Chronic Bronchitis Chapter 11

PART II
Obstructive Airway Diseases
Slide 1
Copyright 2006 by Mosby, Inc.
Emphysema
Bronchitis
Slide 2
Asthma
Chronic obstructive pulmonary disease.
Bronchitis, emphysema, and asthma may

present alone or in combination.
Chapter 11
Chronic Bronchitis
Slide 3
Chronic bronchitis. Inset, Weakened distal airways in emphysema,

a common secondary anatomic alteration of the lungs .
Anatomic Alterations of the Lungs
Slide 4
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)
Etiology
Slide 5
Cigarette smoking
Atmospheric pollutants
Infection
Gastroesophageal reflux disease
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
Figure 9-11. Excessive bronchial secretions clinical scenario.

Slide 7
Figure 9-10. Bronchospasm clinical scenario (e.g., asthma).

Slide 8
Clinical Data Obtained at the

Patients Bedside
Vital signs
Slide 9
Increased respiratory rate
Increased heart rate, cardiac output, blood

pressure

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
Figure 2-36. The way a patient may appear when using the
pectoralis major muscles for inspiration.
Slide 11
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
are kept open by the effects of positive pressure created by pursed lips during expiration.
Digital
Clubbing
Figure 2-46. Digital clubbing.

Slide 13

Patients Bedside
Peripheral edema and venous distention
Slide 14
Distended neck veins
Pitting edema
Enlarged and tender liver
Distended
Neck Veins
Figure 2-48. Distended neck veins (arrows).

Slide 15
Figure 2-47. Pitting edema. From Bloom A, Ireland J: Color atlas of diabetes, ed 2,
London, 1992, Mosby-Wolfe.
Slide 16

Patients Bedside
Slide 17
Cough, sputum production, hemoptysis
Chest assessment findings
Hyperresonant percussion note
Diminished breath sounds
Diminished heart sounds
Decreased tactile and vocal fremitus
Crackles/rhonchi/wheezing
Figure 2-12. Percussion becomes more hyperresonant with alveolar hyperinflation.

Slide 18
Slide 19
Figure 2-17. As air trapping and alveolar hyperinflation develop in obstructive

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

Laboratory Tests and Special
Procedures
Slide 20
Pulmonary Function Study:

Expiratory Maneuver Findings
Slide 21
FVC
FEVT
FEF25%-75%
FEF200-1200
PEFR
MVV
FEF50%
FEV1%
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
Arterial Blood Gases

Mild to Moderate Chronic Bronchitis
Slide 23
Acute alveolar hyperventilation with

hypoxemia
pH
PaCO2
HCO3
(Slightly)
PaO2
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.
Arterial Blood Gases

Severe Chronic Bronchitis
Chronic ventilatory failure with hypoxemia
pH
Normal
Slide 25
PaCO2
HCO3 (Significantly)
PaO2
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
Acute Ventilatory Changes

Superimposed on Chronic Ventilatory
Failure
Slide 27
Acute alveolar hyperventilation on chronic

ventilatory failure
Acute ventilatory failure on chronic

ventilatory failure
Oxygenation Indices
QS/QTDO2
Slide 28
VO2
C(a-v)O2
Normal
O2ER
SvO2
Normal
Hemodynamic Indices
(Severe Chronic Bronchitis)
Slide 29
CVP
RAP
PA
PCWP
Normal
CO
SV
SVI
CI
Normal
Normal
Normal
Normal
RVSWI
LVSWI
PVR
SVR
Normal
Normal
Abnormal Laboratory Tests and

Procedures
Hematology
Increased hematocrit and hemoglobin
Electrolytes
Slide 30
Hypochloremia (chronic ventilatory failure)
Increased bicarbonate (chronic ventilatory failure)
Sputum examination
Increased white blood cells
Streptococcus pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
Radiologic Findings
Chest radiograph
Slide 31
Translucent (dark) lung fields
Depressed or flattened diaphragms
Long and narrow heart
Enlarged heart
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.
Slide 32
Radiologic Findings
Bronchogram
Slide 33
Small spikelike protrusions
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
General Management of
Chronic Bronchitis
Patient and family education
Behavioral management
Slide 35
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

GOLD Standards
Global Initiative for Chronic

Obstructive
Lung
Disease
Slide 36
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
Figure 11-4. (Close-ups). (From GUIDELINES Pocketcard: Managing Chronic

Obstructive Pulmonary Disease. Baltimore, 2004, Version 4.0, International
Guidelines Center.)
Slide 38

Guidelines Center.)
Slide 39

Guidelines Center.)
Slide 40

Guidelines Center.)
Slide 41
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
Classroom Discussion
Case Study: Chronic Bronchitis
Slide 43

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PART II

Obstructive Airway Diseases

Copyright 2006 by Mosby, Inc.

Chronic obstructive pulmonary disease.

Bronchitis, emphysema, and asthma may

Chronic bronchitis. Inset, Weakened distal airways in emphysema,

Copyright 2006 by Mosby, Inc.

Anatomic Alterations of the Lungs

Chronic inflammation and swelling of the

Excessive mucus production and

Partial or total mucus plugging

Hyperinflation of alveoli (air-trapping)

Smooth muscle constriction of bronchial

Gastroesophageal reflux disease

Copyright 2006 by Mosby, Inc.

Overview of the Cardiopulmonary

Copyright 2006 by Mosby, Inc.

Figure 9-11. Excessive bronchial secretions clinical scenario.

Copyright 2006 by Mosby, Inc.

Figure 9-10. Bronchospasm clinical scenario (e.g., asthma).

Copyright 2006 by Mosby, Inc.

Clinical Data Obtained at the

Increased respiratory rate

Increased heart rate, cardiac output, blood

Copyright 2006 by Mosby, Inc.

Clinical Data Obtained at the

Use of accessory muscles of inspiration

Use of accessory muscles of expiration

Increased anteroposterior chest diameter

Copyright 2006 by Mosby, Inc.

Copyright 2006 by Mosby, Inc.

Figure 2-41. A, Schematic illustration of alveolar compression of weakened bronchiolar

Figure 2-46. Digital clubbing.

Copyright 2006 by Mosby, Inc.

Clinical Data Obtained at the

Distended neck veins

Enlarged and tender liver

Copyright 2006 by Mosby, Inc.

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

Copyright 2006 by Mosby, Inc.

Copyright 2006 by Mosby, Inc.

Clinical Data Obtained at the

Cough, sputum production, hemoptysis

Chest assessment findings

Hyperresonant percussion note

Diminished breath sounds

Diminished heart sounds

Decreased tactile and vocal fremitus

Copyright 2006 by Mosby, Inc.

Figure 2-12. Percussion becomes more hyperresonant with alveolar hyperinflation.

Copyright 2006 by Mosby, Inc.

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

Clinical Data Obtained from

Copyright 2006 by Mosby, Inc.

Pulmonary Function Study:

Copyright 2006 by Mosby, Inc.

Pulmonary Function Study:

Copyright 2006 by Mosby, Inc.

Arterial Blood Gases

Acute alveolar hyperventilation with

Copyright 2006 by Mosby, Inc.

Time and Progression of Disease

Point at which PaO22

Copyright 2006 by Mosby, Inc.