Physiologic mechanisms in aortic insufficiency. I. The effect of changing heart rate on flow dynamics. II. Determinants of Austin Flint murmur.

We studied the dynamic changes in mitral flow patterns and in mitral valve motion before and after producing acute, reversible aortic insufficiency (AI) in nine open-chest dogs. Phasic mitral flow, the mitral valve echocardiogram, and intracardiac phonocardiogram and other hemodynamic variables were measured. During moderate AI (mean regurgitant fraction 52 +/- 5%) (+/- SD), the antegrade filling volume decreased from 31 +/- 7 to 24 +/- 6 ml (p less than 0.01), but the peak protodiastolic mitral flow rate increased from 139 +/- 37 to 157 +/- 42 ml/sec (p less than 0.01), reflecting the shift of a larger fraction of total mitral filling volume to early diastole. In six dogs, atrial pacing was used to examine the hemodynamic effects of tachycardia. Increasing the heart rate from 90 to 120 beats/min increased cardiac output from 2.64 +/- 0.56 to 3.3 +/- 0.831/min (p less than 0.05) and decreased left atrial pressure from 24 +/- 8 to 17 +/- 7 mm Hg (p less than 0.05). Increasing heart rate to 150 beats/min compromised mitral filling, reduced cardiac output and increased left atrial pressure. Moderate tachycardia improves cardiac performance in AI by reducing regurgitant volume, without significantly reducing transmitral filling volume. The mitral valve echocardiogram showed only a small decrease in cusp opening amplitude during AI. A low-pitched left ventricular inflow tract murmur was recorded in protodiastole and corresponded in time to the rapidly increasing mitral flow. We conclude that the major determinant of the turbulence responsible for the creation of the austin flint murmur is the antegrade mitral flow stream and its mixing with the retrograde aortic flow.