Aortic Regurgitation
The following describes changes that occur in the left ventricular
pressure-volume loop when there is
aortic regurgitation. In
aortic valve regurgitation (red loop in figure), the aortic valve does not close completely at the
end of systolic ejection. As the ventricle relaxes during diastole, blood
flows from the aorta back into the ventricle so the ventricle immediately begins
to fill from the aorta. Therefore, there is
no true phase of
isovolumetric relaxation because as the
ventricle relaxes, even before the mitral valve opens, blood is entering the
ventricle from the aorta thereby increasing ventricular volume. Once the
mitral valve opens, filling occurs from the left atrium; however, blood continues to flow from the aorta into the ventricle throughout diastole because
aortic pressure is higher than ventricular pressure during diastole. This
greatly enhances ventricular filling so that end-diastolic volume is increased
as shown in the pressure-volume loop. When the ventricle begins to contract
and develop pressure, blood is still entering the ventricle from the aorta
because aortic pressure is higher than ventricular pressure; therefore, there is
no true isovolumetric contraction because volume continues to increase. Once the
ventricular pressure exceeds the aortic diastolic pressure, the
ventricle then begins to eject blood into the aorta. The increased end-diastolic volume
(increased preload) activates the
Frank-Starling mechanism
to increase the force of contraction, ventricular peak (systolic) pressure, and stroke volume
(as shown by the
increased width of the pressure-volume loop). As long as the ventricle is
not in failure, end-systolic volume may only be increased a small amount (as
shown in figure) due to the increased afterload (
ventricular
wall stress). If the
ventricle goes into
systolic failure,
then end-systolic volume will increase by a large amount and the peak systolic
pressure and stroke volume (net forward flow into aorta) will fall. 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
