for the presence of a foreign body before every two
alone, the rescuer delivers cycles of 30 compressions breaths. In a hospital scenario, the presence of a meal
followed by 2 ventilations. If two (or more) people are tray should alert the rescuer to a possible airway
performing the resuscitation, the person performing obstruction. The rescuer(s) should continue the
compressions should deliver 30 (counting out loud sequence of 30 compressions to 2 ventilations until:
while doing so to cue the person performing ventila-
• Someone confirms the presence of a DNR and
tions) and then pause for the delivery of two breaths.
the resuscitation can be stopped.
After 5 cycles of 30 compressions and two breaths, the
• A physician determines that further resuscitation
rescuers should change positions due to the strenuous
attempts are futile and should be stopped.
nature of the performance of compressions. That
• Someone relieves the rescuer.
change should ideally take less than 5 seconds. The
• Or spontaneous circulation alone or both
airway should be opened using the head tilt-chin lift
spontaneous circulation and breathing return.
method unless the rescuer suspects potential C-spine
If only spontaneous circulation returns, the
trauma (Figure 31-1A). In that case, he should use the
rescuer should deliver one breath every
jaw thrust; however, should the jaw thrust not provide
6–8 seconds or approximately 8–10 per minute.
a patent airway, the rescuer should use the head
It should be noted that the American Heart
tilt-chin lift, as ventilation is a priority at this time
Association now recommends that lay persons
(Figure 31-1B). If there is an airway obstruction,
(non-professionals) performing CPR should
the rescuer should continue to perform cycles of
administer only compressions (a procedure
known as “hands-only CPR,” which can be
performed by any rescuer for the first 5 minutes
of a witnessed adult cardiac arrest) and not
attempt any ventilations.
As compressions are now determined to be the
more important action in CPR, there should be
minimal interruption of compressions, even for the
delivery of breaths. “Push hard and push fast” is the
new mantra for resuscitation. In addition, the Ameri-
can Heart Association recommends avoiding excessive
ventilation. This is a significant departure from past
practice when therapists were encouraged to hyperven-
tilate the patient. There are two physiologic reasons
for limiting ventilation. For one, positive pressure
Best Practice
(A) Terminating Resuscitation

Efforts
Modern ethicists have agreed that stopping a
medical treatment (in this case cardiopulmonary
resuscitation) is no different from not beginning
it at all. Formerly, almost all hospital personnel
believed that once you started some treatment,

stopping it was more difficult than not having be-
gun. For example, if someone were intubated and
placed on mechanical ventilation in an emergency
situation, extubating that person required him
to be weaned from mechanical ventilation. The
(B) reality now is that once a valid DNR is found for
FIGURE 31-1 (A) Head tilt, chin lift maneuver. (B) Jaw someone, resuscitation can cease immediately.
thrust maneuver.
FIGURE 31-2 The recovery position, used when the victim has spontaneous breathing and circulation: The position allows
maintenance of the airway and lets secretions drain from the mouth by gravity.
ventilation increases mean intrathoracic pressure. This the lateral decubitus position (Figure 31-2). The victim is
impedes venous return and thus cardiac output since placed on a level surface on his or her side with the
the venous-intrathoracic pressure gradient is the main inferior arm extended straight up. The position of the
determinant of venous return in the arrest situation. arm provides several benefits:
In addition, excessive ventilation decreases PCO2,
• It helps to cushion the head.
resulting in a left shift of the oxyhemoglobin dissocia-
• It helps position the head to maintain a patent
tion curve. This decreases the availability of oxygen
airway.
to the tissues.
• It keeps the mouth tilted down to let secretions
If the victim is breathing spontaneously at least
or vomitus drain out, thus minimizing the
10 or more times per minute, then the victim should
likelihood of aspiration.
be placed in the recovery position, technically known as
Performing Basic Life Support
Several techniques for basic life support are different two rescuers for children and infants, the
for children and infants. The American Heart As- ratio is 15 compressions:2 ventilations.
sociation defines an infant as someone younger than • The pulse is palpated at the brachial artery
1 year old. A child is between 1 and 8 years old. on an infant because the infant’s neck is
short, a fact that makes palpating the carotid
• Ventilation rates for both infants and children
artery more difficult in infants.
are the same as for adults: 8–10 per minute
or one every 6–8 seconds. The airway obstruction sequence in infants and
• Ventilation for the infant, however, is effected children differs somewhat from that of adults also.
by mouth–to-mouth-and-nose ventilation due
• In both cases, the finger sweep is never
to the small size of the infant’s mouth.
automatic. The rescuer inspects the child or
• Compression depth generally one-half of the
infant’s pharynx for the presence of a foreign
anteroposterior diameter of the thorax. This
body. If one is actually seen, then the rescuer
depth is estimated at 1.5 inches for infants
attempts removal with a finger.
and 2 inches for children.
• In an infant, because of the anatomy and the
• Compressions are performed with the in-
likelihood of damaging the liver, abdominal
dex and middle fingers or by the two hands
thrusts (the Heimlich maneuver) are not
encircling technique using both thumbs in
done; chest compressions, done exactly as
an infant and the heel of one hand in a child.
though one were performing them in cardiac
As with adults, the ratio of compressions to
arrest, are used instead and are alternated
ventilations for infants and children for one
with back blows (Table 31-1).
rescuer is also 30:2. However, if there are
TABLE 31-1 Specifications for CPR

performance
Ventilation Compression
Rate Compression Rate Depth
Adults 8–10 per minute At least
(every 6–8 seconds) 2 inches
100 per minute
Child 8–10 per minute 2 inches
(every 6–8 seconds)
100 per minute
Infant 8–10 per minute 1.5 inches
(every 6–8 seconds)
100 per minute
The victim’s knees should be bent to maintain stability
on the side. The rescuer should continue to monitor
the adequacy of breathing and be prepared to assist
ventilation if the respiratory rate drops to fewer than FIGURE 31-3 The “official” sign for choking.
10 per minute.
ADULT AIRWAY OBSTRUCTION to the floor. In the conscious victim, the rescuer should
The one circumstance in which the rescuer’s efforts then deliver the Heimlich maneuver (abdominal
(if successful) are rewarded almost immediately is in thrusts) until either the foreign body is expelled or the
the case of the conscious person with a complete upper victim loses consciousness.
airway obstruction. For adults, the risk factors for this Note: For someone who is pregnant or obese, the
situation include: rescuer should perform chest thrusts instead of abdom-
inal thrusts.
• Alcohol ingestion. If the victim loses consciousness, the rescuer
• Talking while eating. should call for help and then begin the sequence of
• Ill fitting dentures (a condition which causes the CPR, with one change: The rescuer should inspect the
person to cut progressively larger pieces of meat victim’s mouth for the presence of a foreign body each
and attempt to swallow with minimal chewing). time before attempting to deliver ventilation.
The adult with a complete upper airway obstruction By the time a patient needs either ventilation or
may look surprised and be unable to make a sound. both compressions and ventilation, the therapist has
The victim may (or may not) be giving the “official” missed a golden opportunity (or a number of them).
choking sign of placing the thumb and forefingers of The motto in health care today is health promotion/
both hands around the neck (Figure 31-3). First disease prevention. In other words, keeping people
confirm complete obstruction by asking the victim healthy is less expensive than treating them once they
whether he or she is choking. If the victim is able to become ill. The concept parallels preventive mainte-
cough forcefully and is not cyanotic, he or she should nance in an automobile. The problem is that we deal
be allowed to continue to try to expel the obstruction with individuals who may or may not do the things
without assistance. that prolong their lifespan, especially if the actions are
If, however, there is poor air exchange or cyanosis, inconvenient—even though who would not want to
the victim needs assistance. Take a position directly live longer given the chance?
behind the victim, turned 90º to the victim. In this
position, should the victim lose consciousness and fall,
the rescuer can control the victim’s descent to the floor CHILD AIRWAY OBSTRUCTION
without anyone’s being injured. The rescuer can The sequence for treating a complete upper airway
support the weight of the victim on the closer thigh obstruction in a child is exactly the same as that for an
simply by guiding the victim with the arms, at the same adult. The only difference is that chest thrusts are not
time moving backward and lowering the victim gently performed on a child.
Best Practice
Health Promotion/Disease Prevention in Adults
The respiratory therapist must try to teach people pamphlet that the respiratory therapist can give to
healthful behaviors, for both themselves and also patients to reinforce the stop-smoking message.
their children, for whom they have responsibil- Hypertension is another cause of CAD. The first
ity. For adults, the behaviors are best described as step in controlling blood pressure knows what it is.
heart healthy behaviors and address the cardiac risk An easy way to have blood pressure taken sev-
factors that can be modified. In 2004, the Report eral times a year is to donate blood! A person can
of the Surgeon General identified smoking as the donate blood every 56 days (American Red Cross,
main cause of coronary artery disease (CAD) and 2010) and can therefore have blood pressure taken
that cessation of smoking by adults would probably in a relatively no-stress environment as many as
have the most significant effect of any behavior on seven times each year, while performing a signifi-
the rate of CAD in the United States. Helping people cant public service. Continuing to take prescribed
stop smoking should be high on the priority list for medication is the most important step in controlling
respiratory therapists. To assist in this endeavor, the hypertension. Of course, if people do not feel ill,
Tobacco-Free Lifestyle Roundtable of the Ameri- they frequently stop taking prescribed medication
can Association for Respiratory Care has created a for any condition.
INFANT AIRWAY OBSTRUCTION complete obstruction has been confirmed, the rescuer
In dealing with an infant with complete upper airway should:
obstruction, the completeness of the obstruction • Place the infant face down over his or her arm
needs to be inferred by the lack of sound coming with the head lower than the hips.
from a small person whose face and body language • Administer up to 5 back blows (Figure 31-4A).
show extreme anxiety. A risk factor for upper airway • Turn the infant supine while carefully support-
obstruction for infants, as well as for small children, is ing the head with the head lower than the
the presence of small objects that the infant or child
can reach and then place in the mouth. Once a
(A) (B)
FIGURE 31-4 (A) Back blows for removal of a foreign body airway obstruction. (B) Chest thrusts.
• Administration of drugs and fluids by IV, IO, and

Best Practice (with some limitations), intra-tracheal.
• Monitoring of cardiac rhythm.
Critical Incident Stress • Electrical therapy, which includes defibrillation,
cardioversion, and pacing.
Debriefing
We frequently forget the stress which resuscita- Upon completing an ACLS course, the participant
tion places on the professionals providing the should be able to direct the resuscitation for the first
resuscitation. Whereas on television about 80% 10 minutes of a cardiac arrest. Although other situa-
of victims are resuscitated successfully, in real tions are included in the course, competency in
life 80% of resuscitations are unsuccessful. management of the full cardiopulmonary arrest is
Prehospital care includes a process called critical the key. Most adults are found in VF when they suffer
incident stress debriefing (CISD). The CISD gath- cardiac arrest as a result of a medical problem (as
ers all those involved in a rescue or resuscitation opposed to a traumatic arrest); in children and
a few days after the incident and allows them to infants, the cardiac arrest is more likely secondary to
talk about their performance and especially their a respiratory problem. The two important areas that
feelings following an incident that goes beyond ev- therapists might not be managing but should know
eryday events. An example of an especially stress- how to treat are acute stroke and acute coronary
ful incident might be the fire department whose syndromes (ACS). The time-dependent nature of the
emergency responder finds that one of the victims treatments for both of these situations requires that
of a fatal automobile collision is one of their own someone suffering from either of these illnesses have
members. A professional is brought in to conduct access to medical care as soon as possible. (The
the CISD. Health care givers in the hospital tend window for treatment of stroke is only 3 hours from
to neglect taking care of their own mental health. the onset of signs and symptoms.) The therapist, know-
People can develop post-traumatic stress disorder ing the signs and symptoms of stroke and ACS, is in a
if they are not allowed to work through their feel- position to expedite that medical care for friends and
ings after a particularly stressful resuscitation in relatives.
the hospital such as the attempted resuscitation A reasonable question is why RTs should take ACLS
of a child, which is always a stressful situation. training when most hospitals do not allow them to
intubate, defibrillate, or administer drugs via IV, IO, or
endotracheal routes. The reality is that the respiratory
therapist may be the best trained and educated person
hips and administer up to 5 chest thrusts at the scene of a cardiac arrest. For example, the nurses
(Figure 31-4B). on most medical-surgical floors might see one cardiac
• Repeat this sequence until either the obstruction arrest in a calendar year. They might not quickly
is removed or the infant loses consciousness. remember where the electrodes are supposed to be
placed on the patient. Yet respiratory therapists go to
If the infant becomes unconscious, the rescuer
every cardiac arrest in the hospital. For example, the
should have someone activate the emergency
author was at work when a cardiac arrest was paged.
response system. The infant should be placed on a
Upon responding, he found a female in full arrest with
hard surface, and the rescuer should begin CPR with
the monitor already connected showing v-tach. No one
compressions with the same caveat as that for adults–
was doing anything, even though the correct action at
inspect the mouth for a foreign body each time prior
that point was defibrillation as soon as possible. Even if
to delivering breaths.
forbidden to perform a particular action, the RT can
indicate the correct action to take and encourage a
Advanced Cardiovascular credentialed person to take it.
Three other points about ACLS are important.
Life Support
• First, ACLS is worth little without excellent BLS.
Advanced Cardiovascular Life Support (ACLS)
The ABCs of resuscitation encompass ensuring
encompasses the tasks and techniques used in cardiac
an adequate airway, providing adequate breath-
resuscitation that go beyond what a rescuer can do with
ing, and augmenting circulation as appropriate.
the hands and mouth (or pocket mask). ACLS includes
People become enamored of the gadgets for use
(but is not limited to):
in ACLS and forget the importance of BLS in the
• Endotracheal intubation or other means of overall picture. Do not fall short on the basic
securing the airway. skills.
• Second, ACLS is driven by rhythm algorithms. overly concerned when a resuscitation effort
Each rhythm has an algorithm giving the does not follow the American Heart Association
procedure for resuscitating that rhythm. If the script exactly.
rhythm changes, then the therapist changes to
the appropriate algorithm.
• Third, the title of the publication containing all VENTRICULAR FIBRILLATION (VF), AND
the procedures for resuscitation is Guidelines for PULSELESS VENTRICULAR TACHYCARDIA (V-TACH)
Cardiopulmonary Resuscitation and Emergency In the latest guidelines, VF, v-tach, asystole, and PEA
Cardiac Care (American Heart Association, are grouped together in the Cardiac Arrest algorithm.
2010). When first published, the title of the The big picture of the difference is that VF and v-tach
publication contained the word “standards.” should receive electrical therapy (defibrillation) while
However, realizing the legal and medical there is no electrical therapy for PEA and asystole.
implications, the American Heart Association The most common initial rhythm for the adult in
changed that word to “guidelines.” The change cardiac arrest is ventricular fibrillation. Thus, the
indicates that, practically, a clinician may respiratory therapist should be facile in diagnosing
deviate from the stated protocols when doing so and treating this rhythm. The following case study
is appropriate and warranted based on the highlights the important aspects of treating this
situation and the patient’s condition. Do not be dysrhythmia.
CASE STUDY 31-1

John S. is a registered respiratory therapist with a nurse enter the room with the crash cart. John asks
current ACLS card who is working the night shift in one of them to take over ventilation and the other to
Progressive Community Hospital. He arrives to attach the electrodes to Mr. J.’s chest. The other
administer aerosol bronchodilator therapy to night shift therapist arrives and assumes compres-
Mr. C. J., a patient who was just admitted to a sion duties from John. John notes that the rhythm
medical-surgical floor with an acute exacerbation displayed on the monitor is VF (Figure 31-5). He
of COPD. He enters the room and cheerily greets opens the gel pads and places one to the right of
Mr. C. J., who is in semi-Fowler’s position in his Mr. J.’s sternum and the other on the left side
hospital bed with his eyes closed. Receiving no of his chest at the apex of the heart, about 22 cm
response, John puts on gloves and gives Mr. J. a (9 in) below the axilla. He sets the defibrillator to
shake and calls to him quite loudly. Still getting no 200 joules and charges the paddles. He places the
response, John goes to the hallway and calls out, paddles on Mr. J.’s chest over the gel pads with
“I’ve got a code here—Room 1313!” He returns to good pressure (25 pounds is the listed value),
the room and grabs the pocket mask off the cork chants in a loud voice (while scanning the bed to
board at the foot of the bed. He then lowers the bed assure that there is no one in contact with either
to the flat position as low as possible. He checks for the bed or the patient), “I’m clear. You’re clear.
a pulse for no more than 10 seconds. We’re all clear. Defibrillating!” He discharges the
Feeling no pulse, he removes the head of the paddles. He advises the team performing compres-
bed and places it behind Mr. J.’s back. He delivers sions to resume CPR. The nursing supervisor arrives
30 compressions. John S. then applies the pocket and begins to record the events.
mask and delivers two slow breaths over one second Note: Older defibrillators deliver energy in what
each. Just then the patient’s nurse and the charge is known as a monophasic waveform (current travels
FIGURE 31-5 EKG showing ventricular fibrillation.
(continues)
(continued)
in only one direction). Newer defibrillators (includ- By this time, things should have settled down. The
ing AEDs) deliver energy in a biphasic waveform RT is working with the minimum number of people
(current travels in both directions). These biphasic needed to perform such a resuscitation properly.
defibrillators have been found to be more effective There should be one person each to:
at terminating VF or v-tach at lower energy doses
• Ventilate.
than monophasic defibrillators. This is advanta-
• Perform compressions.
geous since the less energy delivered to the myocar-
• Administer drugs and defibrillate.
dium, the less likely it is to be damaged in the
• Record the chronology of events (the scribe).
process.
• Lead the group.
John requests the charge nurse to start an IV
and administer 1 mg of epinephrine every three to Having a clearly designated leader is important.
five minutes once she has established the line, (Some hospitals place a white hard hat on the code
while he prepares and checks his equipment for cart; whoever is wearing it is in charge.) Clear
endotracheal intubation. Once he has intubated the leadership is especially critical in hospitals with
patient, he confirms the position of the endotra- medical students and house officers; failure to
cheal tube by a number of means. designate who is in charge can lead to confusion
Once the intubation is accomplished, the and a less than optimal resuscitation.
therapist documents (charts):
Questions
• The date and time.
1. If the RT were unable to lower the bed to the
• The size, and type (Miller or Macintosh) of
flat position, what alternatives would he have to
blade used.
position Mr. J. properly for CPR?
• The size tube.
• The ease of visualization of the cords. 2. What are the hazards of placing insufficient
• All indicators that were checked to confirm pressure on the defibrillator paddles?
proper placement of the tube. 3. Who has a greater role in carbon dioxide
• The distance mark in cm at the corner of elimination when a patient is in cardiac arrest:
the mouth. the person ventilating or the one performing
compressions?
Best Practice
Confirmation of Endotracheal Tube Placement
Confirmation of proper endotracheal tube placement long before the chest film is read. Otherwise, other
should be done by a number of means: efforts might be futile. In a patient with at least
spontaneous circulation (though not necessarily
• Auscultation of equal breath sounds
spontaneous breathing), the use of a CO2 detector
• Lack of gurgling auscultated over the epigas-
is the best technique. The detector can be electronic,
trium (referred breath sounds might be heard
as is common in the operating room, or colorimetric,
just below the diaphragm!).
which is more convenient for the resuscitation cart
• Inspection of equal thoracic expansion.
(Easy Cap™). The colorimetric detector is placed
• Visualization of condensation on the inside of
between the manual resuscitator and the patient’s
the tube
endotracheal tube. It is purple when there is no
• Seeing the tube pass between the vocal cords.
carbon dioxide and turns tan and then yellow with
• The use of an esophageal detector device
increasing concentrations of carbon dioxide
(EDD, described later in this chapter).
(Figure 31-6).
The respiratory therapist asks the nursing supervi- Normally in the body, carbon dioxide is present
sor to request a STAT portable chest X-ray. Although as a gas only in the lungs. But what if the person
a chest X-ray is the gold standard for ensuring the has eaten pretzels and drunk beer before being intu-
proper location of an endotracheal tube, a clinical bated in the esophagus? According to the manufac-
determination of proper position has to be done turer, if the endotracheal tube is accidentally placed
(continues)
(continued)
into the esophagus, four or five breaths will wash (Figure 31-7). If a bulb is used, the bulb is squeezed
out any such carbon dioxide. Then the Easy and then attached to the endotracheal tube.
Cap™ will read zero carbon dioxide (purple). The
• If the tube is in the trachea, the bulb rapidly
problem in this case is that 5 L or more of air has
reinflates as the trachea is held open by its
been insufflated into the stomach, and such air
cartilaginous rings.
is looking for a route out of the stomach, bringing
• If the tube is in the esophagus, the bulb
other gastric contents with it, a situation which
reinflates slowly if at all, because the
complicates airway management. At the very least,
esophagus collapses around the end of
that much distension of the stomach will impede
the tube.
subsequent efforts to ventilate the patient. So
the rescuer must ensure proper placement of the If the EDD has the syringe, the rescuer pulls
endotracheal tube at the outset. rapidly back on the syringe.
If the patient has no spontaneous circula- • If the tube is in the trachea, the syringe pulls
tion (full cardiopulmonary arrest), the excretion of back easily to full capacity.
carbon dioxide is determined more by the adequacy • If it is in the esophagus, the syringe stops
of compressions (and thus circulation) than by quickly—as little as 10 mL.
the adequacy of ventilations. In these situations,
the rescuer should use another device, called the If the tube is determined to be in the esophagus:
esophageal detector device (EDD). This consists of • Remove it immediately.
either a 60-mL syringe with a catheter tip (commonly • Reventilate the patient for 2 minutes.
referred to as a Toomey syringe) or a rubber bulb; • Reintubate.
either one has an endotracheal tube connector
FIGURE 31-6 The Easy Cap™ colorimetric CO2 detector is

purple at 0.5% CO2, tan from 0.5 to 2% CO2, and
yellow at 2% CO2.
Image used by permission from Nellcor Puritan Bennett LLC, Boulder,
Colorado, doing business as Covidien.
Drug Sequence for VF/Pulseless v-tach. Suppose,

in the preceding case, the monitor still shows VF after
5 cycles of 30 compressions and 2 ventilations. Here is
what might happen:
• John defibrillates at 200 joules; CPR is resumed
immediately after. FIGURE 31-7 Termed an Esophageal Detector Device (EDD),
• He asks the med nurse to administer 300 mg of a 60-mL syringe with a catheter tip or a rubber bulb can
amiodarone. (Refer to Table 31-2 for a synopsis be used to determine endotracheal tube placement.
of drugs used in adult resuscitation.) Courtesy of Ambu, Inc., Linthicum, Maryland
TABLE 31-2 Drugs most commonly used in adult resuscitation delivered by

either IV or IO route
Drug Classification Action Dosage
Epinephrine Sympathomimetic ␣, ␤1, ␤2 stimulator 1 mg q 3–5 minutes
Lidocaine Antiarrhythmic Decreases ventricular 1–1.5 mg/kg; max
irritability 3.0 mg/kg/24 hours
Amiodarone Antiarrhythmic Decreases ventricular 300 mg second dose
irritability of 150 mg
Magnesium Sulfate Antiarrhythmic for Decreases ventricular 1–2 g over 10 min
torsades de pointes irritability
Procainamide Antiarrhythmic Decreases ventricular 20–30 mg/min to a max
irritability (also used of 17 mg/kg
in supraventricular
dysrhythmias)
Atropine Parasympatholytic Parasympathetic blocker 1 mg/dose to max 3 mg
Bicarbonate Alkalinizing agent Buffers acids Calculated from base
excess and vascular
volume)—½ this dose is
given initially
Narcan Narcotic antagonist Blocks narcotic receptor 2 mg repeated as
(naloxone) sites necessary
Vasopressin Sympathomimetic ␣, ␤1, ␤2 stimulator 40 mg—may replace
first or second dose of
epinephrine
Note: Lidocaine may be used instead of amiodarone as an antiarrythmic. Initial dose of lidocaine is 1–1.5 mg/kg with subsequent doses of 0.5–0.75 mg/kg up
to a maximum of 3 mg/kg.
• After about another 2 minutes of CPR, seeing in 50 mL of normal saline—and only if the
that the rhythm is unchanged, John again rhythm is torsades de pointes or there is
defibrillates a 200 joules. measured or suspected hypomagnesemia.
• Another 1 mg of epinephrine is followed by one
more defibrillation after five cycles of CPR,
assuming the rhythm is unchanged.
Best Practice
• A dose of 150 mg of amiodarone is delivered,
followed by 5 cycles of CPR and then defibrilla- Scribe
tion if the rhythm is unchanged. The scribe is critical to have on the resuscita-
• Five cycles of CPR are delivered following tion team. The epinephrine is given every 3 to
another 1 mg dose of epinephrine; defibrillation 5 minutes throughout any cardiac arrest. In
is again performed at 200 joules if the rhythm this case, it is given between one of two anti-
remains unchanged. arrhythmic drugs. Without someone watching the
• The sequence continues with five cycles of CPR clock and logging each therapeutic intervention,
followed by a rhythm check and defibrillation if the resuscitation could get out of control. It is
warranted. (Note: The therapist has 23 seconds also very difficult, if not impossible, to accurately
to deliver 30 compressions and 10 seconds of reconstruct the chronology of events during a
off-the chest time to deliver two breaths. Thus, resuscitation after the fact. This post hoc re-
five cycles should take approximately 165 construction is, however, common in patients in
seconds or two minutes and 45 seconds. The cardiac arrest who have been resuscitated in the
American Heart Association persists in saying field and brought in by ambulance, since there is
“5 cycles or two minutes of CPR”.) not enough room in the back of an ambulance for
• Should the resuscitation reach this point, the the full resuscitation team.
next drug delivered is magnesium sulfate: 1–2 g
The reality is that things rarely reach this stage. The VF • It causes other adverse effects due to the extracel-
or pulseless v-tach usually resolves, either into some lular alkalosis that it causes.
sort of perfusing rhythm or into asystole, with no • It exacerbates central venous acidosis.
further cardiac response to the resuscitation efforts. • It may deactivate catecholamines (specifically
epinephrine), which are administered at the
• The magnesium sulfate is followed by five cycles same time.
of CPR and then defibrillation at 200 joules, if • Finally, bicarb produces carbon dioxide when it
indicated. buffers acids. This respiratory acidemia may
• Finally, procainamide may be given (the only result in a paradoxical tissue acidosis due to the
drug given as an infusion during complete reverse diffusion of carbon dioxide, especially in
cardiac arrest) at 20 mg/min up to 17mg/kg. For the cardiac and cerebral circulations. Therefore,
an 80 kg person, then, infusing this amount at adequate ventilation must be assured before
this rate would take over 45 minutes! (The bicarbonate administration.
procainamide may be infused at 50 mg/min,
which in this example would reduce the time
needed to 18 minutes.) Termination of Resuscitative Efforts. When should
resuscitation be stopped? Of course, if a valid DNR
Thirty-five years ago, sodium bicarbonate (bicarb) was appears, then resuscitation should be stopped
administered every 5 minutes, just like epinephrine. immediately.
However, bicarb has fallen out of favor for routine use Otherwise, the general answer is when there is no
in a full cardiopulmonary arrest. To understand its further response from the cardiovascular system. As
banishment, the RT needs to understand the rating long as the patient can be successfully defibrillated, the
system for drugs and treatments that the American resuscitation continues even though the patient
Heart Association has adopted. periodically reverts to VF. However, it is clearly medi-
• Class I is definitely helpful. cally futile to continue resuscitating the patient, and
• Class IIa is acceptable, probably helpful. the effort should be terminated if:
• Class IIb is acceptable, possibly helpful. • The patient has been in asystole with no
• Class III is not indicated, may be harmful. response to therapy for a period of time.
The American Heart Association also mentions drug • All potential causes have been ruled out (see the
overdoses, especially with tricyclic antidepressants as asystole algorithm).
additional appropriate times for bicarbonate adminis- • And the entire algorithm has been run.
tration; in a full arrest, this does not seem pertinent.
Within this system: ASYSTOLE
• For a hypoxic lactic acidosis, bicarb is considered Probably the next most common rhythm that rescu-
Class III. ers see is asystole. Of course, “asystole usually is a
• For a known preexisting bicarbonate sensitive confirmation of death rather than a rhythm to be
acidosis (such as someone in renal failure), it is treated” (American Heart Association ACLS Instruc-
Class IIa. tor’s manual). So respiratory therapists must be able
• If the patient is intubated and the resuscitation to recognize indications for ending the resuscitation.
has been proceeding for some time, or if the Asystole (known in lay terms as flatline) is easy to
patient has had ROSC after a prolonged interval, recognize (Figure 31-8). To be sure of the diagnosis
bicarb is deemed Class IIb. of asystole, it should be confirmed that all electrodes
are firmly attached to the patient. (People often
Bicarb can have seven adverse effects on the body,
inappropriately and imprecisely refer to them as
all of which should be given consideration when it is
leads, but a lead is the potential difference between
administered during a full arrest (American Heart
two electrodes.)
Association, 1992).
The lead most commonly monitored in
• Bicarbonate shifts the oxyhemoglobin dissocia- emergencies is lead II (the right arm and left leg).
tion curve to the left, inhibiting the release of This lead is popular because it is the limb lead
oxygen to the tissues. that provides the best P-waves. In fact, when most
• It has not been shown to enhance the ability to monitor/defibrillators are turned, on they are in lead
defibrillate or to improve survival rates in animal II, but the operator can switch to lead III (left arm
models. and left leg), lead I (left arm and right arm), or
• It can induce hyperosmolarity and hypernatremia. paddles.
FIGURE 31-8 EKG showing asystole.
Definitive Therapy. Once pulselessness has been breath sounds and chest rise? Obtaining an arterial
determined, it is time to begin compressions, intuba- blood gas is probably not a useful exercise during a full
tion, and obtaining an IV access. One mg of epineph- cardiac arrest for three reasons: (1) the time involved in
rine is given via IV/IO or 2 mg via the endotracheal obtaining the results, (2) the controversy over exactly
tube once access is available. what constitutes good arterial blood gas values in the
context of full cardiopulmonary arrest, and (3) because
Causes of Cardiac Arrest. The rescuer has to run down of the venous pulsations in the femoral vein secondary
the list of possible causes of cardiac arrest to determine to cardiac compressions, blood may be mistakenly
whether there is any immediately correctable one. This sampled from the vein instead of the artery. Besides,
list can be remembered as the 6 Hs and 5 Ts. hypoxia denotes insufficient oxygen delivery to the
tissues; arterial blood gas values give us only the ability
• Certainly hypoxia (1) can be immediately
to determine content and not the transport or delivery
addressed. Check the basics: Is the resuscitation bag
in the absence of a value for cardiac output (see Chap-
connected to an oxygen source? Is that source actually
ters 16 and 19). Some people, in fact, feel that venous
turned on? Is there adequate ventilation, as judged by
blood gases (not necessarily mixed venous from the
pulmonary artery) provide a better picture of the
metabolic conditions at the tissue and cellular level.
Best Practice
• Two other conditions—hypo- and hyperkalemia
Drug Administration (2)—would be known ahead of time by means of
routine lab tests:
What if IV is not an option? What if, for instance,
an elderly diabetic has no visible peripheral • If the patient is determined to be hyperkalemic,
veins? Intubating the trachea takes priority over the resuscitation effort could pretty much be
starting an IV if only one person has to do both. ended at that time. Lowering the serum potas-
The endotracheal tube provides both airway con- sium of someone in cardiac arrest is not really
trol and a means for administering some drugs. feasible.
Five liquid and one gaseous drug can be given • If the patient is hypokalemic, potassium could
by means of an endotracheal tube. The gaseous be administered to raise the serum level.
one is, of course, oxygen. The others go by the
If the patient has a preexisting acidosis (excess
acronym of LEAN-V (or LANE-V): lidocaine,
hydrogen ions) (3), buffering with bicarbonate is
epinephrine, atropine, narcan, and vasopressin.
indicated. To estimate the base deficit, use the follow-
The dose of any drug administered through the
ing formula:
endotracheal tube should be 2–2.5 times that
given intravenously. The one caveat is that a vol- total base deficit ⫽ 0.25 L/kg ⫻ base deficit
ume of no more than 10 mL should be instilled mEq/L (from an ABG) ⫻ body weight (kg)
down the endotracheal tube at one time. To
avoid having the drug expelled into your face, the The factor of 0.25 estimates the volume of extracellular
best plan is to give 5 mL, bag a few times, and fluid. Bicarbonate typically is in preloaded syringes
administer another 5 mL. Note that the optimal with about 45 mEq in 50 mL. Because this calculation
doses of these drugs given via the endotracheal is an approximation, administer one-half of the
tube have not been determined; IV/IO delivery calculated amount and reevaluate the patient's
is preferred because there is more reliable drug acid-base status.
delivery and pharmacologic effect. Hypothermia (4) is probably the one condition
whose presence would lead to the prolongation of the
resuscitation efforts. This becomes more common as • To determine of the presence of cardiac tampon-
outside temperatures fall. As the saying goes, “You are ade, (2) insert a needle into the pericardium and
not dead until you are warm and dead!” The patient’s aspirate. Of course, this procedure is the province of a
core temperature should be 30–32oC before it is physician. If cardiac tamponade is the cause, the
determined that the person is dead. In fact, at lower improvement in the patient’s condition should be
temperatures, surface (skin) electrodes may reveal no immediate.
electrical activity in the heart; needle electrodes may
• The respiratory therapist should be able to
be necessary to determine the cardiac rhythm. The
rapidly to assess the presence of a tension pneumothorax
rewarming process may take some time, as external
(3), but there would have to be some suspicion that
rewarming is inappropriate in any setting, whether
this is a problem. A typical patient at increased risk for
prehospital or in the hospital. Internal rewarming can
tension pneumothorax:
be accomplished by:
• Is postoperative lobectomy.
• Warm gastric, peritoneal, colonic, and bladder
• Has severe bullous disease.
lavage.
• Has been generating high peak pressures on
• The provision of humidified gas warmed above
mechanical ventilation.
body temperature for ventilation.
• Or has had a subclavian line recently inserted.
• The use of warmed IV fluids.
Cardiopulmonary bypass can also be used if the There is no time for an X-ray. Diagnosis and treatment
following conditions are all met: must be immediate or the patient will die. The signs of
a tension pneumothorax include:
• All else fails.
• There is optimism for the patient’s recovery if • Breath sounds are decreased or absent over the
rewarmed. affected side.
• And the procedure is available. • There is decreased movement of the affected
side.
In the case of hypothermia, the team should stop electri- • If the RT can judge the percussion note, there
cal therapy and hold any further drug therapy until the would be hyper-resonance over the affected side
body temperature is at least 30oC. as well.
• Hypovolemia (5) can be empirically determined • A late sign is tracheal displacement away from
by delivering a bolus of 250–500mL of normal saline the effected side due to movement of the entire
or lactated Ringers. Any response to this should cause mediastinum
the delivery of another fluid challenge bolus. The Treatment is simple and within the purview of the
bolus should be infused fairly rapidly. Remember respiratory therapist (assuming the RT has been
that IV pumps have a maximum infusion rate of credentialed by the hospital to perform the procedure):
999 mL/hour; the infusion of 500 mL would take needle decompression.
a half hour via a pump. It is faster, therefore,
simply to run the IV wide open and watch the • Find the second or third intercostal space in the
bag closely. midclavicular line (straight laterally from the
angle of Louis or sternal notch).
• Hypoglycemia (6) (serum glucose 70 mg/dL in • Insert a 14- or 16-gauge IV catheter over the
adults or 40 mg/dL in infants) is more a potential superior edge of the inferior rib (to avoid the
problem in infants and neonates. neurovascular bundle that runs in a groove
• If the patient had taken a drug overdose (toxins) (1), in the inferior edge of the superior rib)
such as tricyclic antidepressants, digoxin, ␤ blockers, or (Figure 31-9).
calcium channel blockers. Suspect a drug overdose in the • The clinician may hear a rush of air.
patient with a history of psychiatric problems who is • The needle is left in place as you have now
taking one of these drugs. There may be little to do in changed a tension pneumothorax into an open
these cases as removal of that drug from the blood would pneumothorax, not an ideal situation but a
be as difficult as treating hyperkalemia. There needs to be better one.
some circulation for the drug to be metabolized or This results in rapid improvement if tension pneumo-
excreted. There are a few types of drugs for which there thorax is the problem.
are direct antidotes, such as narcotics (naloxone/Narcan)
and benzodiazepenes (romazicon/Flumazenil). Cer- • Massive pulmonary embolism (thrombosis) (4)
tainly, if there is an antidote, it should be administered needs to be suspected by recent clinical history. The
at that time. common denominator in pulmonary embolism is
PULSELESS ELECTRICAL ACTIVITY

Pulseless electrical activity (PEA), which can be associ-
ated with a variety of rhythms, used to be called
electromechanical dissociation (EMD). However, a
1 variety of situations can produce electrical activity in
2 the absence of a pulse; hence the name change.
3 The key in treating PEA is to eliminate the poten-
4 tial causes in a methodical fashion. (See the list
following the section on asystole on p.866.)
BRADYCARDIAS
For an adult, the official definition of bradycardia is a
heart rate less than 60 beats per minute. However,
highly conditioned athletes may have a resting heart
rate in the forties; a person in congestive heart failure
may have a resting heart rate of 110 per minute just to
maintain minimal perfusion. The important determi-
nation is whether the patient has serious signs and
symptoms associated with this heart rate such as:
• Chest pain
• Shortness of breath
• Altered level of consciousness
• Low blood pressure
• Signs of shock
FIGURE 31-9 Proper location for needle decompression for • Pulmonary congestion (crackles auscultated in
tension pneumothorax at the second or third intercostal lung bases)
space, hugging the superior edge of the inferior rib. • Congestive heart failure
• Acute MI
If the bradycardia is symptomatic, regardless of the
inactivity. (Even otherwise healthy individuals have rate, then the therapist should intervene. The RT
developed pulmonary emboli after prolonged airplane should, of course, examine the electrocardiogram
trips without physical activity.) Added risk factors are (EKG) (see Chapter 19). If there is third-degree AV
smoking, recent surgery, phlebitis, the use of birth heart block, the patient needs a transcutaneous pacer as
control pills, cardiovascular disease, obesity, pregnancy, temporizing therapy on the floor. A physician can
trauma, and polycythemia (with smoking and birth insert a transvenous pacer to stabilize the heart rate
control pills being a particularly bad combination). If until the patient can be taken to the OR and a perma-
the embolism is so massive as to result in cardiac nent pacer installed. In the case of type II second-
arrest, it is likely fatal in that the only treatment is degree AV block (Mobitz II) with the absence of serious
surgical embolectomy. signs and symptoms, a pacer is still a good idea because
the condition may progress to third-degree AV heart
• Acute myocardial infarction (MI) (thrombosis) (5). block. Once the therapist has determined that interven-
This would be suspected from the patient’s medical tion is appropriate, the intervention should proceed
history, including: through the following sequence.
• A history of coronary artery disease (CAD).
• Previous MI. Definitive Treatment. Initially, atropine should be
• Family history of MI (especially at or before the administered. If the person had a heart transplant,
age of 55). atropine has no effect on the denervated heart. Atro-
• The reason for admission to hospital. pine should be administered in increments of 0.5 mg
• Previous coronary revascularization surgery or up to a maximum of 3 mg. It should be administered
percutaneous coronary intervention (PCI). as rapid IV push; slow administration or administra-
• Cardiac catheterization reports. tion of a bolus of less than 0.5 mg can cause a para-
• EKG changes. doxical decrease in heart rate. The limitation of
• Medications. administering medication as a bolus is that the effect
CASE STUDY 31-2

A 50-year-old woman is hospitalized on a medical- The resident asks the medication nurse to hang
surgical floor for chemotherapy for breast cancer 1 L of normal saline and run it wide open into the
following a course of radiation therapy. She has just 16-gauge port of the central line. The resident asks
had a triple lumen subclavian line placed for central for a 5-inch spinal needle to perform a pericardio-
venous access. Jan, the respiratory therapist, is called centesis. Jan auscultates and finds diminished
to her room because she has been found uncon- breath sounds on the side of the central line. Chest
scious, apneic, and pulseless. Jan quickly begins excursion also is diminished on that side. Above the
compressions after lowering the head of the bed and chaos that is typical in a resuscitation in a patient’s
placing the head of the bed under the patient for a room, the percussion note is difficult to appreciate.
firm surface. Once the code cart arrives with a Jan asks for a 14-gauge 2-inch IV catheter. She
monitor, a nurse places three electrodes (one under quickly preps the area of the third intercostal space
each clavicle at the midclavicular line and one at the with an alcohol prep pad and inserts the catheter
left costal margin at the midaxillary line) and turns on perpendicular to the chest, hugging the top of the
the monitor, displaying sinus rhythm. Jan requests an fourth rib. As she enters the plural space, she hears
8-mm endotracheal tube and the intubation equip- a hiss as air leaves the thorax. Jan informs the
ment. Jan also requests 1 mg of epinephrine to be resident, who pauses before attempting a pericar-
administered into the patient’s central line. diocentesis. Nearly 500 mL of normal saline have
Another therapist arrives and intubates the run in. The rhythm is unchanged, but Jan asks the
trachea. (Note: Given the new emphasis on deliver- therapist who is doing compressions to stop. She
ing excellent compressions without interruption, feels for a carotid pulse and finds a weak one. The
intubation is not a high priority if adequate ventila- resident requests another 500-mL fluid bolus and a
tion can be easily delivered via a face mask.) Once blood pressure. The initial pressure Jan obtains is
intubation is completed and the proper tube 90/40 mmHg.
placement is confirmed, the medical admitting
resident enters the room and confers with Jan. The
Questions
three possibilities are:
1. In someone with end-stage renal disease, what
• Iatrogenic tension pneumothorax (from inser- cause for cardiac arrest is uppermost in Jan’s
tion of the central subclavian line). mind?
• Pericardial tamponade from radiation therapy
2. In someone with no blood flow (except as
or metastases.
performed by external cardiac compression),
• Hypovolemia.
can drug overdose or hyperkalemia, as causes
In this setting, all three potential causes can be of cardiac arrest, realistically be treated such
addressed simultaneously. that the patient can recover? Why?
can be difficult to predict and cannot be modified once • Next, the current is decreased in 5-mA incre-
the drug is given. Additionally, if no further therapies ments until capture is just lost and then returned
are instituted, the heart rate will decrease in about 15 to the last level to minimize the current being
minutes to what it was initially. delivered. Remember that the patient may not be
After atropine, transcutaneous pacing is the entirely grateful; transcutaneous pacing is a
intervention of choice. Place the pacer pads in the same painful procedure. Analgesia and sedation may
location as for defibrillation. Note: Insure that the pads be appropriate. Confirmation of the presence of
are specified as able to be used for pacing. a pulse along with the electrical activity should
not be done at the carotid artery as the muscle
• Once the RT turns the pacer on and starts it, the
movement which accompanies transcutaneous
unit marks each QRS, usually with a bright dot
pacing can be misconstrued to be a pulse. Note:
or line on or above the QRS.
A patient who has undergone transcutaneous
• The rate should be set at 80/min.
pacing will be very sore the following day due to
• The current is increased in 10 mA increments
contraction of large numbers of skeletal muscles
until capture occurs (usually over 70-80 mA)—
because of the cutaneous delivery of current.
that is, each pacer spike is followed by a wide QRS.
Best Practice
Oxygen Therapy
For anyone who suffers the sudden onset of signs or quote one of the pioneers in oxygen therapy,
symptoms suggesting a cardiovascular problem, the John Haldane: “Hypoxia not only stops the
first interventions are O2-IV-monitor. In the emer- machine, it wrecks the machinery” (Hal-
gency situation, there is no such thing as too much dane, 1919). In other words, the worst thing
oxygen. Thus, a nonrebreather or a high-flow, high- that can happen to the patient is to become
concentration aerosol system should be applied to hypoxic. Respiratory therapists should do
the patient. For those concerned about potential their utmost to ensure that this does not
depression of the hypoxic stimulus to breathe in happen.
patients with chronic obstructive pulmonary disease
Intravenous access should be obtained while
(COPD), remember two important facts:
the patient is as stable as possible. Starting an IV
• Only a small minority of patients with COPD becomes very difficult if there is a decrease in blood
are actually carbon dioxide retainers whose flow to the extremities. An alternative is IO access.
breathing is stimulated due to lack of oxygen Finally, ACLS treatments are based on algorithms
(Scanlan, et al., 1999). determined by the cardiac rhythm. All three inter-
• If someone’s breathing is depressed, the RT ventions can be effected in just a few minutes and
can intubate and mechanically ventilate. To provide the basis for everything that follows.
If pacing does not have the desired effect, continue • Decreased level of consciousness.
the drug sequence. In order, the drugs and dosages are: • Low blood pressure.
• Indications of shock, pulmonary edema, or
• Dopamine in an infusion of 5–20 ␮g/kg/min
acute MI.
(a Class IIb intervention).
• Epinephrine in an infusion of 2–10 ␮g/min If the patient is unstable, then the therapist should
(a Class IIb intervention). prepare for immediate cardioversion. A heart rate of
150 implies instability; the therapist should proceed
directly to cardioversion.
TACHYCARDIAS
Probably the most complex of all the ACLS algorithms Cardioversion. Cardioversion is the synchronized
is for tachycardias. Although it is initially a fairly daunt- delivery of electrical energy to the heart to change a
ing piece, just take it step by step. rhythm. If the cardioversion is elective, then the patient
Under any circumstances, assess ABCs first, and could be premedicated with (usually) a benzodiaz-
deal with any defects found. As with any potential epine (such as midazolam or Versed) or a barbiturate
cardiac problem, the rescuer should: (such as methohexital or Brevital) plus a narcotic for
analgesia. However, if the patient is unstable, then this
• First apply O2-IV-monitor.
becomes an urgent procedure—taking the time to
• Then obtain vital signs (including what some are
administer drugs delays the application of the electrical
now calling the fifth vital sign: pulse oximetry).
therapy to restore effective circulation; in addition,
• Set up a 12-lead EKG.
most sedatives and analgesics have adverse effects on
• Perform a physical examination.
the cardiovascular system. At any rate, the therapist
• Obtain a chest radiograph.
should make provisions for securing the patient’s
• Review the patient’s history.
airway should this procedure become necessary. In
other words, a manual resuscitator with mask should
Stable or Unstable? The first determination is whether
be connected to oxygen and intubation supplies
the patient is stable or unstable. As soon as the thera-
should be at the bedside and checked beforehand.
pist finds indications of instability, the assessment
The patient is connected to the monitor/
should be interrupted to treat the problem. As with the
defibrillator with EKG electrodes in the standard
bradycardias, serious signs and symptoms are:
monitoring positions (just below each clavicle at the
• Chest pain. midclavicular line and at the left costal margin at the
• Shortness of breath. midaxillary line).
• The therapist turns on the defibrillator and confirms an R-wave and discharges. The delay
activates the synchronizer. The device begins to can be disconcerting if one is expecting an
indicate in some way that it is finding R-waves. immediate discharge as happens when
This can simply be a flashing light (as on defibrillating.
PhysioControl LifePack 5) or a bright dot on the • If the initial cardioversion is unsuccessful, the
R-wave and a flashing “SYNC” on the monitor therapist should increase the energy level (from
screen (as on PhysioControl LifePack 10). The 50 to 100 or from 100 to 200 joules) and attempt
rescuer should be aware of the function of his cardioversion again. Remember that the synchro-
hospital’s particular model because some nizer may need to be turned on again; otherwise
defibrillators disable the synchronizer after each you are delivering an unsynchronized shock
delivery of energy; others remain in the synchro- which may cause the rhythm to deteriorate
nized mode until it is turned off. into v-fib.
• The initial energy level should be selected: 50 to
200 joules (watt-seconds) depending upon the
Drug and Nondrug Treatments. If the patient is
presenting rhythm.
determined to be stable, the therapist can move a little
There are two techniques used to cardiovert. In the more slowly. With all the preliminary investigations
past, the therapist took paddles and applied them with completed, it is time to treat the rhythm.
about 25 pounds of pressure to the patient’s thorax • Patients in chronic atrial fibrillation should also
with gel pads or conductive gel (which looks like be anticoagulated because it has been found
toothpaste) just as for defibrillation. The safer and thus that they have more than five times greater risk
preferred method is the hands-off technique. of stroke than someone not in that rhythm
(Harvard Health Letter, 1998).
• For hands-off cardioversion, connect the elec-
• If the rhythm displays a wide QRS (0.12
trodes to the cable (if necessary—some come
seconds) and only if it is regular and monomor-
preconnected) before attaching the electrodes to
phic, then adenosine can be considered. If the
the patient because it is often difficult to connect
rhythm has a wide QRS but is not regular, the
the cable once the electrodes are on the patient’s
therapist should consider an antiarrythmic
skin.
infusion.
• Large electrodes are attached to the patient by
their adhesive border in one of two locations: Antiarrhythmic infusions for stable wide-QRS
either to the right of the sternum and at the apex tachycardia:
(as previously described for defibrillation) or at Procainamide infused at 20–50 mg/min until one
the front midsternum and back. The location is of four situations occurs: the arrhythmia is suppressed,
specified by the manufacturer and marked both hypotension occurs, the QRS width increases 50%,
on the outside of the foil packet containing the or the maximum dose of 17 mg/kg has been delivered.
electrodes and on the electrodes themselves. Amiodarone 150 mg delivered over 10 minutes;
(There are two alternative locations for the pads repeat as needed if VF or v-tach recurs; follow up with
underneath the scapula on either side.) an infusion of 1 mg/min for 6 hours.
• Once the patient is connected to the defibrillator Sotalol 1 to 1.5 mg/kg: Although package insert
and the initial energy level is selected, the recommends slow infusion, the literature supports
therapist charges the unit. infusion of the maximum dose over 5 minutes or less.
• Then the RT places the paddles on the patient (if If the QRS is narrow, vagal maneuvers lead the
using paddles) and chants: “I’m clear, you’re clear, therapeutic parade. The therapist can ask the patient to
we’re all clear. Shocking!” During this announce- bear down (Valsalva maneuver). An alternative is
ment, the operator is scanning the stretcher carotid sinus massage. The therapist should auscultate
for someone who is not paying attention. first before performing this maneuver because this is
The therapist has to be sure that he or she is also contraindicated in those with a bruit, which indicates
clear because the operator is the one most often the presence of partial obstruction due to peripheral
shocked during defibrillation or cardioversion. vascular disease. It is also best to do only one side at a
• The therapist holds down both buttons on the time because bilateral carotid sinus massage has been
paddles (it is somewhat awkward to do) or known to lead to cardiac arrest due to greatly increased
pushes the “discharge” button on the machine vagal tone.
itself if using hands off until the machine If the vagal maneuvers do not “break” the rhythm,
discharges (listen for the relay click inside). It the next rung on the therapeutic ladder is adenosine.
may take a second or so before the machine Each dose of adenosine is given by rapid IV push; the
first is 6 mg. The therapist should immediately flush it (formerly children’s) 81 mg non enteric-coated aspirin
with 20 mL of normal saline. The therapist should also may be life saving.
understand that the first rhythm after administration of
adenosine is asystole. The good news is that the Initial Assessment and Connection of Patient to
half-life of adenosine is only about 5 seconds, so it AED. Prior to attaching the AED, the rescuer needs to
goes away very quickly. A second dose at double the confirm that the victim is unresponsive, apneic, and
initial dose is given after 2–3 minutes if the initial one pulseless. The AED should not be attached to the
has no effect. victim who does not meet all three criteria.
• If the complex is still narrow and the patient • The rescuer should place the AED next to the left
remains stable, a beta blocker or calcium chan- side of the victim’s head.
nel blocker is the next drug of choice. • The pads should be connected to the cable (if
they are not already connected in the package).
All pathways ultimately lead to cardioversion if
Where the pads should be placed is indicated on
traveled all the way. Under these circumstances,
the outside of the package and on the pads
assuming the patient remains stable, premedicate the
themselves (just as pads used for transcutaneous
patient. A short-acting benzodiazepine such as Versed
pacing have their location noted). The pads are
(midazolam) is the drug of choice. It provides mild
placed in the same locations as for manual
sedation and is also an amnesiac; its short duration
allows the patient to recover more quickly.
ACUTE CORONARY SYNDROMES (ACS) Best Practice

The key to dealing with what are now grouped as acute
coronary syndromes is the urgency of treatment. For Decisions Involving
coronary reperfusion (percutaneous coronary interven-
tion or PCI) or thrombolytic therapy) to minimize the Resuscitative Care
size of the myocardial infarct, the patient has to have The bottom line is delivering the best patient
the intervention in less than 12 hours after the onset of care possible. Who actually delivers the care
symptoms. Since denial causes people to delay seeking or who determines the appropriate care to give
medical attention in the first place, they use up valu- is not important. If a therapist knows the right
able time. The emergency department must have a thing to do, then the therapist can help the
system already in place to deal with the patient who is patient achieve a better outcome (live rather than
complaining of chest pain. die). Never be hesitant to make suggestions or to
The key drugs used in treating acute coronary voice an opinion.
syndromes are: For example, the respiratory therapist arrives
at a code that has just been called. Moving to
• Oxygen.
the head of the bed to ventilate, he discovers
• Morphine.
that the floor nurses have already attached the
• Nitroglycerine.
patient to a monitor, which is showing v-tach.
• Aspirin.
The patient’s nurse confirms that the patient has
• Heparin.
no pulse. There is no coronary certified nurse on
• -blockers.
the scene yet; the hospital does not credential
• Thrombolytic agents.
respiratory therapists to perform defibrillation.
• Angiotensin-converting enzyme (ACE) inhibitors.
The medical resident has just walked into the
The mechanical intervention is percutaneous room. What is the appropriate treatment right
coronary intervention (PCI). The American Heart Asso- now? Of course, it is defibrillation. The therapist
ciation emphasizes the initial treatment by saying: quickly summarizes the situation to the resident
“MONA (morphine, oxygen, nitroglycerine, aspirin) (“We have an unresponsive, apneic, pulseless
greets all patients with chest pain” (ACLS Instructor’s woman in v-tach who needs to be defibrillated”)
Manual, 2010). The reader may wonder what role the and asks the nurses to find the gel pads for the
respiratory therapist might play in the emergency defibrillator. The therapist has expedited the
treatment of acute coronary syndromes. As in many delivery of the appropriate treatment to this
situations, and in the previous example, knowing what patient, possibly saving her life. If the therapist
to do may be as important as being able to do it. If the knew nothing about ACLS, he would have simply
person with the suspected ACS is a friend or relative, continued to ventilate or perform compressions.
having the person chew one adult (325 mg) or two
Spotlight Sequence of Operation.

On • The AED should now be turned on. (Some AEDs
automatically turn on when the cover is raised.)
Automatic External At this point, the victim needs to be completely
Defibrillation still; the AED cannot analyze the rhythm if the
An automatic external defibrillator (AED) is a patient is moving. (CPR must be stopped or, if
device that requires minimal training to operate. the patient is in the back of an ambulance, the
The operator does not have to know how to vehicle must be pulled off the road and
interpret an EKG (although some have EKG stopped.)
display screens). The device actually talks the • Depending on the model, the AED may auto-
operator through the proper sequence of actions matically go into analyze mode, or the rescuer
(Figure 31-10). may have to push the “Analyze” button.
• The AED responds to only one of two rhythms,
VF or v-tach, usually with a rate of 150. If
either of these rhythms are present, the AED
defibrillation, that is, to the right of the sternum usually makes a decision quickly. A long pause
and at the apex of the heart; they can also be after the AED begins analyzing the rhythm
placed anteriorly and posteriorly. usually indicates that the rhythm is not treatable
• A towel, a razor, a pair of gloves, and a pocket with defibrillation. If the AED decides it is a
mask should be included in the AED kit. The defibrillatable rhythm, it begins to charge. Once
towel is used to dry off the wet or diaphoretic charged, it indicates “Shock Advised—Push
victim; the razor is used to shave the chest if Button to Shock.” Some completely automatic
necessary. An alternative to shaving (assuming models analyze, charge, and defibrillate without
there is more than one set of electrodes) is to any action by the operator, but these are in the
place one set of electrodes firmly on the chest minority.
and then forcefully remove them, thus removing • Just as with a manual defibrillator, the operator
the hair. (Good skin contact is important to should chant “I’m clear! You’re clear! We’re all
avoid arcing and possible skin burns. Most clear! Shocking,” while scanning the victim to
people have seen a patient after a resuscitation ensure no one is in direct contact before defibril-
with paddle-shaped burns on the chest.) The lating. If the victim is on metal seats (such as at a
adhesive pads achieve energy delivery compa- stadium), the rest of the people in that row
rable to handheld paddles without the pressure should be asked to stand during defibrillation.
because these pads are flexible and the entire • Once the shock is delivered, the rescuers should
surface is sticky. The pads therefore can contact a immediately begin CPR for another 5 cycles. The
larger surface area than the metal paddles can. AED will time this and inform the rescuers when
2 minutes have elapsed.
• This sequence of CPR-rhythm evaluation-defi-
brillation continues as long as the victim
remains in v-tach or VF; a nondefibrillatable
rhythm may be NSR, v-tach with a slow rate,
asystole, or indeed any rhythm but VF or v-tach.
Return of spontaneous circulation (ROSC) is the
best indication to stop AED use. However, the
pads should remain in place as the therapist
continues to monitor the pulse in case defibrilla-
tion becomes necessary again.
American Heart Association AED Initiative. The

American Heart Association has a major initiative to

increase awareness and use of AEDs by people who are
not medically trained. The first-priority group consists
of people such as police officers, firefighters, personnel
in sports stadiums, and managers of large apartment
FIGURE 31-10 An automated external defibrillator (AED). buildings who are likely to come across job situations
in which there is need to defibrillate. Next in line are Attach the electrodes as was done in the scenario or use
people with relatives who have conditions that might the paddles for a so-called quick look. It is better to
result in the need for defibrillation. (Unfortunately, attach the standard monitoring electrodes first rather
the literature does not demonstrate increased survival than acquiring the EKG through the paddles for three
among those with home defibrillators.) Ultimately, the reasons.
AHA vision is that an AED will be located anywhere
there is a fire extinguisher or telephone. The reason is • First, it is easy to forget to switch from paddles
that the two most important determinants of survival back to lead II and think the patient is in
in adult cardiac arrest are time to CPR and time to asystole, thus not defibrillating the patient at the
defibrillation. The success rate for defibrillation is earliest possible time.
90% after 1 minute, but it falls to zero after about • Second, the electrodes are needed anyway, and
10 minutes. Thus, speed is of the essence in determin- attaching them takes only a few seconds.
ing the need for defibrillation and actually defibrillating. • Last, with the high epinephrine level in the
AEDs also clearly have a place in the hospital. One therapist’s blood due to the excitement of the
may question the wisdom of buying more defibrillators situation, some muscle tremor may result, which
when every crash cart has one and people are around mimics v-fib on the monitor.
who can use them. Think about the sequence of events If the therapist decides to use the paddles:
during a cardiac arrest in the hospital outside the
critical care units. A nurse who finds a patient in • The lead selector switch on the monitor/
cardiac arrest must alert someone to page a code. That defibrillator is set on “Paddles.”
person calls the code phone number, and the operator • The paddles are applied to the patient’s chest
then pages the code team. When their beepers sound, with good pressure over gel pads and the rhythm
the members of the code team (including the CCU or is analyzed. If it is VF or v-tach, defibrillation can
ICU nurse) must stop whatever they are doing and get be carried out immediately.
to the location of the arrest. Thus, several minutes have
elapsed before someone who is credentialed to operate Enhancing Conduction. To achieve good contact with
the manual defibrillator arrives, significantly lowering the patient’s chest and to avoid burns to the skin, the
the chances for a successful defibrillation. therapist should use something to enhance conduction
The timing is very different with an AED at the between the paddles and the skin. Probably the
nursing station and all nurses trained to use it (about messiest is electrode cream applied to the paddles. The
a 2-hour class for people with medical backgrounds). downside of using electrode cream is that the patient’s
Upon discovering a patient in full cardiac arrest, the chest is very slippery following application of the
nurse shouts for someone to bring the AED. After paddles, and performing compressions is difficult
delivering 5 cycles of 30 compressions and 2 breaths, unless the chest is wiped off, further delaying the
the nursing staff can deliver the first (and possibly resumption of compressions.
only) shock. With the cost of AEDs falling, it is only Next in terms of convenience is saline-soaked
a matter of time before they will appear at general 4 4s. Their advantages are:
nursing stations. Presently, many manual monitor/
defibrillators are able to function in AED mode. Thus, • They are not slippery.
there does not have to be a separate AED purchased. • They cling to the chest wall.
One place where AEDs have special significance is • The ingredients are readily available everywhere
aboard an airplane. If a passenger suffers a full cardiac in the hospital and are inexpensive.
arrest while on an airplane, landing is not even an They do tend to leak saline, however.
option as far as treatment goes. It could take as long as Last on the list of conduction enhancers are gel
a half hour under the best of circumstances before the pads. They are probably the most expensive conduction
plane arrives at the gate of an airport. More airlines are enhancement but the most convenient. They cling to
placing AEDs on their planes as time passes. (Qantas the thorax, are not slippery, and do not drip.
was the first; American, Hawaiian, and Air Zimbabwe,
among others, also have them.) Hands-Off Versus Paddles. The other decision in
defibrillation is whether to use hands-off versus using
paddles. Everyone is familiar with the paddles the
DEFIBRILLATION rescuer holds on the victim’s chest (with 25 pounds of
Defibrillation was briefly described in the scenario of pressure). The rescuer presses the buttons on the
the patient in persistent VF. The therapist can deter- paddles to discharge them for either cardioversion or
mine the patient’s initial rhythm in one of two ways: defibrillation. The major danger with this technique is
electric shock, and the operator is the one most likely • Pulse oximetry gives the therapist a pulse
to be shocked. There is special danger if the therapy is indication as well as oxygenation monitoring.
performed in a moving ambulance because the ambu- • Heart rate and blood pressure should be moni-
lance could lurch in an unpredictable way, throwing tored every 5 minutes.
the rescuer into contact with the metal stretcher frame. • Finally, at least one EKG lead should be dis-
To obviate some of the danger of using the paddles played, preferably lead II, which provides the
for electrical therapy, use the hands-off technique. For best P-waves (lead II is the difference between
this technique, the rescuer needs to connect the pads to the right arm and the left leg). An alternative
the monitor/defibrillator in the receptacle where the is V1, modified V1, or MCL1 (modified chest
paddles are connected. lead 1)—all different names for the same chest
or precordial lead. These chest leads use the V1
• The electrodes are placed on the patient’s thorax,
position as the positive electrode (located in the
either to the right of the sternum (about at the
fourth intercostal space just to the right of the
middle) and at the apex (in the midaxillary line
sternum) with one of the other electrodes as the
on the lower third of the thorax) or anterior and
negative. This chest lead similarly gives the best
posterior. The pads and the foil package in
P-waves as does lead II of the precordial leads.
which the pads come both have line drawings
• Monitoring level of consciousness or responsive-
showing the proper placement of the pads.
ness also enhances the clinical picture.
• Defibrillation or cardioversion is then accom-
plished by pressing the button on the monitor/ Of course, this whole scenario assumes that the
defibrillator at a safe distance from the patient. hospital permits the therapist to administer these kinds
The rescuer still chants “I’m clear! You’re clear! of drugs and intubate. Such authorization requires a
We’re all clear! Shocking!” and scans the patient number of factors. First is state licensure (everywhere
for anyone who is not paying attention. but Alaska) that allows the therapist to administer
these drugs under the respiratory therapy scope of
practice. Next is a medical director who is supportive
Conscious Sedation. As in the case of tachycardia,
of the enhanced responsibilities. Very importantly, the
some procedures (which include cardioversion and
department leader must embrace these activities. Then
transcutaneous pacing as well as bronchoscopy)
the staff have to be willing to learn new duties and
require conscious sedation. This involves administering
be eager to expand their responsibilities. Lastly, the
drugs to provide:
medical board must be forward thinking enough to
• Pain relief—generally narcotics such as entrust such advanced duties to respiratory therapists.
morphine sulfate or fentanyl.
• And sedation—generally benzodiazepines such
as Versed (midazolam) or Ativan (alprazolam) Pediatric Advanced Life Support
or as an alternative Diprivan (propofol) are used An important age-specific competency for respiratory
while maintaining the patient in an arousable therapists is pediatric advanced life support (PALS).
state. Benzodiazepines are also amnesiacs so the The basic concept of PALS is stated in the old saying
conscious patient will not remember the cardio- that “children are not just little adults.” For instance, a
version. fluid challenge for an adult is typically 250–500 mL,
which turns out to be about 3–6 mL/kg; that for a child
This state is specifically differentiated from general
is 20 mL/kg.
anesthesia, in which the patient is unconscious and
pain free. During the administration of conscious
sedation, the respiratory therapist must monitor the BROSELOW TAPE
patient; the key phrase is patient assessment. The person
One piece of essential equipment for use in pediatric
monitoring the patient should have no other responsi-
resuscitation is the Broselow tape. The therapist mea-
bilities, including delivering electrical therapy or
sures the supine victim from crown to heel with the
assisting during bronchoscopy. Especially during
tape. Based on where the victim’s height falls on the
electrical therapy, adverse changes in the patient’s
tape, the RT can read precalculated drug doses and the
cardiovascular system may occur, and the RT needs to
size of endotracheal tube and suction catheter. These
be prepared to intubate. The intubation equipment
values are calculated based on the 50th percentile for
should be readily at hand; no one should have to look
weight based on height in a population of 20,000
for it.
children. Use of this tape can bring order to the
• The most important functions to monitor are determination of drug dosages and tube sizes in
airway, breathing, and circulation (as always). pediatrics.
There is no good ALS without good BLS. So the • Capillary refill. This should be less than 2 seconds
first requirement of PALS, just as in ACLS, is that the in a warm environment and extremities should
participants can perform excellent BLS, especially be warm.
ventilation with bag and mask. Refer to the beginning • Urine output (if available). This should be
of this chapter with age-specific competencies for 1–2 mL/kg/hr.
specifics on child (age 1–8 years) and infant (age less • Blood pressure. Systolic should be age specific
than 1 year) BLS, including relief of foreign body within normal limits: 0–1 month, 60 mm Hg;
airway obstruction. 1 month–1 year, 70 mm Hg; 1–10 years, 90
(2 age in years).
• Level of consciousness (LOC). The LOC can
INITIAL PATIENT ASSESSMENT rapidly be determined by the AVPU scale
AND PREVENTION (Alert, responds to Voice, responds to Pain,
As in many situations, the prevention of respiratory or Unresponsive).
cardiac arrest is preferable to the need for resuscitation
This whole evaluation should take only a minute or so.
once the child has arrested. The basic preventive
Should the rapid assessment reveal problems,
measure is assessing the patient for the signs and
treatment needs to be quickly initiated.
symptoms of impending respiratory failure and
circulatory shock and initiating the appropriate • If the therapist determines that the child is in
treatments. The therapist should look at: possible respiratory failure, the child should be
allowed to assume a position of comfort with
• General appearance. Does the child appear
a caregiver. Repositioning minimizes oxygen
comfortable or ill, active or flaccid?
demand and helps in maintaining the airway.
• Respiratory rate. A rate over 60 is always abnor-
Oxygen should also be provided as tolerated,
mal; irregular respirations are also a poor sign.
monitored with pulse oximetry.
Tachypnea relative to the age group may be the
• If the therapist determines that respiratory failure
first sign of respiratory distress. A rate below
is probable, the child should be removed from the
10 in an ill or injured child is a poor prognostic
caregiver, the airway secured, and ventilation
sign.
assisted with 100% oxygen. In addition, cardiac
• Skin color and temperature. The skin should be
monitoring should be initiated and vascular
pink, warm, and dry. Pallor, mottling, or cyano-
access obtained.
sis (also of mucus membranes) or a fall in
• If the child is in shock, either compensated or
oxyhemoglobin saturation indicates inadequate
decompensated, the therapist should ensure an
oxygen delivery, blood flow, or both. Diaphore-
adequate airway, ventilate with 100% oxygen,
sis is indicative of sympathetic discharge in
obtain vascular access, and provide volume
cardiovascular emergencies.
expansion. Vasoactive drugs may be necessary.
• Evidence of increased respiratory effort. Nasal
flaring, grunting, use of accessory muscles,
tracheal tug, and intercostal and suprasternal
retractions all indicate increased respiratory FLUID THERAPY AND DRUGS
effort. Vascular access is necessary as part of most resuscita-
• Connection with environment. The child should tions for the delivery of fluids for volume resuscitation,
regard the speaker when addressed and, if old drugs or both. The routes for administering drugs can
enough, respond to questions. Infants may be be a central vein, peripheral vein, intraosseous, or
looking around and babbling and cooing. endotracheal. In a child younger than 6 years old, the
Unusual irritability or lethargy or the failure to therapist should not waste time establishing a periph-
respond to painful procedures are poor signs in eral vascular line if access is difficult. An intraosseous
the infant. line can be used for administration of anything deliver-
• Adequacy of tidal volume. Inspection and ausculta- able via intravenous line, including volume replace-
tion should reveal subjectively sufficient movement, because blood from the bone marrow of the
ment of the thorax with each breath. tibia passes into the central circulation via the popliteal
• Rate and quality of peripheral pulses. The rate for vein.
the awake infant or child should be age specific Fluids for resuscitation are normal saline or
within normal limits: up to 3 months, 85–205/ lactated Ringer’s solution. Unless hypoglycemia has
minute; 3 months to 2 years, 100–190/minute; been determined, solutions containing glucose are not
2–10 years, 60–140/minute. Pulses should be appropriate due to an association between hyperglyce-
readily palpable. mia and poor neurologic outcome. When vascular
access cannot be immediately obtained, drugs that can the infancy of critical care, practitioners thought that,
be delivered via the endotracheal tube indicated by the since the body worked to maintain pressure, so should
mnemonic LEAN (or LANE). they. However, when the body has already effected
Drugs other than epinephrine are given much less significant vasoconstriction, adding vasoconstrictors is
frequently during pediatric resuscitation. detrimental in two ways:
• Atropine is useful in symptomatic bradycardia. • Although arterial pressure may actually increase,
• Narcan (naloxone) is given for the infant with the net effect on the patient’s condition is
respiratory depression caused by narcotics. The negligible.
clinician should be aware that naloxone has a • The increase in systemic vascular resistance
shorter half-life than narcotics, so one may need (SVR) may actually decrease cardiac output
to repeat its administration. because an overloaded heart is unable to eject
• Sodium bicarbonate should be given only later blood against the increased afterload.
in the resuscitation, once adequate ventilation is
Thus, clinicians sometimes tread a fine line between
established with documented severe metabolic
maintaining sufficient pressure to perfuse the cerebral
acidosis, hyperkalemia, or tricyclic antidepres-
and coronary circulations adequately while maintain-
sant overdose. (Contrast this to the situation
ing flow to the remainder of the organs, which are
25 years ago when sodium bicarbonate was
sensitive to ischemia in varying degrees.
routinely given every 5 minutes during an arrest.)
In treating any type of shock, the first priority is to
• Calcium used to be administered after every
be sure that “the tank is filled”—that there is enough
other drug had been given during a resuscitation
fluid (blood) to circulate. This is especially true in
without effect. Now, calcium is given only for
septic shock, in which volume expansion is the first-
documented hypocalcemia, hypermagnesemia,
line therapy. In children and infants, the tank can be
hyperkalemia, or calcium channel blocker
relatively large. As noted, the fluid challenge for a child
overdose.
is 3–6 times that of an adult (on a weight basis, 20 mL/
kg as opposed to 3–6 mL/kg). Children who are very
Shock: A Flow Definition. Adequate perfusion to the hypovolemic or in severe septic shock may need more
body relies on three things: than 60 mL/kg. The clinician must be sure that suffi-
cient volume is on board (the patient is euvolemic).
• A pump that can supply adequate flow, because
At that point, the clinician may start thinking
cardiac output is never great enough to supply
about positive inotropes, of which three are commonly
everywhere simultaneously.
used. Once their use has been optimized, it is time for
• A vascular bed that is able to change size to
vasopressors as a last resort.
allocate blood flow.
Epinephrine may be the inotrope or vasopressor of
• Sufficient fluid (blood) to fill the system.
choice in several clinical circumstances. It is useful in
Every type of shock causes a problem with one (or symptomatic bradycardia, anaphylactic shock, hypo-
more) of these conditions. For example: tension, and cardiac arrest. Its use may be limited by
the development of tachycardia or tachydysrhythmias.
• Cardiogenic shock involves a malfunctioning
At doses less than 0.3 ␮g/min, it is primarily a positive
pump.
inotrope; at higher doses, the vasoconstrictor effect
• Septic shock results from the inability of the
predominates.
body to constrict the arterioles to allocate blood
Dobutamine is useful in the child in cardiogenic
flow.
shock with normal blood pressure. Its vasodilatory
• Hypovolemic shock results from insufficient
effects may cause a fall in blood pressure or failure to
blood volume to fill the vascular space due to
increase an already low pressure. Its dosage range is
excessive blood or fluid loss.
from 2–10 ␮g/kg/min. Dopamine at low doses (2 ␮g/
The human body has no flow sensors in the vascular kg/min) increases renal and splanchnic flow; at high
system; the sensors are baroreceptors or pressure doses ( 10 ␮g/kg/min), it is a vasoconstrictor. In the
sensors. The priority of the system is to maintain middle range (2–10 ␮g/kg/min) it adds positive
arterial pressure to perfuse the circulations that matter inotropy to the increased renal blood flow. Because it
the most: the brain and the heart. Because both organs causes the release of endogenous catecholamines, it
extract a large amount of oxygen from the blood may not work in the patient who is in chronic conges-
passing by, maintaining pressure is of paramount tive heart failure (CHF) or shock. The clinician would
importance in the continued performance of both see this if a dose of 20 ␮g/kg/min has no effect. In
organs. However, in shock, perfusion is inadequate. In this case, epinephrine is the better choice.
RESUSCITATING THE NEWBORN OUTSIDE TABLE 31-3 Risk factors indicating

THE DELIVERY ROOM potential need for neonatal resuscitation
Everything else being equal, it is best to resuscitate
newborns in the delivery suite, where all the equipment Antepartum Factors
and people with special skills in this area reside. How- Mother’s age > 35 years
ever, from time to time, a newborn needs to be resusci- Post-term gestation
tated in other venues. As an example, the pregnant
Maternal diabetes
mother in her third trimester who is in the intensive care
unit gives birth unexpectedly. The objectives for infant Multiple gestation
resuscitation, regardless of where it takes place, are to: Pregnancy-induced hypertension
• Eliminate preventable morbidity. Pre-eclampsia
• Restore effective ventilation, perfusion, and Size-dates discrepancy
oxygenation. Chronic hypertension
• Maintain body heat by reducing heat loss to the
Anemia or isoimmunization
environment (a major consideration in the
newborn). Previous fetal or neonatal death
Drug therapy such as:
Maintaining a neutral thermal environment is of
paramount importance in resuscitating the newborn Lithium carbonate
for two reasons: Magnesium
• Neonates are wet when born, and the wetness Adrenergic blocking drugs
enhances evaporative cooling. Bleeding in second or third trimester
• Neonates have a large surface area-to-volume Maternal infection
ratio, which enhances radiation cooling. Maternal substance abuse
If a radiant warmer is not available, the therapist can Hydramnios
use warmed towels, aluminum foil, or warmed IV bags Fetal malformation
(there is always a microwave around) wrapped in
towels. It should go without saying that all involved in a Oligohydramnios
neonatal resuscitation should observe standard precau- Diminished fetal activity
tions during the entire procedure. As in many situa- Premature rupture of membranes
tions, it pays to be prepared. Before it is needed, No prenatal care
equipment for neonatal resuscitation should be gath-
ered and conveniently organized. Part of preparation is Intrapartum Factors
anticipating the situations in which resuscitation might Emergency cesarean section
be expected. For a list of such situations, see Table 31-3. Nonreassuring fetal heart patterns
Breech or other abnormal presentation
Directed History. The respiratory therapist should
Use of general anesthesia
obtain a directed resuscitation-oriented history. Four
items may affect the initial resuscitation: Prolonged rupture of membranes (more than 24 hours
before delivery)
• Is the infant premature? Immature lungs increase
Narcotics administered to mother within 4 hours
the likelihood that resuscitation will be needed.
of delivery
• Are there multiple fetuses? These will require
multiple resuscitation teams. Precipitous labor
• Has the mother received narcotics in the last Meconium-stained amniotic fluid
4 hours? The administration of narcotics raises Prolonged labor (more than 24 hours)
the likelihood of respiratory depression in the
Prolapsed umbilical cord
newborn.
• Is the amniotic fluid meconium-stained? The Prolonged second stage of labor (more than 2 hours)
newborn will require rapid suctioning to remove Abruptio placenta
meconium from the airway. Placenta previa
Initial Interventions. An inverted pyramid, proceed-

ing from basic to advanced, illustrates the relative
frequency with which interventions are needed in rate of 120 per minute, with ventilations inter-
resuscitating neonates. spersed at a ratio of 3:1.
• Once the heart rate rises above 80 per minute,
• Starting at the top of the pyramid, every new-
compressions can be stopped.
born needs to be dried and warmed.
• Next, the infant should be positioned supine In contrast to adult resuscitation, neonatal resusci-
with the head in a neutral position. (Hyperex- tation depends mostly on adequate ventilation. The
tension of the neck can result in occlusion of the only drug routinely used is epinephrine. Epinephrine
airway.) This position can be achieved by placing can be given via the IV, endotracheal tube (ETT), or
a towel or blanket to elevate the torso 0.5 inch. intraosseous route (IO). (See Table 31-4 for doses of
• Finally, the therapist should stimulate the infant, these drugs.) Bicarbonate is used to adjust acid-base
beginning with gentle flicking of the soles or status once the infant has stabilized. Another “medica-
gently rubbing the back. In most cases, there tion” is volume expanders, either normal saline or
should be a vigorous response from the neonate blood.
(crying). Once the neonate has been stabilized, the therapist
• If the infant is breathing adequately but cya- continues to monitor the newborn’s condition. Four
notic, the respiratory therapist should administer problems, indicated by the mnemonic DOPE, can
blow-by oxygen. cause subsequent deterioration in the resuscitated
• If, on the other hand, the infant is not breathing infant:
adequately or at all, has a heart rate <100, or
• Displaced endotracheal tube (This is easy to do
remains cyanotic despite oxygen administration,
with such a short trachea; simply moving from
the therapist should immediately begin bag-
full flexion to full extension may displace the
mask ventilation. A rate of 40–60 per minute
tube.)
should be used, with assessment of efforts by the
• Obstructed endotracheal tube
adequacy of chest expansion, the presence of
• Pneumothorax (from overzealous ventilation)
good bilateral breath sounds, and improvement
• Equipment failure
in heart rate and color.
• If there is no improvement in the infant’s In addition, the therapist should be on the lookout for
condition after a brief trial, then it is time to gastric distension (almost guaranteed after positive
intubate. pressure ventilation with a mask) and inadequate
ventilatory support (it is easy to become complacent,
Next down the pyramid is chest compressions.
but vigilant monitoring must be continuous).
• Once adequate bag-mask ventilation is estab- This is now the time for a more complete evalua-
lished and done for about 30 seconds, the tion of the neonate.
therapist determines the need for circulatory
• A chest X-ray after the intubation
assistance. Frequently, the infant heart rate
• Routine lab studies, especially glucose
increases with good ventilation.
• Maintenance of the neutral thermal environment
• However, if the heart rate is less than 60 or is
• Determination and adjustment of acid-base
60–80 with no increase (see neonatal normals
status
for heart rate), then the respiratory therapist
begins compressions. The complete absence of a
pulse is not necessary. The neonatal heart is CARDIAC RHYTHM DISTURBANCES
relatively unable to increase its stroke volume; Rhythm changes are not the usual primary cause of
cardiac output is therefore very much dependent cardiac arrest in neonates. Most cardiac arrests are the
on rate. result of hypoxia, acidosis, or both, and they are
• The compressions should be performed with two secondary to ventilatory problems. The first decision is
thumbs with the hands encircling the chest at a whether the neonate is stable or unstable. A neonate is
TABLE 31-4 Drugs most commonly used in neonatal resuscitation

Drug Classification Action Dose
Epinephrine Sympathomimetic ␣ ␤1, ␤2 stimulator Initial dose: IV/IO: 0.01 mg/kg
ET: 0.1 mg/kg, Subsequent doses: IV/IO/ET: 0.1 mg/kg
Bicarbonate Alkalinizing agent Buffers acids 1–2 mEq/kg only for prolonged resuscitation
unstable if he or she has a rhythm either that may (Note: These two drugs should not routinely be
deteriorate to cause shock or that is actually causing administered together.)
shock (either compensated or decompensated) or • Should these treatments fail to convert the
circulatory arrest. To keep things simple, these unstable rhythm, synchronized cardioversion is the
rhythms fall into one of three categories: next step.
• Bradyarrhythmias if they are too slow For symptomatic bradycardia:
• Tachyarrhythmias if they are too fast
• Collapse rhythms if there is cardiac arrest • Epinephrine is the drug of first choice. The RT
(anything with no pulse) must remember to treat the patient, not the
monitor. The rate, whether fast or slow, is not as
Because cardiac output in neonates is very rate depen- important as its effect.
dent, the bradycardia simply does not provide a • The next drug for children is atropine. Atropine
sufficient number of stroke volumes per minute for must be pushed rapidly, or its administration
adequate cardiac output. The tachycardia interferes may result in a paradoxical slowing of heart rate.
with ventricular filling by shortening diastole too
much, resulting in a decreased stroke volume. (Refer to Table 31-4 for drug dosages.)
Treatment options for pediatric patients are relatively The group of collapse rhythms consists of
simple. asystole, VF, pulseless v-tach, and pulseless electrical
For the tachycardia with a narrow QRS: activity (PEA), formerly called electromechanical
Vagal maneuvers should initially be considered but dissociation).
should not delay other treatment. In the case of collapse rhythms, the priorities are:
• Adenosine is the drug of first choice at 0.1 mg/kg • Initiating chest compressions.
with the maximum dose of 6 mg. Adenosine • Securing the airway and insuring adequate
should be delivered by rapid push immediately ventilation.
followed by a rapid flush of 5–10 mL NS. A • Obtaining vascular access, either IV or IO.
second dose is given at 0.2 mg/kg, with the • Giving epinephrine every 3–5 minutes.
maximum dose 12 mg. Treatment for ventricular fibrillation is parallel to
• If there is a regular monomorphic wide-complex that for adults.
tachycardia (possibly ventricular tachycardia), the First, 5 cycles of 30 compressions to 2 ventilations
therapist should first administer adenosine at the for one rescuer or a ratio of 15:2 for two rescuers
doses given above for a narrow-complex tachycar-
dia. Should that fail, expert consultation is advised; • An initial shock, with 2 joules/kg, 4 joules/kg for
drugs potentially administered are either amioda- the second one, and subsequent shocks at 4
rone at a dose of 5 mg/kg over 20–60 minutes or joules/kg up to 10 joules/kg or adult dose. As
procainamide15 mg/kg over 30–60 minutes. with adults, each defibrillation is immediately
followed by 5 cycles of compressions and
ventilations.
Age-Specific Competency • Epinephrine, given to everyone in cardiac arrest,
at a dose of 0.01 mg/kg IV/IO or 0.1 mg/kg
down the endotracheal tube if there is no IV/IO
ECGs in Neonatal/Pediatric access.
Arrhythmias • If v-tach or v-fib persists, amiodarone is the
A tachyarrhythmia with a narrow complex is likely next drug, given as a bolus of 5 mg/kg; it may
to be either sinus tachycardia or supraventricular be repeated twice more if v-tach or VF persists.
tachycardia. Using the rate as an initial guide, the Lidocaine is an alternative antiarrhythmic
rate for a sinus tachycardia is likely to be less drug.
than 220 for an infant and 180 for a child. Also, • Defibrillate between each drug administration.
variability in R-R interval is more likely in sinus Be sure to perform 2 minutes of CPR after each
tachycardia, although at these high rates the defibrillation before assessing rhythm.
variability may be difficult to discern without the • If ventricular fibrillation or ventricular tachycar-
use of calipers. A wide complex tachycardia is dia recurs after resuscitation, a lidocaine drip
almost always ventricular in origin in children (as may be started. If a dose has not been given in
opposed to a supraventricular tachycardia with 15 minutes, the therapist should administer a
aberrant conduction in adults). loading dose of 1 mg/kg and then start a drip of
20–50 ␮g/kg/min.
For PEA, the treatment runs exactly parallel to that PEDIATRIC TRAUMA
for an adult. The therapist: “Injury is the leading cause of death and disability in
• Starts compressions, intubates the trachea, and children” (AHA PALS Instructor Manual, 2010). Having
secures vascular access. a system already in place for handling trauma cases
• Gives epinephrine every 3–5 minutes (although improves outcomes.
most clinicians lean toward 3-minute intervals). Boys are injured more often than girls. The average
• Investigates and treats possible causes. (See the pediatric trauma patient is 7 years old and weighs
list under asystole for adults.) about 50 pounds. Head injuries account for nearly 6
out of 10 cases, with injuries to extremities following at
CASE STUDY 31-3

A 2-year-old boy, weighing about 12 kg, has just • Order a chest X-ray.
been removed from a pond in front of his grandpar- • Monitor with pulse oximetry and vital signs.
ents' house after an unknown immersion time. He is • Because any ventilation using a mask or
unresponsive, apneic, and pulseless. An advanced mouth-to-mouth insufflates gas into the
life support ambulance is requested via the 911 stomach, place a nasogastric or orogastric
system. The grandfather initiates CPR in a some- tube to decompress the stomach and facili-
what clumsy fashion. A neighbor who is a nurse tate ventilation.
hears the grandmother's cries and responds, • Continue monitoring cardiac rhythm—an
beginning effective CPR. important part of this child’s care.
The ambulance arrives after 5 minutes and • Order an arterial blood gas to determine
applies monitor electrodes; the initial rhythm is acid-base status and adequacy of
asystole. One paramedic intubates the child with a ventilation.
4.5-mm endotracheal tube. The second searches • Place the child on mechanical ventilation,
for a vein and readily acquires intravenous access beginning with A/C (or whatever mode is
via an antecubital vein. They give an initial dose of most familiar) with 90% oxygen, a rate of 20,
epinephrine. Within a minute, there is an organized 4 cm H2O PEEP, and a tidal volume of
rhythm with narrow complexes accompanied by a 100 mL (8 mL/kg) and adjusted as appropriate.
faint pulse. The paramedics administer a saline • Determine whether they will need to sedate
bolus of 240 mL (20 mL/kg), which results in a this child to ventilate him appropriately.
stronger pulse. The rhythm is now clearly sinus • Send blood off for a complete blood count
tachycardia with a rate of 130. The child, unfortu- (CBC) and basic electrolyte panel (includ-
nately, responds only to painful stimuli presently. ing sodium, potassium, chloride, total CO2,
He is cut out of his wet clothes, dried, and wrapped BUN, creatinine, and, especially important in
in blankets. He is placed in a heated ambulance children, glucose).
and transported to the regional pediatric specialty
Because this child will likely require critical
hospital. He receives an additional 240 mL fluid
care for a period of time, additional vascular access
bolus in response to another dip in systolic blood
is appropriate via a large line, either peripheral or
pressure. By arrival at the hospital, he is beginning
central.
to take a few spontaneous breaths but still responds
only to painful stimuli.
The paramedics report to the hospital staff, Questions
who congratulate them on a successful textbook 1. What is the usual cause for cardiac arrest in
resuscitation. children? How does this differ from the cause in
Caregivers at the hospital should: adults?
• Start with ABCs, just as the paramedics did. 2. What effect does water immersion have on
• Confirm the proper tube position by clinical cri- outcome?
teria (breath sounds, bilateral chest expansion, 3. What additional considerations must be
good color, tube taped at the appropriate level). addressed for this victim of near drowning?
1 out of 4 (AHA PALS Instructor Manual, 2007). The the 70 mL/kg used for estimating circulating volume
two main reasons children die after traumatic events in an adult.
are airway compromise and unrecognized bleeding.
• Fluid boluses are given at 20 mL/kg of crystal-
Three injuries can affect priorities in resuscitating
loid, or roughly 25% of the circulating volume.
the injured child: potential cervical spine injuries,
• After reassessment, this may be done two more
hemorrhage, and chest trauma. Initially, a rapid survey
times.
of the ABCs should be done. D should be added for
• Plan on replacing lost blood with crystalloids at
disability (rapid neurologic evaluation, such as
a 3:1 ratio because only about one-third of
Glasgow Coma Scale), and E should be added for expo-
crystalloids remains in the vascular space.
sure (maintenance of body heat). A secondary survey
• After three 20-mL/kg boluses, if further fluid
covers head to toe once the therapist has dealt with the
resuscitation is necessary, consider packed red
things discovered in the primary survey that can rapidly
blood cells, initially 10 mL/kg and then 20 mL/kg
lead to death if not treated.
if further volume is needed. (Remember that
normal saline has very little oxygen-carrying
Neurologic Evaluation. The respiratory therapist
capacity compared to any fluid containing red
should be familiar two methods of neurological
blood cells.)
evaluation: the AVPU scale (discussed earlier in this
chapter) and the Glasgow Coma Scale. The Glasgow
Coma Scale (Figure 31-11) enables the therapist to
hone in more closely on the exact level of neuro-
Neonatal Resuscitation Program
logical function. The total possible score ranges The neonatal resuscitation program (NRP) is a joint
from 3, representing the unconscious unresponsive effort of the American Academy of Pediatrics and the
person to 15, which is normal. Some clinicians American Heart Association. The NRP textbook is
suggest that the totals for each section should be actually a self-learning text, with clear objectives at the
specified if the value is less than 15 to provide even beginning of each of the six lessons and quizzes as the
more detail. learner progresses through each chapter. Therapists
who feel they are conversant with the material covered
Fluid Resuscitation. The therapist should also be in any given chapter can simply proceed to the quizzes
familiar with fluid resuscitation for the child in for self-evaluation. However, the text clearly states that
hemorrhagic shock. The estimated circulating the successful completion of the course does not imply
volume for a child is 80 mL/kg, slightly more than that the therapist is competent in neonatal resuscita-
tion. Supervised clinical experience (a preceptorship) is
needed before actually taking sole responsibility for
any component of a neonatal resuscitation.
Eye Opening Spontaneous 4 PRIMARY VERSUS SECONDARY APNEA

To voice 3 Neonatal apnea is a primary cause for neonatal resusci-
To pain 2 tation. Two types of apnea are seen in newborns:
primary and secondary.
None 1
Verbal Oriented 5 • The infant in primary apnea may initiate adequate
Response spontaneous ventilation with just stimulation
Confused 4
and exposure to supplemental oxygen.
Inappropriate words 3 • The neonate in secondary apnea has already
Incomprehensible words 2 progressed through primary apnea and is
None 1 showing a fall in heart rate, blood pressure, and
oxygen saturation. Unless ventilation is
Motor Obeys commands 6
promptly initiated, the infant in secondary
Response Localizes pain 5 apnea will continue to rapidly spiral down to
Withdraws to pain 4 death.

Flexion to pain 3 There are two complications, however: First, the infant
Extension to pain 2 may progress through primary apnea in utero and be in
None 1 secondary apnea at birth. Second, clinically differenti-
ating between primary and secondary apnea can be
FIGURE 31-11 Glasgow Coma Scale. difficult. Therefore, the therapist should assume the
worst and immediately begin aggressive resuscitation As in any resuscitation, it pays to be prepared. The
measures. Should the infant respond and begin equipment and personnel must be in the delivery room
spontaneous ventilation, then efforts can be reduced. at every birth. Once the neonate is born and needs
resuscitation, it is too late to assemble the team and the
necessary equipment.
CHANGES IN LUNGS AND CIRCULATION The first step in preparation is anticipating the need
AT BIRTH for resuscitation. Many antepartum and intrapartum
Major physiologic and anatomic changes occur in the factors suggest that the about-to-be-born fetus will need
lungs and in the circulation at birth. In utero, the more than the normal care immediately after birth
primary gas exchange organ for the fetus is the pla- (refer again to Table 31-3). All the necessary equipment
centa. The lungs are filled with amniotic fluid and only must be present and operational in the delivery room,
about 10% of the total cardiac output goes to the lungs with one set of equipment for each neonate anticipated.
to provide for growth and metabolism (as contrasted Someone who is able to perform a complete resuscita-
with 100% after birth). At birth, two changes must tion must be present at every birth; that person must
occur within the first few breaths. have no other responsibilities and cannot therefore also
First, the fluid must be removed from the lungs care for the mother. As with equipment, there must be
and be replaced with air. There are three mechanisms at least one resuscitator for each expected birth. When
for removing the fluid. During the passage through ante- or intrapartum factors suggest the delivery of an
the birth canal, the thorax is squeezed, expelling some asphyxiated infant, at least one team of two persons
of the fluid out the airway. The infant who is born by should be present at the delivery for every infant
Cesarean section is therefore denied this mechanism expected: a deliverer and a resuscitator.
for fluid removal. The rest of the fluid is absorbed and Once the infant is born, the first important need is
carried away by both the pulmonary lymphatics and to prevent heat loss. Newborns, especially preterm
the pulmonary circulation, mechanisms two and infants, rapidly lose heat to their surroundings. One
three. reason is that they have relatively little subcutaneous
Second, there must be a significant increase in tissue and a thin epidermis. In addition, they have a
blood flow through the pulmonary blood vessels. high ratio of body surface area to mass ratio compared
This is accomplished by a significant decrease in the to adults. Finally, as previously mentioned, newborns
pulmonary vascular resistance (PVR). Again, three are wet when born, a condition that accelerates evapo-
factors reduce PVR. First, when the fluid is removed rative heat loss. The therapist should place the neonate
from the lungs, the external pressure on the pulmo- on a preheated radiant warmer and dry him or her with
nary blood vessels is reduced, allowing them to a warmed towel. This drying provides the added benefit
increase in size. Second, the inflation of the previously of gentle stimulation, which may begin or help con-
airless lungs straightens out the pulmonary blood tinue respirations.
vessels, decreasing their resistance. Finally, the intro- With the infant dry and under the warmer, posi-
duction of air into the lungs raises the alveolar PO2, tioning is the next important step for facilitating the
reversing the hypoxic vasoconstriction. To further maintenance of a patent airway and breathing. The
ensure two series circuits (the blood passes first proper position is on the back (supine) with the neck
through the pulmonary circulation, then the systemic slightly extended. In an adult, maximum hyperexten-
circulation in order), the bypass valves for the pulmo- sion of the neck is the position for establishing a patent
nary circulation, must close. The closure of the ductus airway. In the infant, however, hyperextension obstructs
arteriosus is facilitated by the release of bradykinin the airway because of its flexibility. The position of
from the lung with the first breath and also with the slight extension can be established by placing a small
increase in PaO2. The closure of the formen ovale, a roll under the shoulders to lift the neonate off the
one-way flap valve opening from right to left, occurs mattress about 0.75–1 inch. If there is a large volume
because left atrial pressure will now exceed right atrial of secretions, turn the infant’s head to the side.
pressure because of the increased blood return to the The next step depends on whether the amniotic
left atrium from the lungs. fluid is stained with meconium, especially with pieces
If any of these events does not occur in due course, of meconium, or if the amniotic fluid has the appear-
the infant is unable to transfer enough oxygen from the ance of pea soup. In either case, the deliverer should
atmosphere into the blood and becomes progressively intubate the infant to remove meconium from the
asphyxiated. This failure of change mechanisms lower airway. If the infant is active, suctioning of the
maintains the fetal circulatory pattern with its resultant mouth and nose is not recommended.
insufficient pulmonary circulation. Intervention must At this point, there is a major change from
be prompt if the infant is to survive. normal suctioning procedures. Suctioning is usually
about delivering too much oxygen because

Best Practice hypoxia is the worst thing that can happen to the
neonate. As the infant’s condition improves, the
Converting from Millimeters oxygen can be gradually withdrawn.
to French Should the drying and suctioning (if needed) not
A common problem is conversion from millime- provide sufficient tactile stimulation to initiate breath-
ters (the normal units for an endotracheal tube ing in the newborn, two other methods of stimulation
inner diameter) to French (the normal units for are recommended. The first is either slapping the sole
the outer diameter of suction catheters). The of the foot with one’s hand or flicking the heel with a
simple rule of thumb is to divide French by 3 finger. The second is rubbing the back. These tech-
to arrive at the actual diameter in millimeters. niques should be done only once or twice; if there is
Thus, our 5 French suction catheter is 5/3 or no response, the therapist should start ventilating.
about 1.67 millimeters in diameter. Continuing to provide tactile stimulation without any
response now simply wastes time and decreases the
likelihood of a successful resuscitation.
accomplished with a catheter passed through the

endotracheal tube. For endotracheal tubes less than VENTILATION
4 mm in diameter, the suction catheter should then be Ventilation of the neonate can be accomplished with
5 French (less than one-half the internal diameter of two different types of devices. One is an anesthesia bag,
the endotracheal tube). This is the smallest suction which requires gas flow to inflate it. The other is a
catheter made. self-inflating resuscitator.
Trying to suction meconium through a small
• The anesthesia bag should have an initial flow of
suction catheter is an exercise in futility. A special
5–8 Lpm of oxygen. A pressure manometer
adapter is placed on the endotracheal tube to connect
helps in judging lung compliance. Many anes-
it to the wall by suction once the infant’s trachea has
thesia bags have a pressure popoff that can be
been intubated. The therapist:
set to limit the pressure delivered to the infant’s
• Applies suction as the endotracheal tube is lungs. Of course, if compliance or resistance
withdrawn. changes, then the delivered tidal volume
• Repeats the process of intubating and suctioning changes too; the RT is delivering manual
until no more meconium is aspirated. pressure-cycled ventilation in this case. Thus, the
• Inserts the tube and uses a suction catheter to therapist must maintain a good airway by
remove any small amount of meconium keeping the neonate’s head tilted properly,
remaining. while monitoring ventilation of the infant by
chest expansion, color, and adequacy of breath
For most infants, suctioning is as far as the inter-
sounds.
ventions go. Nonetheless, the therapist should now
• The self-inflating resuscitator should have a
proceed with a rapid cardiopulmonary assessment of
reservoir to allow delivery of a concentration of
the infant. The scheme is simple.
oxygen as close to 100% as possible. The thera-
• If respirations are inadequate, then ventilation pist is delivering manual volume-cycled ventila-
with a manual resuscitator is indicated. tion in this case. Changes in compliance or
• If respirations appear to be adequate, then the resistance can be monitored by the pressure
therapist checks the heart rate. needed to deliver the tidal volume via the
• If the heart rate is less than 100, the RT begins attached manometer. The self-inflating resuscita-
ventilation; if it is greater than 100, the RT tor also has a popoff valve that is preset, usually
assesses color. to 40 cm H2O. The therapist needs to pay
• If the neonate is pink, no treatment is indicated. attention to this to ensure that the infant is
If the neonate has central cyanosis, then oxygen being ventilated, not the room. The reality is that
should be administered. It can be given with a it is difficult to hear the popoff amid the noise of
simple mask applied to the infant’s face or as the delivery suite. Consequently, the therapist
blow-by with green oxygen tubing held between has to keep careful watch on the pressure
the thumb and forefinger in a cupped hand. In manometer. If it is indicating the same pressure
either case, the flow should be at least 5 Lpm; for each time, part of the tidal volume is probably
this short time, the therapist should not worry being vented to the room.
For either ventilating device, the interface insufflated gas can impede ventilation of even the
between the device and the newborn is the mask. A normal neonate by:
proper size mask covers both the mouth and nose • Directly forcing the diaphragm up, decreasing
easily. The too-large mask interferes with the neo- lung compliance.
nate’s eyes; the too-small mask may not cover the face • Moving into the intestines, continuing to apply
properly and may even push down on the nose, pressure to the diaphragm.
partially occluding it. Both ventilating units should • Causing gastric contents to be forced into the
be checked for proper function before they are pharynx, from where they can be aspirated or
needed as follows: forced into the lungs.
• The self-inflating resuscitator should be squeezed Thus, any infant who is ventilated in this fashion
once and released, then checked for rapid should have an orogastric or nasogastric tube inserted.
reinflation. Then, the mask should be blocked
with the hand and the bag squeezed again to
check both the bag’s ability to deliver pressure CIRCULATION
and also the function of the popoff. Once the airway has been opened and ventilation has
• To check the anesthesia bag, turn the flowmeter been ensured, the therapist should, of course, evaluate
on to 5–8 L/min, occluding the mask with a circulation if this has not already been done. Whereas
hand and ensuring inflation of the bag. Then chest compressions should be performed on adults
squeeze the bag to check that the popoff is set to only in the absence of a pulse, chest compressions
somewhere between 30 and 40 cm H2O. should be performed on infants if their heart rate drops
below 80 per minute (or is 60–80 per minute and not
Ventilation can now begin. Once the quick check of increasing). (Again, infants depend on heart rate to
the ventilation device is performed, ventilate the infant maintain adequate cardiac output.)
for 15–30 seconds at a rate of 40–60 per minute, Chest compressions on neonates are preferentially
watching for the rise and fall of the chest. After this performed by encircling the thorax with both hands with
initial period, evaluate the infant’s heart rate. the thumbs on the sternum. Pressure should be delivered
• If it is greater than 100 and the infant has to the sternum, not to the ribs. As with any performance
spontaneous respirations, stop ventilation. of CPR, the person doing compressions should count out
• If the heart rate is between 60 and 100 and loud to allow the one doing ventilation to easily coordi-
increasing, continue ventilation. nate the ventilation with the compressions.
• If the heart rate is 60–100 and not increasing,
evaluate what is being done. INTUBATION
Is the chest rising and are breath sounds The next major step in neonatal resuscitation is intuba-
good? tion of the trachea. For the neonate, there are five
Is the resuscitation device used actually indications for endotracheal intubation:
attached to a flowmeter delivering oxygen?
(Always check the simple things!) • Ineffective bag-and-mask ventilation
• If using an anesthesia bag connected to a • The need for prolonged positive pressure
blender, is the blender set at 100%? ventilation
• If the heart rate is less than 80, the therapist • A known or suspected diaphragmatic hernia
should begin chest compressions. • The need for suctioning of a meconium-stained
• If the heart rate is less than 60, the therapist neonate
should evaluate the preceding items in addition • Infants weighing less than 1000 g at birth (due
to immediately beginning chest compressions. to the very high likelihood they will require
(Remember that the infant’s cardiac output is positive pressure ventilation)
very rate dependent.) Prior to intubating, estimate the size tube needed by
Most of the time, initial ventilation can be effected referring to the chart in Table 31-5. If the therapist opts
with bag and mask. However, if the neonate has a to use a stylette, a practice that is strongly recommended,
known or suspected congenital diaphragmatic hernia it should be secured in the tube so that it does not
(CDH), the better plan is to intubate the trachea. The project beyond the tip and cannot advance any farther
reason is that bag-and-mask ventilation invariably during insertion. A straight laryngoscope blade (Miller)
results in some amount of insufflation of air into the is preferred for infants and children for two reasons:
stomach. If any part of the GI tract is in the thorax, • The epiglottis in an infant and child is longer
this air further compromises ventilation. In fact, the and floppier than that of the adult. Thus, the use
TABLE 31-5 Endotracheal tube sizes for neonates

Tube ID (mm) Weight (g) Gestational Age (weeks) Insertion Depth from Upper Lip (cm)
2.5 1000 28 6.5–7
3.0 1000–2000 28–34 7–8
3.5 2000–3000 34–38 8–9
3.5–4.0 3000 38 9
of the curved (Macintosh) blade may not allow that it obstructs the view of the larynx and
the therapist to visualize the larynx adequately. then the therapist cannot see whether the tube
• Lifting in the vallecula (as is done with the passes through the vocal cords.
curved blade) can move the larynx anteriorly out • If the larynx cannot be visualized adequately with
of view of the operator. just the blade, the therapist may apply gentle
pressure (or ask the assistant to apply pressure) to
The operator should check the laryngoscope to be
the larynx to move it posteriorly into view.
sure that the light is bright and that the bulb is screwed
• The tube should be inserted until the cord
in tightly. The therapist should also be sure to have
marker (the black band near the bottom of the
working suction available because it is too late if the RT
tube) passes through the vocal cords. That the
discovers it is needed. Finally, a manual resuscitator,
position is appropriate can be determined by
attached to a running source of oxygen, should be
adding 6 to the infant’s weight in kilograms
quickly checked as previously described.
and confirming that the tube marker at the
During the intubation procedure, the therapist may
upper lip corresponds to that number (see
find it useful to enlist the aid of an assistant, who might
Table 31-5).
have many duties before, during, and after intubation:
• Once the tube has been placed, the therapist
• Preparation and checking of the equipment used should immediately confirm proper position by:
in intubation Auscultating over the apices for equal, bilateral
• Stabilizing the infant’s head breath sounds.
• Handing equipment and suction to the operator Visualizing adequate chest excursion.
• Providing pressure over the larynx Visualizing lack of stomach distension.
• Monitoring the infant and notifying the operator Hearing no air entry into the stomach.
of deterioration in the infant’s condition • Once proper position has been confirmed, the
• Timing the intubation attempt and notifying the therapist notes the depth of the tube at the upper
operator if it exceeds 20 seconds lip and tube diameter, then secures the tube to
• Assisting with bagging between intubation the infant.
attempts • Finally, the therapist should chart the intubation
• Checking for proper tube placement procedure.
• Securing the tube
Here is the procedure:
DRUG AND VOLUME THERAPY DURING
• The proper position for intubating an infant, in RESUSCITATION
contrast to that for an adult, is exactly the same Medications can be administered via four different
as that for ventilating with a mask: slight exten- routes: umbilical vein (preferred), peripheral vein,
sion of the neck. intraosseous, or endotracheal tube instillation. Endo-
• The therapist inserts the blade to the base of the tracheal administration of medications has not been
tongue and then lifts along the long axis of the fully studied in infants, and intravenous administration
handle. Prying not only does not provide proper is the preferred route. There are two general indications
visualization of the larynx but also may harm for medication administration in infants:
tooth formation.
• When introducing the tube, the operator inserts • The heart rate remains less than 80 despite
it in the right side of the infant’s mouth. The adequate ventilation and 30 seconds of chest
tendency is to follow the straight blade down to compressions.
the larynx. The problem with this technique is • The heart rate is 0.
A limited number of medications is useful in dextrose (D10) can be administered for a blood
neonatal resuscitation: epinephrine, sodium bicarbon- glucose 40 mg/dL. The bolus is followed by an
ate, 10% dextrose (D10), and volume expanders. infusion of 5 mL/kg/hr either IV or IO.
• The normal dose of epinephrine, if administered (Refer to Table 31-5 for other dosages for these drugs.)
endotracheally, should be increased to 0.05– Two possible volume expanders can be used in
0.1 mg/kg in 0.1–1.2 mL total volume. Although neonates: whole blood or normal saline. Either of these
some infants may respond to intravenous doses is given when there is an indication of hypovolemia, as
as high as 0.2 mg/kg, the use of this high a dose evidenced by:
of epinephrine is not recommended.
• Pallor that persists after oxygenation.
• If the resuscitation is prolonged once vital signs
• Low blood pressure (if it is available).
are restored, sodium bicarbonate may be tried. The
• Weak pulse with an adequate heart rate.
bicarbonate should be administered over 1–2
• Poor response to resuscitative efforts.
minutes in a concentration of 0.5 mEq/mL
(one-half normal strength) to minimize the The dose is 10 mL/kg IV/IO given over 5–10
chance of intraventricular hemorrhage. minutes. After giving the volume expander, the thera-
• Additionally, when vital sign are restored pist should see the pallor improve, the pulse strength
following a prolonged resuscitation, 10% increase, and some response to the resuscitative efforts.
CASE STUDY 31-4

Mrs. L., who is pregnant with a fetus of 30 weeks intubates. Jim confirms equal bilateral breath sounds
gestational age, has had problems with gradually with no sound over the epigastrium and adequate
increasing blood pressure and proteinuria. At her bilateral chest movement. One of the nurses bags
latest prenatal visit, due to her increasing peripheral while he tapes the tube. Dr. Carson is now cannulat-
edema, 4 proteinuria, and a blood pressure of ing the umbilical vein. Jim continues ventilation at a
160/110 torr (all signs of severe pre-eclampsia), her rate of 60 per minute. The infant’s pulse is 60 and
obstetrician decided to perform an urgent Cesarean weak; the EKG monitor shows sinus bradycardia. The
section. Mrs. L. is at risk for delivering an asphyxi- nurse begins chest compressions on Baby L., who
ated infant because of her pregnancy-induced hyper- weighs about 1500 g.
tension and the somewhat emergent nature of her After 1 minute, the neonatologist asks the nurse
Cesarean section. Of course, there is also concern to stop compressions to assess the progress of the
about the maturity of the infant’s lungs. resuscitation. Because the heart rate is still 60, a
Because of the possible problems, Jim, a nurse administers 0.015 mg of epinephrine. After
neonatal specialist from respiratory care and Dr. another minute of chest compressions, Baby L.’s heart
Carson, a neonatologist, are present at the delivery. rate is now 100, but her pulse is still very hard to
Mrs. L. is brought to the delivery suite where an palpate. Dr. Carson draws up 15 mL of normal saline
anesthesiologist establishes epidural anesthesia (10 mL/kg fluid challenge) and infuses it slowly into
along with oxygen by cannula and continuous pulse the umbilical vein line. Her color begins to improve,
oximetry monitoring. The obstetrician delivers a and her pulse becomes stronger. A pulse oximeter
somewhat limp, pale female in about 10 minutes shows Baby L.’s saturation to be 90% during ventila-
and hands her to the neonatologist. Dr. Carson tion with 100% oxygen. Jim suggests a chest X-ray to
places her in a prewarmed radiant warmer, dries her assess the infant prior to moving her to the neonatal
off, and positions her on her back with slight intensive care unit. Once the chest film has been
extension of her head. Because she still shows little taken, the team moves Baby L. to the neonatal ICU.
movement, Jim begins bagging her with a Mapleson
(flow-inflating) bag and 100% oxygen. Questions
The neonatologist announces the 1 minute Apgar 1. How could the maturity of the infant’s lungs be
score as 4 and prepares the intubation equipment. predicted prior to delivery?
Jim asks one of the nurses to set the suction regula- 2. How does the necessity of drug administra-
tor to 60 mm Hg. As Dr. Carson is intubating, he tion during an infant resuscitation affect the
asks Jim for some laryngeal pressure and then easily possible outcome?
If the infant does not improve following a couple available who can intubate the trachea. Nor it is it
of fluid challenges, it is time to consider dopamine intended for use for people who:
starting at 5 ␮g/kg/min and titrating to effect up to a
• Are shorter than 5 feet tall.
maximum of 20 ␮g/kg/min.
• Are breathing spontaneously.
• Are not completely unconscious (as it would
Emergency Airway Adjuncts stimulate vomiting).
• Have esophageal disease or have swallowed
In the emergency situation, the airway of choice is the
caustic materials.
oral endotracheal tube. It is readily inserted by properly
• Require resuscitation for prolonged periods of
trained medical professionals and provides an open
time.
airway, airway protection (although it is not a guaran-
tee against aspiration), a route for secretion removal, Before the EOA is removed, the trachea must be
and a connection for positive pressure ventilation. If intubated. The removal of the EOA is frequently
the endotracheal tube is not needed for one of these accompanied by gastric contents, which can then be
reasons during a resuscitation and ventilation is easily aspirated or forced into the lungs by positive pressure
performed using a bag and mask, endotracheal intuba- breathing.
tion is not a priority and can be delayed to the The EGTA has a gastric tube lumen in the middle
postresuscitation time. However, in some circum- to permit decompression of the stomach after bag-and-
stances it is either not practical or possible to insert an mask ventilation by means of the insertion of a gastric
oral endotracheal tube. In these cases, other devices can tube (Figure 31-13). Its use is otherwise similar to that
provide some of the functions of the endotracheal of an EOA. The level of ventilation and oxygenation
tube: esophageal obturator airway (EOA)/esophageal provided by either an EOA or EGTA is generally less
gastric tube airway (EGTA), esophageal-tracheal than that provided when the patient’s trachea is
combitube (ETC), and the laryngeal mask airway intubated.
(LMA).
ESOPHAGEAL TRACHEAL COMBITUBE

ESOPHAGEAL OBTURATOR AIRWAY/ESOPHAGEAL The esophageal tracheal combitube (ETC) is a
GASTRIC TUBE AIRWAY double-lumen tube that is blindly inserted into the
The esophageal obturator airway (EOA) and esoph- pharynx. One lumen is like an endotracheal tube
ageal gastric tube airway (EGTA) were designed (open to the end), and the other lumen ends blindly
about 30 years ago for when there was no one skilled with holes that wind up in the vicinity of the opening
in endotracheal intubation. The EOA, a tube about for the larynx if the tube is placed in the esophagus
25 cm long and 1 cm in diameter, is inserted blindly (like an EOA). Once the tube is inserted, the operator
into the esophagus; it comes in only one size for adults inflates the small balloon on the end of the tube with
(Figure 31-12). Once it is in place, a large cuff is 15 mL of air and the large 100-mL balloon that
inflated, which occludes (obturates) the esophagus. occludes the pharynx. Then the operator determines
Proper placement is verified by auscultation of breath whether the tube is in the trachea. If it is, ventilation
sounds and auscultating over the epigastrium. can be accomplished just as with an endotracheal
A major disadvantage of the EOA is that the rescuer tube.
still must maintain a seal of the mask on the victim’s If the tube is in the esophagus, ventilation can be
face. It is not intended for use when someone is accomplished through the other opening. The esophagus
FIGURE 31-12 Esophageal obturator airway. FIGURE 31-13 Esophageal gastric tube airway.
CUFF APERTURE VALVE The sequence depends on available resources. If

BAR INFLATION
INDICATOR BALLOON
someone is unconscious and unresponsive and the
therapist is alone with an AED at hand, he should call
911, perform 5 cycles of 30 compressions and 2
breaths, then attach the AED and evaluate the rhythm
INFLATION LINE
and shock as appropriate. If there are two rescuers, one
AIRWAY calls 911 and retrieves the AED on the way back from
CONNECTOR calling 911; the other initiates CPR with compressions.
If there are three rescuers, one calls 911, one obtains
and applies the AED, and the third begins CPR—and
MASK so on.
AIRWAY TUBE
FIGURE 31-14 Laryngeal mask airway. REVIEW QUESTIONS

1. What is the order of the first three priorities in
managing an unconscious person?
is sealed by the smaller balloon, and gastric contents 2. Other than endotracheal intubation, what meth-
can be evacuated through that lumen. The ETC pro- ods can the respiratory therapist use to open and
vides ventilation similar to that provided by an endo- maintain someone’s airway?
tracheal tube while preventing the aspiration of gastric 3. What equipment is needed for endotracheal
contents. intubation? How is intubation done?
The two major limitations of the ETC are that it
4. What is the proper sequence for managing a VF/
comes in only one size (making it not suitable for pedi-
pulseless v-tach cardiac arrest?
atric use) and that the trachea cannot be suctioned if
the tube is in the esophagus. 5. What are the priorities in managing cardiac arrest
in a child?
6. How do infant and adult resuscitations differ in
LARYNGEAL MASK AIRWAY terms of their priorities?
The laryngeal mask airway (LMA) is a device that 7. When would you use a laryngeal mask airway or
consists of a small mask with an inflatable rim on the laryngeal-tracheal combitube instead of an endo-
end of a tube (Figure 31-14). It comes in several sizes. tracheal tube?
It is inserted blindly with the mask facing the tongue
until resistance is felt; then the inflatable rim is
inflated. If the LMA is in the proper position, the tube
will rise about 1 cm as the rim is inflated. The mask MULTIPLE-CHOICE QUESTIONS
covers the opening of the trachea and allows ventila- 1. Equipment and personnel for neonatal resuscita-
tion; however, the therapist must remember that the tion should be available:
LMA does not prevent against aspiration. It works well a. immediately in the delivery room.
in about 90% of cases including pediatrics. b. somewhere in the hospital on page.
Several limitations of the LMA need to be kept in c. only if the team anticipates needing them.
mind: d. to be called in if needed.
• Ventilation may not be adequate because the cuff 2. If an infant does not breathe after birth, bag-and-
fails to seal the larynx; either the tongue has mask ventilation should be instituted immediately
been pushed over the larynx, or the epiglottis has because:
been flipped over the larynx. I. the infant may be in secondary apnea.
• If there is inadequate anesthesia when the mask II. the longer the delay, the less likely a
is inserted or removed, laryngospasm may occur. favorable outcome when resuscitation
• It cannot protect well against aspiration. is needed.
III. the infant may have already gone through
primary apnea.
Summary a. I only
In dealing with a patient emergency, the critical b. II only
priorities are circulation, airway, and breathing. The c. I and II
new priority in the pulseless patient is compressions. d. I, II, and III
3. In which of the following situations would imme- 8. When performing a pediatric resuscitation, what
diate cardioversion not be indicated? device can provide the therapist with drug dosages,
a. atrial fibrillation, rate 180, BP 80/40, 3 second ETT size, and suction catheter size?
capillary refill a. PALS pocket handbook
b. supraventricular tachycardia, rate 150, BP b. American Heart Association pocket cards
125/75, alert, warm skin c. Broselow tape
c. atrial flutter, rate 160, BP 90/60, complaint of d. PDR
shortness of breath 9. When an infant is newly delivered, what are the
d. ventricular tachycardia, rate 170, unresponsive, very first priorities?
BP 70/40 a. stimulation, bag-and-mask ventilation,
4. What are the guidelines for giving drugs via compressions
endotracheal tube? b. intubating, cannulating the umbilical vein,
I. The dose should be 2–2.5 times that of the determining cardiac rhythm
IV dose. c. weighing, confirming name, footprinting
II. The drug should be flushed in with 20 mL of d. drying, warming, and positioning
saline. 10. What advantage does the esophageal-tracheal
III. Only narcan, atropine, epinephrine, vasopres- combitube have over the endotracheal tube?
sin (in adults), and lidocaine should be a. It requires no other equipment to insert.
given. b. It provides better ventilation.
a. I only c. It has fewer hazards.
b. III only d. It is cheaper.
c. I and III
d. I, II, and III
5. Why would AEDs be useful in a hospital?
a. They would reduce the amount of training CRITICAL-THINKING QUESTIONS
needed.
b. They would allow patients on floors to be 1. An RT is the first person on the scene with an
defibrillated faster. unconscious, unresponsive person in a shopping
c. They would decrease costs for monitor- mall. Many willing but untrained people are
defibrillators. available to help. What duties should the
d. They would decrease maintenance required for RT assign bystanders? What if someone
defibrillators. knows CPR?
6. If using a manual defibrillator, what precautions 2. An RT is the team leader for the anticipated
should the RT take? resuscitation of an infant about to be born. How
I. Remove any transdermal medication patches. many people should be on the team and what
II. Be sure no one (including the RT) is touching would be their functions? What should be checked
the bed. in preparation for the delivery?
III. Be sure to utilize some sort of conduction 3. A respiratory therapist is employed in a hospital
enhancer. that does not yet allow RTs with an ACLS course
a. I only completion card to fully participate in resuscita-
b. II only tion. Arriving at a code on a medical-surgical floor,
c. I and II the RT finds a woman already attached to a
d. I, II, and III monitor-defibrillator in pulseless v-tach. Someone
7. When giving a fluid bolus of saline or Ringer’s is doing compressions; a nurse hands over the bag
lactate, it is necessary to deliver three times the and mask as the RT goes to the head of the bed.
estimated fluid deficit. Why? What needs to be done next? Whom can the RT get
a. Only about one-third of crystalloids actually to do it?
remains in the vascular space. 4. A therapist is at the local athletic club playing
b. The crystalloids are diluted when they mix with tennis, and he has an AED in the car, having just
the blood. taught a CPR course. Someone comes running over
c. Crystalloids have one-third the effectiveness of to say that a person has a problem on the track. If
colloids. this person is pulseless, should the RT use the AED?
d. The crystalloids are being excreted at a rapid What are the pros and cons of using it in this
rate. situation?
Suggested Readings Cummins RO, Graves JR. (1996) ACLS Scenarios: Core
Concepts for Case-Based Learning. New York, NY:
American Association for Respiratory Care. Clinical Mosby Lifeline.
practice guideline: resuscitation in acute care Division of Injury Control, Center for Environmental
hospitals. Respir Care. 1993;38,12:1179–1188. Health and Injury Control, Centers for Disease
American Association for Respiratory Care. Clinical Control and Prevention. Childhood injuries
practice guideline: defibrillation during resuscita- in the United States. Am J Dis Child. 1990;144:
tion. Respir Care. 1995;40,7:744–748. 627–646.
American Association for Respiratory Care. Clinical Dubin, D. (2000) Rapid Interpretation of EKG’s. Sixth
practice guideline: management of airway emergen- edition. Tampa, FL: Cover Publishing.
cies. Respir Care. 1995;40,7:749–760. Gant NF, Gilstrap LC. Hypertension in pregnancy.
American Heart Association. Advanced Cardiac Life ACOG Tech Bull. 1996;219.
Support. Dallas, TX: American Heart Association; Grauer K, Cavallaro D. (2000) Volume I-ACLS
2010. Certification Preparation. 3rd edition. St. Louis,
American Heart Association. BLS for Healthcare Provid- MO: Mosby-Lifeline.
ers. Dallas, TX: American Heart Association; 2010. Grauer K, Cavallaro D. (2000) Volume II-ACLS A
American Heart Association. Guidelines for Cardiopulmo- Comprehensive Review. 3rd edition. St. Louis, MO:
nary Resuscitation. Dallas, TX: American Heart Mosby-Lifeline.
Association; 2010. Haldane, JS. Symptoms, causes, and prevention of
American Heart Association. Instructor’s Manual— anoxemia. Br Med J. 1919;2:65.
Advanced Cardiac Life Support. Dallas, TX: American Health Consequences of Smoking, The. Cardiovascular
Heart Association; 2010. Disease. A Report of the Surgeon General, publica-
American Heart Association. Instructor’s Manual—Basic tion DHHS (PHS) 84-50204. U.S. Department of
Life Support. Dallas, TX: American Heart Association; Health and Human Services, Public Health Service,
2010. 1983, ppiv, 127–129.
American Heart Association. Instructor’s Manual— Huff, J. (2005). ECG Workout- Exercises in Arrhythmia
Pediatric Advanced Life Support. Dallas, TX: American Interpretation. 5th edition. Philadelphia, PA:
Heart Association; 2010. Lippincott.
American Heart Association, American Academy of Insurance Institute for Highway Safety. Child Restraint
Pediatrics. Textbook of Neonatal Resuscitation. Dallas, Laws. 2010.
TX: American Heart Association; 2010. NIH Consensus Conference. Physical activity
American Heart Association. Textbook of Pediatric and cardiovascular health. JAMA, 1996;276,3:
Advanced Life Support. Dallas, TX: American Heart 738–743.
Association; 2010. Scanlan CJ, Wilkins RL, Stoller JK, eds. Egan’s Funda-
American Red Cross. Blood Facts and Statistics. Washing- mentals of Respiratory Care. St. Louis, MO: Mosby;
ton, DC: American Red Cross; 2010. 1999.
Centers for Disease Control and Prevention. Uninten- United States Department of Health and Human
tional Drowning Fact Sheet, Washington, DC: Services. Physical Activity Guidelines for Americans.
Centers for Disease Control and Prevention. Dallas, TX: American Heart Association; 2008.
CHAPTER 32
Managing Disasters: Respiratory Care

in Mass Critical Care
Thomas J. Johnson
OBJECTIVES
• Define the levels or tiers of disasters and disaster management.
• Describe the Incident Command System and the National Incident Management System (NIMS).
• Describe the injuries associated with natural disasters.
• Describe the medical management of blast and crush injuries.
• List the differences between a natural biological outbreak and a bioterrorist attack.
• Describe the medical responses to a pandemic influenza or other emerging disease.
• Describe the medical countermeasures to chemical agents.
CHAPTER OUTLINE
National Incident Management System Floods
Incident Command System Fire
Hospital Disaster Preparation Man-Made Disasters
The Respiratory Therapist in Response to Explosions
Multiple Casualty Incidents Bioterrorism
Natural Disasters Chemical Weaponry
Earthquakes Disease
Tornadoes Influenza
Hurricanes
891
KEY TERMS
acute respiratory distress high-order explosion (HE) pirfenidone
syndrome (ARDS) hospital emergency incident primary blast injury
anthrax command system (HEICS) Push Packs
blast lung injury (BLI) incident command system (ICS) quaternary blast injury
blast overpressure injuries interferon racemic epinephrine
bronchopleural fistula interleukin-6, 7, 8 ribavirin
cidofovir lewisite secondary blast injury
coccidioidomycosis live attenuated vaccine (LAV) self-contained breathing
cytokine storm low-order explosion (LE) apparatus (SCBA)
diplopia mass casualty incident (MCI) self-evacuation
disseminated intravascular MetHb spalling
coagulopathy (DIC) multidrug-resistant tuberculosis staphylococcal enterotoxin B
dumbels (MDRTB) (SEB)
dysarthria multiple organ system failure systemic inflammatory response
dysphagia (MOSF) syndrome (SIRS)
dysphonia N-acetyl-l-cystine (NAC) tertiary blast injury
emergency mass critical National Incident Management trivalent inactivated vaccine
care (EMCC) System (NIMS) (TIV)
epidemic neuraminidase tumor necrosis factor-alpha
hemagglutinin nitrogen mustard zoonotic
high efficiency particulate off-gassing
air (HEPA) pandemic
D
isasters are medical emergencies for which gency that, due to its complexity, scope, or duration,
respiratory therapists (RTs) must be threatens the organization’s capabilities and requires
prepared. For the American College of outside assistance to sustain [patient] care, safety or
Emergency Physicians (ACEP), the defini- security functions.” Yet if one considered the potential
tion of a disaster is “when the destructive effects of for loss of hospital infrastructure and hospital services
natural or man-made forces overwhelm the ability from a community for an extended period of time, as in
of a given area or community to meet the demand post-Katrina New Orleans, then disaster planning is in
for healthcare.”1 The impact of a disaster, or mass the best interest of the facility and the community it
casualty incident (MCI), affects communities in a serves.7 Loss of electrical, heating-ventilation-air
disparate way through differences in social economic conditioning (HVAC), and water, as occurred in New
status, in cultural norms, and in community York City’s power blackouts, can affect hospitals in a
infrastructure. Events such as the impact of hurricane large and complex region.
Katrina,2 the anthrax bioterror events,3 World Trade Disasters occur in different sizes and in different
Center attacks (February 1993 and September 2001), degrees of severity. Most disasters do not overwhelm
Oklahoma City bombing,4 SARS,5 and pandemic the hospital’s ability to cope. Multivehicle accidents,
influenza6 have galvanized the health care community aircraft accidents, and train wrecks can trigger the
and respiratory care professionals to prepare for hospital disaster plan or emergency operation plan
disasters whether man-made or natural. (EOP), but these can be managed by the staff and
To some, disaster preparedness is getting ready for supplies on hand at the time. Mass casualty incidents
something that has a low-probability of occurrence. The may require the redeployment of staff and resources to
time and dollars spent on training, drills, and equip- emergency departments (EDs) for variable amounts of
ment are often limited to that mandated by the Joint time. An example of this is the MCI response of Rhode
Commission, whose accreditation for hospitals includes Island Hospital to a nightclub fire that generated 215
the requirement of a disaster plan. In its prepublication victims. The rapid, effective response of Rhode Island
version of its chapter on emergency management, the Hospital was the result of disaster drills directed by a
Joint Commission states: “A disaster is a type of emer- surgeon. Of the 64 patients admitted to Rhode Island
CHAPTER 32 ■ Managing Disasters: Respiratory Care in Mass Critical Care 893
Hospital, 28 (60%) were intubated for inhalation Incident Command System

injuries. A step-down unit and a medical-surgical unit
were converted to a 21-bed burn ICU.8 Internally hospitals can and should have a hospital
Respiratory therapists, regardless of where they are emergency incident command system (HEICS) or
employed, must have a working knowledge of disaster incident command system (ICS) to activate and
management. The hospital, long-term acute care coordinate the hospital’s response to an incident. The
(LTAC), home care, and skilled nursing facilities all ICS must have as a first step an emergency operations plan
have different needs and priorities. By preparing for (EOP) and an alert and notification communication
disaster, respiratory care professionals mitigate the system. This plan must consider staff health and safety
impact and develop mechanisms for recovery and the as well as legal and ethical issues. The ICS is a com-
resumption of normal operations. Facilities and mand, communication, safety, and operational system
departments should develop communication and plans that should tie into the NIMS seamlessly. Of course, the
with police, fire/rescue, first responders, as well as ultimate goal of the ICS is the safe, efficient, and
federal, state, and local/tribal agencies. These plans effective management of the disaster. Hospitals can
should incorporate cultural, religious, ethical, and legal expect a total first wave of victims to exceed twice the
considerations. number admitted during the first hour of the MCI.9
Once the incident has been managed, then demobiliza-
tion, recovery, and response evaluation (lessons
National Incident Management learned) should occur. For more information, the
System reader is directed to the Emergency Management
Institute’s Web site (http://training.fema.gov).
In February 2003, President George W. Bush promul- In a 2008 supplement,10 the journal Chest pub-
gated the Homeland Security Presidential Directive 5, lished the findings of the Task Force for Mass Critical
which created the National Incident Management Care Summit Meeting (January 26–27, 2007 in
System (NIMS) with a goal of having a standard Chicago, Illinois). This multidisciplinary group of
incident response for all government levels and 37 experts in the fields of bioethics, critical care
response agencies. NIMS is intended to be a flexible medicine, disaster preparedness and response reported
operational system that facilitates governmental and their recommendations for emergency mass critical
nongovernmental agencies working together at all care (EMCC). Critical care units can expect both a
levels during all phases of an incident, regardless of its surge in patients and an acuity level that will be a
size, complexity, or location. challenge to meet.
Spotlight
On
The Logistics Service Branch of the ICS
• Communication Unit. Prepares and implements incident. The unit orders, receives, stores,
the Incident Communication Plan (ICS-205), and distributes supplies, and services
distributes and maintains communications nonexpendable equipment. All resource
equipment, supervises the Incident orders are placed through the Supply Unit.
Communications Center, and establishes The unit maintains inventory and
adequate communications over the incident. accountability of supplies and equipment.
• Medical Unit. Develops the Medical Plan • Facilities Unit. Sets up and maintains
(ICS-206), provides first aid and light required facilities to support the incident.
medical treatment for personnel assigned Provides managers for the incident base and
to the incident, and prepares procedures for camps. Also responsible for facility security
a major medical emergency. and facility maintenance services: sanitation,
• Food Unit. Supplies the food and potable lighting, cleanup.
water for all incident facilities and personnel, • Ground Support Unit. Prepares the Trans-
and obtains the necessary equipment and portation Plan. Arranges for, activates, and
supplies to operate food service facilities at documents the fueling, maintenance, and
bases and camps. repair of ground resources. Arranges for the
• Supply Unit. Determines the type and transportation of personnel, supplies, food,
amount of supplies needed to support the and equipment.
• Medical air supply.

Spotlight • Vacuum supply.
On • Water supply.
• Food supply.
Task Force for Mass Critical Care • Pharmacologic or other consumable supplies or
In the twentieth century, rarely have mass the ability to be resupplied.
causality events yielded hundreds or thousands of Hospitals and departments should develop and
critically ill patients requiring definitive critical promulgate their EOPs that include preparedness,
care. However, future catastrophic natural mitigation, response, and recovery. That plan must
disasters, epidemics or pandemics, nuclear device include preparations for damage/contamination to all
detonations, or large chemical exposures may or part of the facility and evacuation of all patients,
change usual disaster epidemiology and require a visitors, and personnel. Staff support includes personal
large critical care response. The Task Force on protection and vaccination (even for spouses/partners/
Mass Casualty Critical Care reviews the existing children), family and pet care, communications, as well
state of emergency preparedness for mass critical as the essential food, water, and personal hygiene. One
illness and presents an analysis of limitations, must expect both active and passive resistance to
which are presented in subsequent articles. disaster planning.
Baseline shortages of specialized resources such
as critical care staff, medical supplies, and
treatment spaces are likely to limit the number of
critically ill victims who can receive life-sustaining
The Respiratory Therapist
interventions. The deficiency in critical care surge in Response to Multiple
capacity is exacerbated by lack of a sufficient
framework to integrate critical care within the
Casualty Incidents
overall institutional response and coordination of For the respiratory therapist in an MCI, the major
critical care across local institutions and broader concerns are oxygen and mechanical ventilation
geographic areas.11 resources. The increase in oxygen consumption may be
as much as 200–300% for the duration of an MCI.
Cylinder gas is limited by both storage and by the
number of regulators for the cylinders. Large H and K
cylinders can be used as a manifold for backfeeding a
Spotlight zone of gas outlets.13
On Mechanical ventilation is the hallmark life
support of critical care. So, in emergency mass critical
Emergency Mass Critical Care care, RTs can expect a surge in invasive mechanical
Task Force suggestions: EMCC should include ventilation with very few, if any reserve ventilators in
the following: (1) mechanical ventilation, (2) IV the hospital fleet. Rental supplies availability may
fluid resuscitation, (3) vasopressor administra- exceed EMCC needs; federal, state, and city stockpiles
tion, (4) medication administration for specific of ventilators may be delayed or insufficient due to
disease states (e.g., antimicrobials and anti- the numbers of casualties. Stockpiled ventilators
dotes), (5) sedation and analgesia, and (6) select (Impact Eagle, LP-10, iVent, LTV-1000, LTV 1200, and
practices to reduce adverse consequences of others) may require training time that is not feasible
critical illness and critical care delivery. Also, all in the postevent period. Therefore, preparedness
hospitals with ICUs should prepare to deliver training is essential.
EMCC for a daily critical care census at three
times their usual ICU capacity for up to 10 days.12
Natural Disasters
A natural disaster takes a normal, benign environ-
ment and weaponizes it. When nature unleashes its
Hospital Disaster Preparation unpredictable, uncontrolled, unpreventable phenom-
ena with ferociousness, humans are among its
In preparing for a disaster, the worst-case scenarios
victims. Earthquakes, tornadoes, hurricanes, floods,
must be evaluated, such as the loss of:
and major fires have a regional effect to a degree
• Structural integrity of the facility. depending on their intensity, duration, and size.
• Personnel. Population density, community infrastructure, and
• Main oxygen supply. social economics all play a role in the ability to
32+
24-32
16-24
%g
8-16
4-8
2-4
0-2
Lowest hazard
FIGURE 32-1 Seismic map of the United States—‘% g’ is percentage of seismic field activity.
effectively respond to these incidents. The casualties TABLE 32-1 Earthquake Richter scale
that result develop in waves:
Richter
• The first are the self-evacuation victims. Magnitude Description
• These are followed by the seriously injured 2 Felt by few people; detected by instruments
brought in by first responders and by injured
first responders. 3 Felt by people indoors with dishes and
• Finally, the secondary infections and disease doors distressed
exacerbations follow the primary incident. 4 People asleep awakened, walls cracked,
and trees damaged
5 People flee buildings; damage to some
EARTHQUAKES buildings
With an increasing population living and working in 6 Moderate to major damage with wall and
seismically active regions, the effect of an earthquake of chimney collapse
7 or more on the Richter scale will be devastating
7 All buildings damaged, piping broken,
(Figure 32-1 and Table 32-1). Although earthquakes do
landslides possible
not have a season, they are nonrandom events. Plate
tectonics and seismic activity have and will occur in 8 All structures fall, including bridges, wide
one region more than another. The epicenter is the ground cracks
location of the greatest shaking and earth movement, ⬎8 Ground surface waves actually seen;
but the seismic energy is felt a significant distance from destruction of all constructed objects
the epicenter. The destruction of infrastructure and
building collapse result in high mortality. In the North
Ridge California earthquake in 1994, 15% of the fatal serious ECG changes such as tall, tented T-waves,
injuries occurred due to collapsing freeways (Figure 32-2). prolonged QT intervals, or fatal cardiac dysrhythmias.
The most vulnerable of the population affected Crush injuries can lead to kidney failure and require
by earthquakes are the young (⬍5 years old), old dialysis. All victims of crush injuries with dark, red, or
(⬎65 years old), and those with chronic mental or so-called cola urine should have urine analysis for CPK
physical diseases.14 (CK-3) and urine myoglobin and potassium. Severe
The injury patterns range from minor lacerations crush chest injuries and high Injury Severity Scores15
and injuries to severely traumatic brain injuries and (ISS ⬎25) are reported to have a mortality rate of
crush injuries. As the name implies, crush injuries occur 16%.16 Reported17 percentages of injuries typically seen
when a body or body part is subject to a high degree of after an earthquake include traumatic head injuries
pressure after being squeezed between two or more (22%), lower extremity injuries (19%), crush syndrome
objects. Crush injuries from entrapment under debris (11%), and upper extremity trauma (10%). Hypothermia,
cause ischemia to tissues, resulting in rhabdomyolysis secondary wound infections, gangrene requiring
and then in the release of myoglobin, potassium, and amputation, sepsis, acute respiratory distress
phosphate into the circulation. Hyperkalemia results in syndrome (ARDS), and multiple organ system failure
FIGURE 32-2 The collapse of a freeway following an earthquake in California.

Courtesy of Federal Emergency Management Agency
(MOSF) have increased the complexity of care for An earthquake may be further complicated by
earthquake victims. landslides, tsunamis, breaching of dams, levies, and
The airborne debris thrown into the atmosphere by water main breaks resulting from the damage of the
earthquakes is of special concern for the respiratory quake. Gas and electrical supply may be interrupted,
therapist. Dust and contaminants from collapsing and fires can break out.
structures exacerbate chronic lung disease. Even In the postearthquake period, RTs can expect an
otherwise healthy search and rescue people may be increase in respiratory cases from the inhalation of
exposed to asbestos and other native contaminants. dust, mold spores, asbestos, etc. The stress of an
The North Ridge earthquake in January 1994 resulted earthquake can be anticipated to cause an upsurge in
in over 200 cases and 3 fatalities associated with fatal and nonfatal heart attacks. A significant number
coccidioidomycosis infections from the aerosoliza- of people will self-treat or be treated by neighbors or
tion of soil in the earthquake region.18 volunteers who may arrive for care.
Spotlight
On Spotlight
On
Injury Severity Score
The Injury Severity Score (ISS) is an anatomical
Coccidioidomycosis
scoring system (head, face, chest, abdomen, and Coccidioidmycosis is caused by Coccidioides
extremities including pelvis) that provides an immitis, a soil fungus endemic to California’s
overall evaluation of the trauma patient who has San Joaquin Valley, southern Arizona, New
experienced multiple injuries. First, each injured Mexico, Texas, and northern Mexico. When
region of the body is assigned an Abbreviated spores are inhaled, they migrate to the alveoli
Injury Scale (AIS) score. An AIS score 1–6 (minor, where they transform into thick-walled spherules
moderate, serious, severe, critical, and unsurviv- that cause granulomas and lung cavitation.
able) is assigned to the region. Then, the three Patients experience weight loss (⬎10%),
most severely injured body regions have their night sweats (can be confused with TB), and
score squared, then added together to produce the extreme fatigue. Treatment includes antifungals
ISS score. See the on-line resource of Trauma.org such as Amphotericin B, which is preferred
(www.trauma.org) for scoring trauma victims. in pregnancy [0.3–1 mg/kg/IV (adults)]. The
Source: Baker SP, et al. The Injury Severity Score: a method for
precautions are renal and hepatic compromise,
describing patients with multiple injuries and evaluating emergency bronchospasm, hypoxia, dysrhythmias, and
care. J Trauma. 1974;14:187–196. hypotension.19
TABLE 32-2 Classification of tornadoes: Fujita Scale

F0 Gale Wind and some damage to trees and signs F3 Severe Trains overturned and roofs and walls
Tornado of Tornado of torn off well-constructed houses
65–85 mph 136–165 mph
F1 Moderate Moving cars pushed off roads F4 Houses leveled

Tornado of Devastating
86–110 mph Tornado of
166–200 mph
F2 Significant Roofs torn off, trees snapped or uprooted F5 Incredible Automobile-size missiles fly in excess
Tornado of and cars thrown Tornado of of 100 m; entire communities leveled
111–135 mph ⬎200
All images are Courtesy of Federal Emergency Management Association
TORNADOES injuries from debris and crush injuries requiring

Tornadoes are relatively brief, violent storms that can critical care. As with earthquakes, anticipate exacer-
occur singly or in clusters. They have been classified by bations of chronic diseases and increased incidence
Prof. Theodore Fujita according to wind speed and of heart attacks.
damage potential (see the Fujita Scale, Table 32-2). The
lethality of a tornado varies widely depending on the HURRICANES
wind speed, the size of the community it strikes, the Much like tornados, hurricanes are categorized on a
structures, the degree of shelter that victims had at the numerical scale (Table 32-3). Recent violent and
time, and the victims’ host factors (victims’ ages, destructive hurricanes have heightened disaster planning.
physical condition, and ability to react accordingly to Hurricane Katrina in 2005 had winds of 142 mph and a
the disaster). The May 22, 2011 tornado which exten- 20-foot storm surge that killed 2057 (Figure 32-3), and
sively damaged Joplin, Missouri killing 159 persons the Galveston Hurricane of 1900 resulted in an estimated
was rated as an F5 incident. 8000 dead. Since hurricanes spawn tornadoes hundreds
Tornado victims exhibit injuries ranging from of miles inland, a hurricane’s true path of destruction,
minor lacerations to severe penetrating ballistic injury, and death extend well beyond the coastline.
TABLE 32-3 Saffir-Simpson Hurricane Scale

Category Winds Storm Surge Comments
One 75–95 mph/119–153 kph 4–5 foot Damage to shrubs, trees
/64–82 knots
Two 96–110 mph/154–177 kph 6–8 foot Window and roofing damage
/83–95 knots
Three 111–130 mph/178–209 9–12 foot (evacuation of Mobile homes destroyed.
kph/96–113 knots shoreline areas due to flooding Low-lying escape routes cut
as far as 8 miles inland) 3–5 hours before arrival of the
center of the storm
Four 131–155 mph/ 13–18 ft (requires evacuation Some complete roof failures,
210–249 kph of areas 6 miles or more inland) doors windows; major damage
to structures near shore
Five ⬎155 mph /⬎249 kph /⬎ ⬎18 foot (requires evacuation of Major damage to structures; all
135 knots areas 10 miles or more inland) trees and signs blown down
Source: National Weather Service National Hurricane Center (www.nhc.noaa.gov).
Association had screened approximately 1600

impacted residents and found that 25% had mild
to moderate reduction in lung function. Research-
ers could not determine whether this was the
result of breathing mold and dust caused by
Katrina, seasonal allergies, or an indicator of a
long-term change in respiratory health.
FLOODS
The classic flood disaster in the United States is the
Johnstown, Pennsylvania, flood of May 30, 1889. At
4:07 p.m. on that day, a 40-foot wave of water from a
dam failure and heavy rain killed an estimated 2200
people. Entire communities may find themselves
FIGURE 32-3 Aerial shot of the devastation left behind by underwater in the event of a flood (Figure 32-4).
Hurricane Katrina in the Gulf Coast.
Floods produce casualties similar to those of
Courtesy of Federal Emergency Management Agency
hurricanes. Stress-related exacerbations of chronic
Hurricanes have destroyed infrastructure, resulting

in the loss of power to hospitals and the isolation of
the hospital from resupply of liquid oxygen, medical
consumables, and food.
The aftereffect of hurricanes can produce injuries
and disease.
• Recovery and rescue efforts have resulted in injuries
to first responders and to those who are removing
downed trees and power lines, as well as to those
who are working to reestablish electrical, gas,
communication, and road/bridge infrastructure.
• The resulting flooding waters of a hurricane can
not only hamper relief efforts but also contain
contaminates, toxins, and debris. In the aftermath
of the 2005 Hurricane Katrina, the news media FIGURE 32-4 Flooding can devastate an entire community.
reported that the Louisiana American Lung Courtesy of Federal Emergency Management Agency
diseases can be compounded by infections, hypother-

mia, and psychological stress.
FIRE
Sometimes disasters occur at the same time. The Great
Chicago Fire and the lesser known Peshtigo Fire
happened at the same hour and the same day: October 8,
1871. The estimated deaths from these two events are
probably in excess of the 2400 reported because whole
families were wiped out with no one to report their
loss. Equally appalling are the fires that raged for 4 days
after the San Francisco earthquake, leaving over
250,000 San Franciscans homeless.
Hospital preparedness for an MCI resulting from a FIGURE 32-5 The collapse of the Pentagon is an example
fire is exemplified by the Rhode Island nightclub fire of a low-order explosion.
that resulted in 215 victims of the 439 patrons of the Courtesy of Federal Emergency Management Agency
club. There were 96 deaths at the scene of the fire.
Victims were distributed to 16 regional hospitals.20
Surgical and burn/smoke inhalation medical responses Pressure history of high explosive (HE) and thermobaric
should be part of the EOP. explosive (TBE) detonations
TBE vs. HE:
-Lower peak pressure
P2
-Longer pulse duration
Man-Made Disasters
Man-made disasters are incidents that overwhelm the
health care system’s capacity due to a malfunction in
something created by another human being or a P1
Pressure
planned attack devised by human beings. Industrial Thermobaric Explosive (TBE)

accidents and terrorist events are classified as man-
made disasters.
High Explosive (HE)
EXPLOSIONS ambient
Explosions resulting from industrial or transportation
accidents, warfare, and terrorism produce similar injuries.
The severity of the resulting injuries depends on:
t1 t2 t3 t4 t6
• The type of explosives used.
Time
• The proximity of the victims to the blast.
• The shielding between blast and victim. FIGURE 32-6 Pressures associated with high-order explosives.
• The blast environment (closed place versus open
area explosions). Terrorists have access to munitions that can
There are two categories of explosions: low-order produce a high-order explosion (HE), which is an
explosion (LE) and high-order explosion (HE). explosion that produces extreme pressure waves
Low-order explosions (LE) are the result of a traveling faster than the speed of sound (1116 ft/sec
rapid expansion of gases from an ignition. LE creates a or 761 mph) (see Figure 32-6). Examples of materials
subsonic explosion and does not have an over pressur- that produce an HE are:
ization wave. Examples are pipe bombs, gunpowder,
• TNT.
and most pure petroleum-based bombs such as
• C-4.
Molotov cocktails. Although an LE may not have the
• Semite.
extreme violence of the HE, its lethality is undeniable.
• Nitroglycerin.
An extreme example of a low-order explosion is the
• Dynamite.
one resulting from the impact of fuel-filled aircraft on
• Ammonium nitrate fuel oil
the World Trade Center and Pentagon buildings, with
the horrific damage, deaths, and injuries. The resulting Explosions that occur in closed places, such as
building collapse killed thousands (Figure 32-5). cafes, buses, and subways, have a higher mortality
The collapse of a building results in both crush (49% mortality) and more severe injuries in survivors
injuries and relatively few survivors. than open area bombings, where the mortality rate is
about 8%. Even in outdoor explosions, the victims’ initiated with 6 ATA pressure for 15–30 minutes,
proximity to the explosion is critical. Victims who are 6 followed by a decompression with oxygen to 2.8 ATA.25
m from the explosion receive 9 times less overpressure The blast lung triad of respiratory distress, hypoxia,
than those who are only 3 m away. However, all victims and a so-called butterfly or bat wing infiltrate appear-
within 20 m of the blast should be evaluated for ance on chest X-ray has been described for over 30 years
traumatic brain injury (TBI). If the blast wave is reflected in the medical literature. Meanwhile, the severity of the
off a surface, then it can be amplified as much as BLI can be categorized by P/F ratio, chest X-ray, and the
20 times. The blast wave as it passes through tissue presence or absence of a bronchopleural fistula.26
or materials of different density causes spalling or Signs and symptoms are:
shattering, of the inside tissue matrix without penetra-
• Tachypnea.
tion. Spalling can result in pneumothorax, broncho-
• Dyspnea.
pleural fistulas, and acute gas embolism.21 Spalling also
• Cyanosis.
occurs inside vehicles involved in roadside bombing.
• Hemoptysis.
The vehicle skin is not pierced by the blast, but the
• Decreased level of consciousness.
materials inside the vehicle spall, or break up,
• Decreased breath sounds with or without fine
becoming shrapnel that injures or kills the occupants.
crackles.
The injuries resulting from an HE can be classified
as primary, secondary, tertiary, and quaternary. At the same time, diminished heart sounds, low blood
pressure with systolic pressure only slightly above
• Primary blast injuries, sometimes called blast
diastolic, and distended neck veins (Beck’s triad)
overpressure injuries, occur only with an HE.
indicate cardiac tamponade.
Primary blast injuries result from the positive-
The basic ABCDE (airway, breathing, circulation,
pressure wave of an HE that rapidly expands to
defibrillation-diagnosis-decontamination, and expose/
over 20 atm (20 ⫻ 760 mm Hg). This is immedi-
examine) must be followed.
ately followed by a subambient pressure that
exacerbates the blast injury. In addition, the blast • Airway compromise is immediately life-threatening.
wave moves at three to five times the speed of • Hypopnea and apnea require mechanical
sound! This shock wave travels faster in liquids ventilation.
and solids, rendering the brain, lungs, intestines, • Cardiac status, as determined by heart rate and
and tympanic membrane particularly vulnerable blood pressure, is vital.
to damage. • Defibrillation may not be as prominent, but
• Secondary blast injuries are caused by ballistic decontamination of the victim may be. Contam-
debris, by shrapnel, by improvised shrapnel such ination in wounds can produce sepsis or toxic
as nails, nuts, and bolts, or even, in the case of a reactions and can prove fatal in spite of good,
suicide bombing, by bones and body parts. The aggressive, competent critical care.
decontamination of the ballistic debris is an • Expose all skin surfaces to examination for
early intervention that is essential for both the evulsions, lacerations, and penetrating injuries.
patient and the health care provider. Decontaminate the victim. Monitor the end-tidal
• When the victim’s body is thrown by the blast wave, CO2 for increased deadspace due to emboliza-
the resulting injuries are tertiary blast injury. tion by clots, air, or fat.
• Burns, crush injuries, and toxic inhalations result
At the first sign of respiratory decompensation:
in quaternary blast injuries.22
• Perform rapid-sequence intubation with cervical
Blast Lung Injuries. The major causes of immediate spine immobilization.
deaths in explosions are blast lung injury (BLI) and • Mechanical ventilation should be initiated using
air embolism that results from a BLI. Air embolism is volume control (6 mL/kg PBW), pressure control
conjectured to result from cellular damage between the with PIP ⱕ 40 cm H2O.
alveoli and pulmonary capillaries.23 The air embolism • Consider PLVC, IRV, or APRV.
of a BLI had been previously thought to be caused by • Start PEEP at 5–14 cm H2O. If oxygenation does
positive pressure; however, a recent study24 has found not increase, consider adding inhaled nitric
that air embolism can occur very early in the event, oxide (iNO). Adjust the respiratory rate (f) up to
before positive pressure breathing support. Treatment 22 to keep the pH ⱖ 7.20. If the pH cannot be
can be as simple as left decubitus or Trendelenburg maintained with permissive hypercapnia, then
positions with high FIO2 or very effective hyperbaric consider HFPPV or HFOV.
oxygen therapy. If hyperbaric oxygen therapy is avail- • Limit fluid resuscitation to prevent alveolar
able for patients with acute gas embolism, it should be flooding a worsening P/F.27
CASE STUDY 32-1

A bombing in a shopping mall has triggered an MCI 2. What is the value of end-tidal capnography with
alert in the hospital. Initial police and rescue reports this patient?
indicate that the blast appears to be from a high- 3. What treatment options must be considered for
grade military weapon—Semtex or C-4. this patient?
The first victim arriving by ambulance is a
4. If intubation and mechanical ventilation
teenaged boy who is cyanotic and coughing up pink
is indicated, what settings should be
frothy secretions. His vitals are HR 130, f 30, B/P
used?
100/70, 36.9oC with decreased B/S in both lungs.
He has shrapnel injuries to his legs and buttocks. 5. If standard mechanical ventilation fails to
improve oxygenation and/or ventilation, what
Questions alternatives can be used?
1. What are the RT’s immediate assessment and
treatment priorities?
CASE STUDY 32-2

The terrorist bombing of the city’s power and Questions
electrical office building results in a partial building 1. What pathologies are suggested by her history
collapse. Nearly 12 hours after the event, a victim and vital signs?
is extracted alive and is being transported to the ED.
2. What immediate medical interventions
The victim is a woman who has suffered head and
are indicated?
chest injuries and who had her left arm pinned
under a block of rubble. Paramedics report GCS 3. What complications can be expected with these
10 with occasional loss of consciousness, HR 140, types of injuries?
B/P 90/60, and SpO2 92%. She has short runs of 4. What would indicate the need for intubation
polymorphic ventricular tachycardia (Torsade de and mechanical ventilation?
pointes) that resolve spontaneously. The EKG 5. What mechanical ventilation strategies can be
telemetry is: anticipated?
Psychosocial Issues in the Treatment of Blast to preinjury asthma, COPD, smoking history,
Injuries. The long-term sequelae can occur up to and other factors.
11 months or more after the event. • Cultural and language barriers can confound the
patient assessment and the recovery.
• Lung function can return to normal or exhibit a
• Providing “psychological first aid” (e.g., address-
mild restrictive defect on pulmonary function
ing physical needs other than medical care,
test (PFT). Most pulmonary limitations are due
social support, language and cultural sensitivity,
and a sense of decision making) can be a great The bioagents most likely to succeed are:
help.
• Smallpox.
• By limiting exposure to the media or media
• Anthrax.
reports of the event, the patient may have the
• Plague.
psychological space to develop effective coping
• Tularemia.
mechanisms.
• Botulinum.
• Post-traumatic stress has not been shown to be
• Mycotoxin.
reduced consistently by critical incident stress
• Viral hemorrhagic fevers.34
debriefings.
However, history has shown that even Salmonella,
Brucellosis, and others have been weaponized.35
BIOTERRORISM The Centers for Disease Control and Prevention
A biowarfare attack is suggested by an outbreak of a (CDC) has organized these agents by priority, ease
rarely fatal disease that has high virulence and a high of dissemination/transmission, mortality and
mortality rate, such as tularemia. Multiple superinfections morbidity and major public health impact. Note
that cannot be easily explained suggest a biological that, in the CDC’s Category C of emerging pathogens
attack. Even more alarming would be a single case of is multidrug-resistant tuberculosis (MDRTB). The
smallpox since it has been declared eradicated in 1980 categories’ definitions and a list of these agents may
by the World Health Organization. A suicide “bomber” be found in the CDC Web site (http://www.cdc.gov).
with smallpox could inflict a terrible bioterror event.28 Interesting also is the fact that the anthrax
The first documented bioterrorist attack occurred attacks did not precipitate a declaration of a
in the United States in the fall of 1984. A cult called the local state of emergency despite the strain and
Rajneeshee contaminated 10 salad bars in Wasco financial burden the attacks placed on the impacted
County, Oregon. Over 700 people were sickened, but communities.36
there were no fatalities.29 Other cults/terrorist groups
(such as the Aum Shinrikyo (Supreme Truth) that
attacked the Tokyo subways with the nerve agent sarin Anthrax. Anthrax has been a medical problem
throughout recorded history. In its spore form, it
on March 20, 1995) also tried biological agents such as
can survive in the soil for decades. It is primarily a
botulinum toxin and even Ebola.30 Fortunately, they
cutaneous disease derived from infected herbivores
were unsuccessful. Then in the aftermath of the tragedy
and occasionally can affect the gastrointestinal tract.37
of September 11, 2001, a series of anthrax attacks
Inhalational anthrax is extremely rare. However, once
occurred, from Florida to Connecticut.31 This was the
inhaled, the spore is engulfed by alveolar macrophages
second significant documented bioterror attack in the
and carried to the lymph, where it germinates and
United States with far-reaching impact. Two branches
releases its toxins.
of the federal government were temporarily shut down,
In its inhalational form, anthrax presents like the
as were several postal offices, 18 individuals contracted
flu or pneumonia. Diagnosis is accomplished by lab
anthrax (11 inhalational and 7 cutaneous), more than
tests and by exclusion. As in the case of a natural
33,000 required postexposure prophylaxis, and direct
outbreak, diagnosis requires the astute clinician to
costs approached $3 billion.32
suspect anthrax disease in the non-animal-contact
These attacks propelled the civilian medical
cases because natural outbreaks occur among
community into the arcane world of bioweapons. With
abattoir workers, farmers, and ranchers. Chest X-ray
the potential for massive numbers of victims and panic
abnormalities, such as a widened mediastinum,
in both lay and medical personnel, all health care
paratracheal fullness, and pleural effusions or
personnel at the forward edge of the medical response
infiltrates, are highly indicative of inhalational
must have knowledge of this phenomenon. Possible
anthrax, although early in the disease these may
indicators include:
be subtle.38
• A disease that either is unusual or does not occur Until 2001, surviving inhalation anthrax after the
naturally in a given area. symptoms appeared was virtually unknown. Symptoms
• Multiple disease entities in the same patients. of fever, chills, drenching sweats, profound fatigue,
• Large numbers of casualties inhabiting the chest discomfort, and nausea or vomiting were com-
same area. mon findings in the 2001 victims. Rhinorrhea and
• A massive point-source outbreak. productive cough were uncommon findings. Arterial
• An apparent aerosol route of infection. blood gases were not highly alarming with pH of 7.45,
• Dead sentinel animals. PaCO2 27 mm Hg, PaO2 80, and SbO2 97% on room air
• The absence of a natural vector in the area.33 with one anthrax victim.39
Treatment has special requirements. If the victim survives, the dried pustules fall off, and
they must be considered highly contagious.
• Decontamination requires standard precautions.
Smallpox is highly contagious but not quite as
Victims’ clothing should be bagged, labeled,
contagious as its viral cousin, chickenpox, a virus of the
and held for the FBI because it is evidence. The
Herpes zoster family. The disease therefore requires
victims’ hair should be washed if it has not been
respiratory precaution by all.
washed since the exposure.
The Soviets weaponized smallpox and were actively
• Early antibiotic chemotherapy is essential, and
weaponizing it until at least 1990.42 Smallpox is spread
multidrug resistance must be assumed.
through droplet nuclei with devastating effects. Until
• Pleural effusions can be managed by chest tube
1972, however, smallpox offered the terrorist or rogue
thoracostomy. Drainage from the chest tubes or
government limited effectiveness as a weapon because
elsewhere can be a route of infection to the
everyone in the United States over the age of 1 was
therapist, nurse, or physician.40
vaccinated. Nevertheless, these facts created a real
By using routine supportive respiratory care and concern in the military medical community.43
innovative triple chemotherapy (ciprofloxacin or The smallpox vaccine (vaccinia virus) can be
doxycycline, rifampin, and clindamycin or azithromycin administered postexposure, preferably within 7 days.
or vancomycin), over 54.5% recovered. The expected Vaccination is the only effective postexposure treat-
survival rate had been less than 15%.41 ment, and all other standard treatments are supportive.
(In fact, the term “vaccination” comes from the Latin
Smallpox. Smallpox was declared eradicated by the vacca meaning “cow,” since the Edward Jenner vaccine
World Health Organization (WHO) in 1980, and was derived from cowpox in 1789.)
vaccination programs were terminated. So there is an A recent study reported that the antiviral agents,
ever increasing susceptible population. Even a single including ribavirin and cidofovir, could be employed as
case of smallpox is a clear indicator of a bioterrorist aerosol therapy for the treatment of victims. Aerosol-
attack. ized cidofovir (Vistide) by small particle nebulizer44
A smallpox victim: in doses of merely 0.5–5 mg/kg of body weight was
more effective against smallpox, cowpox, camelpox,
• Is febrile, with headache, malaise, back pain,
and monkeypox than larger doses or even subcutane-
and vomiting.
ous injection.45 The respiratory care professional must
• Has lesions on the face, limbs, hands and feet,
be prepared to manage these victims.
even on the palmar surfaces of the hands and
feet, and the lesions are in the same stage of
The Plague. The bubonic plague created a stir in
development. The lesions start as papules
November 2002 when two tourists from New Mexico
(2–3 days) and advance to pustular vesicles on
came down sick with Yersinia pestis (originally called
the face and extremities (Figure 32-7).
Pasteurella pestis) in New York City. The news media
Spotlight
On
Smallpox
• Incubation Period: 7–17 days
• Droplet and airborne precautions: 17 days
• Presentation: Fever, back pain, vomiting,
malaise, headache, rigors; papules
(2–3 days) to pustular vessicles face and
extremities
• DX: Giemsa or modified silver stain, PCR,
and viral isolation IHC
• TX: Immediate vaccination, aerosol
cidofovir 0.5–5 mg/kg, and supportive care.
Source: Bray M. Treatment of aerosolized cowpox virus infection in
FIGURE 32-7 Child with smallpox. mice with aerosolized cidofovir. Antiviral Research. 2002;54,3:
Courtesy of the Centers for Disease Control and Prevention Public Health Image 129–142.
Library/Dr. Michael Schwartz
covered this story avidly.46 The victims were success- This bioagent of terror, the pneumonic plague, is
fully treated, and their disease was naturally acquired contagious and requires respiratory precautions. Even
from infected rodents. Both the U.S. and former Soviet in its bubonic form, the patient may require mechani-
military believe that aerosolized Yersinia pestis would cal ventilation, as in the New York City case. Fortu-
result in the highly contagious and highly fatal form of nately, when identified through Gram stain, DNA
the plague, the pulmonic plague.47 The WHO reported amplification (polymer chain reaction or PCR), and
in 1970 that if 50 kg of Yersinia pestis were to be IHCA, the plague is treated with streptomycin. Yet a
released as an aerosol over a city of 5 million, it would misdiagnosis could be fatal. During the last 50 years, 4
cause about 150,000 cases of the pneumonic plague, of the 7 (57%) victims of the pneumonic plague
which would result in 36,000 deaths.48 died.50 Suctioning, coughing, and draining of tubing
The bubonic plague causes classic lesions called require proper barrier precautions. Effective therapies
buboes, usually in the inguinal area because the flea for the bubonic manifestation of the plague include
vector bites the ankles. Although many consider it a streptomycin, gentamycin, tetracycline, and chloram-
disease of only historical interest, the plague still phenicol. There may also be a role for aerosolized
occurs naturally even in the United States. With tobramycin.
three clinical presentations, bubonic, primary septice-
mic, and pneumonic, the gram-negative bacillus
Yersinia pestis can be identified through laboratory
smears of peripheral blood or lymph node needle Spotlight
aspirate. On
• The bubonic form manifests itself through The Pneumonic Plague
tender, enlarged (1–10-cm) lymph nodes with
• Incubation period: 2–3 days
surrounding erythema.
• Droplet precautions: Respirator and HEPA
• Septicemic plague can be a primary infection or
filtration for ventilators
the result of hematogenous spread of the
• Presentation: High fever, chills, hemoptysis,
bubonic plague. In its primary form, it chal-
toxemia, shock, stridor, B/S crackles, ARF.
lenges the clinician since it lacks the plague-
Onset to death is around 36 hrs! There is no
related bubo.
time for buboes to appear!
• The plague in its pneumonic manifestation is the
• DX: Gram stain, C&S, immunoassay for
concern of all medical professionals. In the
capsulated antigen, DNA amplification
preantibiotic outbreak of the pneumonic plague
(PCR), immunohistochemical stains (IHC)
in Manchuria during 1921, “the expected life of
• TX: Gentamycin 30 mg/kg/day IM; pediatric
the victim was a mere 1.8 days.”49 Once again,
2.5 mg/kg/dose (infants and children Q8h)
the diagnostic marker of buboes may not appear
IV or IM
in the pulmonic plague victim.
The signs and symptoms are as follows:
• The victims present with what appears to be a
severe, rapidly progressing pneumonia after an
incubation period of 1–6 days.
CASE STUDY 32-3
• They are febrile and short of breath.
• They have chest pain and a cough, which may The RT is treating a COPD with CHF, fever,
include hemoptysis. headache, rash, and lesions on the face and
• At this point, tachycardia, tachypnea, dyspnea, limbs in the ED. The examining cardiologist
and cyanosis appear. notes Janeway lesions (nontender hemorrhagic
• Some victims may have cervical buboes. lesions) on the palms and soles and says, “She
• The condition can progress to shock. doesn’t have bacterial endocarditis.”
• Multiple organ system failure (MOSF),
Questions
disseminated intravascular coagulopathy
(DIC), and acute renal failure (ARF) are 1. What is the suspected infection?
possible. 2. What precautions are required?
• Pleural effusions occur in over 50% of the cases. 3. What respiratory care is required?
Patients should be in respiratory isolation until they 4. What will help confirm the diagnosis?
show clinical improvement for 24 hours.
secretions. Look for the classic triad of botulinum

CASE STUDY 32-4 intoxication:
• Symmetrical, descending paralysis with bulbar
A 55-year-old male who works in the hospital’s palsies of (the so-called 4Ds): diplopia,
shipping-receiving is admitted to the ED. He dysarthria, dysphonia, and dysphagia.
presents with a nonproductive cough, stridor, and • An afebrile patient.
cyanosis: 390C, HR 110, f 28; EKG sinus • Clear sensorium.54
tachycardia; Lab: Hct 41%, WBC 7500,
CK-MB 1; CXR shows lymphoadenopathy and Airway control is therefore a priority that would not be
pleural effusions. complicated by bronchorrhea. The RT can expect to
mechanically ventilate these patients for extended
Questions periods.
1. What is the suspected infection? Differential diagnosis is vital. By means of serology,
2. What precautions are required? toxin assays, and anaerobic cultures, botulism can be
identified and readily treated with the pentavalent toxoid
3. What respiratory care is required? vaccine. Standard Universal Precautions suffice because
4. What will help confirm the diagnosis? secondary aerosols from patients are not considered
hazardous. Botulinum toxin is inactivated by sunlight
within 3 hours, and decontamination with soap and
water is effective because it is not dermally active. An
aerosol attack is the most likely scenario in a botulinum
Tularemia. Francisella tularensis, or tularemia, was attack; however, it could be used to attack food as well.
first described in 1911 by G. W. McCoy in Tulare Again, the Soviet Union55 and the Aum Shinrikyo
County, California. Tularemia causes two forms 56
cult both worked avidly to develop Venezuelan
of the disease in humans: ulceroglandular and equine encephalitis (VEE) and other hemorrhagic
typhoidal. viruses (VHF, Hantaan, Marlburg, etc.) into weapons
Although noncontagious, tularemia is a bioweapon of mass destruction and terror.
that causes lesions on the skin and mucus membranes
• With VEE, the victim presents with a general
and that is accompanied by fever (85%), chills (45%),
malaise, labile fever, rigors, headache, and
cough (38%), and myalgias (31%). Approximately
photophobia. The treatment is supportive with
80% of typhoidal tularemia patients develop
standard universal precautions.
pneumonia.51
• VHF is far more dangerous, with respiratory
Easily identified by serology, sputum C&S and PCR
precautions upgraded to airborne isolation
and IHC, tularemia is treated with gentamycin and
and decontamination with hypochlorite and
streptomycin.52 Bronchopleural fistulas and calcifica-
phenolic disinfectants.
tions can complicate care. Airway care and mechanical
• Interestingly, ribavirin has been demonstrated to
ventilation require anticipation of these problems. A
be effective in treating the Hantaan virus.57 The
restrictive defect and air leaks require careful bedside
principles of hemodynamic, respiratory, neuro-
monitoring.
logic, and hematologic support apply.
• Intravenous ribavirin is effective against Lassa
Botulinum Toxin. Human vanity has brought a toxin,
fever with side effects of anemia with reduced
Botox (botulinum), into the chemical cosmetic arena
oxygen transport. The drug should not be given
instead of into the emergency room. It is licensed for
to pregnant women because it is embryo-lethal.
the treatment of strabismus, blepharospasm, and
• Ribavirin has poor in vitro and in vivo activity
cervical torticollis.53 Its licensing may, unfortunately,
against Ebola and Marburg, as well as against
increase its availability to a terrorist.
dengue and yellow fevers. Human monoclonal
Botulinum toxin poisoning can result in a
antibodies seem to hold the most promise at
presentation similar to variations of Guillian-Barré
this time.58
syndrome with one important difference: It is a
rapidly descending paralysis, leading to respiratory Once again, creative use of antiviral agents, such as
failure. It can be confused with myasthenia gravis, cidofovir, as an aerosol might be critical in saving these
tick-borne paralysis, or even nerve agent paralysis. victims of bioterror.
However, miotic pupils and copious respiratory
secretions accompany nerve agent paralysis, whereas Staphylococcal Enterotoxin B. Staphylococcal
in botulinum intoxication there is a decrease in enterotoxin B (SEB) causes symptoms and toxicity
when inhaled in very low doses. Standard Universal Impact of Bioterrorism on the Health Care
Precautions are required. SEB is not dermally active, Community. Bioterror attacks present the health care
and secondary aerosols are not a hazard. community with two unique problems for which it
Its symptoms include sudden onset of fever, chills, must be prepared: mass casualties requiring effective
dyspnea, and retrosternal chest pain. Identified by ELISA, management and ventilatory support by medical
or PCR (DNA amplifications), these victims require: personnel who are burdened with existing patients and
a diagnostic blizzard of genuine and psychogenic
• Intensive respiratory care, including oxygen,
casualties. In addition, bioterrorism presents the
BiPAP, or mechanical ventilation with PEEP.
medical professions and especially respiratory care with
• Close hemodynamic monitoring and excellent
unique challenges and learning.
fluid management.
• Manual resuscitators can manage respiratory
A new drug, pirfenidone, seems to block the effect
support initially; however, the respiratory and
of SEB, especially the development of pulmonary
nursing staffs will be quickly overwhelmed.
fibrosis that complicates ventilator management with a
• HEPA (high-efficiency particulate air) filtering
restrictive defect.59
of exhalate from manual resuscitators may well
forestall the risk to therapists, nurses, and
Spotlight physicians caring for biocasualties.
On • In the chaos of the attack, roads, bridges,
tunnels, and airports may be closed, as they were
Pirfenidone on September 11, 2001. Rental ventilators may
• Initial study at the United States Army not arrive in time. The government Push Packs
Medical Research Institute for Infectious may not arrive for 12 hours or 10 days after the
Diseases demonstrated effectiveness disaster has been identified.
against SEB (Hale ML, et al. Infect Yet this threat presents the profession with an
Immun. 2002;70:2989–2994). outstanding opportunity to clearly demonstrate its vital
• In March 2004, the Food and Drug importance to hospitals, the public health, and the
Administration classifies pirfenidone American public. As more is learned about the agents
as an orphan drug for idiopathic of bioterror, it becomes obvious that respiratory care
pulmonary fibrosis (Nagai S, et al. Intern can play a significant role in the diagnosis, initial care,
Med. 2002;41,12:1118–1123). management, and follow-up care of the victims of
• Several studies demonstrate effectiveness bioterror. The opportunities for expansion of the scope
in bleomycin lung fibrosis (Kakugawa. of practice are legion. The unfortunate reality that
Eur Resp J. 2004), oleic acid ALI (Mei SJ. bioterror will occur again demands that respiratory care
Pharmacl Exp Ther. 2004), kidney fibrosis, professionals be prepared.
and multiple sclerosis (Bowen JD. Mult
Scler. 2003). Zoonotic Disease. Diseases that are caused by host
animals are called zoonotic, and they almost always occur
in humans who have close contact with the host animal.
Even in most farming communities, these zoonotic
CASE STUDY 32-5 diseases rarely occur. However, if urban office workers
come down with brucellosis, glanders, or tularemia, then a
The therapist is called to the ED for intubation terrorist release should be seriously considered.
and mechanical ventilation of a 30–year-old GBS
or MG patient. He has ptosis, diplopia, difficulty Differentiating Epidemics, Pandemics, and
speaking, and upper body paralysis. His wife Seasonal Disease from Bioterrorism. Differential
reports that the symptoms started last night with diagnosis is difficult. Differentiating naturally occurring
nausea, constipation, and difficulty urinating. disease from bioterrorism is challenging and requires
the clinician to have a high index of suspicion.
Questions Naturally occurring diseases and climatic events can
1. What other diagnosis should be considered? further confound the situation.
2. What precautions are required? • Pandemics start with one or more index cases;
3. What respiratory care is required? then there is a logarithmic growth in the number
4. What will help confirm the diagnosis? of victims, perhaps partly due to a seasonal
surge.
• Bioterrorism produces a large number of victims Respiratory therapists engaged in home care
in a very short time. These victims have a should follow the Standard and the Droplet Precau-
common geographic point where the terrorists tions when entering a home to provide services to an
released the agent. On the other hand, natural infectious patient. Professional judgment determines
outbreaks from contaminated water, food, whether a surgical N95 respirator should be worn upon
or drink can have single geographic point entering the patient’s home. Good hand hygiene has
source too. been cited as the single most important practice in
infection control.62
Infection Control in Biological Events. Infection
control is an evolving science that requires frequent CHEMICAL WEAPONRY
updates and training. Emerging diseases such as severe
acute respiratory syndrome (SARS), avian influenza, A 1969 United Nations report defined chemical
and others require early epidemiologic identification warfare agents as “[c]hemical substances, whether
and implementation of infection control (IC) to reduce gaseous, liquid or solid, which might be employed
their spread by means of the infection of other patients because of their direct toxic effects on man, animals
and the staff. and plants.” The use of chemicals in our daily lives
The two forms of disease transmission that are of requires bulk shipments by rail, truck, or ship and
most concern are contact and airborne transmission. the large volume storage, all of which subject to
accidental release into the air, as in the Bhopal
• In skin-to-skin contact, transmission occurs incident of 1984. Perhaps a more alarming event was
when the therapist touches patients to assess, the sarin nerve agent release by an apocalyptic cult,
turn, or position them. Contact transmission the Aum Shinrikyo, in the Tokyo subway system in
can occur through contaminated hands and March of 1994, which resulted in 5000 casualties and
fomites. 12 deaths.63
• Airborne transmission occurs via droplet The history of poison gas warfare (i.e., chemical
nuclei containing the infectious agent, warfare) is not confined to the battlefields of World
such as TB.60 War I, where it is the most infamous. During the
The respiratory therapist must be aware that Ethiopian campaign in 1935–1941, the Italian Army
aerosol-generating procedures such as nebulizer used mustard agents (vesicants/blister agents) on the
treatments, suctioning, intubation, and bronchoscopy Ethiopians. More recently, Iraq used lethal combina-
have a real potential for disseminating droplet nuclei. tions of nerve and mustard agents against both the
In the Canadian SARS experience, viral transmission Iranians (Iran-Iraq War) and Iraqi Kurdish populations.
from the patient to health care personnel occurred Some nations considered chemical warfare agents as a
during an intubation procedure. Consider additional “poor man’s nuclear weapon.” Table 32-4 summarizes
precautions for hospital personnel or reducing aerosol- categories of chemical agents.
generating procedures to only those essential for The possible indicators of a chemical release or
patient care. attack are as follows:
Environmental and administrative controls other • Are there mass casualties/fatalities with minimal
than Universal Standard Precautions should be estab- or no physical trauma?
lished as early in a biological event as possible. • Are first responders casualties?
• The early detection of infectious disease, • Are there dead animals and/or vegetation in
the vaccination of health care personnel, the area?
pharmaceutical prophylaxis, and isolation
or cohorting of infectious patients are all
essential. TABLE 32-4 Basic categories of
• Emergency departments and clinics should chemical agents
promote the use of masks by symptomatic
Pulmonary Agents: chlorine, phosgene, cyanide
persons or patients during transport.
• Guidance in the use of personal protective Vesicant Agents: Lewisite and the nitrogen
equipment (PPE), the cleaning of equipment, mustard agents
handling lab specimens, and postmortem care Nerve Agents: Tabun (GA), Sarin (GB), and VX
must be preestablished. Lachrymators: CN (Mace), CS
• There is some evidence to show that the
Insecticides: Malathion, parathion, and sevin
use of ultraviolet light can lower transmission
rates.61 Defoliants: Agent Orange, Round-up, etc.
• Are there reports of unusual odors, smoke, or Next, pralidoxime is administered via autoinjector.
vapor clouds? (If you smell it, then you are a Pralidoxime chloride is a cholinesterase reactivator.
victim too! A phenomenon of off-gassing occurs Nerve agent victims with myasthenia gravis require very
when chemicals on a victim vaporize and affect close monitoring when pralidoxime is used. Conscious
rescuers or health care professionals.) patients should be informed that mild to moderate
pain may be felt at the injection site. In an organophos-
Note: Most military-grade chemical weapons have no
phate pesticide or nerve agent, toxidrome pralidoxime
smell associated with them.
is potentially curative.64
Patients should be monitored for a reduction or
Chemical Warfare/Terrorism Nerve Agents:
elimination of symptoms in 5–10 minutes. If symptoms
Sarin (GB), Soman (GD), Tabun (GA), or VX.
Nerve agents are chemically related to organophos-
phate insecticides. Sarin and Tabun were developed
by German scientists (hence the “G” prefix to its
abbreviation) who were working on controlling
Spotlight
mites on plants. At the end of World War II, the On
Soviet Army captured the German chemical muni-
tions plant and thus acquired these agents. The
The Nerve Agent–Poisoned Child
United States countered with its own research and Pralidoxime:
produced the highly lethal, VX. A droplet of VX on • Pediatric dosage:
the skin is fatal in seconds to minutes. Nerve agents • 20–40 mg/kg IV over 10 minutes
penetrate clothing to produce symptoms or even • 5–10 mg/kg/h for 24 hours after initial
death and can be effective even through heavy winter bolus
clothing. • Route:
All of these agents cause a cholinergic crisis by • IV preferred
blocking anticholinesterase. Victims exhibit signs and • IM possible (Mark I kits)
symptoms within a minute or sooner after exposure. In
some, the first signs might be seizures and death. Since Atropine:
these agents have volatility similar to water or motor • Range: 0.01–0.04 mg/kg
oil, vaporization may be limited. • Never give less than 0.1mg!
Victims of nerve agent toxicity have the following • 0.02 mg/kg, IV every 5 minutes
signs and symptoms: • Until bronchorrhea, bronchospasm, and
• Headache hemodynamically significant bradycardia
• Blurred vision from pinpoint pupils (miosis) are controlled
• Tight chest (smooth muscle constrictions) with
bronchospasm and copious secretions
• Diaphoresis
• Lacrimation
• Salivation Spotlight
• Unexplained runny nose On
The treatment of these victims is time-sensitive,
requiring the administration of both atropine
Mnemonic for Diagnosing Nerve
(2 mg/IM) and pralidoxime (2-PAM), both of which Agent Exposure
are in the Mark 1 Nerve Agent Antidote Kit (NAAK) Mnemonic for Muscarinic Signs—Dumbels
autoinjectors that can be administered through heavy
clothing. • Diarrhea
Atropine should be administered first. Intramuscu- • Urination
lar injection into the thigh muscle (vastus lateralis or • Miotic pupils
rectus femoris muscles) can reverse muscarinic effects • Bronchospasm, bronchorrhea, bradycardia*
of nerve agents (i.e., bronchospasm, bradycardia, and • Emesis
excessive secretions). Think dumbels for muscles for • Lacrimation
muscarinic. (See the Spotlight On Mnemonic for • Salivation
Muscarinic Signs—Dumbels.) Atropine can be instilled *Bradycardia was not present in the victims of Tokyo sarin attack.
via an endotracheal tube if necessary.
TABLE 32-5 Chemical agent targets Vesicant toxidrome can result in:
of toxicity • Leukocytopenia.
Toxic Agent Target(s) • Decreased RBC (decreased oxygen transport).
• Decreased platelets.
Nerve agents Airways, breathing,
• Sepsis.
(Sarin, VX, etc.) disability (NMJ)
• Airway obstruction.
Cyanides (asphyxiants) Breathing (cellular) • Atelectasis.
Pulmonary agents Airway, breathing • Disseminated intravascular coagulopathy (DIC).
(phosgene) (alveolar level) • Multiorgan system failure (MOSF).
Riot control Airway, breathing
Close monitoring of the victims’ airway status is vital
Insecticides Airways, breathing, since airway compromise can occur at any degree
(organophospates) disability (NMJ) of injury.
Herbicides Airway, disability
(Carcinogenic) Cyanide. Severe cyanide intoxication results in:
• A brief period of hyperpnea.
• Seizures.
• Hypopnea.
persist, then a second administration of atropine and
• Dysrhythmias.
pralidoxime should be administered. A total of
• Apnea and death.
3 doses of the drugs may be required. In the Tokyo
event, most victims responded to single doses of In mild exposures, only nauseam vertigo, dyspnea, and
atropine and pralidoxime. muscle weakness occur.
Table 32-5 lists targets of toxicity involving expo- The symptoms are a result of the fact that cyanide
sure to chemical agents. stops the cellular oxidative process by blocking
cytochrome a,a3 and dramatically reducing the
Blister Agents (Vesicants). In this category, the production of ATP. The effect is lactic acidemia and
chemical rapidly binds with proteins, including DNA, tissue death. Therefore, oxygen consumption is
to produce damage. Nitrogen mustard and lewisite, severely reduced in affected cells. Mixed venous
for example, were intended to bypass gas mask defense (pulmonary artery) blood oxygen levels can have
by attacking exposed skin. saturations above 76% and partial pressures in excess
“Depending on the vesicant, clinical effects may of 46 mm Hg.
occur immediately (as with phosgene oxime or lewis- Before treatment of dermal exposure cases:
ite) or may be delayed for 2 to 24 hours (as with • Remove all the victim’s clothing, jewelry, and
mustards). Following exposure, the most commonly shoes.
encountered clinical effects include dermal (skin • Bag-and-tag all personal possessions.
erythema and blistering), respiratory (pharyngitis, • Wash affected areas with large quantities of water
cough, dyspnea), ocular (conjunctivitis and burns), and mild liquid detergent, paying attention to
and gastrointestinal (nausea and vomiting).”65 skin in skin folds.
Treatment must be quick.
With aerosol exposures, remove clothing that might
• The early and gentle decontamination
have trapped or adsorbed vapors. If the patient is
(ideally within minutes of exposure) reduces
asymptomatic, washing is usually unnecessary, but if in
damage.
doubt, decontaminate the victim.
• Cut off clothing rather than pulling over the
Treatment requires the removal of cyanide
head or over uncontaminated skin.
from the cytochrome a, a3 by methemoglobin by
• Racemic epinephrine aerosol is effective for
administering the antidote sodium nitrite. Sodium
stridor.
nitrite oxidizes hemoglobin’s Fe⫹2 to produce
• N-acetyl-l-cystine (NAC) by aerosol may
methemoglobin’s Fe⫹3 (MetHb). MetHb results
provide some amelioration of inhalation
in “chocolate brown blood” appearance. This
injuries; however, research is still being
permits the resumption of cytochrome activity
conducted.
and the production of ATP. Sodium thiosulfate
Note: there is no antidote for mustard poisoning; treatment accelerates the catabolism of displaced cyanide
is similar to that for a burn injury. by the liver.
Personal protection includes: Phosphene. The onset of symptoms can vary from
2 to 6 hours, and some victims can be asymptomatic
• HVAC to control the off-gassing that occurs
for 48 hours. All exposed victims must be observed for
when chemicals vaporize from a victim’s body or
48 hours! Children are more vulnerable to phosgene.
clothing.
The signs and symptoms of phosgene intoxication
• Butyl rubber gloves with Teflon, Responder, or
include:
Tychem Protective clothing.
• In some severely contaminated cases, self- • Hoarseness.
contained breathing apparatus (SCBA) to • Stridor.
provide clean pressurized air to emergency • Laryngospasm.
personnel. • Wheezing (reactive airways disease syndrome or
RADS).
The medical management of the cyanide victim
• Cyanosis and fine crackles of noncardiogenic
includes:
pulmonary edema.
• Administration of 10 ml of 3% sodium nitrate IV
over 5–15 minutes while monitoring blood Laboratory evidence of phosgene exposure includes:
pressure for sodium nitrate–induced • Anemia.
hypotension. • Evidence of hemolysis.
• That is followed by 50 ml of 25% sodium • Increased bilirubinemia and/or MetHb.
thiosulfate IV over 10 minutes. • Decreased P/F ratio or increased PA-aO2.
• Keep MetHb levels below 35% (low Hb) and
45% (normal Hb/Hct level). Treatment for phosgene exposure includes:
• In poorly responding patients, a second half- • Oxygen.
dose of both sodium nitrate and sodium thiosul- • Aerosolized bronchodilators.
fate may be administered. • CPAP/Bi-level pressure support (start with 4/8).
• Determine the victim’s Hb level! If MetHb
⬎30/35% (adult) or ⬎25% (children), treat it All ED personnel should wear protective eye wear and
with 1–2 mg/kg IV methylene blue. gloves, especially with liquid phosgene exposure.
• Vitamin B12 can provide excellent therapeutics Pharmacologic therapy includes:
with minimal side effects, especially for pregnant
• Leukotriene receptor-blockers.
women and children.
• Methylprednisolone.
• Oxygen theoretically should not help; however,
• Ibuprofen.
early use of high FIO2 has good outcomes.
• N-acetylcystine (NAC) lavage to mitigate lung
• Also recommended but possibly not feasible
injury.
with an MCI is hyperbaric oxygen.
Children’s stridor responds very well to racemic
epinephrine via aerosol 0.25–0.75 ml of 2.25%
Q 20 min.66
Spotlight
On Chlorine. A dense yellow-green gas with a pungent
odor, chlorine was the ideal killer in the trenches of
Managing the Cyanide- World War I. Being heavier than air, it sought out
Poisoned Child victims in deep trenches and bunkers. Even in
industrial or rail accidents, chlorine seeks low ground
• 100% oxygen
and basements.
• IV 0.33 mL/kg sodium nitrite
The signs and symptoms are as follows:
• 1.65 mL/kg of 25% sodium thiosulfate*
(Adjust the dose for Hb level** and keep • Immediately upon contact, eye and URT irrita-
MetHB <30%.) tion (a burning and choking sensation) ensues.
• Repeat at half dose if symptoms persist. • It is often followed by nausea, vomiting, and
• Vitamin B12 can reverse cyanide toxicity. dyspnea on exertion (DOE).
Watch for anaphylactoid reactions! • Cough and then hoarseness.
*Isom GE, Johnson JD. Sulphur donors in cyanide intoxication. • Pulmonary edema follows in as little as
Clinical and Experimental Toxicology. 1987. 30 minutes or up to 2–24 hours.
**Berlin CM. Treatment of cyanide poisoning in children pediatrics.
1970;46:793. Survivors may have permanent reactive airways disease
(RAD) and either restrictive or obstructive PFT defects.
Treatment is as follows:
• Thorough decontamination with soap and water
CASE STUDY 32-8
is required, ideally before the victims arrive in
the ED. Some 35 people from the airport are in the ED.
• Administer nebulized beclomethasone There was one death in the ED, and one DOA.
(20 mcg/kg)67 or budesonide68 as soon as There is no apparent physical trauma. Para-
possible to improve compliance and P/F. medics report several immediate deaths at the
• Therapists should consider racemic epinephrine airport. Several have lost consciousness, are
for stridor, Bi-level (APRV) pressure support, and convulsing, and are virtually apneic. Others are
intubation MV. Inhalation injury should resolve vomiting, drooling, and tearing; several have
in 3–5 days. uncontrollable diarrhea and shortness of
breath.
Note: Nebulized NaHCO3 for neutralizing HCL result-
ing from chlorine intoxication is unproven. Questions
1. What agent or agents could be responsible?
2. What therapeutics must be taken immediately?
3. What are the RT’s priorities?
CASE STUDY 32-6
The therapist is paged to the ED STAT. There are
55 adults and children from the neighborhood
that was being sprayed for West Nile virus
mosquitoes. The RT is ordered to treat the ones Disease
with hoarseness and paroxysmal cough. While Outbreaks of disease can at times overwhelm the
auscultating one of the victims, she observes that health care system and have devastating effects on
the patient and others have runny noses and are entire populations.
tearing. Their facial and hand skin appears
reddened. She smells garlic. • An epidemic affects a large number of people in
a given population or community. AIDS is an
Questions example of an epidemic that hit the United
1. What agent or agents could be responsible? States in the 1980s.
• A pandemic effects a wide geographic location
2. What PPE level is required?
and an exceptionally high proportion of people.
3. What immediate treatment must be rendered? The H1N1 influenza of 2009 is an example of a
pandemic. Confirmed cases affected 214 coun-
tries and overseas territories.
INFLUENZA
CASE STUDY 32-7 The CDC reports that annually an average of 36,000
Americans die of influenza and that an average of
The respiratory therapist is called to the ED 226,000 hospitalizations result from seasonal influ-
STAT. Upon arrival, he sees six patients who have enza (during late fall to early spring). Annual influenza
arrived simultaneously via car. Two have lost vaccination is strongly recommended with:
consciousness, one is convulsing, and three are
tachypneic (f 34), reporting severe headaches. • Either trivalent inactivated vaccine (TIV)
SpO2 ~90%. A nurse remarks that the victim’s for people over 6 years or in a high-risk
venous blood looks almost as red as your ABG group.
on one victim. • Or the live attenuated influenza vaccine
(LAIV) for healthy, nonpregnant persons.69
Questions
It is prudent for respiratory therapists to protect
1. What agent or agents could be responsible? themselves with the vaccine.
2. What PPE level is required? Influenza viruses are transmitted from person
3. What immediate treatment must be rendered? to person via large particle droplets (greater than
5 microns) from coughs and sneezes as well as from
hand to nose. Large droplets have a range of less than Some survivors suffered from residual postinfluenza
1 m and remain airborne for a very short time and can encephalitis.
be a source of surface contamination leading to the In 1957 another pandemic, the AH2N2 (Asian flu)
hand-nose route of transmission. However, droplets resulted in 70,000 deaths in the United States. In the
less than 5 microns, as might result from the use of Asian flu pandemic, the highest mortality was in the
small volume nebulizers, can remain suspended in the school age and elderly populations. The AH2N2
air for a considerable amount of time. pandemic of 1969 had a much lower fatality rate. As
The typical incubation period is 1–4 days; however, seen in these pandemics, the virus can share genetic
the adult patient is shedding viruses before symptoms material and mutate, thus frustrating vaccine develop-
appear. Children can shed the virus before they are ill ment and requiring annual inoculation.
and for more than 10 days after symptoms appear. In 2009, the most recent flu pandemic from the
Influenza deaths are low among children less than H1N1 virus resulted in over 25,000 deaths worldwide.
5 years of age, as compared to adults over 65 When a pandemic strikes, several aspects of
(0.4 deaths compared to 98.3 deaths per 100,000 hospital policy and EOP must be preestablished.
persons).70
• First heating-ventilation-air conditioning
Influenza results in:
(HVAC) must have an excess of 6 air exchanges
• Fever. per hour and filtered.
• Myalgias. • Flu shots must be administered to all staff as
• Headache. early in the flu cycle as practicable.
• Malaise. • An adequate supply of gowns and N95 masks
• Nonproductive cough. must be in the hospital’s stock.
• Sore throat and rhinitis. • Aerosols and aerosol therapy must be reduced or
• Exacerbation of preexisting cardiac or pulmonary eliminated.
diseases. • All exhalation from mechanically ventilated
• Secondary bacterial infection. patients must be filtered using a high efficiency
particulate air (HEPA) filter.
There are two types of influenza viruses: A and B. These
• The staff should decontaminate or shower and
are further subtyped by their surface antigens: hemag-
change clothes before going home.
glutinin and neuraminidase.
The AH5N1 or a similar influenza virus triggers a
• Hemagglutinin permits the virus to bind with
cytokine storm (releasing tumor necrosis factor-
and to enter the cell to be replicated. Hemagglu-
alpha, interleukin-6, 7, 8, and interferon), an
tinin, a protein, has 16 types; types H5 though
immunological overreaction that leads to ARDS. The
H7 are the most dangerous.
strong immune response to viral infections results in a
• Neuraminidase facilitates the release of newly
high mortality rate.72 The severity of the ARDS is
replicated viruses to escape the cell and to infect
indicted by:
other cells. There are 9 versions of the N protein
with the N1 being the most dangerous. • A P/F ratio of less than 200.
• Blood lactate greater than 2.2 mmol/L.
The variations in paring of H and N proteins permit a
• Pulmonary infiltrates on chest films.
possible 144 versions of the Type A influenza virus alone!
Therefore proinflammatory cytokines seem to be
Pandemic Influenza. Starting in April–May 1918 and the culprit that results in ARDS, SIRS (systemic
resuming in the fall 1918 and well into February 1919, inflammatory response syndrome), and multiorgan
the so-called Spanish Flu (AH5N1) raged around the system failure (renal failure, disseminated intravascular
world. The bodies of the victims of the 1918–1919 coagulopathy, and respiratory failure). Complicating
pandemic buried in the permafrost of Alaska and the situation is renal impairment with decreased urine
Siberia provided the DNA of the virus. The 1918–1919 output (requiring careful fluid management), creati-
pandemic provides a template for diagnosis. The nine ⬎ 100, urea ⬎ 6, and uric acid ⬎400. Lympho-
AH5N1 infection was characterized uniformly by fevers cytes can decrease to 0.04 and monocytes to 0.03.73
of 102ºF (38.9ºC), bronchial pneumonia, septicemia,
and CNS involvement with the highest attack rate in Bird Flu, a Zoonostic Variant. Close contact among
persons between 14 and 40 years of age. In an era humans, birds, and pigs can have the unfortunate
where travel was slow, Eskimo villages were wiped out, result of sharing viruses. The contact creates the
and the island of Fiji suffered 8000 deaths. There were optimal environment for viruses to share proteins and
an estimated 20–40 million deaths worldwide.71 emerge as a pandemic. During 2004, Vietnam reported
22 cases and 15 deaths from avian H5 strain. Later, MCI because of the many unknowns as the event
Thailand reported 12 cases with 8 deaths. This mortal- unfolds. By establishing an early diagnosis and
ity rate was 67–68% with a potential to be ten times providing prompt, prepared aggressive care, the
more lethal than the 1918–1919 pandemic. worst case can be forestalled. Accurate record keeping
and the bagging and tagging of victims’ personal
Suggested Medical Management of the possessions assist in the investigation that will follow
Pandemic Victim. the event.
The regular use of surge ventilators purchased by
• First, scrupulous infection control procedures
state or local governments for EMCC precludes or
must be taken. Vaccination with even standard
reduces training time. Among the ventilators purchased
influenza vaccines is prudent until a specific
by state and local governments are the Viasys-Pulmo-
vaccine can be developed, manufactured, and
netics LTV 1200 and the Versamed iVent. Both are
distributed.
excellent volume-pressure-cycled ventilators with PEEP
• Treating the cytokine storm requires 200 mg
and oxygen options and an internal battery with about
hydrocortisone, 10 mg chlorpheniramine,
1 hour’s worth of use. However, both require annual
0.5–3.0 mg metaraminol in divided doses and
servicing by company-certified technicians, mandatory
titrated for effect, and 1 gm acetaminophen—all
battery recharge, and temperature-humidity-controlled
intravenously.
storage.76
• In previous cases, neither bronchospasm nor
The federal government’s emergency National
laryngeal edema was evident; therefore broncho-
Strategic Stockpile Push Packs are 2-ton preloaded
dilators may not be necessary. If they become
and prepositioned supply containers of medicines,
necessary, then minimize the use of aerosol.
equipment, and ventilators (no oxygen) that can be
Consider the use of MDI with a spacer, even with
at a site within 12 hours of an emergency. Push
mechanical ventilators. Nebulized particles of
Packs include the LP-10 and the Impact Eagle754
less than 5 microns remain suspended in the
transport ventilator which, while easy to operate,
breathing environment for a considerable period
still requires in-service education that must be
of time.
accomplished prior to a disaster of either natural
• In SARS and in some Avian flu cases, patients
causes or of human intent. The Eagle754 is a touch
responded to bilevel pressure with supplemental
screen operation ventilator with internal battery
oxygen. However, there are concerns for the virus
(rechargeable) and compressor; it is therefore ideal
being spread via the patient’s exhalate.
for emergency situations. With an automatic pressure
Mechanical ventilation of patients should fall transducer, the 754 can support patients to an
under the ARDSnet recommendations because the altitude of 25,000 feet. It is approved for use with
P/F ratios will be in the ALI (⬍300) or ARDS (⬍200) adults and pediatric patients, including infants.
range. Ventilation with tidal volumes of 6 ml/kg PBW Additionally, the Impact Eagle provides the intensive
using assist-control mode is a good starting point. care–level of mechanical ventilation that nurses,
PEEP levels are conventionally 5–12 cm H2O; however, respiratory therapists, and intensivists have come to
the positive effects of PEEP on oxygenation (PaO2, expect from their ventilators: alarms and graphics
SbO2, and CaO2) must be weighed against the negative display.77
effects on blood pressure and cardiovascular func- Medicine and respiratory care in particular are
tion.74 “Drying” the lung with conservative fluid constantly evolving sciences with new research and
administration and aggressive use of diuretics and/or clinical experience that constantly broaden knowledge,
dialysis has been shown to help reduce the duration of skills, and pharmacologic treatment. They require
mechanical ventilation in ARDS patients.75 respiratory therapists to maintain and update their
knowledge and proficiency. The reader is strongly
encouraged to confirm information contained in this
Summary chapter for updates, evidence-based studies, and
Disasters of any cause or size require a coordinated, clinical competencies.
prepared response if both the victims and the hospital
are to survive. The NIMS and the hospital’s ICS are the
command and control elements of disaster response. Study Questions
Most disasters are Tier 1 and can be managed by
REVIEW QUESTIONS
prepared and drilled staff.
Standard Precautions, aerosol protection, and 1. What is the difference between a natural and a
patient decontamination are more important in an human-made disaster?
2. List at least five biological and five chemical agents 7. Victims of HE who are 3 m from the explosion are
that can be used in a terrorist attack and the likely to suffer which of the following injuries?
physiological effects that each produces. a. TBI, pneumothorax, bronchopleural fistulas,
3. What is the role of the respiratory therapist on a and acute gas embolism
disaster response team? b. mold, bacterial, and fungal infections
c. hypobaric or decompression injuries
d. none of these
MULTIPLE-CHOICE QUESTIONS 8. A large number of people have been seeking care in
1. Several adult victims of a cyanide terrorist your hospital for Guillian-Barré syndrome (GBS).
attack have MetHb levels of greater than 35%. What may be occurring?
Which of the following is the best treatment a. an unusual outbreak of the disease
option? b. the effect of the flu vaccination program
a. Administer 100% oxygen via bilevel c. a bioterror event, not GBS
pressure 4/8. d. a mass hysteria event
b. Administer a half dose of sodium nitrate and 9. Several ED patients report the symptoms of blurred
sodium thiosulfate. vision and difficulty with speaking, enunciating,
c. Administer vitamin B12 intravenously. and swallowing. What do their symptoms suggest?
d. Administer methylene blue IV until MetHb is a. botulinum intoxication
less than 30%. b. cyanide intoxication
2. Primary blast injuries are the result of which of the c. myasthenia gravis crisis
following? d. food poisoning with salmonella
a. shrapnel or suicide bomber’s body parts 10. Twenty patients from this morning’s commuter
causing penetrating injuries train are in your ED. They exhibit tearing, rhinor-
b. violent pressure wave of HE rhea, drooling, and excessive productive cough.
c. burns or crush injuries from explosions Several are vomiting. On examination, they have
d. blast victim being thrown by the blast wave pinpoint pupils, wheezing, and low heart rates.
3. The most important practice to reduce the What do their symptoms suggest?
transmission of infectious agents is: a. pandemic influenza outbreak
a. hand hygiene. b. bioterrorist use of tularemia
b. use of ultraviolet lights. c. terrorist use of a nerve agent
c. HVAC with 6 to 10 air exchanges per hour. d. terrorist use of a blister or vesicant agent
d. use of N-95 masks.
4. The care of a patient with inhalation anthrax CRITICAL-THINKING QUESTIONS
requires the use of:
a. droplet precautions. 1. What can the respiratory therapist do to assure that
b. Standard Precautions. culturally sensitive situations can be avoided even
c. biohazard level IV controls. during a mass casualty event?
d. cidofovir aerosol. 2. What is the role of the respiratory therapist in a
5. In a mass casualty incident (MCI), which of the dual-agent bioterror attack?
following are the major concerns of the respiratory 3. What actions can the nurse–respiratory therapist
care service? perform to successfully manage pediatric casualties
a. oxygen therapy supplies and mechanical of a disaster?
ventilators 4. What are the difficulties to be expected with the
b. a stockpile of gowns, masks, and gloves pregnant/elderly/disabled/chronically ill in a mass
c. a stockpile of aerosol bronchodilators casualty incident?
d. cancellation of elective surgery and PFTs
6. While crush injuries are common in earthquakes,
for what type of pathologies must a respiratory
therapist prepare?
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handle.dtic.mil/100.2/ADA424230 .apgea.army.mil
77. Impact Instrumentation, Inc. http://www U.S. Public Health Service Office of Emergency
.impactinstrumentation.com Preparedness. www.ndms.dhhs.gov
CHAPTER 33
Adult Critical Care

Ken D. Hargett and Joy Kraus Hargett
OBJECTIVES
• Identify assessment criteria for patients entering into a critical care unit.
• Understand admission and severity scoring guidelines utilized for patient assessment.
• Understand the role of the respiratory therapist in the critical care unit.
• Understand the opportunities for respiratory care involvement in the critical care unit.
• List special procedures that affect the care of the patient in the critical care unit.
CHAPTER OUTLINE
Entry of the Patient into the Critical Care System Multidisciplinary Competencies
Assessment and Stabilization of the Patient Shared Policies and Procedures
Unit Admission and Severity Scoring Guidelines Critical Paths
Establishing Appropriate Respiratory Care Cost Containment Ideas
Detailed Assessments Information Systems, Data Management, and
Intensive Care Unit Design and Function Computerized Patient Records
Department Organization Management of the ICU Patient
Personnel Considerations Surgical Considerations
Tools for Success in the Intensive Care Unit Medical Considerations
Clinical Practice Guidelines Cardiovascular Considerations
Therapist-Driven Protocols Renal Considerations
Quality Improvement Activities Neurological or Neuromuscular Considerations
KEY TERMS
care plans critical paths severity scoring guideline
clinical practice guidelines multidisciplinary competencies therapist-driven protocol (TDP)
918
CHAPTER 33 ■ Adult Critical Care 919
T
he arena of critical care medicine is an ever In the initial patient assessment, the respiratory
changing specialty, particularly as it relates to therapist must quickly ensure that the patient is being
respiratory care. As technology continues to treated safely. For example, patients who have been
advance and research provides new alterna- received from the operating room must be evaluated
tives to treatment, respiratory therapists (RTs) must be for the return of normal vital signs and, if they are not
prepared to always be improving their care and acting present, supported with the appropriate interventions
as an integral part of the patient care team. This chapter until normal vital signs return. Patients appearing with
evaluates the expectations of the respiratory therapist a depressed respiratory rate or tidal volume should be
who is assigned to work with adult patients in critical evaluated for mechanical ventilation via invasive or
care. This chapter reviews: noninvasive means.
Appropriate respiratory care should always be
• The assessment of patients admitted to the
assessed upon the patient’s entry into the critical care
critical care area, the monitoring of them during
unit. The basic components of a respiratory assessment
their stays in the critical care unit, and the variety
are:
of special procedures performed in that unit.
• Intensive care unit (ICU) design and function, to • Vital signs (heart rate, respiratory rate, pulse
give the respiratory care department members oximetry).
ideas and information on which to base their • Breathing pattern [depth of respirations, chest
activities as fully integrated players on the movement (symmetrical/asymmetrical), breath
ICU-oriented health care team. sounds].
• Tools that assist respiratory therapists or respira- • Skin color.
tory care departments to provide value to the
intensive care unit.
• The various body system functions that affect the
patient’s care and that have implications for CASE STUDY 33-1
respiratory therapists and the care they render.
Note: In this chapter, the terms “critical care unit,” C. C. is a 72-year-old, 70-kg male brought to the
“intensive care unit,” and “ICU” are used synonymously. ICU postcoronary artery bypass surgery. He was
still heavily sedated with a propofol drip and
placed on mechanical ventilation in the SIMV
Entry of the Patient into the mode with a rate of 10, tidal volume 700 cc,
Critical Care System FIO2 0.6, pressure support of 5 cm H2O, and
A patient entering the critical care unit of a hospital is a PEEP of 5 cm H2O. The patient has a history of
common but still tense situation for the health care COPD. Bedside report from the anesthesiologist
provider, whether one is a novice or a seasoned caregiver. indicated that the patient was slightly fluid
Good critical thinking skills, judgment, and experience overloaded with bounding pulses, as evidenced
are important qualities for the health care provider, by a prominent PMI on the chest.
including the respiratory therapist, to have in order to be An immediate ventilator check shows the
successful in caring for the critical care patient. following:
Exhaled VT 675 cc
PIP 32 cm H2O
ASSESSMENT AND STABILIZATION PEEP 5 cm H2O
OF THE PATIENT Flow 70 Lpm
Assessment of the patient entering the critical care Total rate 30
system is essential to providing the right care, regardless Sensitivity 1
of patient origination: Spontaneous rate 20
Spontaneous exhaled volume 50 cc
• The emergency department.
• Surgery (which includes planned or unplanned Questions
surgical procedures). 1. How would the RT determine whether the
• Other diagnostic or treatment procedures ventilator is autocycling?
(cardiac catheterization laboratory, noninvasive 2. What is the most likely cause of the auto-
cardiology, chemotherapy, or radiation proce- cycling?
dures, etc.).
• Current hospital patients with worsening health 3. How would the RT correct the autocycling?
conditions.
• Level of consciousness. • The SOFA score utilizes the evaluation of 6

• Airway status. systems (respiratory, cardiovascular, hepatic,
• Cardiovascular status. coagulation, renal, and neurologic) to predict
the probability of mortality.1
This rapid initial assessment ensures the respira-
tory therapist that the patient is safe and that Regardless of the systems used, the intent is to quanti-
immediate needs are addressed as the patient settles tate the severity of illness.2
into the unit, detailed assessments (discussed later Although these systems may work well for deter-
in this chapter) require more time but allow the mining nursing ratios, they may not be well suited for
respiratory therapist to develop the most appropriate respiratory care departments in determining therapist-
care plan. to-patient ratios. Many respiratory care departments
have developed a numerical type of rating system that
counts the numbers of tasks that the respiratory
UNIT ADMISSION AND SEVERITY therapist has to perform. The RT is then assigned
SCORING GUIDELINES work based on the number of tasks that can be com-
pleted in a given time period.
Usually, a patient is admitted to an intensive care As is the case in many hospitals, respiratory
unit because of the ICU’s advanced technology or therapists may be assigned to take care of several
specialty care capability. Some institutions have critically ill patients in one area. In some cases,
criteria to determine whether a patient should be critically ill patients may require less respiratory
admitted into the intensive care unit or to ascertain care intervention than more stable intensive care
the patient’s acuity level. These rating systems may patients. This does not preclude the possibility that
be foreign to respiratory therapists because this a very unstable patient may require the extensive
practice is not often used in determining respiratory involvement of both the nurse and the respiratory
care workloads. The rating systems may be in the therapist to be stabilized. The degree of RT involve-
form of a severity scoring guideline or severity ment therefore depends on the types of services
rate scale, which evaluates the level of care required provided by the respiratory care department. For
for the patient and to determine the nurse-to- example, if the respiratory care department is
patient ratio or how many patients the nurses responsible for hemodynamic monitoring, blood
may care for. gas sampling, blood gas and electrolyte analysis,
Several rating systems have been developed and and advanced airway care procedures (intubations,
studied for their effectiveness. Scoring systems are tracheostomy tube changes, etc.), the therapists may
commonly used in research protocols to validate the be more involved with higher-level tasks than those
equality of patient populations or as predictors of working for departments that do not provide such
outcomes. For the general adult ICU patient, severity services. Stable intensive care patients being weaned
scoring systems are available: from the mechanical ventilator generally require
• Simplified Acute Physiology Score (SAPS) more RT involvement in such procedures as ventila-
• Acute Physiology and Chronic Health Evaluation tor weaning or discontinuance, airway management,
(APACHE) and psychological support and encouragement.
• Sequential Organ Failure Assessment (SOFA)
• Mortality Probability Model (MPM)
Other systems are available for pediatrics, cardiac ESTABLISHING APPROPRIATE
surgery, or trauma patients. RESPIRATORY CARE
Some of the commonly used systems are as To support the patient in the recovery process, it is
follows: important to establish the appropriate respiratory care
for patients as soon as possible after admission into
• A very common public domain rating scale, the
the critical care unit. Often, respiratory therapists who
APACHE II system, evaluates 12 physiological
work in the ICU have very busy days, providing many
variables (APS) and determines outcomes based
levels of care to patients. Day-to-day respiratory care
on an evaluation of the patient’s health status.
duties include basic respiratory care procedures,
Each of these parameters has a rated score
such as:
based on the degree of deviation from
normal physiological values. The total score • Oxygen administration.
indicates the severity of illness or acuity of • Aerosolized medication therapy.
the patient. • Other treatment modalities, such as chest
• The APACHE III and IV are proprietary versions physical therapy, intrapulmonary percussive
and have more parameters. ventilation, and incentive spirometry.
More advanced respiratory care procedures may

include:
• Mechanical ventilation (including assessments
made for weaning).
• Physiological monitoring (pulse oximetry,
end-tidal CO2 monitoring, invasive and nonin-
vasive hemodynamic monitoring).
• Specialized procedures (ventilator patient
transports, tracheostomy care, airway care,
metabolic monitoring, invasive blood gas and
electrolyte monitoring, blood gas punctures, and
analysis).
Because these duties require expertise and adequate
time to perform, therapists need support in determin-
ing the appropriate care for patients.
Patient care plans are useful tools in establishing
appropriate respiratory care. They are used in many
circumstances, and the respiratory care world should be
no exception. Whether written or computerized, care
plans help therapists organize the shift, so that, on any
given day, they know what each patient requires, as
well as which practitioners will take care of the patient
during the patient’s stay in the ICU.
• Care plans can be general or specific. For exam-
ple, a general care plan for ventilated patients can
be utilized throughout many intensive care
units. However, specific criteria can be included
for the patient’s particular disease process.
• Care plans can incorporate protocols (discussed
later in the chapter).
• The information on the care plan should take
into consideration the direction that the medical
staff or physician feels the patient is moving
toward.
• Care plans can be incorporated into documenta-
tion that therapists already provide, such as a
ventilator flow sheet (Figure 33-1).
As the patient’s stay in the intensive care unit
continues, therapists should be aware of the long-term
goals of the medical plan established for the patient. A
Best Practice
Department Standards
Departments should develop standards for
determining the appropriate assignment of daily
activities for the respiratory therapist based on
the number of interventions that the therapist

has to make with the patients. The departments
should also have provisions for immediate adjust-
ments of workload to ensure appropriate coverage
of needed patient care.
FIGURE 33-1 Care plan incorporated into ventilator flow sheet.
thorough review of the medical record is essential. This should be able to recognize immediate problems
review should include physician orders, history and (incorrect tube placement, pneumothorax, lung
physical examination, nurses’ notes, and diagnostic consolidation, etc.). Respiratory therapists must
findings. These care plans can guide the respiratory become skilled at identifying straightforward but
therapist in determining the type of care activities important medical conditions.3 With good critical
required by the patient and enable the practitioner to thinking skills, RTs can relate the patient’s symptoms
progress the patient through the process in an orga- with CXR findings to determine problematic situations.
nized fashion. This is an invaluable service in medical treatment and
Documentation on a critical care flow sheet for patient outcome.
mechanical ventilation is essential in providing infor-
mation to respiratory therapists, physicians, nurses, and Acid-Base Balance. The arterial blood gas is essential
other health care providers, whether for the current in the diagnosis and treatment of oxygenation and
management of the patient or for use in quality acid-base balance. The respiratory therapist is the ideal
enhancement projects. A ventilator flow sheet, which health professional to evaluate a patient’s acid-base
includes the care plan, minimizes document duplica- balance and to be the expert in arterial blood gas
tion. Ventilator flow sheets, along with other types of punctures, arterial blood gas analysis and quality
medical record documentation, can be computerized, control, and acid-base interpretation. Many of the skills
thus enhancing communication and accessibility to needed are taught extensively in respiratory care
patient information by a number of health care education programs throughout the country. Respira-
professionals. tory therapists have authored several textbooks on
acid-base balance and arterial blood gases. A survey of
respiratory care departments in 1992 showed that 83%
DETAILED ASSESSMENTS
of respiratory care departments provided blood gas
Respiratory therapists can offer their expertise to analysis.4 Acid-base and arterial blood gases are
enhance patient care in several ways, such as: discussed in Chapter 16.
• Assessment of chest X-rays (CXR).
• Acid-base balance. Readiness to Wean. The respiratory therapist is the
• Readiness for weaning. best practitioner for determining a patient’s readiness
• Metabolic monitoring. for weaning. The therapist’s daily duties in the inten-
sive care unit are directly related:
Chest X-Rays. CXRs are one of the most useful clinical • Mechanical ventilation
assessment tools available in the intensive care unit. • Pulmonary function testing
Few bedside caregivers, with the exception of the • Pulmonary mechanics
physician, are as adept in reviewing radiological • Airway care such as suctioning or tracheostomy
findings found on the CXR as the respiratory therapist. care
As a bedside caregiver in the unit, the therapist should • Aerosolized medication treatments
be one of the first individuals to view the CXR and • Weaning trials
Often during these procedures, the therapist assesses
Best Practice the patient’s status and documents the observations.
This documentation, like the ventilator flow sheet, can
assist the respiratory therapist in determining the
Ventilator Flow Sheets weaning activities that are beneficial to the patient.
Ventilator flow sheets should be more than a
place to record ventilator settings. The flow sheet Metabolic Monitoring: Nutritional Assessment.
should be the resource where the patient status Patients in the ICU, especially mechanically ventilated
is reviewed and on which the results of various patients, are at risk for malnutrition. Many of the
indicators of the patient’s respiratory status can clinical conditions that present in the ICU cause
be recorded for reference. A well designed flow numerous disturbances in the normal metabolism.
sheet can facilitate weaning or document the Clinicians in the ICU often find it difficult to determine
failure to progress. When properly used, the flow the correct amount and type of nutrients that patients
sheet can help maintain the continuity of care need during their clinical course.
from shift to shift and assist in the implementa- The relationship of improper feeding with poor
tion of protocols. Documentation is also a key outcomes, such as increased length of stay, mortality,
safeguard in the event of a legal question. and morbidity, have been reported in numerous
articles.5 The effect of poor nutritional status on a
patient’s ability to wean from mechanical ventilation elective surgery, trauma, and burns, have all been shown
has also been reported.6 With the continued develop- to increase metabolic demand by as much as 150%.
ment of accurate bedside instruments, more and more Sepsis also increases metabolism by as much as 200%.7
ICUs have started programs in nutritional assessment Daily activities in the ICU also have a significant effect on
to guide the feeding of most patients. caloric requirements.
Typically, the caloric requirements of a patient are The Harris-Benedict equation, developed in 1919,
calculated by means of the Harris-Benedict equation. has been shown to be very inaccurate in determining
For men, the equation is: the actual patient’s requirements. Hess and colleagues
66.5 ⫹ (13.75 ⫻ weight) ⫹ (5.003 ⫻ height) reported that the actual measured requirements of a
⫺ (6.775 ⫻ age) specific patient population were as much as 60%
greater than the calculation.8 Other studies have
For women, it is: indicated that the calculated value is very inaccurate in
655.1 ⫹ (9.563 ⫻ weight) ⫹ (1.85 ⫻ height) specific patient conditions.9 The incorrect use of the
⫺ (4.67 ⫻ age) Harris-Benedict equation often results in severe under-
or overfeeding of the patient.
These formulas are used to approximate the patient’s Malnourishment of the ventilated patient has
daily requirement in kilocalories (Kcal) per 24 hours. significant consequences.
A patient’s clinical condition is then taken into account
to adjust the calculation. Many clinical factors, such as • Underfeeding results in the patient’s inability to
generate adequate diaphragm strength to sustain
respiration. Table 33-1 indicates the possible
CASE STUDY 33-2 consequences to underfeeding the ventilated
patient in the ICU.
E. H. is a 40-year-old female 15 days post-MVA • In addition, an increase in infections, particu-
with a closed head injury and resolved lung larly pneumonia, is seen in patients who are
contusion. She was trached at day 10 and inadequately nourished.
remains in a coma on ventilatory support. A size
Overfeeding, especially with a high carbohydrate
8 Shiley low-pressure disposable inner cannula
formula, results in the production of excessive amounts
tracheostomy tube is in place. She is on SIMV of
of carbon dioxide. Excess carbon dioxide production,
8, pressure support of 15, FIO2 of 0.3, and PEEP
especially in COPD patients who are already suscep-
of 5 cm H2O.
tible to CO2 retention, makes weaning from the
The therapist in the neurosurgery unit who is
ventilator difficult.
going off duty tells the incoming RT that he has
The following lists show the hazards associated
just completed suctioning and trach care on Ms.
with overfeeding and underfeeding the ventilated
H. The new RT is called to the room by the nurse
patient. The possible hazards of overfeeding are:
because of a continuous ventilator alarm. The
alarms that are activated are the low-pressure • Increased CO2 production.
disconnect, the low exhaled tidal volume, and • An increase in the necessary level of ventilator
the low exhaled minute volume alarm. The support.
patient has a pulse oximeter reading of 84% and • A potential increase in incidence of barotraumas.
a falling heart rate. • An increase in the work of breathing.
Questions
1. What are the possible causes of the alarms? TABLE 33-1 Respiratory quotient
2. What is the first action the RT should take?
RQ ⬎ 1.00 Lipogenesis or hyperventilation
3. If adequate ventilation cannot be restored
RQ 0.90 Primary carbohydrate oxidation
through the tracheostomy tube, what actions
should be taken? RQ 0.85 Fat, protein, and CHO oxidation
RQ 0.80 Primary protein oxidation
RQ 0.70 Primary fat oxidation
Best Practice RQ ⬍ 0.70 Ketogenesis, alcohol oxidation
The value of the measured respiratory quotient is
All alarms should be responded to immediately. indicative of the substrates being metabolized.
There is no such thing as a “false alarm.” Generally, an RQ of ⬎ 1 indicates overfeeding and an
RQ ⬍ 0.70 indicates starvation.
The possible respiratory consequences of malnutrition been used to determine both oxygen consumption
are: during various modes of mechanical ventilation and
oxygen delivery.11,12
• Diaphragm and other muscle weakness.
• Impaired response to hypoxemia and
hypercarbia.
• An increase in respiratory infections. Intensive Care Unit Design
• An increase in atelectasis. and Function
• A decrease in weaning capabilities.
• An increased chance of pulmonary edema. The ICU is structured to provide a higher level of
management and surveillance than the normal floor
Metabolic monitoring is accomplished with an patient receives. ICUs may be open, closed, or
instrument called an indirect calorimeter. Several comanaged.
versions are on the market. The device consists of:
• Open units have all qualified staff physicians
• A high-speed, very accurate oxygen analyzer. admit and care for their patients, with consults
• A volume measuring device. only as requested. The primary care/admitting
• And a carbon dioxide analyzer. physician directs the care to their patients. A
The device measures oxygen consumption (V⭈O2) and medical director or ICU team may handle such
CO2 production. From these values the respiratory issues as triage decisions due to increased census
quotient can be calculated. or decreased staff availability.
• In a closed unit, the medical director and ICU team
CO2 Produced are responsible for the admission, discharge, and
Respiratory Quotient ⫽ _________________
Oxygen Consumed total care of the patient. Care for the patients is
formally turned over to the medical director and
The normal values are a CO2 production of 200 mL/min associates, who assume responsibility.
and an oxygen consumption of 250 mL/min. This gives • A comanaged unit is a blend that allows the
us a normal RQ (respiratory quotient) of 0.8. The RQ primary care physician to utilize the ICU physi-
is related to the amounts of fat and carbohydrate that cian team to assist in the management of the
are being metabolized by the patient. Table 33-1 shows patient.
the substrates that are mostly metabolized by the
patient at various measured RQs. A recent movement has been for patients in the ICU to
If the nitrogen excretion is known from a 24-hour be managed by physicians with specialized training.
urine sample, then the actual caloric requirement of These board-certified intensivists may have medical,
the patient can be calculated by means of the Weir surgical, or anesthesia backgrounds. Organizations like
formula. The resting energy expenditure (REE) is com- the Leapfrog Group, which is a consortium of insur-
puted, utilizing the oxygen consumption (V⭈O2), the ance purchasers, recommend intensivist coverage for all
carbon dioxide production (V⭈CO2), and the urinary ICUs.13 However, recent data support that the closed
nitrogen (UN), as follows: unit model results in better outcomes and reduced
mortality.14
REE (kcal/24 hours) ⫽ [3.94(VO2) ⫹ 1.1(VCO2)] A number of characteristics make an ICU functional.
⫻ 1.44 ⫺ 2.17(UN)
• The care should be multidisciplinary, and
As denoted by its name (resting energy expendi- teamwork is highly important.
ture), REE requires that the patient is at rest for the • Caregivers should work in a coordinated manner
monitoring period, which usually requires about to ensure the best possible care.
20 minutes. Another important aspect of obtaining • The unit must be able to support a wide range of
accurate results is that the patient must reach a condi- medical issues, including mechanisms to treat
tion called steady state. This is the period during the ventilatory, circulatory, renal, gastrointestinal,
data collection when oxygen consumption becomes hematological, and neurological failure.
stable, indicating that a patient’s minimal activity level • There should be appropriate monitoring and
and ensuring that the accurate collection of all exhaled supportive equipment.
gas can be made. • Administrative, technical, and clerical support
Many benefits have been derived from well imple- are necessary.
mented metabolic monitoring programs. Decreased • On-going training and quality monitoring are
length of stay and decreased utilization of very expen- essential.
sive hyperalimentation and enteral feedings have been • The medical staff should provide coverage 24 hours
demonstrated.10 Additionally, metabolic monitors have per day, whether directly or in a consulting role.
With respect to this last point, telemedicine, or the while placing key practitioners in specific areas. Besides
utilization of long-distance physician coverage, is excellent clinical and critical thinking skills, respiratory
utilized in some hospitals. Telemedicine physicians therapists who are successful in the ICU environment
provide consults to the physician staff at a time when have the following qualities:
an attending physician may not be on site. This tool
• Rapport with other health care providers.
can provide intensive care expertise in hospitals where
• Eagerness to work in the area.
services are limited, such as in some rural locales. It
• Eagerness to take on new projects. Willingness to
may also provide access to new or developing medical
learn.
fields where expertise is limited. In some institutions,
• Compassion and empathy for the patients.
residents may provide some of the coverage. Nurse-to-
patient ratios should be developed according to Some institutions with centralized respiratory care
standards or needs. departments choose to provide a unit-based practitio-
ner model, in which a select number of practitioners
are permanently or semipermanently assigned to a
DEPARTMENT ORGANIZATION specific ICU. This is similar to respiratory therapists
The respiratory care department must take an active who work directly for the ICU, such as in a hospital
role in the new health care environment and provide with a decentralized department. In a model utilized at
customer-focused patient care.15 The respiratory care St. Luke’s Episcopal Hospital in Houston, Texas,
department should be organized so that respiratory therapists are assigned to work zones to a particular
therapists are involved in the direct day-to-day patient “zone,” or area of the hospital, for a given number of
care activities (previously discussed in the chapter), as weeks or months. The zone may be an acute care floor
well as other projects. or ICU. The therapist works in the zone for that time
Depending on the department structure and on period. Respiratory therapists are effective in the
fluctuations in the day-to-day respiratory care activity, various work areas based on:
some respiratory therapists may provide high-level
• Their clinical skills (decision making and critical
activities. These employees may hold titles such as
thinking).
clinical respiratory care supervisors, clinical respiratory
• Their rapport with other health care providers
care specialists, or respiratory care liaisons. Whatever
(nurses, physicians).
the title, placing highly trained therapists with excellent
• Their desire to work in the area.
critical thinking skills in key positions helps the
• The contributions they are able to make.
department prove its worth. These activities can
• Their interdependence with other bedside
include:
clinicians.13
• Patient care rounds with physicians or other
Another model, used at The Methodist Hospital
multidisciplinary groups.
in Houston, Texas, places department therapists in a
• Discharge planning rounds.
service line structure. Therapists may work for the
• Development of care plans.
medicine or surgical service line, but all therapists work
• Respiratory therapy education and competency
under a centralized respiratory care department. The
verification.
therapists in the service line work both on the floors
• Resident or medical student teaching.
and in the ICUs where those patients are housed;
• Patient and family education.
however, they work primarily in the service line to
which they are assigned.
PERSONNEL CONSIDERATIONS Depending on the duties and functions of the
respiratory therapy department, some specialty areas
Personnel orientation and training are essential to the
such as a cardiovascular recovery room or pulmonary
success of the respiratory therapist in the critical care
ICU, may have therapists zoned in the area for more
unit. In some institutions, therapists may work only in
than their designated time frames or permanently.
intensive care units, some may rotate between the acute
Utilizing a zoned approach requires the department
care areas and the intensive care units, while others
to establish rotation time frames that work best for
work strictly in acute areas. Depending on the size of
them.
the institution and the number of critical care areas
Following are advantages of zoning respiratory
available, the appropriate number of staff have to be
therapists:
trained. Some institutions have many intensive care
units that may be similar or dissimilar in nature. The • Uniformity in day-to-day patient care
organization of the department should allow for • Completion of research or educational projects
cross-training of therapists throughout all work areas specific to that unit
• Expertise in specific competencies required for quality and provide value to the institution. Because of
the area the educational training development received by
• Rapport with other members of the health care respiratory therapists, they are an ideal caregiver to take
team assigned to the unit on high-level tasks. Their cross-training into nursing
• Familiarity with the patients who remain in the roles and nurses into traditional therapists’ roles can
unit for a length of time maximize services provided for the patient.
In many institutions, the number of respiratory
Rotation out of the area, however, is essential to
therapists employed is greatly less than the number of
provide sufficient staff coverage in times of vacation or
nurses employed. Also, respiratory therapists assigned
illness or to give primary respiratory therapists the
to the critical care area might not always be matched
chance to work in other areas of the system in response
to the number of nurses. Some suggestions on cross-
to their request or to departmental needs. Rotating
training follow, tailored for adult intensive care
unfamiliar people to an area new to them may cause
circumstances:17
stress; however, this can be alleviated with a good
orientation program or an opportunity to work in the Respiratory Therapist Only
area on a regular or occasional basis.
Therapists can also provide clinical leadership • Respiratory management of mechanically
activities owing to their educational training. Due to ventilated patients
their scientific background, RTs are the logical caregiv- • CPAP, IPPB
ers to become experts in: • Arterial puncture
• Arterial line insertions
• Modes of ventilation. • Aerosolized medication delivery to mechanically
• Alternative gas therapy (nitric oxide, heliox). ventilated patients
• Permissive hypercapnia. • Endotracheal intubation
• Prevention of ventilator-associated pneumonia • Intrahospital transport of ventilated patients
and acute lung injury. • Administration of exotic gases and drugs by
• Tracheal gas insufflation.16 inhalation: nitric oxide, heliox, surfactant,
• Ventilator graphical analysis.17 ribavirin
Respiratory therapists are certainly the experts in • Continuous inhaled bronchodilators
the areas of oxygen therapy, aerosol therapy, pulse • Bronchoscopy assist
oximetry, and mechanical ventilator management. In • Indirect calorimetry
these modalities, respiratory therapists can be the
Shared Cross-Training (Respiratory Therapist
educators of other health care professionals. Though
and Registered Nurse)
fairly mundane to the respiratory therapist, simple
respiratory care must often be taught to nurses and • Assisting with insertion of chest tubes, central
physicians. This may be in the form of formal cross- lines, arterial lines, intubations and extubations,
training programs or simple in-service educational tracheostomies
classes. • Pulmonary assessment
Respiratory therapists may also add value by • Phlebotomy
contributing to formal educational training programs • Cardiac output determination
that are attended by nurses and physicians preparing • Aerosolized medication delivery to nonmechani-
for advanced credentials. Intensive care nurses may cally ventilated patients
prepare for such specialty examinations as the CCRN • Suctioning
(critical care registered nurse) examination. This • Chest physical therapy
examination encompasses a large number of respira- • Weaning
tory and pulmonary questions. The respiratory thera- • CVVH and CVVHD
pist is the ideal person to teach pulmonary anatomy • 12-lead ECG
and physiology, acid-base balance, pulmonary func- • IV starts
tion, and respiratory care procedures. Therapists can • Troubleshooting biomedical equipment
offer these types of services to physicians, medical (e.g., monitors, ECG machines)
students, and residents. Respiratory therapists can also • IABP
serve as instructors for classes and coordinate advanced • Oxygen setup
cardiac life support (ACLS) programs. • ECLS
The cross-training of therapists in traditional • Cuff pressures
nursing duties may be an option at some institutions. • Vital signs
However, new roles should be ones that enhance • Baths
Registered Nurse Only Successful TDP implementation takes its cue from the
use of AARC clinical practice guidelines.
• Admissions
By utilizing the CPGs, a best practice model can be
• Blood and medication administration
developed. However, best practice may require institu-
tions to individually assess programs for success,
Tools for Success in the Intensive because sometimes research shows that the same
outcomes can be based on different approaches. For
Care Unit example, in 1994 and 1995, two landmark articles on
A variety of tools are available to ensure that the the gradual withdrawal of mechanical ventilator
respiratory therapist can be a welcomed addition to the support appeared in the literature.19,20 These tech-
health care team in the ICU. niques were different from each other, each showing an
effective weaning technique. Because conflicts are seen
in the literature from time to time, institutions may
CLINICAL PRACTICE GUIDELINES need to establish their own best practice model that fits
Policies and procedures, developed by the respiratory well into their organization with its specific patient
care department or by the critical care unit, should population.
guide departments in establishing appropriate respira- A source for clinical practice guidelines from the
tory care activities. A good starting place in the devel- AARC is available from the Respiratory Care Journal Web
opment of the appropriate policies is in the use of the site (www.rcjournal.com). These guidelines and those
clinical practice guidelines (CPGs). CPGs used in from related health care organizations have been
respiratory care were developed under the direction of organized into one Internet Web site: the National
the American Association for Respiratory Care (AARC) Guideline Clearinghouse. These guidelines were also
and are based on scientific research and levels of published in the Federal Register on April 13, 1998.21
evidence. Evidence-based medicine is essential in Due to the number of guidelines available (more than
providing appropriate care to patients. Research and 500 as of October 1999), respiratory therapists now
publications are graded according to the level of have access to guidelines that have been established by
evidence they represent. other professional organizations.
• Level I is a double-blinded placebo-controlled,
multicenter trial. QUALITY IMPROVEMENT ACTIVITIES
• Level II is peer-reviewed nonrandomized, concur- It is increasingly imperative to balance improvements
rent or cohort investigations. in clinical effectiveness with the availability of
• Level III is peer-reviewed state-of-the-art review resources.22 Quality improvement projects are generally
articles, surveys, meta-analysis, or substantial useful in demonstrating the effects that respiratory
case series. therapists can have on patient outcomes. Such projects
• Level IV is nonpeer reviewed opinions, anec- may include, for example (discussed later in this
dotal information, or official statements of chapter):
organizations.
• Reducing hospital-acquired pneumonia and the
CPGs are employed to provide assistance to respira- implementation of ventilator bundles.
tory care departments in standardizing respiratory care • The use of ventilator weaning protocols.
procedures and in developing or refining policy and • Joint Commission preparation.
procedure. CPGs can also be used as monitors for
effectiveness of care. Standardization of care also can Respiratory care departments need to become an
provide assistance in the development of training or integral part of these types of clinical and quality
competency verification programs. These programs, improvement activities so that RT-related standards,
whether for the therapist only or for a multidisciplinary such as the CPGs, are utilized to their fullest extent.
group of health care providers, can be taught effectively Also, engaging the respiratory care departments in a
if standards of care are set up appropriately.18 quality project initiative at its very start can ensure the
department’s involvement and enhance the role of the
therapist as a patient advocate.
THERAPIST-DRIVEN PROTOCOLS
The therapist-driven protocol (TDP) can enhance Reducing Hospital-Acquired Pneumonia. Ventilator-
departmental efficiency and operation in the critical associated pneumonia (VAP) has been the focus of
care unit. The respiratory therapist–driven protocol is a hospital-associated pneumonia for some time. In 2002,
method to provide a particular service (such as oxygen the CDC’s National Nosocomial Infection Surveillance
therapy) in a predesigned algorithm or decision matrix. System (NNIS) reported VAP rates ranging from 2 to
15%, depending on the type of patient and medical

issue surrounding that patient. This results in: Best Practice
• Increased mortality rates.
• Increased length of stay and consumption of Quality Improvement
resources. Respiratory care needs to become a part of the
• Increased cost of care, estimated at approxi- solution instead a part of the problem. Integra-
mately $40,000 more for patients who acquire tion of the RC department as part of the quality
VAP compared to those who do not. improvement team lends credibility and legitimacy
to the respiratory care department as a whole.
To avoid this significant detriment to patient care,
the Institute for Healthcare Improvement (IHI) has
described components of the Ventilator Bundle, which
is aimed at preventing ventilator-associated pneumo-
on enhancements that need to occur in quality activi-
nias. According to IHI, implementing these compo-
ties, and assists in policy and procedure development.
nents together helps in achieving better outcomes for
There is a great deal of information available on the
patients. The four components are:
Joint Commission Web site (www.jointcommission.org).
• Elevation of the head of the bed.
• Daily sedation “vacations” and assessment of
extubation potential. MULTIDISCIPLINARY COMPETENCIES
• Peptic ulcer disease prophylaxis. The respiratory care department can flourish in quality
• Deep venous thrombosis prophylaxis.23,24 improvement activities. In turn, multidisciplinary
projects can enhance the performance of the depart-
ment as well as that of the intensive care unit. One
Ventilator Weaning Protocols. Ventilator weaning
such project reported was a multidisciplinary joint
protocols have been used extensively throughout the
competency program in caregiver performances in code
United States and reported in the literature.25–28 Many
blue situations.30 Although not specific to an intensive
of the ventilator weaning protocols have had a positive
care unit, this program can enhance the skill of any
effect on the reduction of intubation times, length of
practitioner. The program, initially developed by the
stay, and patient outcomes. These activities have caught
nursing service, was designed to give nurses an oppor-
the attention of the medical community, and more
tunity to practice code blue skills (beyond that of basic
medically directed ventilator weaning projects are being
CPR procedures) annually in a controlled setting.
initiated. A recent project underwritten by the Society of
Because personnel other than nurses attend code
Critical Care Medicine (SCCM), called Project Impact,
blue procedures in the hospital, other disciplines
has reported a decrease in ventilation times with
needed to be involved in the competency training as
physician-directed protocols, as compared to RN/RRT
well. Therefore, the respiratory care and pharmacy
protocols. Information on this project can be found at
departments, which participate in cardiopulmonary
the Society for Critical Care Web site (www.sccm.org).
resuscitation procedures in the hospital, were invited to
More recent approaches to ventilator weaning
join the group. The respiratory care department is
include the utilization of spontaneous breathing trials
responsible for the ACLS program coordination and
(SBTs) instead of the gradual withdrawal of ventilator
training in the hospital and could help ensure that
support. This approach has been shown to decrease the
appropriate ACLS guidelines are utilized. The special
length of mechanical ventilation. The technique
expertise of the pharmacy department on medication
involves placing all eligible patients (FIO2 ⬍ 0.6, PEEP
administration was also beneficial to the program’s
⬍8, hemodynamically stable) in a spontaneous
success. Participation of all these disciplines was
breathing mode and monitoring the rapid shallow
essential in providing a quality educational program
breathing index (RSBI). Patient pass if their RSBI stays
utilizing a team approach.
less than 105 for 30–90 minutes. If they pass, patients
Programs such as this one provide an individual
should be extubated.29
handbook to each participant, an open-book test, an
ECG test, and hands-on validation, which is monitored
Joint Commission Preparation Teams. The respiratory by instructors. The instructors are nurses, respiratory
care department can be engaged in Joint Commission therapists, and pharmacists. Respiratory therapists may
preparation at the grassroots levels. The involvement of teach essential tasks such as emergency airway manage-
respiratory therapists on the hospital core Joint Com- ment to nurses and pharmacists. Nurses or pharmacists
mission team keeps the department informed of may conduct the review for respiratory therapists on
hospital accreditation activities, provides information crash cart items.
To make revisions for the following year, after the respiratory therapists should become involved in the
annual program is complete, the team members review development of pathways, which target respiratory
the program’s strengths and weaknesses, as reported patients. Paths that involve respiratory diagnoses
by the trainers and attendees. This joint program (asthma, COPD, pneumonia, trached ventilator-
measures the competency of many individuals in an dependent patients) or patients with potential
institution and can lead to the development of pulmonary problems (postoperative patients, for
multidisciplinary competencies, which are standards example) should incorporate the AARC CPGs if
or competency verification activities that are or can be possible. One such critical path is shown in Figure 33-2.
used by multiple groups, such as nursing and respiratory Reports in the literature have shown that
care departments. Multidisciplinary competencies can therapist-driven protocols incorporated into a critical
lead to the establishment of institutional standards of path can decrease hospital cost and length of stay.32
competency verification. This activity is a great indicator Pathways may also lead to the development of order
for Joint Commission team activities. sets or standard orders, which should enhance the
One such idea for multidisciplinary competency functionality of the respiratory care department in the
verification is in the area of specimen sampling. With appropriate administration of therapy, patient billing,
the current trend toward more bedside sampling and and charge capture. An example is found in Table 33-2.
point-of-care testing, individuals need to be trained to
use new equipment, and their performance needs to be COST CONTAINMENT IDEAS
verified. Pathology departments have traditionally been
responsible for much of the laboratory testing in Cost containment efforts are essential in curtailing
hospitals and are the experts in testing. At the same costs in a very expensive health care environment. In
time, many respiratory care departments provide blood 2007, total health care spending represented 17% of
gas analysis in the hospital. These departments can be the United States gross domestic product (GDP). Total
great resources and developers of testing, training, and spending was $2.4 trillion, or nearly $8000 per per-
competencies, which have moved out of the laboratory son.33 The current climate in health care stresses that
and to the bedside. intensive care units function at high efficiency and
optimize quality while decreasing risks and expendi-
tures.2 Mechanisms to identify which patients might be
SHARED POLICIES AND PROCEDURES able to be moved through the system quickly or which
Because a variety of professionals often share many may have potential complications are keys to moving
tasks, policy and procedural activities have to be intensive care patients into more appropriate levels of
considered. If disciplines share responsibilities, such as care. These mechanisms should be in place before or at
suctioning or ABG sampling, the policy and procedures the time of admission. Multidisciplinary cooperation is
for each discipline should duplicate each other. Accredi- key to successful patient care management. For exam-
tation agencies such as the Joint Commission examine ple, one cost savings idea might be to schedule multi-
the consistency of policies between departments, and disciplinary rounds in the ICU, allowing caregivers
standards of care should be uniform throughout the from a variety of disciplines to provide input into
hospital. Working through this process may be time- progressing the patient through the system. Cost
consuming and may take a great deal of coordination, savings have also been reported by utilization of
but it is well worth the effort during surveys by accredi- respiratory care protocols.28,34
tation agencies. Having one area responsible for the Cost containment ideas can be incorporated from
content of the policy, with review from other disci- studies in the literature. According to one report, an
plines, might facilitate and ease the integration of area of consideration is the use of inhaled bronchodila-
policies. Having multiple reviewers is important to tors during mechanical ventilation.35 Cost comparisons
enhance the effectiveness of the policy and procedure have been made that evaluate the costs of utilizing a
program and to provide timely updates of information metered-dose inhaler (MDI) versus a small-volume
and expertise relative to each of the disciplines. nebulizer (SVN) therapy.35–37 However, departments
should determine their own individual costs to ascer-
tain whether this is a justified project. Individual
CRITICAL PATHS institutional costs, such as labor and cost of materials,
Critical paths, otherwise known as care paths or may vary significantly among institutions.35
pathways, can act as a consistent mechanism in which As health care institutions strive to control costs,
to treat patients with similar diagnoses. The critical reports are beginning to surface that describe the use
path, a management tool used for almost 30 years, of products beyond the suggested life of the products,
mixes clinical practices and time guidelines into a which is generally specified by the manufacturer. Some
coordinated plan for care.31 Given their expertise, health care organizations are challenging these claims
930
FIGURE 33-2 Ventilator-dependent critical path. (continues)

Courtesy of St. Luke’s Episcopal Hospital, Houston, Texas
931

TABLE 33-2 Example of standardized order sets for respiratory care services
COPD ADMISSION ORDERS—
RESPIRATORY CARE ORDERS
ABG now, if not done in ER
Pulse oximetry spot check on admission
Titrate FIO2 for O2 saturation ____%
Oxygen therapy via O2 @ ___liters per nasal cannula or O2 @ ___ % per venti-mask
Medications:
Respiratory care to assess patient for use of MDI protocol
Bronchodilators metered-dose inhaler with spacer (Please refill for take-home use.)
____Albuterol (Ventolin, Proventil) ___puffs q ___ hours
____Ipratropium (Atrovent)____ puffs q ____ hours
If patient is unable to use MDI, then handheld nebulizer with
____Albuterol 2.5 mg/3.00 NS q ___ hours while awake
____Albuterol 2.5 mg/3.00 NS q ___ hours around the clock
____Ipratropium 0.5 mg/3.00 NS q ___ hours while awake
____Ipratropium 0.5 mg/3.00 NS q ___ hours around the clock
and doing clinical studies to support their efforts. One systems (RCIS) have been in use for several years and
product under recent consideration for so-called have provided mechanisms that allow the caregiver to
off-label use is the closed system suction catheter. spend more time at the patient bedside.15 With the
Studies have been done on extending the time period RCIS, in the number of manual data entries is reduced.
between replacements beyond the manufacturer’s Respiratory therapists have reported that documenting
recommended time period.38–40 These studies describe in a clinical information system in an ICU can produce
the time extension of the change intervals, which the time savings and uniformity of charting that is not
appear to lead to no increase in ventilator-associated seen when utilizing manual charting systems.41
pneumonia rates or decrease in functionality of the The RCIS can also be used for research applications,
device. Other reports suggest that ventilator circuits productivity, and billing activities. Depending on the
may be changed at a reduced frequency without an capabilities of the health care information system, the
increase in hospital acquired pneumonia rates.40 This RCIS may be able to be integrated into the hospital
practice has been implemented in a number of institu- system. Maximizing productivity from integration of
tions throughout the country. individual systems is essential to prevent the loss of
In any event, the legal ramification of utilizing a patient information.42 Capturing ventilator data directly
product beyond its suggested life is an important from the ventilator and integrating them into a cardiac
consideration. The risk management department has to monitor or hospital information system can provide a
be contacted regarding such activities. Also, the infec- more accurate medical record, which allows review of
tion control department should offer advice on using medical care during selected time periods. This comput-
direct patient care products with a potential for infec- erized patient record is the wave of the future. It can
tious disease. Other departments where changes are improve decision-making activities, based on retrospec-
likely to have a direct effect should also be contacted, tive and concurrent data. In addition to functioning as a
such as the purchasing department, which obtains the data reporting tool, it can assist in quality monitoring,
product, or patient care supply department, which which in turn can lead to quality improvement activi-
supplies the product. ties. Computerized patient records may also improve
documentation in terms of medical-legal activities.43
INFORMATION SYSTEMS, DATA MANAGEMENT,

AND COMPUTERIZED PATIENT RECORDS Management of the ICU Patient
Information systems or data management systems are A patient in critical care has many medical needs that
playing an important role in providing timely data require vigilant monitoring and management. These
collection in the ICUs. Respiratory care information patients may have conditions that affect multiple
systems and may require medical or surgical proce- tory therapists are most often involved with specific
dures for care and treatment. pulmonary disease entities. Acute respiratory failure in
COPD patients or patients admitted in status asthmati-
cus often end up in the ICU. Often, these patients
SURGICAL CONSIDERATIONS require some type of mechanical ventilation, by either
A variety of new surgical procedures are announced in invasive or noninvasive means. Many patients who
the news daily. As new techniques and procedures are have COPD are elderly and also have special
developed, the challenge for the bedside caregivers is to age-related needs.
continue to provide the best care possible as the patient
recovers. Although providing details of the latest
surgical enhancements is beyond the scope of this CARDIOVASCULAR CONSIDERATIONS
chapter, the following considerations should be made. The heart receives oxygen via the coronary blood flow.
Due to its mechanics, the heart uses most of the oxygen
• Respiratory therapists need to pay particular
available in the coronary circulation and little reserve
attention to patients who have undergone surgical
exists. Because of this phenomenon:
procedures, owing to the possible decline in
pulmonary function.44 This decline may extend • Patients with coronary artery disease or heart
past the actual surgical procedure and be related to failure usually require supplemental oxygen
other causes, such as the delivery of anesthesia, therapy in the intensive care unit.
surgical wound dressings, postoperative pain and
analgesia, and patient immobilization. Individuals
with preexisting lung disease may be particularly
susceptible, owing to their decreased lung function, CASE STUDY 33-3
and they may require a higher level of respiratory
care than patients without lung disease.45 Critical Care Management of the
• Surgical procedures that involve the thoracic and COPD Patient
upper abdominal areas have the most significant
effect on pulmonary function and cause more S. S. is a 68-year-old male with severe COPD 2
severe respiratory complication.45 days postlung volume reduction surgery. He was
• The reason for surgery—whether planned or in the surgical ICU and had been on a PB 7200
unplanned (trauma or cardiac arrest, for ventilator since his surgery. He was hemodynami-
example)—dictates the evaluation of the patient cally stable and still has bilateral chest tubes
before surgery. Patients with existing lung disease with minimal air leak. He had been progressing
often have pulmonary function testing or other well and was being weaned off the ventilator
evaluations before surgery to enhance anesthesia from assist control to SIMV with pressure
delivery and assist in the care plan afterward. support.
The physician ordered the rate on the
Other areas to consider include: ventilator to be decreased to 6 breaths per
• Postoperative changes in lung volume. minute and to add 20 cm H2O pressure support.
• Changes in gas exchange abnormalities. Immediately after making the ventilator changes,
• Breathing patterns. the therapist noticed that the exhaled volume
• The assessment of pulmonary function, such as widely fluctuated and read much lower than
vital capacity measurements, acid-base balance, expected. The therapist also noticed that the
and breathing patterns. spontaneous breaths inspiratory time seemed
• The aggressive treatment of other complications, very long. The chest tube bubbling was now
such as aspiration, hypothermia, and hemody- much greater. The patient’s pulse oximeter
namic instability. saturations did not change, but the end-tidal
CO2 was much lower than previously.
Respiratory therapists should be adept at assess-
ment and critical thinking skills in order to manage Questions
this type of patient. 1. What is the most probable cause related to
the activation of pressure support?
MEDICAL CONSIDERATIONS 2. How can a chest tube air leak be quantified?
Equally as challenging to manage as the surgical 3. Why would the patient’s oxygenation not
patient is the medical patient. Patients can be admitted change but the end-tidal CO2 reading drop?
into the ICU for a variety of reasons; however, respira-
• After open-heart surgery, such as coronary artery NEUROLOGICAL OR NEUROMUSCULAR

bypass or heart valve replacement, patients CONSIDERATIONS
require mechanical ventilatory support and Many patients in intensive care may have disorders of
oxygen therapy after extubation until pulmonary the neurological or neuromuscular system. Spinal cord
status is normalized. trauma may result in paralysis depending on the extent
• Some patients require extensive support, such as and location of injury. Injury above the third cervical
intra-arterial balloon pump (IABP) or left segment leads to respiratory muscle paralysis and death
ventricular assist devices (LVAD) in order to unless immediate resuscitative actions (ventilation)
support the actions of the heart and may also occur.39
need advanced respiratory modalities, such as The Glasgow Coma Scale (GCS) is used to assess
mechanical ventilation.46 unconscious. This widely accepted standardized tool
assesses the level of consciousness, based on patient
responses to eye opening and verbal and motor skills.
RENAL CONSIDERATIONS The score ranges from 3 to 15, with 15 being consid-
Mechanical intervention can affect renal function and ered normal.46
fluid balance. Mechanical ventilation can cause reduc-
tions in atrial natriuretic peptide (ANP) and an
increase in plasma antidiuretic hormone (ADH), which
Summary
ultimately affect urine output and fluid retention. The critical care environment is a challenge for any
Mechanical ventilation, which decreases cardiac output caregiver. With new technologies arriving daily, keeping
and blood pressure, may cause a decrease in renal up is hard. Caregivers who accept new challenges well
perfusion, which ultimately decreases urine output.45 should survive in this environment. Respiratory
therapists are trained to function in the critical care
environment and should flourish in the setting.
Best Practice Study Questions

REVIEW QUESTIONS
Utilizing CPGs in Lung
1. What qualities are important for respiratory
Inflation Therapy therapists who desire to work in intensive care
Postoperative care may include therapies rang- units?
ing from supplemental oxygen to mechanical
2. What clinical practice guidelines address lung
ventilation. After extubation, some type of lung
inhalation techniques?
inflation therapy is usually indicated. Physi-
cian practice or preference or regional practices 3. How does an information system enhance patient
may dictate the particular type of lung inflation care?
therapy utilized in a hospital. In any event, if 4. How can respiratory therapists provide benefits to
protocols are not in place, therapist-directed the health care organization in the intensive care
protocols that address lung inflation techniques setting?
are of benefit. The AARC has developed several 5. What role do respiratory therapists play in cost
therapist-driven protocols that may benefit lung containment?
inflation. Often many surgical patients who do
not progress through the system in the expected
manner become patients with a variety of medi- MULTIPLE-CHOICE QUESTIONS
cal issues. Utilizing the following CPGs enhances
1. Which is not an advantage of zoning therapists to
best practice.
selected work areas?
• Incentive spirometry (Respiratory a. uniformity in patient care on a day-to-day
Care, 1991) basis
• Postural drainage therapy (Respiratory b. completion of research or educational projects
Care, 1991) specific to that unit
• Use of positive airway pressure adjuncts c. no expertise required in specific competencies
to bronchial hygiene therapy (Respiratory for the area
Care, 1993) d. rapport with other members of the health care
team assigned to the unit
2. Which of the following is not a feature of care plans? cardiac surgical patients. Chest. 2003;123:
a. They can guide the respiratory therapist in 1229–1239.
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3. A well designed ventilator flow sheet can do all the 5. Robinson G, Goldstein M, Levine G. Impact of
following except: nutritional status on DRG length of stay. JPEN. J
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8. Hess D, Daugherty A, Large E, Agarwal N. A
a. diaphragm and other muscle weakness.
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b. impaired response to hypoxemia and
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hypercarbia.
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c. increase in respiratory infections.
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15. Sabo J. Respiratory Care in the 1990s: Respiratory
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what every RCP should know. AARC Times. Suggested Readings
1995;19:24–29. Branson RD, Hess DR, Chatburn RL, eds. Respiratory
32. Hargett K, Meents C, Wheeler D, Hale K. Integra- Care Equipment. Philadelphia, PA: Lippincott
tion of therapist driven protocols into a critical Williams and Wilkins; 1999.
pathway: the effect on cost and reduction in length Marini J. Weaning Techniques and Protocols. Respir
of stay [abstract]. Respir Care. 1996;41:949. Care. 1995;40:233–238.
33. National Coalition on Healthcare. Health insur- Scott F. Cost cutting strategies in the ICU. Adv Manage
ance costs. www.nchc.org Respir Care. 1997;6:39–44.
34. Reid R, Evey L. Cost savings associated with Sibbald W. The “whys” and “wherefores” of measuring
implementation of a chest physiotherapy (CPT) outcomes in respiratory critical care. Respir Care.
protocol [abstract]. Respir Care. 1999;44:1265. 1998;43:1092–1098.
35. Hess D. Inhaled bronchodilators during mechani- Society of Critical Care Medicine Coalition for Critical
cal ventilation: delivery techniques, evaluation of Care Excellence. ICU Cost Reduction Practical Sugges-
response, and cost-effectiveness. Respir Care. 1994; tions and Future Considerations, Vol. 2. Mount Pros-
39:105–122. pect, IL: Society of Critical Care Medicine, 1995.
CHAPTER 34
Subacute and Long-Term Care

Kathleen S. Wyka
OBJECTIVES
• List the care elements of a subacute care program.
• List three groups of respiratory patients accepted into the subacute care setting.
• List three elements of admission for access to the subacute care setting.
• Identify four ventilators that may be used in the subacute setting.
• Identify the two accrediting agencies in subacute care.
• Identify the two tools that determine the daily rate that a subacute facility may earn from CMS.
• Define long-term care (LTC).
• Differentiate the various long-term care facilities on the basis of the patient care provided.
• Explain the reimbursement mechanism for long-term care.
CHAPTER OUTLINE
Definition of Subacute Care Weaning
Core Elements of an Ideal Subacute Care Program Discharge Planning
Accreditation and Regulation of Facilities Reimbursement
Respiratory Therapist’s Involvement in Current Practices in View of PPS
Subacute Care
Long-Term Care
Respiratory Care Acuity Levels and Modalities Long-Term Care Facilities
Patient Selection Respiratory Care Personnel
Patient Evaluation Reimbursement
Specialized Ventilator Care Facilities
KEY TERMS
assisted living length of stay (LOS) postacute care
capitated care long-term care (LTC) resource utilization group
case management managed care organizations (RUG-III)
critical pathway (MCOs) subacute care
diagnosis-related group (DRG) minimum data set (MDS)
937
I
n the past, acute care was clearly differentiated person’s underlying long-term conditions and
from long-term and home care. Patients stayed in overall situation.
the hospital until they were well enough to go Generally, the individual’s condition is such
home on their own or be transferred to a long- that the care does not depend heavily on high-
term care facility. Long-term care and home care technology monitoring or complex diagnostic
required very little technical or complicated patient procedures. Subacute care requires the coordinated
care. The introduction of new health care delivery services of an interdisciplinary team including
systems, such as managed care and prospective pay- physicians, nurses, and other relevant professional
ment systems, however, encouraged hospitals to disciplines who are trained and knowledgeable to
discharge patients sooner and with more technical or assess and manage these specific conditions and
complicated care needs than in the past (“quicker and perform the necessary procedures. Subacute care is
sicker”). These needs could not be met by existing given as part of a specifically defined program,
long-term and home care programs; therefore a new regardless of the site . . . It requires frequent . . .
category of care arose: Subacute care usually refers to patient assessment and review of the clinical course
low-technology, uncomplicated inpatient care, but the and treatment plan for a limited. . . time period,
term is sometimes used synonymously with postacute until the condition is stabilized or a predetermined
care, which includes all care given after the acute care treatment course is completed.2
stay, no matter where the care occurs. The field of
According to this definition, subacute care can take
subacute care has experienced rapid growth since the
place just about anywhere, from acute care or specialty
middle of the 1980s. This growth seems to be fueled
hospitals to skilled nursing facilities (SNFs) and from
partly by changes in health care payment systems (see
rehabilitation programs to outpatient programs and
Chapter 1) and partly by the rapid growth of the aging
home care settings. The definition allows for a wide
population.
range of patients, for almost all age brackets, and for
many traditionally acute care procedures, including
infusion therapy, respiratory care, cardiac services,
Definition of Subacute Care wound care, rehabilitation services, postoperative
recovery programs for knee and hip replacements, and
The term “subacute” care was formerly used to describe
cancer, stroke, and AIDS care.3
hospitalized patients who failed to meet established
criteria for a medically necessary acute stay but who
were not stable enough to go either home or to a
nursing home. Now the phrase is used almost exclu- Core Elements of an Ideal
sively to refer to patients treated in any setting other
than an acute care bed. So subacute, or postacute, care Subacute Care Program
is nothing new; rather, it is a discrete classification on In a report to the federal government entitled Subacute
the continuum of care. It is “a level of care—skilled care Care: Policy Synthesis and Market Area Analysis, Manard
for patients with complex needs—that some nursing and coworkers listed four core elements of an ideal
facilities, home care providers and others have been subacute care program but pointed out that the field is
providing for years under a variety of different names.”1 evolving daily and the core elements may change. The
Subacute care can be classified as the traditional first ideal core element is organization:
high-end skilled nursing care that was formerly done in
First, ideal subacute care is an organized program.
the hospital but is now done in an alternative site. It
It is more than any type of care provided to
serves patients who require less intensive care than the
high-end Medicare patients. Some programs are
traditional acute care but more attention than tradi-
organized around specific disease categories (e.g.,
tional nursing home care.
stroke or cancer); others are organized around
The Joint Commission has established accredita-
specific interventions (e.g., pain management or
tion criteria and standards for subacute care facilities.
wound care), and some are organized around other
The American Health Care Association in Washington,
more or less homogeneous patient characteristics
D.C., and The Joint Commission have jointly approved
(e.g., pediatrics or medically complex). In general,
the following definitive definition of subacute care.
providers tend to distinguish between rehabilita-
Subacute care is goal-oriented treatment rendered tion subacute patients, which include conditions
immediately after, or instead of, acute hospitaliza- such as hip replacement, spinal cord injuries, and
tion to treat one or more specific active complex brain injuries. These patients tend to require more
medical conditions or to administer one or more rehabilitation services such as physical, occupa-
technically complex treatments, in the context of a tional, and speech therapies. Conversely, medical
CHAPTER 34 ■ Subacute and Long-Term Care 939
subacute patients tend to have conditions that care and case managers, whose jobs involve both
require intensive medical and nursing care, but resource use monitoring and more traditional
fewer other therapies. This group of patients care-coordination activities. Care techniques . . .
includes those with cardiovascular diagnoses, also include the use of Acare maps™ and/or critical
cancer, ventilator care, wounds, and IV therapy.4 pathway protocols, program evaluation based on
measured outcomes, and an emphasis on continu-
Long-term care facilities often provide rehabilitation ous quality improvement.4
subacute care, and hospitals and nursing homes most
often provide medical subacute care. Respiratory care In skilled nursing facilities, on-site case managers who
obviously has a place in medical subacute care because are highly trained, skilled clinical professionals are vital
of respiratory therapists’ ability to assess and treat for coordinating the efforts of physicians, clinical team
complex cardiopulmonary problems and their knowl- members, patients, and family. (Case management is
edge of cardiopulmonary physiology. Since the time a method of medical management in which a person is
the Manard report was written (1995), respiratory care assigned patients with the same types of problems to
has also found a place in the rehabilitative subacute standardize care.) Respiratory therapists are logical case
care area (see Chapter 36). managers for a subacute care unit that is organized
The second core element of subacute care is focus around the specific intervention dealing with cardio-
on outcomes: pulmonary disease or a unit that is devoted to ventila-
tor care. Managed care organizations are pressing for
In the ideal, a subacute care program is intensely critical pathways as a technique for timing the
focused on achieving specified, measurable sequence of interventions in the care plan of the
outcomes. The outcomes or goals may. . . vary for patient to achieve positive outcomes. Respiratory care,
each patient (e.g., healing a wound or restoring the again with the leadership of the AARC, has provided
patient to a particular level of functioning) . . . . thorough cardiopulmonary clinical practice guidelines,
Subacute programs in the ideal stress . . . achieving which are the cornerstone of critical pathways and
outcomes in a particularly efficient and lower cost protocols. Many of the AARC guidelines can be found
manner.4 in the References and Suggested Readings throughout
With regard to the efficiency and cost, the American this book.
Association for Respiratory Care (AARC) has empha- Many health care workers claim that managed care
sized the need to educate ourselves to the language of has been the single most important driving force to
managed care. Managed care organizations (MCOs) alternative site care, such as subacute care. The introduc-
(organizations that provide health care coverage) want tion of capitated care, which limits the amount of
positive patient outcomes at the lowest possible cost. health care dollars that can be paid over a patient’s life,
Respiratory therapists have traditionally provided to both institutions and physicians has generated the
positive patient outcomes at a low cost but have failed to
adequately measure the costs. Measurement of patient
outcomes and the documentation of costs enable
respiratory therapists to help subacute care facilities Spotlight
maintain efficient and effective utilization of resources. On
The third core element of subacute care is special
resources: Cost Effectiveness of
Special resources . . . generally include physical
Respiratory Therapy
plant features such as a distinct unit . . . and more The Muse report indicates that respiratory
and better trained staff [than in a traditional therapists provide high-quality care with definite
nursing facility], especially physicians and nurses.4 positive patient outcomes. Using data from
1996, the report demonstrates that persons who
The AARC research initiative demonstrated that receive treatments from respiratory therapists
respiratory therapists are “better trained” than tradi- tend to have more positive outcomes and lower
tional nursing facility staff in cardiopulmonary patient costs (i.e., use fewer health care services) than
assessment and treatment and can provide quality care those who do not receive care from respiratory
with positive outcomes at a lower cost.5 therapists.
The fourth core element of subacute care is Source: Muse & Associates. A Comparison of Medicare Nursing
Home Residents Who Receive Services from a Respiratory
a set of techniques thought essential to achieving Therapist with Those Who Do Not. Washington, DC: Muse & Assoc;
stated goals. These techniques include the use of July 1999.
interdisciplinary teams to plan and provide patient
aggressive search for less expensive health care. The requirement that subacute care patients undergo a
financial pressures of capitated care have fueled the 3-day hospital stay before being transferred to a
search for improvements in two aspects of subacute care: subacute facility. This requirement comes from the
lower cost and higher quality. Capitation has moved Social Security Act definition of posthospital extended
into the Medicaid market, and managed care organiza- care services: “extended care services furnished an
tions understand that money can be made if the patient individual after transfer from a hospital in which he
is kept out of the acute care hospital. Keeping patients in was an inpatient for not less than 3 consecutive days.”7
an acute care setting when they do not require acute care Managed care companies also want to eliminate this
is a waste of money, but sending the patient home too requirement. For example, “some large, fully capitated
early may result in readmission. Discharging patients to medical groups that contract to staff hospital emer-
subacute care facilities instead of to their homes can gency rooms have directives to transfer any patient who
help prevent costly readmissions as long as the subacute doesn’t require acute care services—invasive procedures
care institutions provide quality care. or complex diagnostics, for example—directly from the
The health care industry continues to move toward ER to a subacute unit.”8
integrated health networks, which offer certain finan-
cial advantages to acute care facilities. Acute care
facilities that cannot convert beds into subacute care Accreditation and Regulation
often form alliances with existing facilities that do have
subacute care beds. Since hospitals have a much higher of Facilities
cost base because of the needs of acute care patients, Subacute facilities may be accredited by the Joint
the ability to move stable patients to a subacute care Commission or the Commission for Accreditation of
facility, such as a nursing home, can save hospitals Rehabilitation Facilities (CARF). The Joint Commission
money. Current trends show that managed care is a private not-for-profit organization that evaluates
companies, in an effort to contain costs, are shifting and accredits more than 17,000 health care organiza-
increasing numbers of hospital patients into subacute tions and programs, including home care providers and
care beds in nursing homes. subacute care facilities.9
For common diagnosis-related group (DRG) Subacute care facilities gain Joint Commission
procedures, subacute care can save thousands of accreditation by being scored on sets of standards.
dollars.6 In addition, increased revenue can be gener- Standards cover all areas of the subacute care facility,
ated by charging for the subacute care. Management from nursing care to laundry services and from the
companies contract with hospitals and skilled nursing physical plant to spiritual services. If a facility complies
facilities to convert skilled nursing beds to subacute with all related standards a 3-year accreditation is
care beds. The management company provides the granted. Facilities not in full compliance are awarded
expertise on subacute care reimbursement and regula- either conditional accreditation (deficiencies require
tions that may be lacking from the partner institutions. remediation or corrective action) or no accreditation.
Before any new subacute care facilities are built, CARF focuses on accrediting agencies and organiza-
most states require that a certificate of need (CON) be tions providing a variety of rehabilitation services.
obtained. Currently only 14 states do not require one. Three subcategories were developed, taking into
A CON is a requirement that a facility must file with its account the different levels and types of rehabilitation
respective state’s department of health to receive (acute or subacute), the location (hospital or SNF), and
authorization to institute a particular service or level of patient outcome goals.10
care. As an example, in New Jersey, a bill was passed in The National Committee for Quality Care
1996, allowing hospitals to either convert or designate (NCQA), another accrediting body, was formed to
as subacute up to 7% of the total medical-surgical beds ensure quality in managed care organizations. If
or 12 beds, whichever is greater (NJ Senate Bill No. subacute care organizations or their parent organiza-
368, 1996). The rationale is that the institution is not tions under which they operate wish to contract with
adding any beds; it is only converting existing beds to a MCOs, they must be aware of the NCQA standards and
lower level of acuity. how to meet them.10
SNFs are highly regulated health care entities; Federal and state governments have always regu-
however, the regulations are not specifically tailored to lated subacute care facilities and will continue to do so
subacute care. Rather the regulations used are for as the field grows. By regulating subacute care, the state
hospitals and nursing homes. Nursing homes and has the opportunity to control growth surges, thereby
managed care companies find some of these require- preventing excessive numbers of subacute care beds.
ments unreasonable. For instance, nursing home Each state incorporates its own policies on regulating
providers of subacute services want to eliminate the subacute care centers.
may be classified into three distinct groups depending

Best Practice on the level of respiratory care they need:
• Basic respiratory care
Accreditation • Intermediate respiratory care
Even though accreditation by The Joint Commis- • Ventilatory care
sion (TJC) is optional, it is to the advantage of the
Basic respiratory care includes modalities such as:
subacute care facility to be accredited because
many managed care organizations (MCOs) look • Oxygen therapy.
for this accreditation. The Joint Commission is • Bland aerosol administration.
becoming the standard for most MCOs. • Delivery of aerosols to the upper airway.
• Intermittent positive pressure breathing (IPPB).
• Postural drainage.
Patients at this level may be admitted to the subacute
facility to continue with the rehabilitation process
RESPIRATORY THERAPIST’S INVOLVEMENT before being discharged to their home. Most patients
IN SUBACUTE CARE requiring basic respiratory care traditionally are taken
Different levels of subacute care have implications for care of by RNs and LPNs.
respiratory care. Table 34-1 shows four levels along Patients in the intermediate respiratory care group
with the respiratory therapist’s involvement. may have a tracheostomy requiring care and may
require aerosol administration. These patients may also
be admitted to the subacute facility to continue with
weaning trials from the tracheostomy tube, eventually
Respiratory Care Acuity Levels leading to decannulation. Patients who are admitted to
and Modalities subacute facilities with tracheostomies are often cared
for by respiratory therapists.
Subacute respiratory care generally follows three basic
Specific bedside respiratory care modalities for
acuity levels, each with its own appropriate level of
basic and intermediate-level patients in the subacute
respiratory therapist and equipment commitments:
setting include:
airway management patients (basic), complex respira-
tory patients (intermediate), and ventilator-dependent • Oxygen therapy.11
patients (the highest acuity level). All of these patients • Nasotracheal suctioning.12
require frequent respiratory assessment to ascertain the • Postural drainage therapy.13
need for such respiratory procedures as bronchodilator • Delivery of aerosols to the upper airway.14
therapy, oxygen therapy, bronchopulmonary hygiene, • Assessing the response to bronchodilator therapy.15
and airway management. • Directed cough.16
The subacute setting uses many of the same • Selection of an appropriate aerosol delivery device.17
respiratory care modalities as the acute care setting. • Bland aerosol administration.18
These modalities range from routine bedside respira- • Incentive spirometry.19
tory care to care for the ventilator-dependent patient. • Intermittent positive pressure breathing.20
Certain subacute facilities may accept only specific • Use of positive airway pressure adjuncts to
types of respiratory patients. These respiratory patients bronchial hygiene therapy.21
TABLE 34-1 Four levels of subacute care and respiratory therapist involvement
Traditional General Chronic Long-Term Transitional
Location Within hospital or Nursing home Chronic care facility Long-term care facility
freestanding
Respiratory High: provides same Teaching and training Consultant role to More intensive than acute
therapist level as acute care, functions; can be nurses care; most patients have
involvement with interdisciplinary extended to long-term some type of respiratory
teamwork and or home when patient therapy
patient education problem leaves
Source: From Bunch D. Phenomenal growth of subacute care offers new opportunities for RCPs. AARCTimes. March 1996:48.
Patients in the ventilatory care group may be consist of a nurse, a case manager, a physical therapist,
admitted to the subacute facility for extended weaning an admissions coordinator, and a social worker. The
from mechanical ventilation or for long-term mechani- respiratory therapist needs to complete an initial
cal ventilation. Any subacute care facility that accepts assessment form to gather all the information needed
ventilator patients should have respiratory therapists to prepare for the possible admission of this patient to
on staff. Acute care facilities manage patients with an the facility.
average length of stay (LOS) of 4–7 days, whereas The subacute facility should be ready to accept any
subacute facilities focus on longer stays, with an patient who requires a multitude of services to progress
average LOS of 60–90 days. and prepare for discharge to the home or to the long-
Specific procedures related to ventilatory support term setting. Some of the most common diagnoses
in the subacute setting include: encountered in the subacute setting are:
• Endotracheal suctioning of mechanically • Spinal cord injuries.
ventilated patients.22 • Joint replacements.
• Humidification during mechanical ventilation.23 • Femur fractures, including hip fractures.
• Patient-ventilator system checks.24 • Major multiple trauma.
• Transport of the mechanically ventilated • Congenital anomalies.
patient.25 • Traumatic brain injury (TBI).
• Providing patient and caregiver training.26 • Strokes or cerebral vascular accidents (CVAs).
• Discharge planning for the respiratory care • Neurological disorders, including multiple
patient.27 sclerosis, motor neuron disease, muscular
dystrophy, polyneuropathy, and Parkinson’s
PATIENT SELECTION disease.
When looking at prospective patients for the subacute Common services needed to accommodate these
setting, the admissions team must look at the follow- patients are:
ing elements of admission:
• Physical, occupational, and speech therapy.
• Evaluation of the patient for the appropriateness • IV therapy; wound care.
of care • Cardiac rehabilitation.
• Formulation of an admissions plan and a • Ventilator and pulmonary rehabilitation.
potential discharge plan • Pain management.
• Determination that financial resources are • Dialysis.
adequate • Chemotherapy.
PATIENT EVALUATION SPECIALIZED VENTILATOR CARE FACILITIES

Many of the patients discharged from an acute to The highest level of subacute respiratory care is offered
a subacute facility have a multitude of medically in a specialized ventilator care facility. Some facilities
complex problems, including respiratory-related accept only long-term ventilator patients; others may
complications. An example of this type of patient is a accept long-term as well as weaning ventilator patients.
75-year-old male who was admitted to the acute care
setting with a history of chronic obstructive pulmonary
disease (COPD) and a primary admitting diagnosis of
a fractured hip. Surgery was performed to repair the
Best Practice
fractured hip, and the patient completed a normal
postoperative course while in the acute care setting. The Preadmission Evaluation
time had come for discharge from the acute care The nurse case manager and the respiratory
setting, but the patient could not be discharged home therapist need to perform an on-site evaluation
because of his inability to ambulate. The decision was of any patient being considered for a subacute-
made to transfer the patient to a subacute facility where based ventilator unit. At this stage, the patient
he could continue the rehabilitation process. At the has already exhausted his or her stay in the acute
same time, he would receive respiratory care to keep his care facility and probably has failed all ventilator
COPD under control. weaning attempts. In the preadmission on-site
The admissions team of a subacute facility, espe- evaluation, the team must gather all the informa-
cially one that accepts ventilator-dependent individu- tion needed to portray a complete picture of the
als, should be multidisciplinary and have a respiratory patient.
therapist. The balance of the admissions team should
Most long-term ventilator patients can be managed

on portable positive pressure ventilators such as the Best Practice
Phillips Respironics PLV Continuum ventilators
(Figure 34-1), Nellcor Puritan-Bennett Achieva All professional personnel working with ventilator
(Figure 34-2), and 540 Portable ventilators. Patients patients should be aware of the battery life of both
who are admitted to weaning ventilator care facilities internal and external batteries used to power the
may use units such as Nellcor Puritan-Bennett ventilator. Additionally, these personnel should
(740, 760, and 7200 series) ventilators the Bird T-Bird also ensure that both audio and visual alarms are
AVS/VSO2/VS Series ventilators (Figure 34-3), functional and at proper volume to assure that
and the Pulmonetic LTV 1000, 1150 and 1200 ventila- alarms will be heard by appropriate personnel.
tors (Figure 34-4). Of these ventilators, all are portable
except the Nellcor Puritan-Bennett 740, 760, and 7200
series. Portable ventilators are compact, can be battery
operated (internal and external), and can be trans-
ported with the patient. Nonportable ventilators are AC
power dependent.
FIGURE 34-3 T-Bird AVS/VSO2/VS Series ventilators.

Courtesy of Bird Products Corporation
FIGURE 34-1 Continuum ventilator.

FIGURE 34-2 Achieva ventilator. FIGURE 34-4 Pulmonetic Systems LTV 1000 mechanical
Image used by permission from Nellcor Puritan Bennett LLC, Boulder, Colorado, ventilator.
doing business as Covidien. Courtesy of Pulmonetic Systems
Weaning can be reduced and a fenestrated tube can

be used.
With the advent of portable ventilators that can provide 8. Institute capping trials to lead to decannulation
synchronized intermittent mandatory ventilation of the tracheostomy tube.
(SIMV), pressure support ventilation, and continuous 9. Once the patient is decannulated, begin nasal
positive airway pressure (CPAP), many of the same oxygen to keep the arterial saturation at an
weaning modalities that are used in the acute setting acceptable level.
can be continued in the subacute setting. Monitoring
techniques such as pulse oximetry, capnography or
capnometry during mechanical ventilation, and Discharge Planning
sampling for arterial blood gas analysis are all accurate
methods of evaluating the progress of the weaning The respiratory therapist can have an integral role in
patient in the subacute setting. discharge planning at the subacute level. The respira-
A typical weaning scenario might progress as follows: tory therapist needs to be involved in the discharge
process from the day of admission to the day of
1. Patient is admitted on continuous mechanical discharge.
ventilation on assist-control. Once patients reach their maximum potential in
2. Weaning parameters are performed, indicating the subacute setting, arrangements need to be made for
that the patient may be strong enough to tolerate their anticipated discharge to the next level of care,
SIMV. whether it is home or a long-term care unit. If patients
3. SIMV and pressure support ventilation are are going to be transferred to a long-term care unit, the
initiated. discharge planner must make sure that the facility can
4. SIMV rate and pressure support ventilation are provide the necessary care. For example, if the patient
titrated as tolerated. has a tracheostomy with 40% oxygen via an aerosol
5. Once SIMV4 and pressure support are tolerated, trach collar, the long-term care facility must have
CPAP or tracheostomy collar trials can begin. the knowledge and the equipment to manage this
6. If tracheostomy collar trials are tolerated during patient—such as piped-in oxygen or oxygen concentra-
the day, the patient may need to be rested on the tors, compressors, and oxygen analyzers.
ventilator during sleep. On the other hand, if the same patient is going
7. Once the patient is able to tolerate a tracheostomy home, the patient and the family should be taught how
collar for 24 hours, the size of the tracheostomy to provide the care. The patient and caregivers need to
be given a structured, written education program that
they can easily understand. Written material can be
assembled in a complete, easy-to-read manual. Any
Spotlight education presented to the patient or caregivers must
On be documented in the medical record on a form such
as a Resident Education Flow Sheet.
Costs of Ventilator Weaning
Some of the health care costs associated with
ventilator weaning in the subacute facility can be
lowered with the following:
Best Practice
• Performing fewer arterial blood gas analy-
ses and using pulse oximetry and capnog-
raphy more. The cost of arterial blood gas Plan of Care
analyses is reduced by not having to incur The first 48 hours after admission are crucial
the cost of a full laboratory analysis. in the discharge process. During this time, all
• Typical ventilators in the subacute setting the disciplines are required to submit their care
cost anywhere from $6000 to $18,000. plans after performing careful evaluations of the
These ventilators provide SIMV, CPAP, patient. The respiratory therapist must also for-
and pressure support in a compact and mulate a care plan after reviewing such informa-
portable size as opposed to the larger tion as past health history, past hospitalizations,
hospital ventilators, which cost more social history, and the wishes of the family to
than $20,000. bring their family member home.
Once all educational objectives have been accom-

Spotlight plished, the patient and the caregivers must be able to
On demonstrate what they have learned. The respiratory
therapist can then develop a complete list of equip-
Successful Patient Education ment and supplies needed to take care of the patient at
The respiratory therapist should present the home. The interdisciplinary team then meets again to
education to the patient and caregivers in review the final discharge plan, including equipment,
different formats, such as written material, caregivers, and transportation on the day of discharge.
videotape presentations, and hands-on
demonstration. All the material must be specific
to the age of the caregivers and the patient and
Reimbursement
must be easy to understand for all involved. Medicare, Medicaid, private insurers, health mainte-
The subject and results of these sessions nance organizations (HMOs), and preferred provider
should be recorded in the patient’s chart or organizations (PPOs) all cover services offered at the
record. subacute level. The HMOs and other managed care
organizations are using subacute care facilities because
CASE STUDY 34-1

J. is a 63-year-old Hispanic male who was admitted ventilator at night. By the twelfth day, his tracheos-
to the subacute facility after a 4-month stay in an tomy tube was changed to a fenestrated tube to
acute care hospital. His admitting diagnosis was facilitate capping and eventual decannulation. By
respiratory failure secondary to COPD and pneumo- day 14, J. was on nasal oxygen, which was discon-
nia. J. was admitted with a Foley, gastrostomy, and tinued 2 days later because he was able to maintain
tracheostomy tube in place, and his skin was intact. an oxygen saturation of 95%.
Physical, occupational, speech, and respiratory During the course of ventilator weaning, all
therapists evaluated him, and a care plan was therapists worked with J. to facilitate increased
initiated. The assessments were as follows: muscle strength, increased oral nutritional intake,
and training in activities of daily living. On day 21,
PT: Patient was unable to ambulate and
he was transferred to the hospital for removal of the
required maximum assist for transfers.
tracheostomy and gastrostomy tubes. Two days
OT: Patient required maximum assist with later, he came back to the subacute facility for the
dressing, bathing, and grooming as well as continuation of his rehabilitation program and
all ADLs. completion of his discharge plan to home. Within
ST: Patient required speech training using 6 days, he was discharged home with the services
a Passy Muir speaking valve and dysphagia provided by a local home health agency.
studies in an effort to increase his oral nutri-
tional intake. Questions
RT: Patient tolerated increased CPAP trials 1. During on-site evaluation in the acute setting,
while on the ventilator. His ventilator settings what was the best method for the respiratory
were: CPAP @ 0, PS ⫹10 cm H2O, FIO2 0.35 therapist to determine J.’s needs before
(8 a.m.–10 p.m.) and assist/control @ 10, Vt admitting him to the subacute setting?
700 cc, FIO2 0.35 (10 p.m.–8 a.m.). 2. What monitoring techniques could be used to
He was doing so well that, within 2 days, he measure respiratory fatigue during the weaning
progressed to a trach collar during the day and was process of mechanical ventilation in the
maintained on A/C at night so that he could rest. subacute setting?
After the third day, he tolerated the trach collar so 3. How would the interdisciplinary team determine
well that it was not necessary to return him on the a game plan for J.?
their costs are lower than they would be in the acute 16 – 18 RUC $392.28
9 – 15 RUB
care setting. Typically, the subacute costs are 40–60% ADL: ultra high
720 minutes 4 – 8 RUA
less than the hospital-related acute care costs. In
16 – 18 RVC
addition, subacute care may generate more income ADL: very high 9 – 15 RVB
than other nonacute care settings. Reimbursement for a 500 minutes 4 – 8 RVA
typical nursing home bed may be $150 a day or more ADL: high
13 – 18 RHC
9 – 12 RHB
depending on region or facility, whereas reimburse- 325 minutes 4 – 7 RHA
ment for a bed in a subacute facility may cost up to
15 – 18 RMC
$800 a day or more, depending on the services needed, ADL: medium 8 – 14 RMB
150 minutes 4 – 7 RMA
such as ventilator care, IV therapy, or specialized
wound care. ADL: Low
14 – 18 RLB
4 – 13 RLA $180.05
In the past, respiratory care in the subacute setting 45 Minutes
was reimbursed in one of two ways.
+ TREATMENTS 4 – 5 ----SE3 $260.25
• The most popular method was for the subacute ADL= 7 2 – 3 --------SE2
1 or more ---SE1 $195.86
care facility to have a transfer agreement with a
hospital to obtain Medicare reimbursement. The SUCTIONING
TRACH
respiratory care staff was then provided to the VENT
subacute facility by that transfer hospital. IV MED
IV MED
• In the other method of payment for respiratory 17–18
care services, the subacute care facility contracted SSC $191.50
YES
ADL 15–16
with an outside management company, which SSB
would provide the respiratory therapists, equip- 7–14 SSA $178.20
ment, supplies, and policies and procedures to

yes = CC2 = $190.42
run the respiratory care department. The facility 17–18 depressed
no = CC1
then reimbursed the management company on A
yes = CB2
either a per diem rate or any other rate as set 12–16 depressed
D
forth on their contract. no = CB1
L
4–11 depressed yes = CA2
In 1998, the Centers for Medicare & Medicaid
Services (CMS) cut reimbursement in the subacute care no = CA1 = $149.20
arena, adversely affecting payment for respiratory care.
CMS changed from a cost-per-charge reimbursement Resource Utilization Group – RUG- sample chart
system to a prospective payment system (PPS). With
Treatments, e.g., suctioning, trach., vent, combined with ADL equals a
this transition, the transfer agreement was eliminated. higher rate than the lowest rehab RUG score.
PPS rates consist of a federal rate and a facility-specific
rate. The federal payment rate covers all costs of FIGURE 34-5 Resource utilization group (RUG-III) case mix
furnishing covered skilled nursing services with the classification system.
exception of educational costs. This includes Part B Courtesy of Gerry Cannon, RN, BS, Hospicomm Inc., Quality Assurance
services furnished under an arrangement with the
subacute facility to subacute inpatients. Therefore,
except for physician’s services and other practitioners
exempted under the law, the unbundling of services standardized resident assessment instrument (RAI)
allowed under the previous payment mechanism are called the minimum data set (MDS) (Figure 34-6).
no longer permitted. Over 100 assessment items are used to provide
The resource utilization group (RUG-III) information on the patients’ nursing care needs,
case-mix classification system consists of 44 categories therapies, medical diagnoses, cognitive status, behav-
that capture resource use (nursing and treatment time) ioral problems, and activities of daily living (ADL)
of subacute patients and is intended to provide an impairments. Subacute facilities must prepare the
improved method of tracking the quality of care. The MDS clinical assessment by day 5 of a patient’s
44 RUG categories are classified from the most clini- admission to the facility and must perform ongoing
cally complex to the least complex groups. RUG-III assessments within certain time frames. The patient
groups are used in determining the payment scheme data gathered on the MDS are analyzed to determine
(Figure 34-5). the appropriate RUG-III category for the patient and
Patient assessment plays a crucial role in deter- therefore the per diem rate the facility will receive
mining the case mix. The assessment process uses a during the patient’s stay.
FIGURE 34-6 First page of the minimum data set (MDS) form.
Courtesy of Briggs Corporation
Current Practices in View of PPS formerly called domiciliary, family care, or rest
homes. These homes vary in size from more
The PPS changes in reimbursement mechanisms have than 100 residents to smaller ones caring for
resulted in the dissolution of many respiratory pro- 2–6 residents.
grams in the subacute setting because respiratory care is • Assisted living. A living residence for group
not individually recognized as a reimbursable therapy. housing and services for 2 or more unrelated
Instead it is included within the extensive services and adults that makes available at least one meal per
special care groups. Some subacute facilities have day, housekeeping services, and personal care.
eliminated their respiratory care staff and are using Individuals in this type of residence may obtain
specially trained nursing staff to care for their patients. respiratory care equipment such as compressor/
Subacute facilities that accept ventilator patients are nebulizers, oxygen systems, or positive airway
still employing respiratory therapists to facilitate the pressure (PAP) therapy devices from a home care
weaning process. These facilities will continue to be the company. However, depending on facility
forerunners in subacute respiratory care with more and regulations and/or state law, residents must be
more referrals of the compromised pulmonary patient. able to safely use and maintain this equipment.
Assistance may be provided by properly trained
Long-Term Care staff members, and home care respiratory
therapists may visit, assess the individual, and
Long-term care (LTC) is defined as a broad scope of provide follow-up care. Health insurance payors,
medical and nonmedical services that are provided to including Medicare, reimburse the home care
individuals with a chronic illness or disability. These company directly for equipment provided in
individuals cannot care for themselves over extended assisted living arrangements. Some states
periods of time. LTC may also involve custodial and recognize different types of assisted living
nonskilled care that includes assistance with normal residences that include adult care homes, group
activities of daily living such as bathing, dressing, and homes for developmentally disabled adults, and
use of the bathroom. The most common form of multiunit assisted housing with services. Facili-
long-term care is found in the home where either ties providing assisted living are usually private
family members or caregivers are available to assist the pay and may cost an individual $35,000 or more
individual on a daily basis. It is also provided in the per year, depending on the residence.
community at specialized centers (assisted living • Continuing care retirement communities (CCRC).
facilities) and in nursing homes. Residences typically providing independent
LTC can be delivered to patients of any age, but the accommodations that include full apartments,
majority of patients receiving this type of care are efficiency apartments, villas, or cluster homes. A
elderly. variety of services are provided such as commu-
The Centers for Medicare & Medicaid Services nity dining, recreation, social events, housekeep-
(CMS) reported that in 2006, 9 million men and ing, transportation, and health-related services
women in the United States over the age of 65 years (testing and treatment). An entrance fee may be
needed some type of long-term care. By 2020, this charged along with a monthly fee. The entrance
number, according to CMS, will increase to 12 million fees may or may not be refundable. The majority
older Americans. Most of these individuals (an esti- of CCRCs are private pay, although some may
mated 70%) will be cared for in the home by family offer subsidized units.
members and/or caregivers. The U.S. Department of • Nursing homes. Facilities that provide nursing or
Health and Human Services (DHHS) also estimates convalescent care for a specified number of
that people 65 years and older will have a 40% chance persons unrelated to the licensee. Nursing
of entering a nursing home and that approximately homes provide long-term care of chronic
10% of the people entering a nursing home will reside conditions or short-term convalescent or reha-
there for 5 or more years.28 bilitative care for which medical and nursing
types of care are indicated. Most residents of
LONG-TERM CARE FACILITIES nursing homes need long-term care; however,
some are admitted for shorter stays following
Long-term care is often thought of as being delivered in
hospitalization for convalescent or rehabilitative
a facility or institution, including the following:
care. Nursing homes must be state licensed, and
• Adult care homes. Residences for elderly and Medicaid pays for certain health care services
disabled adults who require 24 hour supervision and nursing home care for older persons in most
and assistance with activities of daily living states. Eligibility, however, is based on income
and personal care needs. These facilities were and personal resources.
• Long-term care ventilator units. These facilities units, require the respiratory care practitioner to be
provide long-term ventilatory care for patients able to work independently. RTs can be successful in
who are not able to be weaned from ventilatory their facility by setting up a program that fits well with
support and who do not have family or caregiv- the needs of surrounding area hospitals. These pro-
ers that are able to provide this level of care in grams need to accept both weaning and long-term
the home setting. Specialized units throughout ventilator patients.
the United States provide care for pediatric, Many managed care organizations are constantly
adult, and elderly patients in need of long-term, seeking specialty ventilator units to contract with in an
high-technology respiratory care. effort to reduce the overall health care costs to their
subscribers. Managed care organizations are also
RESPIRATORY CARE PERSONNEL looking for facilities that are accredited by the Joint
Respiratory therapists (RTs) working in long-term care Commission as a sign of excellence. Because the field
do so on either a full-time, part-time, or consulting of subacute care continues to grow, there will continue
basis. Many facilities involved in LTC rely on outside to be changes in regulation and reimbursement.
vendors to provide diagnostic tests and other related Finally, with the growing aging population in the
services. Unless the facility specializes in long-term United States, there has been an increasing need for
ventilatory support, respiratory care equipment usually long-term care (LTC). Although LTC can be provided to
has limited availability; most use portable oxygen individuals of any age, most recipients of LTC are
systems and suction units. RTs tend to work indepen- elderly and are cared for in the home, assisted living
dently with minimal supervision but with a heavy residences, specialty units, and nursing homes. The
emphasis on patient care planning. In terms of docu- respiratory therapist can provide care in any of these
mentation, LTC, as with subacute care, requires initial venues and becomes a valuable member of the inter-
justification, ongoing follow-up, and detailed financial disciplinary team.
recordkeeping. Long-term care facilities are state
licensed and accredited. RTs on staff are often called on
to assist with any licensing and accrediting processes as Study Questions
part of the interdisciplinary, professional team that REVIEW QUESTIONS
provides care at the facility.
1. What are the three groups of respiratory patients
accepted into the subacute setting?
Reimbursement 2. What are the three elements of admission for
There are a variety of ways to pay for long-term care. access to the subacute setting?
However, the individual must think ahead and plan 3. List some of the ventilators that may be used for
accordingly. Many people enroll in long-term care long-term and weaning ventilator patients.
insurance policies that help to pay future long-term 4. What are the two accrediting agencies in subacute
care expenses such as those for a nursing home. care?
Premiums can be expensive. Private insurance plans are
5. What are the two tools that determine the daily
available, but individuals need to consider enrollment
rate that a subacute facility may earn from CMS?
earlier on in life. Normally, the younger people are
when they first enroll, the lower their premiums will 6. What is long-term care and where can it be provided?
be. Generally, Medicare does not pay for long-term
care. Medicare pays only for a medically necessary
skilled nursing facility or home health care, and the MULTIPLE-CHOICE QUESTIONS
person must qualify for this type of care. Medicaid, on 1. Which of the following is not used by the respira-
the other hand, pays for certain health services and tory therapist in the subacute setting?
nursing home care for elderly people with low incomes a. initial assessment form
and limited assets. Medicaid is a state and federal b. pulse oximeter
government program, and, as such, payment varies c. transfer agreement
from state to state. d. MDS assessment
2. Subacute facilities are regulated by all of the
following agencies except which?
Summary a. state departments of health
With the advent and proliferation of subacute care, we b. TJC
have found that the respiratory therapist definitely has c. CORF
a role. Many specialty units, such as ventilator care d. ACHMS
3. All of the following ventilators can provide porta- 12. Long-term care is generally not paid for by:
bility in the subacute setting except which? a. Medicaid.
a. Pulmonetics LTV 1000 b. private long-term care insurance policies.
b. Nellcor Puritan-Bennett 7200 c. Medicare.
c. Bird TBird d. private pay.
d. Nellcor Puritan-Bennett Achieva
4. Which of the following is not a member of the CRITICAL-THINKING QUESTIONS
interdisciplinary team in the subacute setting? 1. How are ventilators in the subacute setting, such as
a. respiratory therapist the Nellcor Puritan-Bennett 7200 and the Bird
b. nurse TBird, different from ventilators in the acute care
c. occupational therapist setting?
d. medical laboratory technician
2. What is the role of the respiratory therapist as an
5. Subacute care facilities are accredited by: interdisciplinary team member in a subacute
a. state departments of health. program?
b. sponsoring hospitals.
3. How does weaning a ventilator patient in the
c. TJC.
subacute setting differ from weaning in the acute
d. ACHMS.
care setting?
6. Ventilator weaning modalities in subacute care
4. What methods could respiratory therapists use to
facilities may include all of the following except
“sell” themselves to subacute and long-term care
which?
programs that do not employ RTs in their facilities?
a. pressure support
b. CPAP
c. SIMV References
d. volume control
1. Shriver K. What’s new in subacute care? Modern
7. MDS stands for which of the following? Healthcare. January 1995;26:34–38.
a. medical delivery standard 2. Buttaro T., et al. Clinical Management of Patients in
b. maximum data set Subacute and Longterm Care Settings. St. Louis:
c. minimum data set Elsevier; 2006:2.
d. Medicare deviation standard 3. Tokarski C. Riding the express. Hospitals Health
8. The MDS is used: Networks. July 1995; 69:20–23.
a. for assessment and care screening. 4. Manard B, et al. Subacute Care: Policy Synthesis and
b. to establish minimum standards of care. Market Area Analysis. Fairfax, VA: Lewin-VHI; 1995.
c. to establish maximum standards of care. 5. Muse & Associates. A Comparison of Medicare
d. to determine discharge criteria. Nursing Home Residents Who Receive Services from
9. A classification system that sets the per diem rate a Respiratory Therapist with Those Who Do Not.
that the facility is paid by Medicare for treating a Washington, DC: Muse Assoc; 1999.
particular patient is termed: 6. Epstein J. License to steal. Finan World. September
a. RUG. 1995;164:34–35.
b. DRG. 7. Post-hospital extended care services. Social
c. PPS. Security Act. Sec.1861. [42 U.S.C. 1395x(h)]
d. MDS. http://www.socialsecurity.gov
8. Maher L. Is subacute care worth your money?
10. Which of the following is a predetermined method
Busin Health. July 1995;13:18–24.
of payment based on diagnostic-related groups
9. http://www.jointcommission.org/AboutUs/
regardless of the amount of care given?
Fact_Sheets/joint_commission_facts.htm
a. RUG
10. Pratt, JR. Long-Term Care, Managing Across the
b. DRG
Continuum. Sudbury, MA: Jones & Bartlett;
c. PPS
2010:112.
d. MDS
11. Which one of the following is not a long-term care clinical practice guideline: oxygen therapy in the
facility? home or extended care facility. Respir Care. August
a. the home 2007;52(1):1063–1068.
b. nursing home 12. American Association for Respiratory Care. AARC
c. assisted living facility clinical practice guideline: nasotracheal suctioning.
d. continuing care retirement community Respir Care. September 2004;49,9:1080–1084.
13. American Association for Respiratory Care. AARC 23. American Association for Respiratory Care. AARC
clinical practice guideline: postural drainage clinical practice guideline: humidification during
therapy. Respir Care. December 1991;36: mechanical ventilation. Respir Care. August
1418–1426. 1992(8);37:887–890.
clinical practice guideline: bland aerosol adminis- clinical practice guideline: patient-ventilator system
tration. Respir Care. May 2003;48,5:529–533. checks Respir Care. August 1992;37,8:882–886.
clinical practice guideline: assessing response to clinical practice guideline: in-hospital transport of
bronchodilator therapy at point of care. Respir Care. the mechanically ventilated patient. Respir Care.
December 1995;40:1300–1307. June 2002; 47,6:721–723.
clinical practice guideline: directed cough. Respir clinical practice guideline: providing patient and
Care. May 1993;38:495–499. caregiver training. Respir Care. July 1996;41,7:
17. American Association for Respiratory Care. AARC 658–663.
clinical practice guideline: selection of a device for 27. American Association for Respiratory Care. AARC
delivery of aerosol to the lung parenchyma. Respir clinical practice guideline: discharge planning for
Care. July 1996;41,7:647–653. the respiratory care patient. Respir Care. December
18. American Association for Respiratory Care. AARC 1995;40,12:1308–1312.
clinical practice guideline: bland aerosol adminis- 28. Centers for Medicare and Medicaid Services. U.S.
tration. Respir Care. May 2003;48,5:529–533. Department of Health and Human Services.
19. American Association for Respiratory Care. Annual cost of long term care survey (conducted
AARC clinical practice guideline: incentive by Genworth Financial). 2007.
spirometry. Respir Care. December 1991;36:
1402–1405.
20. American Association for Respiratory Care. AARC Suggested Readings
clinical practice guideline: intermittent positive Argondezzi T. Long term care: finding the perfect fit. Ad
pressure breathing. Respir Care. May 2003;48, Respir Care Pract. August 1998;11:20–21.
5:540–546. Krachman SL. Initiating weaning: appropriate measures
21. American Association for Respiratory Care. AARC promote successful extubation. Adv Manag of Respir
clinical practice guideline: use of positive airway Care. June 1999;8:24–25.
pressure adjuncts to bronchial hygiene therapy. Lewis DL. Transfer agreements. Adv Manag Respir Care.
Respir Care. May 1993;38:516–521. March 1997;6:35–38.
22. American Association for Respiratory Care. AARC Taraszewski R. Subacute respiratory care. Adv Manag
clinical practice guideline: endotracheal suctioning Respir Care. March 1996;5:30–33.
of mechanically ventilated adults and children Wiseman L. MDS, RUGs and PPS Clinical and Financial
with artificial airways. Respir Care. May 1993;38, Strategies. Wilmington, NC: Professional Education
5:500–504. Seminars; 1998.
CHAPTER 35
Respiratory Home Care

Kathleen S. Wyka and David A. Gourley
OBJECTIVES
• Identify the major factors leading to the growth of home respiratory care.
• Describe the responsibilities of the key members of the discharge planning team.
• List the Medicare guidelines for reimbursement of oxygen therapy equipment.
• Differentiate the three systems for home oxygen therapy.
• List the diagnoses of patients successfully managed in a home ventilator program.
• List the basic equipment and supplies needed for a home ventilator patient.
• Define a technology-dependent child.
• List the indications for home apnea monitoring.
CHAPTER OUTLINE
History and Evolution Sleep Apnea Therapy
Selecting Patients for Home Care Nasal Continuous Positive Airway Pressure
Oxygen Therapy Bilevel Therapy
Oxygen Concentrators Home Polysomnography
Liquid Oxygen Systems Home Mechanical Ventilation
Compressed Gas Cylinders Components of a Successful Program
Oxygen-Conserving Devices Current Equipment
Basic Respiratory Equipment Patient and Caregiver Education
Aerosol Therapy Pediatric Home Care
Intermittent Positive Pressure Breathing Age-Specific Criteria
Suction Units Equipment
Percussors Infant Apnea Monitoring
Devices for Cough Assistance
(continues)
952
CHAPTER 35 ■ Respiratory Home Care 953
(continued)
Clinical Respiratory Services Care Planning

Assessment Reimbursement
Patient Assessment Payors
Environmental Assessment Regulatory Bodies, Accreditation,
Patient Education and Licensure
Disease Management Accreditation
KEY TERMS
apparent life-threatening cuirass noninvasive positive pressure
event (ALTE) exsufflation ventilation (NPPV)
care planning Health Care Financing Adminis- oxygen concentrator
Centers for Medicare & tration (HCFA) oxygen-conserving device (OCD)
Medicaid Services (CMS) home medical equipment pneumocardiogram (PCG)
clinical respiratory services (HME) companies technology-dependent children
T
he dynamics of the health care delivery home, providing the patient is willing and capable of
system in the United States over the past two receiving the care or that adequate family or profes-
decades has led to an increasing focus and sional support for the patient exists.1
emphasis on home health care services. The Traditional home health care services are typically
specific delivery of home respiratory care and equip- provided by home health agencies. The services of
ment has grown exponentially during this time. these agencies include:
Respiratory care is a highly technical field, dealing with
• Professional nursing visits for skilled care,
complex and sophisticated medical equipment. Home
• Home health aides,
care is no exception. Therefore, most of this chapter
• Homemaker services,
focuses on equipment used to provide respiratory care
• Physical therapy.
in the home care setting.
There must be a support system to provide this Owing to reimbursement issues, the respiratory
equipment to patients at home and to ensure that therapist is not usually part of these services. Respira-
patients or caregivers are properly and appropriately tory care equipment and services are usually provided
educated. Also, because patients are being cared for in by home medical equipment (HME) companies,
an uncontrolled environment and health care profes- sometimes referred to as durable medical equipment
sionals are usually not the primary caregivers, some (DME) companies. This structure for the delivery of
aspects of the home care environment that are not home respiratory care will apparently continue in the
applicable in other care settings are of extreme impor- foreseeable future.
tance. Lastly, law and regulation significantly make an
impact on the provision of home respiratory care
services. All of these subjects are covered as they apply History and Evolution
to respiratory therapists and their role in the delivery of
Several factors have had a significant impact on the
home care services.
evolution of home respiratory care and the dramatic
In 1990, the Council on Scientific Affairs defined
increase in today’s demand for these services. The
home health care as “the provision of services and
respiratory therapist (RT) must know about them in
equipment to the patient in the home for the purposes
order to understand the current structure, environment,
of restoring and maintaining his or her maximum level
and delivery of home respiratory care. These factors are:
of comfort, function, and health.” This includes
medical and health-related services or care provided in • Advances in technology.
the home and implies that any procedure can be • Health care economics.
delivered, performed, or administered to a patient at • Changing demographics of the critically ill.
AARC Position Statement Home Respiratory Care Services

Home respiratory care is defined as those pre- testing—is the most competent health care pro-
scribed respiratory care services provided in a fessional to provide prescribed home respiratory
patient’s personal residence. Prescribed respiratory care. The complexities of the provision of home
care services include, but are not limited to, respiratory care are such that the public is placed
patient assessment and monitoring, diagnostic at a significant risk of injury when respiratory care
and therapeutic modalities and services, disease services are provided by unqualified persons, either
management, and patient and caregiver education. licensed or unlicensed, rather than by persons with
These services are provided on a physician’s written appropriate education, training, credentials, and
or verbal order and practiced under appropriate competency. Therefore, the AARC recommends that
law, regulation, and medical direction. A patient’s practitioners who are employed to provide home
place of residence may include, but is not limited respiratory care possess the Certified Respiratory
to, single-family homes, mobile homes, multi-family Therapist (CRT) or Registered Respiratory Therapist
dwellings, assisted living facilities, retirement com- (RRT) credential awarded by the National Board
munities, and skilled nursing facilities. The goal of for Respiratory Care, as well as state licensure or
home respiratory care is to achieve the optimum certification where applicable. In addition, the
level of patient function through goal setting, edu- AARC supports efforts to improve access to home
cation, the administration of diagnostic and thera- respiratory care through improvements in public
peutic modalities and services, disease manage- and private insurance coverage, state and federal
ment, and health promotion. reimbursement programs, and enhancement of
It is the position of the American Association services in provider models.
for Respiratory Care that the respiratory therapist— Source: Reprinted from AARC Times, May 2001;25:77. Courtesy of
by virtue of education, training, and competency AARC, Dallas, Texas, 2000.
Advances in technology were certainly one of the DRG system, hospitals are reimbursed at a fixed
most important factors in the early development of rate for each of 485 specific diagnoses. This system
home respiratory care. Before 1970, most respiratory discourages overutilization of services and encourages
equipment was pneumatic, rendering it difficult, if not early discharge from the acute care hospital—“quicker
impossible, for home use.2 The equipment was devel- and sicker.” This system has directly increased the
oped for use by health care professionals and therefore number of patients requiring continued care after
was usually complex. The development of compact, discharge, including many respiratory care modalities.
portable equipment that was simple enough to be The increase in managed care and capitation in the
operated by patients and caregivers of all ages and 1990s has driven the movement to provide health care
educational levels increased its availability and accep- in the least costly setting. Patients requiring high-tech
tance for use in the home. care and services may initially be discharged to
Health care economics has also played a significant subacute care facilities, then moved into the home
role in the growth of home respiratory care. In 1965, environment where these services are routinely
the federal government enacted legislation creating provided.
Medicare and Medicaid benefits. The benefits included A third factor behind the growth of home respira-
reimbursement for durable medical equipment, tory care is the changing demographics of the chronically
including respiratory equipment, in the home. This ill population. Increasing the number of patients need-
created a rapid growth in the number of HME compa- ing continuing care and services at home are such
nies nationwide. Within 10 years, HME companies forces as:
began providing not only respiratory equipment, but
• The increase in chronic pulmonary disease as a
also the care and services of the respiratory therapist as
result of cigarette smoking and environmental
an adjunct to equipment use.
factors.
In 1983, the Health Care Financing Administra-
• The growth of the elderly population with
tion (HCFA), now known as the Centers for Medicare
ongoing health care needs.
& Medicaid Services (CMS), introduced a prospective
• The improved survival rates of patients with
payment system for the reimbursement of hospitals
pulmonary disorders.
called diagnosis-related groups (DRGs). Under the
These services are necessary to prevent hospitalization for admission, which include the patient’s home care
and to improve the function and quality of life. needs, caregiver support, geographical location,
With the Baby Boomer generation reaching retirement reimbursement, and the home environment.
age, the predictions are for continued significant If a patient is currently in a health care facility, a
growth of this population segment and therefore discharge planner or case manager is usually the first
increased demand for home respiratory services. member of the home care team to identify the patient
as an appropriate candidate for discharge. The choice
SELECTING PATIENTS FOR HOME CARE of home care may be based on patient diagnosis or
therapy required. Tables 35-1 and 35-2 include these
The success of providing respiratory care in the home selection criteria.
depends on appropriate patient selection and a To facilitate a successful, coordinated discharge, the
planned and coordinated discharge. This is more appropriate members of the discharge planning team
accurately viewed as the admission process to the should meet and begin the plan for the patient’s
home care provider. The provider sets specific criteria discharge. Table 35-3 identifies the key members of the
discharge planning team and their responsibilities.
TABLE 35-1 Selection criteria for home
care by patient diagnosis
Obstructive Pulmonary Disease:
TABLE 35-2 Selection criteria for home
Chronic obstructive pulmonary disease care based on therapy
Pulmonary emphysema
Oxygen Therapy:
Chronic bronchitis
Oxygen concentrator
Bronchial asthma
Liquid oxygen (LOX)
Bronchiectasis
Compressed gas
Acute bronchitis
Portable oxygen systems
Bronchiolitis
Oxygen conserving device
Restrictive Pulmonary Disease:
Transtracheal oxygen therapy
Pulmonary fibrosis
Hyperbaric oxygen (HBO)
Sarcoidosis
Aerosol Therapy and Tracheobronchial Toilet:
Cystic fibrosis
Metered-dose inhaler (MDI)
Pneumoconiosis (occupational lung conditions)
Small volume nebulizer
Tuberculosis
Continuous aerosol
Pneumonia, including pneumocystis carinii
IPPB
Lung cancer
Exsufflator
Neuromuscular paralysis and related anomalies,
Suction
including myasthenia gravis, poliomyelitis, and
amyotrophic lateral sclerosis (ALS) Tracheostomy care
Skeletal abnormalities involving the bony thorax, Chest physical therapy (CPT)
such as kyphoscoliosis Sleep Apnea Therapy:
Severe obesity Nasal CPAP
Cardiovascular Conditions: Bilevel therapy
Congestive heart failure Neonatal or Pediatric Modalities:
Postmyocardial infarction Apnea monitoring
Atypical Conditions: Oximetry monitoring
Sleep apnea syndrome Mechanical Ventilation:
Sudden infant death syndrome (SIDS) Positive pressure
Bronchopulmonary dysplasia (BPD) Invasive
Migraine headaches Noninvasive positive pressure
Ulcerative conditions involving the skin Negative pressure
TABLE 35-3 Key members of the discharge The discharge plan should include the following
team and their responsibilities elements:
Team • Therapeutic needs

Member Responsibilities • Equipment needs
• Caregiver needs
Utilization Documents patient’s in-hospital care
• Reimbursement
review board and recommends discharge when
• Patient and/or caregiver education and training
member appropriate.
• Assessment of home environment
Physician Initiates discharge and prescribes • Establish time frame for discharge
home care therapy.
When the discharge plan is completed, the patient is
Social worker May include discharge planning
ready for admission to the home care organization. The
or community health department.
respiratory therapist and HME provider subsequently
Usually functions as team coordinator.
must develop the home care plan to address the initial
Organizes and coordinates all
and ongoing problems and needs of the patient. (This
prescribed patient home care.
process is discussed later in this chapter.)
Contacts all team members and
The American Association for Respiratory Care
outside resources and ensures patient
(AARC) developed a clinical practice guideline (CPG)
can be discharged safely and properly.
in 1995 on discharge planning for the respiratory care
Case Acts as gatekeeper while ensuring patient. The CPG outlines the procedure for the
manager continuity of patient care. Grants development and implementation of a comprehensive
authorization for purchasing costly plan for the safe discharge of the respiratory care
equipment or services and reviews patient from a health care facility and for continuing
outpatient or home care procedures. safe and effective care at an alternate site. The CPG
Registered Develops home care plan, provides includes the method for discharge planning as well as
nurse necessary follow-up, and evaluates patient evaluation, site evaluation, personnel, financial
patient status and response to resources, and education and training.3
prescribed home care. Can function
as team coordinator.
Respiratory Recommends respiratory home care
Oxygen Therapy
therapist based on patient condition and need Home oxygen therapy, which began with the delivery
and may set up home care equipment of oxygen cylinders in the home, is the most common
and therapy as required. Evaluates modality provided by respiratory therapists in the
home care environment and patient home today. In 1980, the nocturnal oxygen therapy trial
response to therapy. Can function as (NOTT) documented the long-term survival of the
team coordinator. COPD patient using long-term oxygen therapy (LTOT).4
LTOT has also been demonstrated to improve noctur-
HME Provides prescribed home care equip-
nal oxygen saturation, reduce pulmonary arterial
provider ment and supplies and possibly respi-
pressure, and lower pulmonary vascular resistance. In
ratory therapists for equipment setup
2000 Petty and Bliss revisited the NOTT study and
and scheduled follow-up. Handles all
found that patients who were highly ambulatory and
emergencies involving equipment.
on continuous oxygen therapy (COT) had a 50%
Clinical Evaluates patient’s emotional status higher survival rate than low ambulatory patients and
psychologist and provides counseling as necessary. a 40% higher survival rate than high ambulatory
Physical Recommends and provides all forms patients using only nocturnal oxygen.5
therapist of prescribed physical therapy. In 1985, CMS developed criteria for reimbursement
Occupational Recommends and provides all forms of oxygen therapy equipment by Medicare in order to
therapist of prescribed occupational therapy. reduce the indiscriminate ordering of oxygen equip-
ment. CMS requires that patients meet specific diagno-
Dietitian or Evaluates patient’s nutritional needs
sis criteria and have a hypoxemia documented by
nutritionist and prepares dietary plan. As
arterial blood gas analysis or pulse oximetry as depicted
necessary, arranges meal delivery.
in Table 35-4. The physician must prescribe the specific
Family or Implements patient home care daily oxygen flow rate (FIO2), duration of usage, oxygen
caregiver and notifies team members of any system, and route of administration. PRN orders are not
changes in patient status or condition. acceptable.
TABLE 35-4 Medicare guidelines for specific to oxygen administration in the home or
reimbursement of oxygen therapy alternate site health care facility, and outlines indica-
tions, precautions, assessment of need, resources,
equipment in the home monitoring, and infection control.6
Acceptable Diagnoses:
Severe lung disease, including chronic obstructive
pulmonary disease, diffuse interstitial lung disease,
OXYGEN CONCENTRATORS
cystic fibrosis, bronchiectasis, and widespread The oxygen concentrator is an electrically powered
pulmonary neoplasm device that physically separates oxygen from the
nitrogen in room air. Initially there were two types of
Hypoxia related symptoms or findings that have an oxygen concentrators:
expected improvement with oxygen therapy, including
pulmonary hypertension, recurring congestive heart • Membrane oxygenators, also called oxygen
failure, chronic cor pulmonale, erythrocytosis, enrichers, are no longer used by HME providers.
impairment of the cognitive process, nocturnal • Molecular sieves are the most common type of
restlessness, and morning headaches concentrator used.
Nonqualifying Diagnoses: Membrane oxygenators (oxygen enrichers) use a
Angina pectoris in the absence of hypoxemia plastic membrane approximately 1 micron thick.
Severe peripheral vascular disease Oxygen and water vapor diffuse easily across the mem-
brane, providing an enriched output of approximately
Terminal illnesses without lung involvement
40% oxygen at flows up to 10 Lpm. To compensate for
Acceptable Blood Gas or Oxygen Saturation Values: this lower concentration, flows approximately three
Arterial PO2 at or below 55 mm Hg times that of a normal oxygen source must be used.
SpO2 at or below 88% The molecular sieve concentrator operates with an
air compressor, delivering room air to one of two sieve
Provisional Coverage:
beds. The sieve beds contain zeolyte pellets made of
Arterial PO2 between 56 and 59 mm Hg or SpO2 at sodium aluminum silicate. The pellets absorb nitrogen,
89% with a secondary diagnosis, including any of the carbon dioxide, carbon monoxide, and water vapor.
following conditions: Oxygen and a small amount of argon flow through the
Dependent edema, suggesting congestive heart failure sieve beds and are stored in an accumulator until
Cor pulmonale delivered to the patient through a flowmeter. The sieve
beds alternate between pressurization to produce
Erythrocythemia with a hematocrit of 57% or higher
oxygen and depressurization to purge the waste gases
Nonqualifying Conditions: by what is called the pressure swing cycle. Figure 35-1
Arterial PO2 60 mm Hg or greater is a schematic of a typical molecular sieve oxygen
SpO2 90% or greater concentrator.
Oxygen concentrators can produce an oxygen
purity level of up to 98% at flows of 1–2 Lpm. The
oxygen purity level (FIO2) decreases as the liter flow
Three systems are available for delivery of oxygen increases. The highest liter flow available from oxygen
in the home. concentrators today is 10 Lpm. Oxygen concentrators
are the most appropriate for low-flow oxygen therapy
• Oxygen concentrators are the most commonly
via nasal cannula or for titration into other systems,
used system.
such as high-humidity tracheostomy collars, CPAP
• Liquid oxygen is a frequently used modality and
units, and portable ventilators. Each oxygen concentra-
preferred by some physicians and patients.
tor manufacturer has specific purity levels for each liter
However, due to reimbursement issues, liquid
flow. These data must be available when performing
oxygen use has declined somewhat in recent years.
operational verification on the equipment. The fre-
• Compressed gas cylinders are used in specific
quency of this verification is also specified by the
situations (discussed later in this chapter).
manufacturer and is usually every 90 days.
Table 35-5 compares the three home oxygen systems, Most concentrators manufactured today include a
including the advantages, disadvantages, and safety built-in oxygen sensor that monitors the oxygen purity
measures to be followed. level. The concentrator has an audible and visual alarm
In 1992, the AARC developed a CPG for oxygen that will alert the patient or caregiver if the purity level
therapy in the home and revised it in 2007. The CPG is drops below a predetermined level, usually 90%. The
TABLE 35-5 Comparison of home oxygen systems

System Advantages Disadvantages Safety Measures
Oxygen concentrator Low-pressure system. Requires electrical power. Do not place unit on its side.
Does not require deliveries. Requires backup cylinder for
Can be easily moved. power failures.
Economical. Has limited flow rate capabilities.
Oxygen purity level decreases at
higher flow rates.
Liquid oxygen No need for electric power. Evaporates if not routinely used. Do not tip reservoir or place
Low-pressure system. Can cause burns if mishandled. portable on its side.
Large quantities of oxygen in Requires periodic deliveries. Fill portable unit carefully.
a relatively small container. Do not keep portable in heat.
Can refill portable unit from
reservoir.
Compressed gas No loss of supply when not Is heavy and cumbersome. Secure cylinders with base
in use.

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Foundations of

Kenneth A. Wyka, MS, RRT, AE-C, FAARC

Paul J. Mathews, PhD, RRT, FCCM, FCCP, FAARC

John A. Rutkowski, MPA, MBA, FACHE, RRT

Cengage Learning is a leading provider of customized learning solutions with

Cengage Learning products are represented in Canada by Nelson Education, Ltd.

To learn more about Delmar, visit www.cengage.com/delmar

Printed in the United States of America

To my wife, Kathy, in sincere gratitude for her continued

To my parents, Paul J. and Ruth Irene (O’Malley) Mathews.

To my wife, Joanne, thank you for your unwavering patience,

Preface xvii 15. Clinical Laboratory Studies 387

31. Emergency Respiratory Care 853 Appendix A: The Respiratory Therapist

Appendix E: Arterial Blood Gases:

Section I Scope of Practice 1

CHAPTER 1 THE HISTORY AND SCOPE OF RESPIRATORY CARE 3

CHAPTER 2 LEGAL, PROFESSIONAL, AND ETHICAL PRACTICE 23

Section II The Applied Sciences 51

CHAPTER 3 APPLIED PHYSICS 53

CHAPTER 4 APPLIED CHEMISTRY 82

CHAPTER 5 APPLIED MICROBIOLOGY 101

CHAPTER 6 CARDIOPULMONARY ANATOMY AND PHYSIOLOGY 116

CHAPTER 7 CARDIOPULMONARY PHARMACOLOGY 171

CHAPTER 8 PULMONARY INFECTIONS 201

CHAPTER 9 AIRF LOW LIMITATION DISEASES 227

CHAPTER 10 DIFFUSE PARENCHYMAL LUNG DISEASES 251

CHAPTER 11 ATELECTASIS, PLEURAL DISORDERS, AND LUNG CANCER 266

CHAPTER 12 DISEASES THAT AFFECT THE PULMONARY VASCULATURE 284

Section III Essential Diagnostics 299

CHAPTER 13 COMPREHENSIVE HISTORY, ASSESSMENT,

CHAPTER 14 RADIOLOGY FOR THE RESPIRATORY THERAPIST 343

CHAPTER 15 CLINICAL LABORATORY STUDIES 387

CHAPTER 16 ARTERIAL BLOOD GASES AND NONINVASIVE MONITORING

CHAPTER 17 PULMONARY FUNCTION TESTING 455

CHAPTER 18 POLYSOMNOGRAPHY AND OTHER TESTS

CHAPTER 19 CARDIAC AND HEMODYNAMIC MONITORING 504

Section IV Essential Therapeutics 555

CHAPTER 20 OXYGEN AND MEDICAL GAS THERAPY 557

CHAPTER 21 HUMIDITY AND AEROSOL THERAPY 597

CHAPTER 22 HYPERINFLATION THERAPY 626

CHAPTER 23 PULMONARY HYGIENE AND CHEST PHYSICAL THERAPY 640

CHAPTER 24 AIRWAY MANAGEMENT 661

CHAPTER 25 PHYSIOLOGICAL EFFECTS OF MECHANICAL VENTILATION 687

CHAPTER 26 INITIATION, MONITORING, AND DISCONTINUING

CHAPTER 27 MECHANICS AND MODES OF MECHANICAL VENTILATION 728

CHAPTER 28 NONINVASIVE MECHANICAL VENTILATION 766

Section V Levels of Care Delivery 795

CHAPTER 29 NEONATAL AND PEDIATRIC RESPIRATORY CARE 797

CHAPTER 30 GERIATRIC APPLICATIONS 835

CHAPTER 31 EMERGENCY RESPIRATORY CARE 853

CHAPTER 32 MANAGING DISASTERS: RESPIRATORY CARE

CHAPTER 33 ADULT CRITICAL CARE 918

CHAPTER 34 SUBACUTE AND LONG-TERM CARE 937

CHAPTER 35 RESPIRATORY HOME CARE 952

CHAPTER 36 PULMONARY REHABILITATION 984

CHAPTER 37 PATIENT TRANSPORT IN RESPIRATORY CARE 1025

Section VI Miscellaneous Applications 1035

CHAPTER 38 PROTECTING THE PATIENT AND THE

CHAPTER 39 HEALTH PROMOTION 1068

CHAPTER 40 FUNDAMENTALS OF PATIENT EDUCATION 1098

CHAPTER 41 MANAGEMENT OF RESPIRATORY CARE SERVICES 1115

APPENDIX A: THE RESPIRATORY THERAPIST IN

• Key Terms are listed so the reader can become CHAPTER 3