Obstructive Pulmonary Disease and General Management Principles
A The acronym for chronic obstructive pulmonary disease (COPD) is applied to patients with long-term chronic obstructive pulmonary disease, who show persistent airway obstruction, normally manifested by decreased expiratory flow rates. The airflow obstruction may be associated with airway hyperactivity and may be partially reversible.
1. COPD is the fourth leading cause of death in the United States, preceded by cerebrovascular disease, cancer, and heart disease.
2. In 2000, the World Health Organization estimated that 2.74 million deaths worldwide were attributed to COPD.
3. Between 1985 and 1995, the number of physician visits for COPD in the United States increased from 9.3 million to 16 million.
4. Approximately 14 million people in the United States have been diagnosed with COPD, and this number has increased by 42% since 1982.
5. There seems to be a greater incidence of COPD in men than in women; however, the percentage of women with COPD is steadily increasing.
6. On autopsy, some degree of emphysema appears in a large percentage of the population.
7. Emphysema is the second leading cause of disability, arteriosclerotic heart disease being first.
1. Smoking: Of all risk factors, smoking shows the highest correlation with COPD; however, individual response to short-term and long-term exposure varies considerably from individual to individual. The reasons for this variation in response are not well understood. Smoking:
2. Pollution: Particulate and gaseous.
3. Passive smoking: Evidence indicates the passive inspiration of smoke from the environment increases the risk of COPD. Passive smoking exposes the individual to the same toxic substance, although in lower concentration than the active smoker.
4. Occupational exposure to dusts and fumes.
5. Infection, which may cause decreased pulmonary clearance, resulting in an increased incidence of recurrent infection.
a. β1-Antitrypsin deficiency, which results in emphysematous changes measurable in the third and fourth decades (see Section II, Emphysema).
7. Allergies (e.g., chronic asthma), which can lead to permanent pulmonary changes.
8. Socioeconomic status: Higher incidence has been demonstrated in low socioeconomic groups.
9. Alcohol ingestion, although no direct link has been demonstrated. Alcohol ingestion:
a. Decreases ciliary function.
b. Decreases alveolar macrophage function.
10. Aging, which causes natural degenerative changes in the respiratory tract resembling emphysematous changes.
D Physical appearance of patient
1. Barrel-chested: A result of increased air trapping
a. Increase in anteroposterior diameter
b. Increase proportional to increase in functional residual capacity (FRC)
2. Clubbing (pulmonary hypertrophic osteopathy): Bulbous enlargement of terminal portion of the digits, altering the cuticular angle, may be present if there have been frequent pulmonary infections.
3. Cyanosis: A result of hypoxemia coupled with secondary polycythemia
4. Decreased and adventitious breath sounds
5. Often a hyperresonant chest
7. Malnourished, secondary to loss of appetite (anorexia)
10. May be edematous with jugular vein distention if congestive heart failure (CHF) present
E General pulmonary function changes (Table 20-1)
TABLE 20-1
Changes in Pulmonary Function Associated with Obstructive and Restrictive Lung Disease
| Pulmonary Function Study | Obstructive Disease | Restrictive Disease |
| TLC | Normal or increased | Decreased |
| VC | Normal or decreased | Decreased |
| FRC | Increased | Normal or decreased |
| RV | Increased | Normal or decreased |
| RV/TLC ratio | Increased | Normal |
| FEV1% | Decreased | Normal |
| MMEFR25%-75% | Decreased | Normal or decreased |
1. Pulmonary compliance is frequently increased.
2. Airway resistance increases as a result of mucosal edema and bronchiolar wall weakening.
3. Prolonged expiratory times when numbers 1 and 2 are present.
5. Increased residual volume (RV).
6. Increased RV/total lung capacity (TLC) ratio.
8. Decreased or normal vital capacity (VC).
9. Decreased or normal inspiratory capacity (IC) and inspiratory reserve volume (IRV) secondary to increased FRC.
10. Increased expiratory reserve volume (ERV).
11. Decreased expiratory flow studies: FEV1%, FEV3%, maximum midexpiratory flow rate between 25% and 75% (MMEFR25%-75%), forced expiratory flow determined between the first 200 ml and 1200 ml of exhaled volume (FEF200-1200), and maximum voluntary ventilation (MVV). The level of reduction is associated with severity of disease (Figure 20-1).
F General radiographic findings (Figure 20-2)
1. Increased anteroposterior diameter
4. Pulmonary vascular engorgement with increased vascular markings
5. Increased retrosternal airspace
6. Normal or increased heart shadow
7. Normal or thin elongated mediastinum
9. Possible peripheral bullae or blebs
10. In severe cases or end-stage disease, frequently right ventricular hypertrophy and CHF
1. In all patients dyspnea on exertion is one of the first noticeable symptoms.
2. As the disease process progresses, dyspnea becomes apparent even at rest.
3. Dyspnea normally increases as the work of breathing progressively increases.
4. The percentage of the oxygen consumed to ventilate is increased, severely limiting the patient’s level of physical exertion as the disease progresses.
1. The ventilatory drive of COPD patients may vary considerably.
2. Some continue to increase their ventilatory efforts as the disease progresses, despite increases in work of breathing.
a. These patients possess normal or increased ventilatory drives. In the past these patients were referred to as “pink puffers.”
b. This group usually does not become carbon dioxide retainers, despite continual disease progression.
c. As a result administration of high FIO2 does not depress ventilation. Normal carbon dioxide responsiveness continues until there is complete failure of ventilatory muscles.
d. These patients present in acute distress, with normal or decreased Pco2. levels.
e. The level of Pco2. rapidly increases when failure overwhelms ventilatory capabilities (Figure 20-3).
3. Conversely, many COPD patients have marked alterations in ventilatory drive.
a. Their sensitivity to oxygen frequently is increased, and carbon dioxide is reduced.
b. This group in the past was referred to as “blue bloaters.”
c. They experience progressive increases to baseline Pco2 levels as their disease progresses.
d. At presentation with an acute exacerbation of the disease, markedly elevated Pco2 levels may be noted. Blood gas interpretation is usually acute respiratory acidosis superimposed on chronic respiratory acidosis with severe hypoxemia.
e. These patients are classified as individuals who will not breathe during failure, whereas those with normal drives simply cannot breathe at the time of failure.
I General pattern of arterial blood gas changes demonstrated by carbon dioxide retainers as their disease progresses from mild to severe:
1. Because of the pathophysiology of COPD, ventilation/perfusion inequalities develop.
2. Mismatching of ventilation and blood flow results in hypoxemia. It should be noted that hypoxemia normally is the first measured blood gas abnormality.
3. Hypoxemia becomes increasingly worse as the disease process progresses, resulting in stimulation of peripheral chemoreceptors.
4. Stimulation of peripheral chemoreceptors may result in hyperventilation, the body’s attempt to correct hypoxemia.
5. If hyperventilation persists, the kidneys compensate for the acid-base imbalance. Blood gas analysis reveals compensated respiratory alkalosis (chronic alveolar hyperventilation) with hypoxemia.
6. Hyperventilation continues until oxygen consumption by the patient’s respiratory musculature exceeds the benefits received by hyperventilation.
7. The percentage of total oxygen consumption used for ventilation becomes greatly increased because the efficiency of the respiratory system is greatly reduced by disease and increased accessory muscle use.
8. The body can no longer maintain the level of alveolar ventilation necessary to maintain adequate oxygen tensions without severely compromising oxygen delivery to other organs.
9. Because of the depressed ventilatory drive of the individual and the high cost of breathing, carbon dioxide is allowed to increase in an attempt to conserve energy.
10. This results in further progression of the hypoxemia.
11. The total oxygen reservoir may be decreased even further.
12. This is counterbalanced to a degree by a reduction in oxygen consumption by the respiratory muscles, a decrease in the patient’s overall level of activity, and secondary polycythemia.
13. Alveolar ventilation continues to decrease. This is evidenced by increasing carbon dioxide levels and further development of hypoxemia.
14. With time the patient begins to retain carbon dioxide. Blood gases at this time reveal compensated respiratory acidosis with moderate to severe hypoxemia.
15. It is at this point when carbon dioxide starts to be retained that the patient’s primary stimulus to breathe may become oxygen.
16. If oxygen were administered in sufficient amounts, the hypoxic stimulus to breathe could be reduced, potentially to the point of apnea in a few select patients.
a. This is an unusual occurrence.
b. Most patients who are CO2 retainers do not function on a hypoxic drive.
c. However, care should always be exercised when administering oxygen, but oxygen should not be withheld from a hypoxemic patient because of fear of further hypoventilation.
17. The disease continues to progress with increasing levels of carbon dioxide retention and more severe hypoxemia.
18. The disease process becomes end stage and terminal. The patient’s level of physical activity is severely limited, and he or she is reduced to a pulmonary cripple (Figure 20-4).
1. Cor pulmonale denotes right ventricular hypertrophy secondary to abnormalities of lung structure and function. CHF may or may not be present.
2. It is a frequent sequel to chronic bronchitis and cystic fibrosis.
a. Developing pulmonary disease results in increasing hypoxemia, which causes constriction of the pulmonary arterioles.
b. Constriction causes pulmonary hypertension. The decreased size of the capillary bed seen with advancing pulmonary disease also contributes to development of pulmonary hypertension.
c. Pulmonary hypertension causes the right side of the heart to work harder. With time, right ventricular hypertrophy develops.
d. Pulmonary hypertension, if not controlled, precipitates the development of right ventricular failure.
e. This results in peripheral edema because of increased resistance to venous return and decreased right ventricular function.
f. Failure of the right side of the heart is more frequently seen in association with pulmonary disease than is left-sided heart failure.
g. However, over time the patient with right-sided heart failure can also develop left-sided heart failure.
A Emphysema is characterized by enlargement of air spaces distal to terminal bronchioles, with loss of elastic tissue and destruction of alveolar septal walls.
1. Smoking (high correlation with emphysema)
2. High correlation with long-term air pollution.
a. Destructive changes occur primarily in the respiratory bronchioles.
b. Incidence is much higher in men than women.
c. Primary lesions appear in the upper lobes.
d. There is a high correlation with centrilobular emphysema and smoking; frequently it is a sequel to chronic bronchitis.
a. Changes at alveolar level where destruction of septa predominates.
b. Effects seemingly generalized in distribution.
c. Seen with α1-antitrypsin deficiency and the natural aging process.
1. Shortness of breath, developing gradually
3. Frequent respiratory infections
E Chest radiography findings (Figure 20-5)
F Pulmonary function studies (as outlined in Section I, General Comments)
G Management (as outlined in Section V, General Management Principles in COPD)
1. Acute inflammation of tracheobronchial tree with production of excessive mucus.
4. Treatment: Usually by administration of antibiotics, expectorants, aerosol therapy, and occasionally antitussives.
5. Normally a self-limiting process without serious complications or residual effects.
1. Chronic cough with excessive sputum production of unknown specific etiology for 3 months per year for 2 or more successive years
2. Caused by frequent acute episodes of bronchitis, which may result from:
a. Onset normally insidious, with patient rarely aware of its development
(1) Size increases in relation to wall thickness; normally gland size is approximately one third of the height of the bronchial walls.
(2) In chronic bronchitis, gland size is approximately two thirds of the height of the bronchial walls.
b. Submucosal gland hypertrophy
c. Increased population of goblet cells replacing ciliated columnar cells (epithelial metaplasia)
a. Early in the disease, radiographic changes are not significant, especially if the disease is associated only with larger airways.
b. If the disease has moved to the periphery, hyperinflation with flattened hemidiaphragms may be noticed.
c. Peripheral pulmonary vasculature may be prominent.
d. Cardiac shadow is enlarged.
e. There is pulmonary vascular engorgement.
f. Chest radiography is usually of little use in establishing diagnosis.
g. A positive patient history usually is the best diagnostic tool.
a. In early stages all pulmonary function studies may be normal, except for slight decreases in expiratory flow rates.
b. As the disease process progresses, pulmonary function results are consistent with those presented in Section I, General Comments.
a. Most important: Removal of patient from irritants.
b. Aerosol and bronchodilator therapy if there is a reversible component to airflow obstruction.
c. Antibiotics if indicated for bacterial infection.
d. Treatment regimen fairly consistent with that outlined in Section V, General Management Principles in COPD.
A Permanent abnormal dilation and distortion of bronchi and/or bronchioles
B Classification: There are three types of bronchiectasis (Figure 20-6).
