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Figure 10 The Pathophysiologic Stages of MR
(A and B) Normal physiology (N) is contrasted with that of acute mitral regurgitation (MR). In acute MR, the volume overload of MR increases sarcomere length (SL), augmenting preload. Increased SL is reflected by an increase in end-diastolic volume (EDV). The new pathologic pathway for ejection into the left atrium (LA) reduces afterload as quantified by end-systolic stress (ESS), allowing the left ventricle to eject more completely. Enhanced ejection is reflected by a fall in end-systolic volume (ESV). As a result, the total stroke volume increases to 140 ml, but because 50% is regurgitated into the LA (regurgitant fraction [RF] 0.50), forward stroke volume (FSV) decreases. Ejection fraction (EF) increases, although contractile function (CF) is normal but not increased. (C) Chronic compensated mitral regurgitation. In this phase of MR, eccentric cardiac hypertrophy produces a further increase in EDV, which allows for a large increase in total stroke volume (190 ml) so that FSV returns to nearly normal. The enlarged and compliant LA can accommodate the regurgitant volume at a lower pressure, so that left atrial pressure declines. CF remains normal, and EF remains increased. (D) Chronic decompensated mitral regurgitation. In this phase, CF has been reduced from muscle damage caused by prolonged severe volume overload. Impaired CF reduces the effectiveness of left ventricular ejection and ESV increases. There is a further increase in diastolic volume, which is not compensatory for the increase in ESV, resulting in a decrease in total and forward stroke volumes. Concomitantly, increased EDV worsens the MR by annular dilation and papillary muscle malalignment and regurgitant fraction increases. Ejection fraction is reduced from the compensated state but often remains within the normal range.
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