Aortic insufficiency: Mgmt
Advanced, Clinical - Cardiovascular, Organ-Based and Clinical Sciences
Aortic insufficiency (AI) is classifiable as acute or chronic. While there is no universally accepted definition for timeline, there are generalizable differences. Acute aortic insufficiency is very poorly tolerated; whereas chronic AI allows for the heart to accommodate.
Gradual onset of AI is normally accommodated by the left ventricle with marketed hypertrophy and eventually dilation. Unfortunately, the reduction in left ventricular (LV) function which happens as a result of AI does not improve after aortic valve replacement. The purpose of aortic valve replacement (AVR) is to halt disease progression, not improve LV function. When severe, there is reduction in diastolic blood pressure due to backfilling of the LV and an increase in end diastolic LV pressure, which results in a significant reduction in coronary blood flow.
Aortic insufficiency produces volume overload of the LV and the effective forward stroke volume (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 ejection fraction (EF) declines and is manifested as gradual increases in LV end-diastolic pressure (LVEDP) and end-systolic volume. Chronic AI usually presents as congestive heart failure.
Acute AI does not allow compensatory dilation or hypertrophy of the LV. 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.
It is most important to assess the severity of a patient’s AI, not only echocardiographically but also from a symptomatology standpoint. AI can be asymptomatic for decades, but once patients start exhibiting symptoms, the expected survival is 5 years without AVR. Primarily, the goal in AI is to reduce the regurgitant fraction of blood returning to the LV. This is best achieved by reducing afterload and time spent in diastole. Relative tachycardia (80-100 bpm) and optimization of preload are most commonly encouraged. Spinal and epidural anesthesia are generally well tolerated so long as intravascular volume is maintained. When pressors are required, it is best to avoid pure alpha agonists like phenylephrine as this will result in an increase in afterload and reflexive bradycardia both of which worsen the aortic regurgitant fraction.
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 advanced chronic aortic regurgitation. 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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