Respiratory

“Roses are red,
Violets are blue,

Without your lungs
Your blood would be, too.”
David D. Ralph, MD
New England Journal of Medicine
MEDICAL-SURGICAL
NURSING
Arni A. Magdamo, MD, MHA,

FPCP
University of the Philippines
College of Medicine, College of Nursing
The Respiratory System
Normal Anatomy and

Physiology
The Respiratory Process
 Respiration is the process by which
oxygen enters the body and is utilized
by the cells for their metabolic
processes. It essentially involves five
interdependent steps.
 Ventilation refers to the entry of air
containing oxygen and other gases into
the lungs.
 Ventilation is followed by the diffusion
of gases from and into the alveoli and
alveolar sacs. Oxygen from the alveoli
passes through the respiratory
membrane and enter the perialveolar
capillaries, while carbon dioxide from
the capillaries diffuses through the
respiratory membrane to leave the
lungs by means of exhalation.
 Circulation makes it possible for oxygen
to reach the distant tissues, and for
carbon dioxide to travel from the tissues
back into the lungs.
 The fourth component of the respiratory
process involves another diffusion of
gases, this time involving the entry of
oxygen into target tissues, and the
entry of carbon dioxide into the blood
stream for delivery back into the lungs.
 Cell metabolism and respiration are the
final steps of the respiratory process
wherein oxygen is utilized by the cells,
and carbon dioxide, along with other
waste products, is produced.
The Upper Respiratory
Tract:
The Nose
 The bridge of the nose is bone, and
most of the external nose is cartilage.
 The nasal cavity houses one of the most
efficient filtering system of the body.
 The external nares is divided by the
nasal septum into right and left
portions.
 The paranasal sinuses and the
nasolacrimal duct open into the nasal
cavity.
 Hairs inside the external nares trap
Tract:
The Nose
 The nasal cavity is lined with
pseudostratified ciliated epithelium that
traps debris and moves it to the
pharynx.
 The nasal turbinates or conchae provide
for an additional filtering mechanism by
creating a turbulent airflow within the
nasal cavity that dislodges inhaled
pollutants and make them adhere to the
sticky mucosal surface of the nasal
cavity.
Tract:
The Nose
 The superior part of the nasal cavity
contains the sensory cells for the sense
of smell.
 A vast network of capillaries, called
Kiesselbach’s plexus, line the mucosa of
the nasal cavity.
Tract:
The Nose
Tract:
The Pharynx
 The nasopharynx joins the nasal cavity
through the internal nares and contains
the opening to the auditory (Eustachian)
tube and the pharyngeal tonsils.
 The oropharynx joins the oral cavity and
contains the palatine and lingual tonsils.
 The laryngopharynx opens into the
larynx and the esophagus.
Tract:
The Pharynx
Tract:
The Larynx
 The larynx is a set of cartilages
collectively called the “voice box”.
 There are three unpaired cartilages.
The thyroid cartilage and cricoid
cartilage form most of the larynx. The
epiglottis covers the opening of the
larynx during swallowing.
 There are six paired cartilages. The
corniculate, the arytenoid, and the
cuneiform cartilages all serve as
attachment sites on which the vocal
cords are anchored.
Tract:
The Larynx
 The vocal cords are structures within
the larynx that vibrate to produce.
There are two main groups.
 The vocal folds are the true vocal cords,
connective tissues that vibrate when air
passes through them to produce the
audible sound.
Tract:
The Larynx
 The vestibular folds are known as the
false vocal cords, because they merely
serve as connective tissue support for
the vocal folds.
 The cords produce sounds of different
pitches when their length is varied.
Tract:
The Trachea
 The trachea, also known as the “wind
pipe,” is a hollow tubular structure that
connects the larynx to the lower
respiratory organs (the respiratory
tree).
 It is a series of 15 to 20 C-shaped
cartilages that are solid anteriorly, and
supported posteriorly by a layer of
smooth muscles which contract or relax
to bring about dilation or constriction of
the airways.
Tract:
The Trachea
 It is lined by pseudostratified ciliated
columnar epithelium which aids in the
filtering of inhaled air.
Tract:
The Trachea
The Lower Respiratory
Tract:
The Respiratory Tree
 The primary bronchi extend from the
trachea to each lung. The right primary
bronchus is shorter, wider and is
oriented more vertically, while the left
primary bronchus is longer, narrower
and is oriented more horizontally.
 There are two lungs. The right lung has
three lobes and ten lobules, while the
left lung has two lobes and nine lobules.
Tract:
 The airway passages of the lungs
branch and decrease in size.
 The primary bronchi form the secondary
bronchi, which go to each lobe of the
lungs.
 The secondary bronchi form the tertiary
bronchi, which go to each lobule of the
lung.
 The tertiary bronchi branch many times
to form the bronchioles.
Tract:
 The bronchioles branch to form the
terminal bronchioles, which become the
respiratory bronchioles, from which the
alveoli branch.
 The epithelium from the trachea to the
terminal bronchioles is ciliated to
facilitate the removal of debris.
 Cartilage helps to hold the tube system
open (from the trachea to the
bronchioles).
Tract:
 Smooth muscle controls the diameter f
the tubes (especially the bronchioles).
 The alveoli are sacs formed by simple
squamous epithelium, and they
facilitate the diffusion of gases.
Tract:
The Lungs
Tract:
The Alveoli
Mechanics of Breathing
 Ventilation is the movement of air into
and out of the lungs. Air moves from an
area of higher pressure to an area of
lower pressure.
 Inspiration occurs when the diaphragm
contracts and the external intercostal
muscles lift the ribcage, thus increasing
the volume of the thoracic cavity.
 Expiration occurs when the diaphragm
relaxes and the internal intercostal
muscles depress the ribcage, thus
decreasing the volume of the thoracic
 Lungs tend to collapse because of the
elastic recoil of the connective tissue,
and surface tension of the fluid lining
the alveoli.
 The lungs normally do not collapse
because surfactant reduces the surface
tension of the fluid lining the alveoli,
and the visceral pleura tends to adhere
to the parietal pleura.
Pulmonary Volumes and
Capacities
 There are four pulmonary volumes: tidal
volume, inspiratory reserve volume,
expiratory reserve volume, and residual
volume.
 The tidal volume refers to the volume of
air that goes into and out of the lungs
during normal respiration (about 500
cc).
 The inspiratory reserve volume is the
amount of air that can be inspired
forcefully after inspiration of the normal
tidal volume (about 3000 cc).
Capacities
 The expiratory reserve volume is the
additional amount of air that can be
expired forcefully (about 1100 cc).
 The residual volume is the volume of air
left in the lungs after maximum
expiration. This is also known as “dead
space” (about 1200 cc).
Capacities
 The pulmonary capacities refer to the
sum of two or more pulmonary volumes.
 The vital capacity is the sum of the IRV,
the TV and the ERV. It is the maximum
volume of air that a person can expel
from his respiratory tract after a
maximum inspiration (about 4600 cc).
VC = IRV + TV + ERV
Capacities
 The inspiratory capacity is the amount
of air that a person can inspire
maximally after a normal expiration
(about 3500 cc).
IC = TV + IRV
 The functional residual capacity is the
amount of air remaining in the lungs at
the end of a normal expiration (about
2300 cc).
FRC = ERV + RV
 The total lung capacity is the sum of all
Capacities
MAXIMUM
INSPIRATION
IRV
IC
VC TOTAL
LUNG
TV CAPACITY
ERV
MAXIMUM
EXPIRATION
FRC
RV RV
Pulmonary Pressures
 Major factors in determining the extent
of lung expansion and compliance
during the processes of inspiration and
expiration:
 Alveolar pressure
 Intrapleural pressure
 Alveolar surfactant
 During inspiration, the thoracic cage
enlarges, enlarging both lungs and
decreasing the pressures.
Pulmonary Pressures
 Boyle’s Law:
During inspiration, the enlargement of
the thoracic cage decreases the
pressure in the alveoli to about –3
mmHg. This negative pressure pulls air
through the respiratory passageways
into the alveoli.
Pulmonary Pressures
 Boyle’s Law:
During expiration, the exact mechanism
and effects occur. Compression of the
thoracic cage around the lungs
increases the alveolar pressure to
approximately +3 mmHg which pushes
the air out of the alveoli into the
atmosphere.
Pulmonary Pressures
 Intrapleural Pressures:
 Intrapleural space is the space between the
lungs and the outer walls of the thoracic
cavity. The pressure here is ALWAYS a few
mmHg less than in the alveoli for the
following reasons:

Surface tension of the fluid inside the alveoli
always makes the alveoli try to collapse.

Elastic fibers spread in all directions through the
lung tissues and tend to contract the lungs.
 These factors pull the lungs away from the
outer walls of the pleural cavity, creating an
average negative pressure of –5 mmHg.
Pulmonary Pressures
 Surfactant:
 Surface active agent
 Detergent that greatly decreases the
surface tension of fluid lining the alveoli.
Essential Requirements for
Ventilation
 Adequate atmospheric oxygen
 Clean air passages
 Adequate pulmonary compliance and
recoil
 Compliance is the expansibility or
stretchability of the lungs.
 Recoil is the ability to collapse away from
the chest wall due to (1) elastic fibers
present in the lungs, and (2) surface tension
of the fluid lining of the alveoli which
accounts for 2/3 of the recoil phenomenon.
Gas Exchange
 The respiratory membranes are thin and
have a large surface area that facilitates
gas exchange.
 The components of the respiratory
membrane include a film of water, the
walls of the alveoli, and interstitial
space, and the walls of the perialveolar
capillary.
Gas Exchange
 The rate of diffusion depends on the
thickness of the respiratory membrane,
the surface area of the membrane, the
diffusion coefficient of the gas, and the
partial pressure of gases in the alveoli
and in the blood.
Transport of Oxygen and
Carbon Dioxide
 97% of oxygen combines loosely with
hemoglobin in the red blood cells and is
carried into the tissues as
oxyhemoglobin. The remaining oxygen
is dissolved and transported in the fluid
of plasma and cells.
 The amount of oxygen that the blood
will absorb before it is fully saturated is
about 20 ml per 100 ml of blood (20
vol%).
Carbon Dioxide
 As the hemoglobin releases oxygen to
the tissues, it is referred to as reduced
hemoglobin.
 Normally, only about 25% of oxygen per
ml of blood is diffused to the tissue (5
vol%). However, this rate of release can
be increased to 75% during periods of
stress or increased exercise.
Carbon Dioxide
 Factors that influence the rate of
oxygen transport from the lungs to the
tissues:
 Cardiac output
 Erythrocyte count
 Exercise
 Hematocrit
Control of Respiration
 The respiratory center in the medulla
oblongata and pons stimulates the
muscles of inspiration to contract.
When stimulation of the muscles of
inspiration stops, expiration occurs
passively.
 Receptors present in the respiratory and
cardiovascular system, as well as in
other parts of the body, receive changes
in the internal milieu and send sensory
signals to the respiratory center.
Receptors are classified as:
chemoreceptors, baroreceptors,
proprioceptors, and stretch receptors.
 The Hering-Breuer reflex inhibits the
inspiratory center when the lungs are
stretched during inspiration.
 Carbon dioxide is the major chemical
regulator of respiration.
 It is possible to consciously control
ventilation, but only up to a certain
degree.
The Cough and Sneeze
Reflexes
The Cough and Sneeze
Reflexes
 Means for keeping the respiratory
passages clean by forcing air very
rapidly outward using these two
reflexes.
 Mediated by respiratory muscles,
voluntary and involuntary, with
regulation by the central nervous
system and sensory receptors lining the
respiratory tract.
The Cough Reflex
Irritant touches the surface of the glottis, trachea or bronchus.
Sensory signals are transmitted to the medulla.
Motor signals are transmitted back to the respiratory system.

The Cough Reflex
Motor signals are transmitted back to the respiratory system.
Respiratory muscles contract rapidly generating

high pressures in the lungs while the vocal cords
remain tightly closed.
Vocal cords open suddenly, allowing pressurized air in the

lungs to flow out in a blast.
The Sneeze Reflex
Irritant comes into contact with sensory receptors in the nose.
Sensory signals are received in the medulla.
Motor signals are generated and transmitted back.

The Sneeze Reflex
Motor signals are generated and transmitted back.
Respiratory muscles contract rapidly generating

high pressures in the lungs while the vocal cords
remain tightly closed.
Vocal cords open suddenly, allowing pressurized air in the

lungs to flow out in a blast through the nose and mouth.
Diagnosis of Pulmonary
Function
Clinical Assessment
Symptoms of Pulmonary
Disease
 Dyspnea
 Sensation of breathlessness that is
excessive for any given level of physical
activity.
 Paroxysmal nocturnal dyspnea
 Inappropriate breathlessness at night.
 Orthopnea
 Dyspnea on recumbency.
 Platypnea
 Dyspnea on the upright position relieved by
recumbency.
Disease
 Persistent cough
 Always abnormal
 Chronic persistent cough may be caused by
cigarette smoking, asthma, bronchiectasis
or COPD.
 May also be caused by drugs, cardiac
disease, occupational agents and
psychogenic factors.
 Complications include (1) worsening of
bronchospasm, (2) vomiting, (3) rib
fractures,
(4) urinary incontinence, and (5) syncope.
Disease
 Stridor
 Crowing sound during breathing.
 Caused by turbulent airflow through a
narrowed upper airway.
 Inspiratory stridor implies extratracheal
variable airway obstruction.
 Expiratory stridor implies intratracheal
variable airway obstruction.
 Stertorous breathing is an inspiratory sound
due to vibration in the pharynx during sleep.
Disease
 Wheezing
 Continuous musical or whistling noises
caused by turbulent airflow through
narrowed intrathoracic airways.
 Most, but not all, are due to asthma.
 Hemoptysis
 Expectoration of blood.
 Often the first indication of serious
bronchopulmonary disease.
 Massive hemoptysis: coughing up of more
than 600 ml of blood in 24 hours.
Signs of Pulmonary
Disease
 Tachypnea
 Rapid, shallow breathing.
 Arbitrarily defined as a respiratory rate in
excess of 18/min.
 Bradypnea
 Slow breathing.
 Hyperpnea
 Rapid, deep breathing.
 Hyperventilation
 Increase in the amount of air entering the
alveoli.
Signs of Pulmonary
Disease
 Kussmaul respiration (air hunger)
 Deep, regular sighing respiration, whether
the rate be normal slow or fast.
 Occurs in diabetic ketoacidosis and uremia,
as an exaggerated form of bradypnea.
 Cheyne-Stokes respiration
 Commonest form of periodic breathing.
 Periods of apnea alternate regularly with
series of respiratory cycles. In each series,
the rate and amplitude increase to a
maximum followed by cessation.
Signs of Pulmonary
Disease
 Biot breathing
 Uncommon variant of Cheyne-Stokes
respiration.
 Periods of apnea alternate irregularly with
series of breaths of equal depth that
terminate abruptly.
 Most often seen in meningitis.
Signs of Pulmonary
Disease
 Singultus
 Sudden, involuntary diaphragmatic
contraction producing an inspiration
interrupted by glottal closure to emit a
characteristic sharp sound.
 Causes:
 Reflex stimulation without organic disease
 Diseases of the central nervous system
 Mediastinal disorders
 Pleural irritation
 Abdominal disorders
 Diaphragmatic stimulation
Signs of Pulmonary
Disease
 Physical chest deformities
 The thorax is usually symmetric, both sides
rise equally on inspiration.
 Chest asymmetry at rest:
 Scoliosis
 Chest wall deformity
 Severe fibrothorax
 Conditions with unilateral loss of lung volume
Signs of Pulmonary
Disease
 Symmetrically reduced chest expansion
during deep inspiration:

Neuromuscular disease

Emphysema

Ankylosis of the spine
 Asymmetric chest expansion during
inspiration:

Unilateral airway obstruction

Pleural or pulmonary fibrosis
 Splinting due to chest pain
 Pleural effusion
 Pneumothorax
Signs of Pulmonary
Disease
 Expansion on the chest, collapse of the
abdomen on inspiration:

Weakness or paralysis of the diaphragm
 Chest collapse, rise of the abdomen on
inspiration:
 Airway obstruction
 Intercostal muscle paralysis
 Flail deformity of the chest
Signs of Pulmonary
Disease
 Pulsus paradoxicus
 The arterial blood pressure normally falls
about 5 mmHg to a maximum of 10 mmHg
on inspiration.
 Exaggeration of the normal response.
 Seen in:
 Severe asthma or emphysema
 Upper airway obstruction
 Pulmonary embolism
 Pericardial constriction or tamponade
 Restrictive cardiomyopathy
Signs of Pulmonary
Disease
 Cyanosis
 Bluish discoloration of skin or mucous
membranes.
 Caused by increased amounts (>5 g/dL) of
unsaturated / reduced hemoglobin.
 Presents as either central or peripheral
cyanosis
Signs of Pulmonary
Disease
 Digital clubbing
 Anteroposterior thickness of the index finger
at the base of the fingernail exceeds the
thickness of the distal interphalangeal joint.
 Helpful clues:
 Nail bed sponginess
 Excessive rounding of the nail plate
 Flattening of the angle between the nail plate and
the proximal nail skin fold
Signs of Pulmonary
Disease
 Percussion sounds (resonance, dullness,
hyperresonance)
 Auscultatory sounds (vesicular,
bronchial, bronchovesicular)
 Adventitious sounds
 Abnormal sounds on auscultation
 May be classified as continuous (wheezes,
rhonchi) or discontinuous (crackles,
crepitations)
Signs of Pulmonary
Disease
 Wheezes
 High-pitched sounds which results from
bronchospasm, bronchial or bronchiolar
mucosal edema, or airway obstruction by
mucus, tumors, or foreign bodies.
 Rhonchi
 Low-pitched sounds caused by sputum in
large airways and frequently clear after
coughing.
Signs of Pulmonary
Disease
 Crackles
 Generated by the snapping open of small
airways during inspiration.
 Fine crackles are heard in interstitial
diseases, early pneumonia or pulmonary
edema, patchy atelectasis and in some
patients with asthma or bronchitis.
 Coarse crackles are heard late in the course
of pulmonary edema or pneumonia.
Signs of Pulmonary
Disease
 Fremitus
 Voice vibrations on the chest wall.
 Localized reduction in fremitus occurs over
areas of air or fluid accumulation in the
lungs.
 Increased fremitus suggests lung
consolidation.
 Bronchophony
 Increased intensity and clarity of the spoken
word during auscultation.
 Heard over areas of consolidation or lung
Signs of Pulmonary
Disease
 Whispered pectoriloquy
 Extreme form of bronchophony in which
softly spoken words are readily heard by
auscultation.
 Egophony
 Auscultation of an “a” sound when the
patient speaks an “e” sound.
Signs of Pulmonary
Disease
TYPICAL CHEST EXAMINATION FINDINGS IN SELECTED CLINICAL CONDITIONS
CONDITION PERCUSSIO FREMITUS BREATH VOICE ADVENTITIOU
N SOUNDS TRANSMISSIO S SOUNDS
N
Normal Resonant Normal Vesicular Normal Absent
Consolidatio Dull Increased Bronchial Bronchophony Crackles

n or , whispered
Atelectasis pectoriloquy,
(with patent egophony
airway)
Consolidatio Dull Decrease Decreased Decreased Absent
n or d
Atelectasis
(with
blocked
Bronchial Resonant Normal Vesicular Normal Wheezing
airway)
Asthma
Signs of Pulmonary
Disease
TYPICAL CHEST EXAMINATION FINDINGS IN SELECTED CLINICAL CONDITIONS
CONDITION PERCUSSION FREMITUS BREATH VOICE ADVENTITIOU
SOUNDS TRANSMISSIO S SOUNDS
N
Interstitial Resonant Normal Vesicular Normal Crackles
Lung
Disease
Emphysema Hyperresona Decrease Decrease Decreased Absent or
nt d d wheezing
Pneumothor Hyperresona Decrease Decrease Decreased Absent

ax nt d d
Pleural Dull Decrease Decrease Decreased Absent or

effusion d d pleural
friction rub
Diagnosis of Pulmonary
Function
Laboratory Assessment
Routine Radiography
 Integral part of the diagnostic
evaluation of diseases involving the
pulmonary parenchyma, the pleura, and
to a lesser extent, the airways and the
mediastinum.
 Usually involves a postero-anterior view
and a lateral view.
 Lateral decubitus views are often useful
for determining whether pleural
deformities represent freely flowing
Routine Radiography
 Apicolordotic views visualize disease at
the lung apices better than the standard
posteroanterior view.
Chest Radiography
Chest Radiography
Ultrasonography
 Not useful for evaluation of the
pulmonary parenchyma.
 Helpful in the detection and localization
of pleural fluid.
Computed Tomography
 Offers several advantages over
conventional radiographs.
 Use of cross-sectional images makes it
possible to distinguish between
densities.
 Better at characterizing tissue densities
and providing accurate size of lesions.
Computed Tomography
Computed Tomography
Magnetic Resonance
Imaging
Pulmonary Function Tests
 Objectively measure the ability of the
respiratory system to perform gas
exchange by assessing ventilation,
diffusion and mechanical properties.
 Composed of the spirometry test and
ventilation-perfusion (V/Q) test.
 Indications:
 Evaluation of the type and degree of
pulmonary dysfunction (obstructive or
restrictive)
 Evaluation of dyspnea, cough and other
symptoms
 Early detection of lung dysfunction
 Surveillance in occupational settings
 Follow-up or response to therapy
 Preoperative evaluation
 Disability assessment
 Relative contraindications:
 Severe acute asthma or respiratory distress
 Chest pain aggravated by testing
 Pneumothorax
 Brisk hemoptysis
 Active tuberculosis
 Spirometry
 Allows for the determination of the presence
and severity of obstructive and restrictive
pulmonary dysfunction.
 The hallmark of obstructive pulmonary
dysfunction is reduction of airflow rates.
 Restrictive pulmonary dysfunction is
characterized by reduction in pulmonary
volumes.
Capacities
MAXIMUM
INSPIRATION
IRV
IC
VC TOTAL
LUNG
TV CAPACITY
ERV
MAXIMUM
EXPIRATION
FRC
RV RV
 Ventilation-Perfusion Lung Scan (V/Q
scan)
 Measures the degree of ventilation of the
individual lung segments and the perfusion
of respective segments to detect any
shunting or mismatch.
 Finds utility in settings where possible
pulmonary embolism is suspected.
Tract:
The Lungs
Arterial Blood Gases
 Measure of acid and base balance in the
blood.
 Also check the saturation of blood with
oxygen.
Biologic Specimen
Collection
 Sputum collection
 Spontaneous expectoration or sputum
induction
 Percutaneous needle aspiration
 Usually carried out under CT or ultrasound
guidance.
 Potential risks include intrapulmonary
bleeding and creation of a pneumothorax.
Biologic Specimen
Collection
 Thoracentesis
 Sampling of pleural fluid or for palliation of
dyspnea in patients with pleural effusion.
 Analysis of the fluid for cellular composition
and chemical constituents like glucose,
protein and LDH.
Biologic Specimen
Collection
 Bronchoscopy
 Provides for direct visualization of the
tracheobronchial tree.
 Rigid bronchoscopy is performed in an
operating room on a patient under general
anesthesia.
 Flexible bronchoscopy may be done under
local anesthesia / sedation.
 Diagnostic uses include histologic
identification or neoplasms and
identification of sources of hemoptysis.
Biologic Specimen
Collection
 Bronchoscopy
 Therapeutic indications are retrieval of
foreign bodies and control of bleeding.
 Bronchoalveolar lavage has been used for
the recovery of organisms that are difficult
to isolate in the usual sputum recovery
methods.
Biologic Specimen
Collection
 Video-Assisted Thoracic Surgery (VATS)
 Operator can biopsy lesions of the pleura
under direct vision for both diagnostic and
therapeutic purposes.
 Thoracotomy
 Frequently replaced by VATS.
 Provides the largest amount of biologic
specimen for histologic study.
Biologic Specimen
Collection
 Mediastinoscopy and Mediastinotomy
 Both performed under general anesthesia
by a qualified surgeon.
 Used for visualization and sampling of
tissues in the mediastinum such as lymph
nodes and neoplasms.
Diseases of the
Respiratory System
Nose, Paranasal Sinuses and

Larynx
Influenza
 Influenza viruses, members of the
Orthomyxoviridae family, include types
A, B and C.
 Outbreaks occur virtually every year
and communicability is influenced by
antigenic shifts and viral mutations that
“confuse” the affected patient’s
immune system.
Influenza:
Clinical Manifestations
 Incubation period of 3-6 days.
 Acute illness usually resolves over 2-5
days.
 Most patients largely recover within 1
week.
 Symptoms and Signs:
 Abrupt onset of headache
 Fever and chills
 Myalgia and malaise
 Cough, sneezing and sore throat
Influenza:
 The major problem posed consists of its
complications:
 Primary influenza viral pneumonia
 Secondary bacterial pneumonia
 Mixed viral and bacterial pneumonia
 Extrapulmonary complications:

Reye’s syndrome

Myositis, rhabdomyolysis and myoglobinuria

Encephalitis, transverse myelitis

Guillain-Barré syndrome
Influenza: Treatment
 Treatment for uncomplicated influenza
is symptomatic
 Salicylates should be avoided in children
because of its association with Reye’s
syndrome.
 Increased oral fluid intake.
 Ascorbic acid
 Antivirals:
 Amantadine (Influenza A)
 Rimantadine (Influenza B)
 Ribavirin (Influenza A and B)
Influenza: Treatment
 Prophylaxis:
 Vaccination against Influenza A and B
 Amantadine and rimantadine
Viral Rhinitis
 The nonspecific symptoms of the
ubiquitous common cold are present in
the early phases of many diseases that
affect the upper aerodigestive tract.
 Rhinoviruses, members of the
Picornaviridae family, are a prominent
cause of the common cold, with
seasonal peaks in the early fall and
spring.
 Infections highest among infants and
Viral Rhinitis
 The infection is spread by contact with
infected secretions or respiratory
droplets or by hand-to-hand contact,
with autoinoculation of the conjunctival
or nasal mucosa.
Viral Rhinitis:
 Incubation period of 1 to 2 days.
 Illness generally lasts 4 to 9 days and
resolves spontaneously.
 Symptoms:
 Headache
 Nasal congestion
 Water rhinorrhea
 Sneezing
 Scratchy throat
 General malaise and occasionally fever
Viral Rhinitis:
 Signs:
 Reddened, edematous nasal mucosa
 Water nasal discharge
 Rhinoviruses are not a major cause of
lower respiratory tract disease.
 Rhinoviruses may cause exacerbations
of asthma and chronic pulmonary
disease in adults.
Viral Rhinitis:
 Complications:
 Transient middle ear effusion
 Secondary bacterial infection
 Because of the mild nature and short
duration of the illness, a specific
diagnosis is not commonly needed;
however, viral cultures can be
performed.
Viral Rhinitis: Treatment
 No proven specific treatment.
 Supportive measures:
 Decongestants should not be used for more
than a week because of rebound congestion
noted after cessation (rhinitis
medicamentosa).
 Antipyretics
 Liberal fluid intake
 Ascorbic acid
Other Viral URTI:
Coronavirus
 Account for 10 to 20% of common colds.
 Most active in late fall, winter and early
spring – a period when the rhinovirus is
relatively inactive.
 Symptoms are similar to those of
rhinovirus, but the incubation period is
longer (3 days) and usually lasts 6 to 7
days.
 Mutations of the virus brought about the
SARS phenomenon.
Other Viral URTI:
Respiratory Syncytial Virus
 Belongs to the Paramyxoviridae family.
 Major respiratory pathogen of young
children and is the foremost cause of
lower respiratory disease in infants.
 Transmitted by close contact with
fingers or fomites as well as through
coarse (not fine) aerosols produced by
coughing or sneezing.
 Incubation period of 4 to 6 days.
 Viral shedding may last two weeks in
children but is much shorter in adults.
Other Viral URTI:
Respiratory Syncytial Virus
 Clinical Manifestations:
 Rhinorrhea
 Low-grade fever
 Mild systemic symptoms
 Cough and wheezing
 25-40% with lower respiratory tract
involvement
 Treatment:
 Antiviral ribavirin for children and infants.
 No specific treatment for adults.
Other Viral URTI:
Parainfluenza Virus
 Single-stranded RNA virus of the
Paramyxoviridae family.
 Important cause of mild illnesses and
croup (laryngotracheobronchitis),
bronchiolitis and pneumonia.
 Cold or hoarseness with cough
 Acute febrile illness with coryza
 Barking cough and frank stridor in children
Other Viral URTI:
Parainfluenza Virus
 Treatment:
 In mild illness, treatment is symptom-based.
 Mild croup may be treated with moisturized
air from a vaporizer.
 More severe cases require hospitalization
and close observation for development of
respiratory distress.
 No specific antiviral treatment is available.
Other Viral URTI:
Adenovirus
 Infections occur frequently in infants
and children with a seasonal distribution
of fall to spring.
 Certain serotypes are associated with
outbreaks of acute respiratory disease
in military recruits.
 Transmission can take place via
inhalation of aerosolized virus, through
the inoculation of the conjunctival sac,
and probably by the fecal-oral route.
Other Viral URTI:
Adenovirus
 Rhinitis
 Pharyngoconjunctival fever (bilateral
conjunctivitis, low-grade fever, rhinitis, sore
throat and cervical lymphadenopathy)
 In adults, the most frequent syndrome is the
acute respiratory disease seen in military
recruits, with prominent sore throat, fever
on the second or third day of illness, cough,
coryza and regional lymphadenopathy.
Other Viral URTI:
Adenovirus
 Diagnosis and Treatment:
 Diagnosis is established by isolation of the
virus.
 No specific antiviral therapy is available.
 A live oral vaccine is available and used
widely to prevent outbreaks among military
recruits.
Acute Bacterial Sinusitis
 Symptoms of rhinitis plus clinical signs
and symptoms that indicate
involvement of the affected sinus or
sinuses such as pain and tenderness
over the involved sinus.
 Occurs when an undrained collection of
pus accumulates in a sinus.
 Typical Pathogens:
 Streptococcus pneumoniae
 Other streptococci
 Haemophilus influenzae
 Staphylococcus aureus
 Moraxella catarrhalis
 Pain on pressure over the cheeks (maxillary
sinuses are the most common sinuses
affected).
 Discolored nasal discharge and poor
response to decongestants.
 Headache “in the middle of the head” or in
the forehead.
 Imaging:
 Transillumination
 Caldwell view (frontal)
 Waters view (maxillary)
 Lateral view (sphenoid)
 Submentovertical view (ethmoid)
 CT scan for recurrent sinusitis
 MRI if malignancy in suspected
Acute Bacterial Sinusitis:
Treatment
 Uncomplicated:
 Outpatient management
 Oral decongestants and nasal decongestant
sprays
 Appropriate oral antibiotics for at least two
weeks
* Amoxicillin provides better sinus
penetration than ampicillin.
 Complicated:
 Failure of sinusitis to resolve after a
completed course of antibiotic treatment.
 Complications:
 Lower respiratory tract infections
 Osteomyelitis and mucocoele
 Intracranial complications
 Malignancy (?)
Allergic Rhinitis
Allergic Rhinitis
 “Hay fever”
 Symptoms mimic that of viral rhinitis
but more persistent and show seasonal
variation.
 Symptoms:
 Watery rhinorrhea
 Eye irritation, pruritus, erythema and
tearing
 Signs:
 Pale or violaceous turbinates
Allergic Rhinitis:
Treatment
 Symptomatic in most cases.
 Oral decongestants
 Antihistamines
 Nasal corticosteroid sprays
 Maintaining an allergen-free
environment
 Air purifiers and dust filters
 Desensitization
Epistaxis
 Bleeding from Kiesselbach’s plexus
 Predisposing factors:
 Nasal trauma (nose picking, foreign bodies,
forceful nose blowing)
 Rhinitis
 Drying of the nasal mucosa from low
humidity
 Nasal septal deviation
 Alcohol use
 Antiplatelet medications
 Bleeding diathesis
Epistaxis
 Treatment:
 Direct pressure on the bleeding site.
 Venous pressure is reduced in the sitting
position, and leaning forward lessens the
swallowing of blood.
 Short-acting nasal decongestant sprays
 Cautery
 Treatment of other possible underlying
causes of bleeding
Acute Laryngitis
 Most common cause of vocal
hoarseness.
 May persist for a week or so after
symptoms of upper airway infection
have cleared.
 Etiologies:
 Viral
 Bacterial (Moraxella catarrhalis,
Haemophilus influenzae)
 Treatment:
Diseases of the
Respiratory System
Diseases of the Airways

Diseases of the
Respiratory System
Obstructive Airway Diseases

Asthma
 Increased responsiveness of lower
airways to multiple stimuli.
 Episodic and with reversible obstruction.
 May range in severity from mild without
limitation of patient’s activity, to severe
and life-threatening.
 Men and women are equally affected.
 Afflicts children more commonly than
adults.
Asthma
 Airway narrowing results from:
 Smooth muscle spasm
 Airway edema and inflammation
 Mucus plugging
 Variants:
 Exercise-induced asthma
 Triad asthma
 Cardiac asthma
 Asthmatic bronchitis
 Drug-induced asthma
Asthma
Asthma
 Pathogenesis:
 Common denominator is nonspecific
hyperirritability of the tracheobronchial tree.
 Airway reactivity increased by:
 Allergenic
 Pharmacologic
 Environmental, occupational
 Infectious
 Emotional
 Activity-related
Asthma
 Episodic wheezing
 Chest tightness
 Dyspnea and cough
 Tachycardia and tachypnea with prolonged
expiation
 Ominous signs: fatigue, pulsus paradoxicus,
diaphoresis, inaudible breath sounds with
diminished wheezing, inability to maintain
recumbency, and cyanosis
Asthma
 Laboratory Findings:
 Increased WBC count with eosinophilia
 Viscid sputum on gross examination
 Curschmann’s spirals on microscopic
examination of sputum
 Charcot-Leyden crystals
 Obstructive pattern on the pulmonary
function tests
 Diminished peak expiratory flow rate
(normal: 450-650 L/min in men; 350-500
L/min in women)
 Respiratory alkalosis and mild hypoxemia in
Asthma
Asthma
Asthma
Asthma
Asthma
 Complications:
 Exhaustion
 Dehydration
 Airway infection
 Cor pulmonale
 Tussive syncope
 Pneumothorax (rare)
Asthma
 Prevention:
 Comprehensive patient education
 Pharmacologic intervention
 Environment control
 Early treatment of chest infections
 Recognition and effective management of
nasal and paranasal disorders
 Discontinuance of cigarette smoking
 Pneumococcal and yearly influenza
immunization for patients with moderate to
severe asthma
Asthma: Classifications
 Mild asthma:
 Intermittent brief symptoms up to two times
weekly.
 Absence of symptoms between
exacerbations.
 Brief symptoms with activity.
 Nocturnal symptoms less than twice a
month.
 PEFR or FEV1 of 80% or more, with less than
20% variability on exacerbations.
 Moderate asthma:
 Symptoms more than one to two times
weekly.
 Exacerbations affecting sleep and level of
activity.
 Exacerbations lasting several days.
 Requirement for occasional emergency
care.
 PEFR values 60-80% of predicted, with 20-
30% variability during exacerbations and
greater than 30% on worst exacerbations.
 Severe asthma:
 Continuous symptoms
 Frequent exacerbations
 Limitations of physical activities
 Frequent nocturnal symptoms
 Requirement for frequent emergency care
 PEFR less than 60% of predicted, with
variability of 20-30% on treatment, and
greater than 50% on severe exacerbations
 Prolonged asthma refractory to conventional
modes of therapy (status asthmaticus)
Asthma: Treatment
 Mild ambulatory asthma:
 Short-acting inhaled β2-agonist drug
 Moderate ambulatory asthma:
 Daily maintenance therapy with inhaled
corticosteroids
 Cromolyn or nedocromil
 Short-acting inhaled β2-agonist drugs for
breakthrough wheezing
 Oral theophylline
Asthma: Treatment
Asthma: Treatment
 Severe ambulatory asthma:
 Daily maintenance therapy with inhaled
corticosteroids
 Daily oral sustained-release theophylline or
oral β2-agonist drugs
 Long-acting inhaled β2-agonist drug
(salmeterol)
 Inhaled anti-cholinergic drug (ipratropium
bromide)
 Short-acting inhaled β2-agonist drug for
breakthrough wheezing

Asthma: Treatment
 Status asthmaticus:
 Supplemental oxygen, 1-3 L/min
 Monitoring with oximetry
 Inhaled β2-agonist agents
 Intravenous aminophylline
 Subcutaneous terbutaline
 Intravenous corticosteroids
 Inhaled corticosteroids
 Oral corticosteroids
 Supportive: hydration, physical therapy, MV
Asthma: Prognosis
 Outlook is excellent because of the
availability of medications.
 Better prognosis in those who develop
asthma early in life.
Chronic Obstructive
Pulmonary Disease (COPD)
 Characterized by airflow obstruction due
to chronic bronchitis or emphysema.
 Classifications:
 Chronic Bronchitis
 Excessive secretion of bronchial mucus.
 Productive cough for 3 months or more in at least
2 consecutive years.
 Emphysema

Abnormal and permanent enlargement of air
spaces distal to the terminal bronchiole, with
destruction of their walls, and without obvious
fibrosis.
Chronic Obstructive
EMPHYSEMA VS CHRONIC BRONCHITIS
EMPHYSEMA CHRONIC
BRONCHITIS
HISTORY Onset of After age 50 After age 35
symptoms
Dyspnea Progressive, Intermittent, mild to
constant, severe moderate
Cough Absent or mild Persistent, severe
Sputum production Absent or mild Copious

Sputum Clear, mucoid Mucopurulent or
appearance purulent
Other features Weight loss Airway infections,
“pink puffer” right heart failure,
obesity
“blue bloater”
Chronic Obstructive
EMPHYSEMA CHRONIC
BRONCHITIS
PHYSICAL Body habitus Thin, wasted Stocky, obese
EXAMINATION
Central cyanosis Absent Present
Plethora Absent Present
Accessory Hypertrophied Unremarkable
respiratory
muscles
Anteroposterior Increased Normal
chest diameter
Percussion note Hyperresonant Normal
Auscultation Diminished breath Wheezes, rhonchi

sounds
Chronic Obstructive
EMPHYSEMA CHRONIC
BRONCHITIS
CHEST X-RAY Bullae, blebs Present Absent
Overall Decreased “Dirty lungs”
appearance markings in the
periphery
Hyperinflation Present Absent
Heart size Normal or small, Large, horizontal
vertical
Hemidiaphragms Low, flat Normal, rounded
Chronic Obstructive
EMPHYSEMA CHRONIC
BRONCHITIS
LABORATORY Hematocrit Normal Increased
INDICES
ECG Normal RAD, RVH, P
pulmonale
Hypoxemia Absent, mild Moderate, severe
Hypercapnia Absent Moderate, severe
Respiratory Absent Present
acidosis
Total lung capacity Increased Normal
Static lung Increased Normal
compliance
Diffusing capacity Decreased Normal
Chronic Obstructive
 Causes:
 Cigarette smoking
 Air pollution
 Airway infection
 Familial factors
 Allergies
Chronic Obstructive
 5th or 6th decade of life
 Excessive cough and sputum production
 Shortness of breath that have often been
present for 10 years or more
 Laboratory findings:
 Secondary polycythemia
 Presence of microorganisms in the sputum
 Spirometry shows obstructive pattern
 Hyperinflation on radiographs
Chronic Obstructive
 Complications:
 Pneumonia and acute bronchitis
 Pulmonary embolization
 Left ventricular heart failure
 Pulmonary hypertension
 Chronic respiratory failure
 Spontaneous pneumothorax
Chronic Obstructive
 Prevention:
 Smoking cessation
 Early treatment of airway infections
 Vaccination against pneumococcal
pneumonia and influenza.
Chronic Obstructive
 Treatment:
 Discontinuance of cigarette smoking
 Patient education
 Relief of bronchospasm

Ipratropium bromide

Maintenance therapy with oral theophylline

Oral corticosteroids
 Aerosol therapy
 Chest physiotherapy
 Treatment of complications
 Home oxygen therapy
Bronchiectasis
 Permanent normal dilatation and
destruction of bronchial walls.
 May be caused by recurrent infection or
inflammation.
 Symptoms:
 Chronic cough
 Copious sputum production, often purulent
 Hemoptysis
 Recurrent pneumonia
Bronchiectasis
 Signs:
 Persistent crackles at the base of the lungs.
 Clubbing is infrequent.
 Copious foul-smelling sputum that
separates into three layers in a cup.
 Crowded bronchial markings on chest x-ray.
 Small cystic spaces near the bronchi on
chest CT scan.
Bronchiectasis
 Treatment:
 Antibiotics
 Daily chest physiotherapy with postural
drainage and chest percussion
 Inhaled bronchodilators
 Surgical resection
 Diagnostic and therapeutic bronchoscopy
 Complications:
 Cor pulmonale
 Amyloidosis
 Visceral abscesses at distant sites like the
brain
Diseases of the
Respiratory System
Lower Respiratory Tract

Infections
Community-Acquired
Pneumonia
 Major health problem despite the
availability of potent antimicrobial
drugs.
 Fever and shaking chills
 Purulent sputum production
 Consolidation on physical examination
 Adventitious breath sounds on auscultation
Community-Acquired
Pneumonia:
Pathophysiology
Community-Acquired
Pneumonia:
Pathophysiology
Community-Acquired
Pneumonia
 Leukocytosis
 Patchy infiltrates on chest radiographs
 “Atypical pneumonia” – clinico-radiographic
dissonance; often caused by Mycoplasma or
Chlamydia pneumoniae; less striking
symptoms and physical findings with non-
purulent sputum production and absence of
leukocytosis despite significant infiltrates on
chest radiography; OR severe symptoms in
the absence of significant radiographic
findings
Community-Acquired
Pneumonia
Community-Acquired
Pneumonia:
Community-Acquired
Pneumonia: Management
 Guidelines for Management:
 Criteria for hospitalization:

Age over 65 years old

Co-existing illness

Alteration in vital signs

Leukopenia or marked leukocytosis

Respiratory failure
 Septic appearance
 Absence of supportive care at home
 Prevention:

Pneumococcal vaccine

Influenza vaccine
Community-Acquired
 Most common pathogens:
 Out-patient, without co-morbidity, < 60
years old

Streptococcus pneumoniae

Mycoplasma pneumoniae

Respiratory viruses

Chlamydia pneumoniae

Haemophilus influenzae

Legionella

Staphylococcus aureus

Mycobacterium tuberculosis
Community-Acquired
 Out-patient, with co-morbidity, age > 60
years old

Streptococcus pneumoniae

Respiratory viruses

Haemophilus influenzae

Moraxella catarrhalis
 Hospitalized patients with CAP
 Streptococcus pneumoniae
 Haemophilus influenzae
 Legionella

Chlamydia pneumoniae
Community-Acquired
 Treatment:
 Should be directed towards the elimination
of the suspected causative organism.
 Respiratory support
 Isolation from immunocompromised, or
potentially immunocompromised patients.
Hospital-Acquired
Pneumonia
 Essentials of Diagnosis:
 Occurs more than 48 hours after admission
to the hospital.
 One or more clinical findings (fever, cough,
purulent sputum) in most patients.
 Frequent in patients requiring intensive care
and mechanical ventilation.
 Pulmonary infiltrates on chest x-ray.
Hospital-Acquired
Pneumonia
 Pseudomonas aeruginosa
 Enterobacter sp.
 Klebsiella pneumoniae
 Escherichia coli
 Treatment:
 Empiric therapy must be started as soon as
pneumonia is suspected.
 Respiratory support
Pulmonary Tuberculosis
 Infection beings when aerosolized
droplets containing viable organisms
are inhaled by a person susceptible to
the disease.
 Constitutional symptoms of fatigue, weight
loss, anorexia, low-grade fever, and night
sweats
 Cough
 Patients often appear chronically ill.
 Post-tussive apical rales.
 Pathogenesis:
 After entry into the lungs in aerosolized
droplets, tubercle bacilli are ingested by
macrophages and transported to regional
lymph nodes, and from there, they
disseminate widely.
 Lesions are contained by a delayed-type
hypersensitivity response (DTH; the tissue-
damaging response), and the cell-mediated
macrophage-activating response.
 The development of host immunity and DTH
is evidenced by acquisition of skin-test
reactivity to tuberculin purified protein
 Pathogenesis (cont’d):
 Granulomatous lesions form and organisms
survive within macrophages or necrotic
material but do not spread further.
 Reactivation may occur at a later time. In
some cases, the immune response is
inadequate to contain the infection, and
symptomatic, progressive primary disease
develops.
 Recovery of Mycobacterium tuberculosis
from cultures, or identification of organisms
by DNA probe
 Acid-fast bacilli in the sputum
 Serologic diagnosis by ELISA
 Apical infiltrates on chest radiographs
 Ghon and Ranke signs
 Tuberculin skin test
 Sputum examination for acid-fast bacilli
(AFB) or direct microscopy is the most
important diagnostic test to request for
a patient clinically suspected to have
PTB.
 Sputum collection:
 Best obtained on three consecutive
mornings.
 Clean and thoroughly rinse the mouth with
water.
 Breathe deeply 3 times.
 Sputum collection (cont’d):
 Best obtained on three consecutive
mornings.
 Clean and thoroughly rinse the mouth with
water.
 Breathe deeply 3 times.
 After the third breath, cough hard and try to
bring up sputum from deep in the lungs.
 Expectorate the sputum into a sterile
container with a well-fitted cap.
 Collect at least 1 teaspoonful.
 Examine the specimen to see that it is not
 Sputum collection (cont’d):
 Supervised nebulization with a warm,
sterile, hypertonic (3%) saline solution is
useful for obtaining specimens from
patients highly suspected of having PTB. It
should be attempted for all cooperative
patients who are smear-negative or unable
to expectorate sputum spontaneously.
 Sputum TB culture and sensitivity tests:
 Smear (-) patients with a strong clinical
possibility of PTB and suggestive chest x-
rays.
 Smear (+) or (-) patients suspected of
multi-drug resistant PTB.
 Smear (+) patients demonstrating the “rise
fall” phenomenon.
 All cases of relapse.
 All cases of re-treatment.
 All cases of treatment failure.
 PTB Classifications:
 Class I: exposure, no symptoms, no
radiographic evidence
 Class II: exposure, (+) symptoms, no
radiographic evidence
 Class III: active PTB; exposure, (+)
symptoms, (+) radiographic evidence
 Class IV: treated PTB
 Class V: indeterminate
Pulmonary Tuberculosis:
Treatment
 Newly diagnosed PTB:
 At present, there is a lack of current
evidence or clear trends in favor of efficacy
and superiority of 4 drugs over 3.
 The use of four drugs daily in the intensive
phase treatment adds an additional
assurance against treatment failure should
there be unexpected drug resistance and
assuming adherence to the treatment
regimen, also helps the loss of additional
drugs.
Treatment
 Newly diagnosed PTB:
 Intensive Phase: 2HRZE(S)/4HR(E)

First 2 months: Isoniazid, Rifampicin,
Pyrazinamide and Ethambutol + Streptomycin
(IM)

Next 4 months: Isoniazid and Rifampicin +
Ethambutol
 Maintenance Phase: 3/6HR

Next 3 months: Isoniazid and Rifampicin

Check clinical profile. May discontinue after a
total of 9 months, or may continue as clinical
evidence dictates.
Treatment
 Areas with high resistance rates:
 National Capital Region, including Laguna
 Cebu
 Davao
 Zamboanga
 Cavite
 Pampanga
 Areas with low resistance rates:
 Palawan
 Mountain Province and Benguet
Treatment
 Empiric therapy for MDR-TB suspect:
 Use of at least some second-line drugs.
 Prescribe drugs which the patient has not
previously taken.
 The initial regimens should consist of at
least three drugs, preferably four or five, to
which the bacilli are likely to be fully
sensitive (injectable aminoglycoside and
pyrazinamide, even if previously used,
because resistance is usually unlikely).
Treatment
 Hospitalization is not necessary in most
patients, but should be considered if the
patient is incapable of self-care.
 Preventive therapy:
 Should be given if the patient is under 35
years of age with a positive tuberculin test
(>10 mm) in the following conditions:
 Foreign-born persons from countries with high
prevalence of TB.
 Medically underserved, low-income groups
 Residents of long-term care facilities
Treatment
 Preventive therapy:
 Isoniazid preventive therapy for 6 to 12
months.
 Vaccine:
 BCG should be given to tuberculin-negative
persons.

Children who are repeatedly exposed to
individuals with untreated or ineffectively treated
TB also benefit from BCG vaccination.
Diseases of the
Respiratory System
Bronchogenic Carcinoma
 Suspected etiologies:
 Cigarette smoking
 Ionizing radiation
 Asbestos
 Heavy metals
 Industrial agents
 Lung scars
 Air pollution
 Genetic predisposition
 Squamous cell carcinoma and
adenocarcinoma are the most common
types (30 to 35% of primary tumors
each).
 Small cell carcinoma and large cell
carcinoma account for about 20 to 25%
and 15% of cases, respectively.
 10 to 25% of patients are
asymptomatic, especially during the
early course of the disease.
 Initial Symptoms:
 Cough
 Weight loss
 Dyspnea
 Chest pain
 Hemoptysis
 Change in the patterns of the symptoms
 Physical findings vary and may be
totally absent:
 Superior vena cava syndrome
 Horner’s syndrome
 Pancoast’s syndrome
 Recurrent laryngeal nerve palsy with
diaphragmatic hemiparesis
 Paraneoplastic syndromes
PARANEOPLASTIC SYNDROMES IN LUNG CANCER
CLASSIFICATION SYNDROME COMMON HISTOLOGIC TYPE
ENDOCRINE AND Cushing’s syndrome Small cell
METABOLIC
SIADH Small cell
Hypercalcemia Squamous cell
Gynecomastia Large cell
CONNECTIVE TISSUE Clubbing and hypertrophic Squamous cell, large cell
AND OSSEOUS pulmonary osteodystrophy and adenocarcinoma
NEUROMUSCULAR Peripheral neuropathy Small cell
Subacute cerebellar Small cell
degeneration
Myasthenia (Eaton-Lambert Small cell
syndrome)
Dermatomyositis All
PARANEOPLASTIC SYNDROMES IN LUNG CANCER
CLASSIFICATION SYNDROME COMMON HISTOLOGIC TYPE
CARDIOVASCULAR Thrombophlebitis Adenocarcinoma
Nonbacterial verrucous Adenocarcinoma
(marantic) endocarditis
HEMATOLOGIC Anemia All
Disseminated intravascular All
coagulation
Eosinophilia All
Thrombocytosis All
CUTANEOUS Acanthosis nigricans All
Erythema gyratum repens All
 Cytologic examination of sputum permits
definitive diagnosis of lung cancer in 40 to
60% of cases.
 CT scan and other imaging techniques.
 Treatment:
 Surgery
 Chemotherapy
 Radiotherapy
 Combination therapy
 Immunomodulation
 Prognosis:
 Over-all five-year survival rate is 10 to 15%.
 Determinants of survival:
 Stage of disease at time of presentation
 Patient’s general health
 Age
 Histologic type of tumor
 Tumor growth rate
 Type of therapy
Diseases of the
Respiratory System
Ventilation and Perfusion

Disorders
Pulmonary
Thromboembolism
 Pulmonary emboli arise from thrombi in
the venous circulation or right side of
the heart, from tumors that have
invaded the venous circulation, or from
other sources.
 More than 90% originate as clots in the
deep veins of the lower extremities.
Pulmonary
Thromboembolism
 Physiologic risk factors:
 Venous stasis
 Venous endothelial injury
 Hypercoagulability
 Oral contraceptives
 Cancer
 Protein C or S deficiency
 Antithrombin III deficiency
Pulmonary
Thromboembolism
 Clinical risk factors:
 Prolonged bed rest or inactivity
 Surgery
 Childbirth
 Advanced age
 Stroke
 Myocardial infarction
 Congestive heart failure
 Obesity
 Fractures of the hip or femur
Pulmonary
Thromboembolism
 Symptoms:
 Pleuritic chest pain (74%)
 Non-pleuritic chest pain (14%)
 Dyspnea (84%)
 Apprehension (59%)
 Cough (53%)
 Hemoptysis (30%)
 Sweats (27%)
 Syncope (13%)
Pulmonary
Thromboembolism
 Signs:
 Tachypnea (92%)
 Crackles (58%)
 Accentuated split second heart sound (53%)
 Tachycardia (44%)
 Fever > 37.8°C (43%)
 Phlebitis (32%)
 Diaphoresis (36%)
 Edema (24%)
 Murmur (23%)
 Cyanosis (19%)
Pulmonary
Thromboembolism
 Results of routine laboratory tests are not
helpful in diagnosing pulmonary
thromboembolism.
 Imaging and special examinations:
 Chest radiography
 Lung scanning
 Venous thrombosis studies
 Pulmonary angiography
Pulmonary
Thromboembolism
 Prevention:
 Critically important
 Identification of those at risk
 Prophylaxis
 Treatment:
 Anticoagulation
 Thrombolytic therapy
 Inferior vena cava filter
Pulmonary
Thromboembolism
 Prognosis:
 May cause sudden death.
 Depends on the underlying disease and on
proper diagnosis and treatment.
 Pulmonary hypertension may be a
complication.
Inhalation of Air Pollutants
 Clinical Findings:
 Exposure to low levels is inconsequential.
 Exposure to high levels produces lower and
upper respiratory tract irritation.
 Treatment:
 Healthy individuals exposed to the usual
ambient levels of air pollution need not
observe special precautions.
 Patients with COPD or severe asthma should
be advised to stay indoors and not engage
in strenuous activity in areas of high
 Prognosis:
 Depends on the severity and type of
exposure.
 Also depends on the patient’s preexisting
pulmonary status.
MAJOR AIR POLLUTANTS, SOURCES AND ADVERSE EFFECTS
NOXIOUS AGENT SOURCES ADVERSE EFFECTS

OXIDES OF Automobile exhaust; Respiratory tract irritation,
NITROGEN gas stoves and bronchial hyperreactivity,
heaters; wood- impaired lung defense,
burning stoves; bronchiolitis obliterans
HYDROCARBONS kerosene
Automobilespace
exhaust, Lung cancer
heaters
cigarette smoke
OZONE Automobile exhaust, Cough, substernal
high altitude aircraft discomfort,
cabins bronchoconstriction,
decreased exercise
performance, respiratory
tract irritation
MAJOR AIR POLLUTANTS, SOURCES AND ADVERSE EFFECTS
NOXIOUS AGENT SOURCES ADVERSE EFFECTS

SULFUR DIOXIDE Power plants, Exacerbation of asthma
smelters, oil and chronic obstructive
refineries, kerosene pulmonary disease,
space heaters respiratory tract irritation,
hospitalization may be
necessary, and death may
occur in severe exposure
Pulmonary Aspiration
Syndromes
 Aspiration of inert materials:
 May cause asphyxia if amount aspirated is
massive.
 Most patients suffer no serious sequelae.
 Aspiration of toxic materials:
 Results in clinically evident pneumonia.
 Treatment is supportive
 “Café coronary”
 Acute obstruction of upper airways by food
that occurs in intoxicated individuals.
 Heimlich maneuver may be life-saving.
Pulmonary Aspiration
Syndromes
 Retention of an aspirated foreign body
 Chronic aspiration of gastric contents
 Mendelson’s syndrome
Disorders of Ventilation
 Obesity-hypoventilation syndrome
(Pickwickian syndrome)
 Sleep-related breathing disorders
 Obstructive sleep apnea
 Hyperventilation syndrome
Acute Respiratory Failure
 Clinical Findings:
 Signs and symptoms of the underlying
disease
 Hypoxemia and hypercapnia
 Dyspnea is the chief symptom.
 Cyanosis
 Restlessness, confusion, anxiety, delirium
 Tachypnea
 Tachycardia, hypertension, cardiac
arrhythmias
 Tremors
Acute Respiratory Failure:
Treatment
 Non-ventilatory respiratory support
 Ventilatory respiratory support
 Tracheal intubation
 Hypoxemia
 Upper airway obstruction
 Impaired airway protection
 Poor handling of secretions
 Facilitation of mechanical ventilation
Treatment
 Ventilatory respiratory support
 Mechanical ventilation

Apnea

Acute hypercapnia

Severe hypoxemia

Progressive patient fatigue
Treatment
 General supportive care
 Nutritional support
 Maintenance of fluid and electrolyte balance
 Psychological and emotional support
 Skin care to avoid decubitus ulcers
 Meticulous avoidance of nosocomial
infections
 Prevention of stress ulcers
Pleural Effusion
 Essentials of Diagnosis:
 Asymptomatic in many cases; pleuritic
chest pain if pleuritis is present; dyspnea if
effusion is large.
 Decreased tactile and vocal fremiti; dullness
to percussion; distant breath sounds;
egophony if effusion is large.
 Radiographic evidence of pleural effusion.
 Diagnostic findings on thoracentesis
Pleural Effusion
 Classifications:
 Exudative effusion (at least one of the
following features):

Pleural fluid protein to serum protein ratio > 0.5

Pleural fluid LDH to serum LDH ration > 0.6

Pleural fluid LDH greater than 2/3 of the upper
limit of the serum LDH.
 Transudative effusion

Very low protein content

Often seen in non-inflammatory states
Pleural Effusion:
Approach to Management
PLEURAL EFFUSION
Perform diagnostic thoracentesis

Measure pleural fluid protein and LDH
Any of the following met?

PF/serum protein > 0.5
PF/serum LDH > 0.6
PF LDH > 2/3 upper normal serum limit
Yes No
EXUDATE TRANSUDATE
Further diagnostic procedures Treat CHF, cirrhosis, nephrosis
Pleural Effusion:
EXUDATE
Further diagnostic procedures
Measure PF glucose, amylase

Obtain PF cytology
Obtain differential cell count
Culture, stain PF
Amylase elevated Glucose < 60 mg/dL

Consider: esophageal rupture, Consider: Malignancy
Pancreatic pleural effusion Bacterial infections
Malignancy Rheumatoid pleuritis
NO DIAGNOSIS
Pleural Effusion:
NO DIAGNOSIS
Negative
Needle biopsy of Consider pulmonary embolus Positive:

pleura (lung scan or pulmonary arteriogram) Treat for PE
Negative Positive:
Treat for TB or CA
Negative
Positive: Treat
PPD for TB
No: Consider SYMPTOMS IMPROVING

Yes
Thoracoscopy or
Observe
Open pleural biopsy
Pleural Effusion
 Treatment:
 Treatment of the underlying condition
 Removal if the effusion is large (therapeutic
thoracentesis or tube thoracostomy)
 Pleurodesis
Pneumothorax
 Types:
 Spontaneous
 Traumatic
 Essentials of diagnosis:
 Acute onset of ipsilateral chest pain and
dyspnea, often of several days’ duration.
 Minimal physical findings in mild cases;
unilateral chest expansion, decreased
tactile and vocal fremiti, hyperresonance,
diminished breath sounds, mediastinal shift,
cyanosis in tension pneumothorax.
 Presence of pleural air on chest x-ray.
Pneumothorax
 Treatment:
 Depends on the severity of the condition.
 Supportive and oxygen supplementation if
needed.
 Tube thoracostomy and pleurodesis.

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“Roses are red,

Violets are blue,

Arni A. Magdamo, MD, MHA,

Normal Anatomy and

Sensory signals are transmitted to the medulla.

Motor signals are transmitted back to the respiratory system.

Respiratory muscles contract rapidly generating

Vocal cords open suddenly, allowing pressurized air in the

Sensory signals are received in the medulla.

Motor signals are generated and transmitted back.

Respiratory muscles contract rapidly generating

Vocal cords open suddenly, allowing pressurized air in the

Consolidatio Dull Increased Bronchial Bronchophony Crackles

Pneumothor Hyperresona Decrease Decrease Decreased Absent

Pleural Dull Decrease Decrease Decreased Absent or

Nose, Paranasal Sinuses and

Diseases of the Airways

Obstructive Airway Diseases

Sputum production Absent or mild Copious

Auscultation Diminished breath Wheezes, rhonchi

Lower Respiratory Tract

Ventilation and Perfusion

NOXIOUS AGENT SOURCES ADVERSE EFFECTS

NOXIOUS AGENT SOURCES ADVERSE EFFECTS

Perform diagnostic thoracentesis

Any of the following met?

Measure PF glucose, amylase

Amylase elevated Glucose < 60 mg/dL

Needle biopsy of Consider pulmonary embolus Positive:

No: Consider SYMPTOMS IMPROVING

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