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PART II

Obstructive Airway Diseases

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Emphysema

Bronchitis Asthma

 Chronic obstructive pulmonary disease.


 Bronchitis, emphysema, and asthma may
present alone or in combination.

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Chapter 11
Chronic Bronchitis

Chronic bronchitis. Inset, Weakened distal airways in emphysema,


a common secondary anatomic alteration of the lungs.
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Anatomic Alterations of the Lungs
 Chronic inflammation and swelling of the
peripheral airways
 Excessive mucus production and
accumulation
 Partial or total mucus plugging
 Hyperinflation of alveoli (air-trapping)
 Smooth muscle constriction of bronchial
airways (bronchospasm)

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Etiology
 Cigarette smoking
 Atmospheric pollutants
 Infection
 Gastroesophageal reflux disease

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Overview of the Cardiopulmonary
Clinical Manifestations Associated
with CHRONIC BRONCHITIS
The following clinical manifestations result from
the pathophysiologic mechanisms caused (or
activated) by Excessive Bronchial Secretions
(see Figure 9-11) and Bronchospasm (see
Figure 9-10)—the major anatomic alterations of
the lungs associated with chronic bronchitis
(see Figure 11-1).

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Figure 9-11. Excessive bronchial secretions clinical scenario.
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Figure 9-10. Bronchospasm clinical scenario (e.g., asthma).
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Clinical Data Obtained at the
Patient’s Bedside
Vital signs
 Increased respiratory rate
 Increased heart rate, cardiac output, blood
pressure

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Clinical Data Obtained at the
Patient’s Bedside
 Use of accessory muscles of inspiration
 Use of accessory muscles of expiration
 Pursed-lip breathing
 Increased anteroposterior chest diameter
(barrel chest)
 Cyanosis
 Digital clubbing

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Figure 2-36. The way a patient may appear when using the
pectoralis major muscles for inspiration.
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Figure 2-41. A, Schematic illustration of alveolar compression of weakened bronchiolar
airways during normal expiration in patients with chronic obstructive pulmonary disease
(e.g., emphysema). B, Effects of pursed-lip breathing. The weakened bronchiolar airways
are kept open by the effects of positive pressure created by pursed lips during expiration.
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Digital
Clubbing

Figure 2-46. Digital clubbing.


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Clinical Data Obtained at the
Patient’s Bedside
Peripheral edema and venous distention
 Distended neck veins
 Pitting edema
 Enlarged and tender liver

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Distended
Neck Veins

Figure 2-48. Distended neck veins (arrows).


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Figure 2-47. Pitting edema. From Bloom A, Ireland J: Color atlas of diabetes, ed 2,
London, 1992, Mosby-Wolfe.
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Clinical Data Obtained at the
Patient’s Bedside
 Cough, sputum production, hemoptysis
 Chest assessment findings
 Hyperresonant percussion note
 Diminished breath sounds
 Diminished heart sounds
 Decreased tactile and vocal fremitus
 Crackles/rhonchi/wheezing

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Figure 2-12. Percussion becomes more hyperresonant with alveolar hyperinflation.
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Figure 2-17. As air trapping and alveolar hyperinflation develop in obstructive
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lung diseases, breath sounds progressively diminish. Copyright © 2006 by Mosby, Inc.
Clinical Data Obtained from
Laboratory Tests and Special
Procedures

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Pulmonary Function Study:
Expiratory Maneuver Findings

FVC FEVT FEF25%-75% FEF200-1200


   

PEFR MVV FEF50% FEV1%


   

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Pulmonary Function Study:
Lung Volume and Capacity Findings

VT RV FRC TLC
N or    N or 

VC IC ERV RV/TLC ratio


 N or  N or  

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Arterial Blood Gases

Mild to Moderate Chronic Bronchitis


 Acute alveolar hyperventilation with
hypoxemia

pH PaCO2 HCO3- PaO2


   (Slightly) 

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Time and Progression of Disease
Disease Onset Alveolar Hyperventilation
100

90 Point at which PaO2


declines enough to
80 stimulate peripheral
oxygen receptors
70
PaO2 or PaCO2

60
PaO2
50

40

30

20

10

Figure 4-2. PaO2 and PaCO2 trends during acute alveolar hyperventilation.
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Arterial Blood Gases

Severe Chronic Bronchitis


 Chronic ventilatory failure with hypoxemia

pH PaCO2 HCO3- PaO2

Normal  (Significantly) 

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Time and Progression of Disease
Disease Onset Alveolar Hyperventilation Chronic Ventilatory Failure
100

90 Point at which disease


becomes severe and patient
Point at which PaO2
begins to become fatigued
80 declines enough to
stimulate peripheral
70 oxygen receptors
Pa02 or PaC02

60

50

40

30

20

10

0
Figure 4-7. PaO2 and PaCO2 trends during acute or chronic ventilatory failure.
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Acute Ventilatory Changes
Superimposed on Chronic Ventilatory
Failure
 Acute alveolar hyperventilation on chronic
ventilatory failure
 Acute ventilatory failure on chronic
ventilatory failure

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Oxygenation Indices

QS/QT DO2 VO2 C(a-v)O2


  Normal Normal
O2ER SvO2
 

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Hemodynamic Indices
(Severe Chronic Bronchitis)

CVP RAP PA PCWP


   Normal

CO SV SVI CI
Normal Normal Normal Normal

RVSWI LVSWI PVR SVR


 Normal  Normal

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Abnormal Laboratory Tests and
Procedures
 Hematology
Increased hematocrit and hemoglobin
 Electrolytes
 Hypochloremia (chronic ventilatory failure)
 Increased bicarbonate (chronic ventilatory failure)
 Sputum examination
 Increased white blood cells
 Streptococcus pneumoniae
 Haemophilus influenzae
 Moraxella catarrhalis
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Radiologic Findings
Chest radiograph
 Translucent (dark) lung fields
 Depressed or flattened diaphragms
 Long and narrow heart
 Enlarged heart

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Figure 11-2. Chest X-ray film of a patient with chronic bronchitis. Note the translucent (dark)
lung fields, depressed diaphragms, and long and narrow heart.
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Radiologic Findings
Bronchogram
 Small spikelike protrusions

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Figure 11-3. Chronic bronchitis. Bronchogram with localized view of left hilum. Rounded
collections of contrast lie adjacent to bronchial walls and are particularly well seen below
the left main stem bronchus (arrow) in this film. They are caused by contrast in dilated
mucous gland ducts. (From Armstrong P, Wilson AG, Dee P: Imaging of diseases of the
chest, St. Louis, 1990, Mosby.)
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General Management of
Chronic Bronchitis
 Patient and family education
 Behavioral management
 Avoidance of smoking and inhaled irritants
 Avoidance of infections
 Respiratory care treatment protocols
 Oxygen therapy protocol
 Bronchopulmonary hygiene therapy protocol
 Aerosolized medication protocol
 Mechanical ventilation protocol
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GOLD Standards

Global Initiative for Chronic


Obstructive
Lung
Disease

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Figure 11-4. Acute exacerbation of COPD (AECOPD): Guideline algorithm (ACCP/ACP-ASIM). CXR,
Chest X-ray; NPPV, noninvasive positive pressure ventilation; PEFR, peak expiratory flow rate;
URI, upper respiratory infection. (From GUIDELINES Pocketcard: Managing Chronic Obstructive
Pulmonary Disease. Baltimore, 2004, Version 4.0, International Guidelines Center.)
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Figure 11-4. (Close-ups). (From GUIDELINES Pocketcard: Managing Chronic
Obstructive Pulmonary Disease. Baltimore, 2004, Version 4.0, International
Guidelines Center.)

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Figure 11-4. (Close-ups). (From GUIDELINES Pocketcard: Managing Chronic
Obstructive Pulmonary Disease. Baltimore, 2004, Version 4.0, International
Guidelines Center.)

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Figure 11-4. (Close-ups). (From GUIDELINES Pocketcard: Managing Chronic
Obstructive Pulmonary Disease. Baltimore, 2004, Version 4.0, International
Guidelines Center.)
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Figure 11-4. (Close-ups). (From GUIDELINES Pocketcard: Managing Chronic
Obstructive Pulmonary Disease. Baltimore, 2004, Version 4.0, International
Guidelines Center.)
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Figure 11-4. Acute exacerbation of COPD (AECOPD): Guideline algorithm (ACCP/ACP-ASIM). CXR,
Chest X-ray; NPPV, noninvasive positive pressure ventilation; PEFR, peak expiratory flow rate; URI,
upper respiratory infection. (From GUIDELINES Pocketcard: Managing Chronic Obstructive
Pulmonary Disease. Baltimore, 2004, Version 4.0, International Guidelines Center.)
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Classroom Discussion
Case Study: Chronic Bronchitis

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