Mitral Regurgitation
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 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 because when the aortic
valve closes and the ventricle
begins to relax, the mitral valve is not completely close so blood flows
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. This 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. These 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, nor do they include the
ventricular dilation (remodeling) that increases ventricular compliance.
Revised 04/05/07
