Aortic insufficiency produces volume overload of the LV and the effective forward SV is reduced due to the backward flow of blood into the LV during diastole. With chronic AI, the LV progressively dilates and undergoes eccentric hypertrophy. The resulting increase in end-diastolic volume maintains an effective SV because the end-systolic volume is unchanged. Eventually, as ventricular function deteriorates, the EF declines and is manifested as gradual increases in LVEDP and end-systolic volume. Chronic AI usually presents as congestive heart failure.
Acute AI does not allow compensatory dilation or hypertrophy of the left ventricle. Effective SV rapidly declines because the normal-sized ventricle is unable to accommodate a sudden large regurgitant volume. The sudden rise in LVEDP is transmitted back to the pulmonary circulation and causes acute pulmonary congestion. Acute AI typically presents as sudden onset of pulmonary edema and hypotension.
The principles underlying the medical management of aortic insufficiency are directed at augmenting forward flow and include afterload reduction and avoidance of bradycardia. Digitalis, diuretics, and afterload reduction, particularly with ACE inhibitors, generally benefit patients with advaced chronic AR. The decrease in arterial blood pressure reduces the diastolic gradient for regurgitation.
Patients with acute aortic insufficiency typically require intravenous inotropic (dopamine or dobutamine) and vasodilator (nitroprusside) therapy.
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