Chapter 033. Dyspnea and Pulmonary Edema (Part 3)

Differential Diagnosis Dyspnea is the consequence of deviations from normal function in the cardiopulmonary systems. Alterations in the respiratory system can be considered in the context of the controller (stimulation of breathing); the ventilatory pump (the bones and muscles that form the chest wall, the airways, and the pleura); and the gas exchanger (the alveoli, pulmonary vasculature, and surrounding lung parenchyma). Similarly, alterations in the cardiovascular system can be grouped into three categories: conditions associated with high, normal, and low cardiac output (Fig. 33-2).Figure 33-2Respiratory System DyspneaControllerAcute hypoxemia and hypercapnia are associated with increased activity in the controller. ...
Nội dung trích xuất từ tài liệu:
Chapter 033. Dyspnea and Pulmonary Edema (Part 3) Chapter 033. Dyspnea and Pulmonary Edema (Part 3) Differential Diagnosis Dyspnea is the consequence of deviations from normal function in thecardiopulmonary systems. Alterations in the respiratory system can be consideredin the context of the controller (stimulation of breathing); the ventilatory pump(the bones and muscles that form the chest wall, the airways, and the pleura); andthe gas exchanger (the alveoli, pulmonary vasculature, and surrounding lungparenchyma). Similarly, alterations in the cardiovascular system can be groupedinto three categories: conditions associated with high, normal, and low cardiacoutput (Fig. 33-2). Figure 33-2 Respiratory System Dyspnea Controller Acute hypoxemia and hypercapnia are associated with increased activity inthe controller. Stimulation of pulmonary receptors, as occurs in acutebronchospasm, interstitial edema, and pulmonary embolism, also leads tohyperventilation and air hunger, as well as a sense of chest tightness in the case ofasthma. High altitude, high progesterone states such as pregnancy, and drugs suchas aspirin stimulate the controller and can cause dyspnea even when therespiratory system is normal. Ventilatory Pump Disorders of the airways (e.g., asthma, emphysema, chronic bronchitis,bronchiectasis) lead to increased airway resistance and work of breathing.Hyperinflation further increases the work of breathing and can produce a sense ofan inability to get a deep breath. Conditions that stiffen the chest wall, such askyphoscoliosis, or that weaken ventilatory muscles, such as myasthenia gravis orthe Guillain-Barré syndrome, are also associated with an increased effort tobreathe. Large pleural effusions may contribute to dyspnea, both by increasing thework of breathing and by stimulating pulmonary receptors if there is associatedatelectasis. Gas Exchanger Pneumonia, pulmonary edema, and aspiration all interfere with gasexchange. Pulmonary vascular and interstitial lung disease and pulmonaryvascular congestion may produce dyspnea by direct stimulation of pulmonaryreceptors. In these cases, relief of hypoxemia typically has only a small impact onthe intensity of dyspnea. Cardiovascular System Dyspnea High Cardiac Output Mild to moderate anemia is associated with breathing discomfort duringexercise. Left-to-right intracardiac shunts may lead to high cardiac output anddyspnea, although in their later stages these conditions may be complicated by thedevelopment of pulmonary hypertension, which contributes to dyspnea. Thebreathlessness associated with obesity is probably due to multiple mechanisms,including high cardiac output and impaired ventilatory pump function. Normal Cardiac Output Cardiovascular deconditioning is characterized by early development ofanaerobic metabolism and stimulation of chemoreceptors and metaboreceptors.Diastolic dysfunction—due to hypertension, aortic stenosis, or hypertrophiccardiomyopathy—is an increasingly frequent recognized cause of exercise-induced breathlessness. Pericardial disease, e.g., constrictive pericarditis, is arelatively rare cause of chronic dyspnea. Low Cardiac Output Diseases of the myocardium resulting from coronary artery disease andnonischemic cardiomyopathies result in a greater left ventricular end-diastolicvolume and an elevation of the left ventricular end-diastolic as well as pulmonarycapillary pressures. Pulmonary receptors are stimulated by the elevated vascularpressures and resultant interstitial edema, causing dyspnea. [newpage]