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PART II

Obstructive Airway Diseases

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Emphysema

Bronchitis

Slide 2

Asthma

Chronic obstructive pulmonary disease.

Bronchitis, emphysema, and asthma may


present alone or in combination.
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Chapter 11
Chronic Bronchitis

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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

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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

Slide 5

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).

Slide 6

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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).


Slide 8

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Clinical Data Obtained at the


Patients Bedside
Vital signs

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Increased respiratory rate

Increased heart rate, cardiac output, blood


pressure

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Clinical Data Obtained at the


Patients Bedside

Slide 10

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.
Slide 11

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Slide 12

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
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are kept open by the effects of positive pressure created by pursed lips during expiration.

Digital
Clubbing

Figure 2-46. Digital clubbing.


Slide 13

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Clinical Data Obtained at the


Patients Bedside
Peripheral edema and venous distention

Slide 14

Distended neck veins

Pitting edema

Enlarged and tender liver

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Distended
Neck Veins

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


Slide 15

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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


Patients Bedside

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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.


Slide 18

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Slide 19

Figure 2-17. As air trapping and alveolar hyperinflation develop in obstructive


lung diseases, breath sounds progressively diminish.
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Clinical Data Obtained from


Laboratory Tests and Special
Procedures

Slide 20

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Pulmonary Function Study:


Expiratory Maneuver Findings

Slide 21

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

N or

IC

ERV

VC

N or

N or
Slide 22

TLC

RV/TLC ratio
N or

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Arterial Blood Gases


Mild to Moderate Chronic Bronchitis

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Acute alveolar hyperventilation with


hypoxemia

pH

PaCO2

HCO3

(Slightly)

PaO2

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Time and Progression of Disease


Disease Onset

Alveolar Hyperventilation

100
90

PaO2 or PaCO2

80

Point at which PaO22


declines enough to
stimulate peripheral
oxygen receptors

70
60

PaO2

50
40
30
20

PaC
O

10
0

Slide 24

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
Normal

Slide 25

PaCO2

HCO3 (Significantly)

PaO2

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Time and Progression of Disease


Disease Onset

Alveolar Hyperventilation

Chronic Ventilatory Failure

100
90

Pa02 or PaC02

80
70
60

Point at which PaO22


declines enough to
stimulate peripheral
oxygen receptors

Point at which disease


becomes severe and patient
begins to become fatigued

O2
C
a

50
40
30

Pa
O

20
10
0
Figure 4-7. PaO2 and PaCO2 trends during acute or chronic ventilatory failure.
Slide 26

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Acute Ventilatory Changes


Superimposed on Chronic Ventilatory
Failure

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Acute alveolar hyperventilation on chronic


ventilatory failure

Acute ventilatory failure on chronic


ventilatory failure

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Oxygenation Indices

QS/QTDO2

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VO2

C(a-v)O2

Normal

O2ER

SvO2

Normal

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Hemodynamic Indices
(Severe Chronic Bronchitis)

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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

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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

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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

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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.)
Slide 34

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General Management of
Chronic Bronchitis

Patient and family education

Behavioral management

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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

Slide 36

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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.)
Slide 37

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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.)
Slide 38

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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.)
Slide 39

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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.)
Slide 40

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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.)
Slide 41

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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.)
Slide 42

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Classroom Discussion

Case Study: Chronic Bronchitis

Slide 43

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