Porth's Essentials of Pathophysiology, 4e

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Respiratory Function

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affords the potential for impaired gas exchange because of mismatching of ventilation and perfusion. The FVC is the amount of air that can be forcibly exhaled after maximal inspiration. In patients with chronic lung disease, the FVC is decreased, the FEV 1.0 is decreased, and the ratio of FEV 1.0 to FVC is decreased. Lung vol- ume measurements reveal a marked increase in RV, an increase in TLC, and elevation of the RV-to-TLC ratio. These and other measurements of expiratory flow are determined by spirometry and are used in the diagno- sis and severity of COPD (see Chapter 21, Fig. 21-15). Other diagnostic measures become important as the disease advances. Measures of exercise tolerance, nutri- tional status, hemoglobin saturation, and arterial blood gases can be used to assess the overall impact of COPD on health status and to direct treatment. The treatment of COPD depends on the stage of the disease and often requires an interdisciplinary approach. 10,44 Smoking cessation is the only measure that slows the progression of the disease. Maintaining and improving physical and psychosocial functioning is an important part of the treatment program. A long- term pulmonary rehabilitation program can significantly reduce hospitalizations and increase a person’s ability to manage and cope with his or her impairment in a posi- tive way. This program includes breathing exercises that focus on restoring the function of the diaphragm, reduc- ing the work of breathing, and improving gas exchange. Physical conditioning with appropriate exercise training increases maximal oxygen consumption and reduces ventilatory effort and heart rate for a given workload. Work simplification and energy conservation strategies may be needed when impairment is severe. Respiratory tract infections can prove life-threaten- ing to persons with severe COPD. A person with COPD should avoid exposure to others with known respira- tory tract infections and should avoid attending large gatherings during periods of the year when influenza or respiratory tract infections are prevalent. Immunization for influenza and pneumococcal infections decreases the likelihood of their occurrence. Although antibiotics are used to treat acute exacerbations of COPD due to bacte- rial infection, there is no evidence that the prophylactic use of antibiotics prevents acute exacerbations. The pharmacologic treatment of COPD includes the use of bronchodilators, including inhaled adrener- gic and anticholinergic agents. 10,44 Inhaled β 2 -agonists have been the mainstay of treatment of COPD for many years. It has been suggested that long-acting inhaled β 2 - agonists may be even more effective than the short-act- ing forms of the drug. The anticholinergic drugs, which are administered by inhalation, produce bronchodila- tion by blocking parasympathetic cholinergic receptors that produce contraction of bronchial smooth muscle. They also reduce the volume of sputum without alter- ing its viscosity. Because these drugs have a slower onset and longer duration of action, they typically are used on a regular basis rather than as needed. Inhalers that combine an anticholinergic drug with a β 2 -adrenergic agonist are available. Oral theophylline may be used in treatment of persons who fail to respond to inhaled

bronchodilators. The long-acting theophylline prepara- tions may be used to reduce overnight declines in respi- ratory function. When theophylline is prescribed, blood levels are used as a guide in arriving at an effective dose schedule. Although inhaled corticosteroids often are used in treatment of COPD, there is controversy regarding their usefulness. There is evidence that inflammation in COPD is not suppressed by inhaled or oral corticosteroids. 44 Because corticosteroids are useful in relieving asthma symptoms, they may benefit persons with asthma con- comitant with COPD. Inhaled corticosteroids also may be beneficial in treating acute exacerbations of COPD, minimizing the undesirable effects that often accompany systemic use. Oxygen therapy is prescribed for selected persons with significant hypoxemia (arterial PO 2 < 55 mm Hg). Administration of continuous low-flow (1 to 2 L/min) oxygen to maintain arterial PO 2 levels between 55 and 65 mm Hg decreases dyspnea and pulmonary hyper- tension and improves neuropsychological function and activity tolerance. 10,44 The overall goal of oxygen ther- apy is to maintain a hemoglobin oxygen saturation of at least 90%. Portable oxygen administration units, which allow mobility and the performance of activities of daily living, are often used in severe COPD. Because the ven- tilatory drive associated with hypoxic stimulation of the peripheral chemoreceptors does not occur until the arte- rial PO 2 has been reduced to about 60 mm Hg or less, increasing the arterial PO 2 above 60 mm Hg tends to depress the hypoxic stimulus for ventilation and often leads to hypoventilation and carbon dioxide retention. Bronchiectasis Bronchiectasis is characterized by a permanent dilation of bronchi caused by destruction of the bronchial muscle wall and elastic supporting tissue 16,46,47 (Fig. 23-11). It is not a primary disease but occurs secondary to a number of abnormalities that profoundly obstruct the airways or produce persistent infection, including atelectasis, obstruction of the smaller airways, diffuse bronchitis, and cystic fibrosis. 15 In the past, bronchiectasis often fol- lowed a necrotizing bacterial pneumonia that frequently complicated measles, pertussis (whooping cough), or influenza. Tuberculosis was also commonly associated with bronchiectasis. Thus, with the advent of antibiotics that more effectively treat respiratory infections such as tuberculosis, and with immunization against pertussis and measles, there has been a marked decrease in the prevalence of bronchiectasis. Etiology and Pathogenesis Two processes are critical to the pathogenesis of bron- chiectasis: obstruction and chronic persistent infec- tion. 15,16 Regardless of which may come first, both cause damage to the bronchial walls, leading to weakening and dilation. On gross examination, bronchial dila- tion is classified as saccular, cylindrical, or varicose. 16,47 Saccular bronchiectasis involves the proximal third to