Regardless of the underlying etiology of mitral regurgitation (MR), a decrease in the coaptation between the leaflets of the valve commonly characterizes all cases of MR.  Acute MR occurs when there is sudden disruption of one or more of the components of the mitral valve, as occurs in leaflet perforation, rupture of a chordae tendineae, or rupture of the papillary muscle.  In the acute phase, the volume and pressure overload in the left atrium is transmitted backward into the pulmonary vasculature to cause an elevation of the pulmonary capillary wedge pressure which causes dyspnea, orthopnea, and rales. In addition, there is decreased forward stroke volume. Chronic MR can be either primary or secondary. Chronic primary MR results from chronic disruption of one or more component of the mitral valve (papillary muscles, chordae tendineae, or valve leaflets), whereas chronic secondary MR results from the dysfunction and dilatation of the left ventricle rather than an intrinsic abnormality in one of the components of the mitral valve.  If the chronic MR develops slowly over months to years or if the acute phase is successfully managed with medical therapy, the patient enters the chronic compensated phase of MR that can eventually deteriorate into a decompensated phase as the left ventricular systolic function worsens.  The markers of MR decompensation are as follows: left ventricular end-diastolic dimension greater than 70 mm, left ventricular end-systolic dimension greater than 45 to 47 mm, and left ventricular ejection fraction (LVEF) less than 50 to 55 percent.
Mitral regurgitation pathophysiology
Tricuspid regurgitation pathophysiology
Aortic regurgitation pathophysiology
Tricuspid stenosis pathophysiology
Bicuspid aortic stenosis pathophysiology
Mitral valve prolapse causes
Mitral stenosis causes
Aortic stenosis pathophysiology