Porth's Essentials of Pathophysiology, 4e

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Disorders of Ventilation and Gas Exchange

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in the residual volume (RV) along with a decrease in the inspiratory reserve capacity (tidal volume + inspiratory reserve volume [IRV]) and forced vital capacity (FVC), such that the person breathes close to his or her func- tional residual capacity (residual volume + expiratory reserve volume; see Chapter 21, Fig. 21-17). As a result, more energy is needed to overcome the tension already present in the lungs, and the accessory muscles (e.g., sternocleidomastoid muscles) are required to maintain ventilation and gas exchange. This increased work of breathing further increases oxygen demands and causes dyspnea and fatigue. Because air is trapped in the alveoli and inspiration is occurring at higher residual lung vol- umes, the cough becomes less effective. As the condi- tion progresses, the effectiveness of alveolar ventilation declines, and mismatching of ventilation and perfusion occurs, causing hypoxemia and hypercapnia. Pulmonary vascular resistance may increase as a result of the hypox- emia and hyperinflation, leading to a rise in pulmonary arterial pressure and increased work demands on the right heart. The physical signs of bronchial asthma vary with the severity of the attack. A mild attack may produce a feel- ing of chest tightness, a slight increase in respiratory rate with prolonged expiration, and mild wheezing. A cough may accompany the wheezing. More severe attacks are accompanied by use of the accessory muscles, distant breath sounds due to air trapping, and loud wheezing. As the condition progresses, fatigue develops, the skin becomes moist, and anxiety and apprehension ensue. Sensations of shortness of breath may be severe, and often the person is able to speak only one or two words before taking a breath. At the point at which airflow is markedly decreased, breath sounds become inaudible, wheezing diminishes, and the cough becomes ineffec- tive despite being repetitive and hacking. 19 This point often marks the onset of respiratory failure. A common error on physical examination is the absence of wheez- ing which signifies severe bronchospasm and represents the lack of air movement. With appropriate treatment, wheezing can be unmasked as air movement improves. Diagnosis andTreatment The diagnosis of asthma is based on a careful history and physical examination, laboratory findings, and pulmo- nary function studies (see Chapter 21). 19–22 Spirometry provides a means for measuring FVC, FEV1.0, PEF, tidal volume, expiratory reserve volume, and inspira- tory reserve volume. The FEV1.0/FVC ratio can then be calculated. The level of airway responsiveness can be measured by inhalation challenge tests using methacho- line (a cholinergic agonist), histamine, or exposure to a nonpharmacologic agent such as cold air. The Expert Panel of the National Asthma Education and Prevention Program (NAEPP) has developed classification systems intended for use in identifying persons at high risk for development of life-threatening asthma attacks and directing asthma treatment 19 (Table 23-1). Small, inexpensive, portable meters that measure PEF are available. Although not intended for use in the

responsiveness (e.g., smog-related asthma). A group of chemicals that can provoke an asthmatic attack are the sulfites used in food processing and as preservatives added to beer, wine, and fresh vegetables. There is a small group of persons in whom aspirin and other NSAIDs evoke the clinical triad of nasal pol- yps, chronic rhinosinusitis, and bronchial asthma. 15,16,27 The mechanism of the hypersensitivity reaction is com- plex and not fully understood, but most evidence points toward an abnormality in arachidonic acid (AA) metab- olism in which aspirin inhibits the bronchodilating cyclooxygenase pathway without affecting the lipoxy- genase pathway, thereby shifting the balance toward the bronchoconstrictor leukotrienes (see Chapter 3, Fig. 3-4). Avoidance of aspirin and all NSAIDs is a nec- essary part of the treatment program. Both emotional factors and changes in hormone lev- els are thought to contribute to an increase in asthma symptoms. Emotional factors produce bronchospasm by way of vagal pathways. They can act as a bron- chospastic trigger, or they can increase airway respon- siveness to other triggers through noninflammatory mechanisms. Reproductive hormones may play a role in asthma in women. Up to 40% of women with asthma report a premenstrual increase in asthma symptoms. 28 Female reproductive hormones have a regulatory role on β 2 -adrenergic function, and it has been suggested that abnormal regulation may be a possible mechanism for premenstrual asthma. Symptoms of gastroesophageal reflux are common in both adults and children with asthma, suggesting that reflux of gastric secretions may act as a bronchospastic trigger. Reflux during sleep can contribute to nocturnal asthma. 19 Manifestations Persons with asthma exhibit a wide range of signs and symptoms ranging from episodes of wheezing and feel- ings of chest tightness to acute immobilizing attacks. The attacks differ from person to person, and between attacks, many persons are symptom free. Attacks may occur spontaneously or in response to various triggers, respiratory infections, emotional stress, or weather changes. Asthma is often worse at night. Studies of noc- turnal asthma suggest that there is a circadian and sleep- related variation in hormones and respiratory function. 29 The greatest decrease in respiratory function occurs at about 4:00 am , at which time cortisol levels are low, mel- atonin levels high, and eosinophil activity increased. 30 During an asthmatic attack, the airways narrow because of bronchospasm, edema of the bronchial mucosa, and mucus plugging. Expiration becomes pro- longed because of progressive airway obstruction. 19–22 The amount of air that can be forcibly expired in 1 sec- ond (forced expiratory volume in 1 second [FEV 1.0 ]) and the peak expiratory flow rate (PEF), measured in liters per second, are decreased. During a prolonged attack, air becomes trapped behind the occluded and narrowed airways, causing hyperinflation of the lungs. This produces an increase