Chapter 033. Dyspnea and Pulmonary Edema (Part 3)

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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 33-2 Respiratory System Dyspnea Controller Acute hypoxemia and hypercapnia are associated with increased activity in the controller. ...

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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 33-2 Respiratory System Dyspnea Controller Acute hypoxemia and hypercapnia are associated with increased activity in the controller. Stimulation of pulmonary receptors, as occurs in acute bronchospasm, interstitial edema, and pulmonary embolism, also leads to hyperventilation and air hunger, as well as a sense of chest tightness in the case of asthma. High altitude, high progesterone states such as pregnancy, and drugs such as aspirin stimulate the controller and can cause dyspnea even when the respiratory 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 of an inability to get a deep breath. Conditions that stiffen the chest wall, such as kyphoscoliosis, or that weaken ventilatory muscles, such as myasthenia gravis or the Guillain-Barré syndrome, are also associated with an increased effort to breathe. Large pleural effusions may contribute to dyspnea, both by increasing the work of breathing and by stimulating pulmonary receptors if there is associated atelectasis. Gas Exchanger Pneumonia, pulmonary edema, and aspiration all interfere with gas exchange. Pulmonary vascular and interstitial lung disease and pulmonary vascular congestion may produce dyspnea by direct stimulation of pulmonary receptors. In these cases, relief of hypoxemia typically has only a small impact on the intensity of dyspnea. Cardiovascular System Dyspnea High Cardiac Output
Mild to moderate anemia is associated with breathing discomfort during exercise. Left-to-right intracardiac shunts may lead to high cardiac output and dyspnea, although in their later stages these conditions may be complicated by the development of pulmonary hypertension, which contributes to dyspnea. The breathlessness 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 of anaerobic metabolism and stimulation of chemoreceptors and metaboreceptors. Diastolic dysfunction—due to hypertension, aortic stenosis, or hypertrophic cardiomyopathy—is an increasingly frequent recognized cause of exercise- induced breathlessness. Pericardial disease, e.g., constrictive pericarditis, is a relatively rare cause of chronic dyspnea. Low Cardiac Output Diseases of the myocardium resulting from coronary artery disease and nonischemic cardiomyopathies result in a greater left ventricular end-diastolic volume and an elevation of the left ventricular end-diastolic as well as pulmonary capillary pressures. Pulmonary receptors are stimulated by the elevated vascular pressures and resultant interstitial edema, causing dyspnea. [newpage]