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In contrast to the dramatic symptoms associated with acute valvular dysfunction, most valvular heart disease encountered in the ED is chronic and incidentally noted on exam. Adaptive responses preserve cardiac function and can delay the diagnosis of chronic valvular disease for decades but contribute to eventual cardiac dysfunction. Compared with the general population, patients with clinically evident valvular heart disease have a 2.5-fold higher death rate and a 3-fold increased rate of stroke.1
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THE NEWLY DISCOVERED MURMUR
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After discovering a new murmur, the first step in the ED is to determine the clinical significance. Benign or physiologic murmurs do not cause symptoms or findings compatible with cardiovascular disease; they are generally soft systolic ejection murmurs that begin after S1, end before S2, and are not associated with abnormal heart sounds. Systolic murmurs may be associated with anemia, sepsis, volume overload, or other conditions causing an increased cardiac output. Evaluation and treatment are focused on the underlying trigger rather than the murmur itself. Patients without chest pain, dyspnea, fever, or other signs attributable to valvular disease do not need emergent echocardiography but should be referred for eventual imaging.
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Any diastolic murmur or new systolic murmur with symptoms at rest is pathologic and warrants emergent echocardiographic imaging. Patients with syncope from suspected aortic stenosis require admission for monitoring and echocardiography (Figure 54-1). Table 54-1 presents a grading system for murmurs. Another consideration in the newly diagnosed murmur is the possibility of endocarditis, especially in suspected valvular insufficiency (see chapter 155, "Endocarditis").
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EPIDEMIOLOGY AND PATHOPHYSIOLOGY
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Mitral stenosis prevents normal diastolic filling of the left ventricle. Despite declining frequency, rheumatic heart disease remains the most common cause worldwide. Rheumatic carditis causes fusion of valvular commissures, matting of chordae tendineae, and eventual calcification and limited mobility of the valve. Valvular obstruction is slowly progressive, often with 20 to 40 years before onset of symptoms. Mitral valve obstruction causes left atrial pressure to rise, resulting in left atrial enlargement, pulmonary congestion, pulmonary hypertension, and frequently atrial fibrillation. In severe disease, pulmonary hypertension may lead to pulmonic and tricuspid valve incompetence, pulmonary edema, right-sided heart failure, and bronchial vein rupture.
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