Early Systolic Regurgitant Murmurs

Rarely, a regurgitant murmur confined to early systole is seen in the presence of a small VSD. This murmur begins in the usual manner at the onset of ventricular systole and stops suddenly in early or middle systole.292 The sudden cessation of the murmur is due to the fact that as ejection continues and ventricular size decreases, the small defect is sealed shut as the ventricular septum thickens during systole and the flow ceases. This murmur is important because it is characteristic of the type of VSD that may disappear with age.

In contrast to the holosystolic murmur of chronic mitral regurgitation, acute severe mitral regurgitation may present as an early systolic spindle-shaped murmur.293 Common conditions producing acute mitral regurgitation include spontaneous rupture of the chordae tendineae of a myxomatous valve, acute or subacute bacterial endocarditis of the mitral valve, papillary muscle rupture or dysfunction secondary to acute MI, and disruption of the mitral apparatus due to chest trauma.294 In each of these conditions, large-

volume flow regurgitates into a relatively normal left atrium that has not had the time to make the adaptive changes in compliance seen in chronic long-standing mitral regurgitation. As a result, an extremely high v wave is generated in the left atrium.

This high v wave abolishes the left ventricular-left atrial gradient during the latter part of systole, resulting in termination of retrograde flow and abbreviation of the systolic murmur. As shown in a patient with acute mitral regurgitation secondary to spontaneous rupture of the chordae tendineae of a myxomatous valve, the murmur ends before A2. Audible expiratory splitting with an accentuated P2 is present at the base, and a loud S4 is recorded at the apex. The presence of the S4 associated with a prominent presystolic impulse on palpation is an important clue that indicates the acute nature of the mitral regurgitation and is rarely present in mitral regurgitation of a chronic nature. The systolic murmur of acute mitral regurgitation, which can mimic ejection murmurs, may have classic radiation to the axilla and back, especially if it is due to prolapse of the anterior leaflet of the valve with flow directed over the posterior leaflet. When the murmur is loud, it may be conducted to the top of the head and to the sacrum along the spinal column. Occasionally, the murmur is conducted to the base of the heart and great vessels, simulating aortic stenosis. The quick-rising carotid pulse with rapid falloff, as well as the wide physiologic splitting of the second heart sound, helps differentiation from aortic stenosis.295

The systolic murmur of organic tricuspid regurgitation is often unimpressive and presents as an early systolic murmur ending well before A2, even in the presence of severe regurgitation.296 In this condition, the RV pressure is nearly normal, and massive regurgitation may be present with only a small pressure differential between the right ventricle and the right atrium. The small pressure head results in a low-velocity flow, minimal turbulence, and a soft, abbreviated murmur. Occasionally, only minimal early systolic vibrations are heard. In most patients, large vwaves are readily apparent in the JVP. The murmur retains the characteristic inspiratory augmentation seen in right-sided regurgitant murmurs and is frequently associated with an S4 that increases in intensity with inspiration. A right-sided S4 and a prominent diastolic tricuspid flow rumble are the rule when the tricuspid regurgitation is acute, as in endocarditis of the tricuspid valve. After total excision of the tricuspid valve for infective endocarditis related to intravenous drug abuse, the systolic murmur is often very unimpressive or may be completely absent. Giant v waves in the neck are easily visible, however, and palpable venous thrills and a murmur at the base of the neck may be present secondary to rapid retrograde flow in the jugular system.297 Other causes of organic tricuspid regurgitation include carcinoid heart disease, RV infarction, chest trauma, and damage of the tricuspid valve during open heart surgery.

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