Afterload in MR

The LV is capable of maintaining stroke volume in chronic MR until advanced stages of the disease because, following the Frank-Starling law, diastolic lengthening increases shortening of the sarcomere. If the regurgitant leak were unrestrictive, this compensating mechanism would be insufficient to maintain forward flow because the preload-recruited stroke volume would be mostly pumped towards the left atrium. In chronic MR, the regurgitant lesion always imposes a significant opposition to backflow. Although its area may vary during systole, in fluid-mechanical terms, the regurgitant lesion in MR behaves as a small, flat and restrictive orifice. Very large free regurgitant lesions, as sometimes found in severe tricuspid insufficiency—showing a laminar regurgitant flow and a very low transtricuspid pressure gradient—are virtually never seen in chronic MR. Furthermore, even in advanced stages of the disease, any decline in cardiac output is compensated by vasomotor reflexes. Consequently, systolic blood pressure remains normal in chronic MR.1

Ventricular pressure translates to afterload by means of wall-stress. Governed by Laplace's law, systolic wall-stress is directly proportional to systolic LV pressure. But systolic wall-stress is also directly proportional to the degree of wall curvature (radius), …