![]() ![]() Computed tomography of the chest is the most appropriate imaging study for diagnosing suspected pulmonary causes of chronic dyspnea. Pulmonary function studies can be used to identify emphysema and interstitial lung diseases. Measurement of brain natriuretic peptide levels may help exclude heart failure, and d-dimer testing may help rule out pulmonary emboli. Initial testing in patients with chronic dyspnea includes chest radiography, electrocardiography, spirometry, complete blood count, and basic metabolic panel. Examination findings (e.g., jugular venous distention, decreased breath sounds or wheezing, pleural rub, clubbing) may be helpful in making the diagnosis. ![]() Patients' descriptions of the sensation of dyspnea may be helpful, but associated symptoms and risk factors, such as smoking, chemical exposures, and medication use, should also be considered. The clinical presentation alone is adequate to make a diagnosis in 66 percent of patients with dyspnea. ![]() The etiology of dyspnea is multi-factorial in about one-third of patients. Most cases of dyspnea result from asthma, heart failure and myocardial ischemia, chronic obstructive pulmonary disease, interstitial lung disease, pneumonia, or psychogenic disorders. Dyspnea that is greater than expected with the degree of exertion is a symptom of disease. The perception of dyspnea varies based on behavioral and physiologic responses. S 4 is from ejection of blood from the atrium into a noncompliant ventricle, as might be encountered in the setting of ventricular hypertrophy related to systemic hypertension, or in the setting of an acute myocardial infarct.Chronic dyspnea is shortness of breath that lasts more than one month. It is particularly common in the setting of CHF. A pathologic S 3 occurs with ventricular systolic dysfunction during the rapid filling phase of diastole or from impact of the left ventricle against the chest wall. Paradoxical splitting (P 2 first and A 2 second) occurs with delayed closure of the aortic valve (e.g., left bundle branch block, aortic stenosis). Wide splitting of S 2 is caused by a greater than normal delay in pulmonic closure (e.g., right bundle branch block, pulmonic stenosis) or earlier aortic valve closure due to decreased left ventricular volume (e.g., mitral regurgitation, ventricular septal defect). S 2 is physiologically split during inspiration (aortic, A 2, first and pulmonic, P 2 second)-increased venous return to the right side of the heart delays closure of the pulmonic valve and decreased return to the left side speeds closure of the aortic valve. In a patient with hypertension (systemic or pulmonary), closing of the associated valve (aortic or pulmonic) is accentuated (louder) in a patient with stenosis, the closing is diminished in strength (softer sound). The S 1 sound is caused by closing of the mitral and tricuspid valves, and the S 2 sound is caused by closing of the aortic and pulmonary valves. An understanding of heart sounds is important in the clinical evaluation of heart disease. ![]()
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