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Slide 1

PART II

Emphysema Bronchitis Asthma

Slide 2  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.

Slide 4

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) Copyright © 2006 by Mosby, Inc.

Slide 5

Etiology

Slide 6

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 7

Figure 9-11. Excessive bronchial secretions clinical scenario.

Slide 8

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

Slide 9

Clinical Data Obtained at the Patient’s Bedside

Slide 10

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 Copyright © 2006 by Mosby, Inc.

Slide 11

Figure 2-36. The way a patient may appear when using the pectoralis major muscles for inspiration.

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 Slide 13

Figure 2-46. Digital clubbing.

Slide 14

Clinical Data Obtained at the Patient’s Bedside

Distended Neck Veins

Slide 15

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

Slide 16

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

Slide 17

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 Copyright © 2006 by Mosby, Inc.

Slide 18

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

Slide 19

Figure 2-17. As air trapping and alveolar hyperinflation develop in obstructive lung diseases, breath sounds progressively diminish.

Slide 20

Clinical Data Obtained from Laboratory Tests and Special Procedures

Slide 21

Pulmonary Function Study: Expiratory Maneuver Findings

FVC



PEFR



FEV T



FEF 25%-75%



MVV



FEF 50%



FEF 200-1200



FEV 1%

Slide 22

Pulmonary Function Study: Lung Volume and Capacity Findings

V T N or



RV FRC TLC

 

N or





IC ERV RV/TLC ratio N or



N or

Slide 23

Arterial Blood Gases

Mild to Moderate Chronic Bronchitis

 Acute alveolar hyperventilation with hypoxemia

pH Pa

 

CO 2 HCO 3 -



(Slightly) Pa



O 2

Slide 24 100 90 80 70 60 50 40 30 20 10 0

Time and Progression of Disease Disease Onset Alveolar Hyperventilation

Point at which PaO 2 declines enough to stimulate peripheral oxygen receptors Pa O 2

Figure 4-2. Pa O 2 and Pa CO 2 trends during acute alveolar hyperventilation.

Slide 25

Arterial Blood Gases

Severe Chronic Bronchitis

 Chronic ventilatory failure with hypoxemia

pH Pa Normal



CO 2 HCO 3 -



(Significantly) Pa O 2

Slide 26 100 90 80 70 60 50 40 30 20

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

Point at which PaO 2 declines enough to stimulate peripheral oxygen receptors Point at which disease becomes severe and patient begins to become fatigued 10 0

Figure 4-7. PaO 2 and PaCO 2 trends during acute or chronic ventilatory failure.

Slide 27

Acute Ventilatory Changes Superimposed on Chronic Ventilatory Failure

Slide 28

Q S /Q T



O 2 ER



Oxygenation Indices

D O 2



Sv O 2



V O 2 Normal C(a-v) O 2 Normal

Slide 29

Hemodynamic Indices (Severe Chronic Bronchitis)

CVP



CO Normal RAP



SV Normal SVI Normal PCWP Normal CI Normal RVSWI



LVSWI Normal PVR



SVR Normal

Abnormal Laboratory Tests and Procedures

Slide 30  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

Slide 31

Radiologic Findings

Slide 32

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 33

Radiologic Findings

Slide 34

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 35

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 Copyright © 2006 by Mosby, Inc.

Slide 36

GOLD Standards

G lobal Initiative for Chronic O bstructive L ung D isease

Slide 37

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 38

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

Slide 39

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

Slide 40

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

Slide 41

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

Slide 43

Document

Transcript Document

PART II

Chapter 11 Chronic Bronchitis

Anatomic Alterations of the Lungs

Etiology

Overview of the Cardiopulmonary Clinical Manifestations Associated with CHRONIC BRONCHITIS

Clinical Data Obtained at the Patient’s Bedside

Clinical Data Obtained at the Patient’s Bedside

Clinical Data Obtained at the Patient’s Bedside

Clinical Data Obtained at the Patient’s Bedside

Clinical Data Obtained from Laboratory Tests and Special Procedures

Pulmonary Function Study: Expiratory Maneuver Findings

Pulmonary Function Study: Lung Volume and Capacity Findings

Arterial Blood Gases

Arterial Blood Gases

Acute Ventilatory Changes Superimposed on Chronic Ventilatory Failure

Oxygenation Indices

Hemodynamic Indices (Severe Chronic Bronchitis)

Abnormal Laboratory Tests and Procedures

Radiologic Findings

Radiologic Findings

General Management of Chronic Bronchitis

GOLD Standards

Classroom Discussion Case Study: Chronic Bronchitis

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