Although acute valvular dysfunction may cause dramatic symptoms, most valvular heart disease encountered in the ED is chronic and incidentally noted on exam. Adaptive responses preserve cardiac function and delay the diagnosis of chronic valvular disease 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
THE NEWLY DISCOVERED MURMUR
After discovering a new murmur, the first step in the ED is to determine its clinical significance. Seek a new murmur in patients with acute dyspnea or weakness. Benign or physiologic murmurs are common and 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 other abnormal heart sounds. Systolic murmurs may be associated with anemia, sepsis, volume overload, or other conditions causing an increased cardiac output. Focus the evaluation and treatment on the trigger. Patients without chest pain, dyspnea, fever, or other signs attributable to valvular disease do not need emergent treatment.
Any diastolic murmur or new systolic murmur with symptoms at rest is pathologic and warrants emergent echocardiography (Figure 54-1). Think of endocarditis, especially in suspected valvular insufficiency. Table 54-1 presents a grading system for murmurs.
TABLE 54-1A Grading System for Murmurs ||Download (.pdf) TABLE 54-1 A Grading System for Murmurs
|Faint, may not be heard in all positions
|Quiet, but heard immediately with stethoscope placement onto the chest wall
|Heard with stethoscope partly off the chest wall
|Heard when stethoscope is entirely off the chest wall
Algorithm for evaluation of newly discovered systolic murmur. CXR = chest radiograph.
EPIDEMIOLOGY AND PATHOPHYSIOLOGY
Mitral stenosis prevents normal diastolic filling of the left ventricle. 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.
Mitral annular calcification is a slowly progressive nonrheumatic cause of mitral stenosis. It is more common among women, the elderly, and those with hypertension or with chronic renal failure.2 Due to its slow progression, mitral ...