The following describes changes that occur in the left ventricular pressure-volume loop when there is mitral regurgitation. In mitral valve regurgitation (red pressure-volume loop in figure), as the left ventricle contracts, blood is not only ejected into the aorta but also back up into the left atrium. This causes left atrial volume and pressure to increase during ventricular systole. Note in the pressure-volume loop that there is no true isovolumetric contraction phase (no vertical line between mitral valve closure and aortic valve opening) because blood begins to flow across the mitral valve and back into the atrium before the aortic valve opens as soon as ventricular pressure exceeds left atrial pressure. Because of mitral regurgitation, the afterload on the ventricle is reduced (total outflow resistance is reduced) so that end-systolic volume can be smaller than normal; however, end-systolic volume can increase if the heart also goes into systolic failure. There is no true isovolumetric relaxation (vertical lines between aortic valve closure and mitral valve opening) because when the aortic valve closes and the ventricle begins to relax, the mitral valve is not completely closed so blood continues to flow back into the left atrium (therefore further decreasing ventricular volume) as long as intraventricular pressure is greater than left atrial pressure. During ventricular diastolic filling, the elevated pressure within the left atrium is transmitted to the left ventricle during filling so that left ventricular end-diastolic volume (and pressure) increases. Ventricular end-diastolic volume is also increased because in chronic mitral regurgitation the ventricle anatomically dilates (remodels) so that ventricular compliance is elevated. Increased end-diastolic volume would cause wall stress (afterload) to increase if it were not for the reduced outflow resistance because of mitral regurgitation that tends to decrease afterload during ejection because of reduced pressure development by the ventricle. The net effect of these changes is that the width of the pressure-volume loop is increased (i.e., ventricular stroke volume is increased); however, ejection into the aorta (forward flow) is reduced. The increased ventricular "stroke volume" (measured as the end-diastolic minus the end-systolic volume) in this case includes the volume of blood ejected into the aorta as well as the volume ejected back into the left atrium.
The changes just described do not include cardiac and systemic compensatory mechanisms (e.g., systemic vasoconstriction, increased blood volume, and increased heart rate and inotropy) that attempt to maintain cardiac output and arterial pressure. Therefore, the red loop depicted in the figure only represents what may occur under a given set of conditions.