Aortic regurgitation usually develops slowly and is progressive (chronic), but it can also develop quickly (acute). Chronic aortic regurgitation may be caused by abnormalities of the aortic valve, the aortic root, or both. Abnormalities in the valve are usually con-genital (bicuspid valve) or due to rheumatic fever. Diseases affecting the ascending aorta cause regur-gitation by dilating the aortic annulus; they include syphilis, annuloaortic ectasia, cystic medial necro-sis (with or without Marfan syndrome), ankylosing spondylitis, rheumatoid and psoriatic arthritis, and a variety of other connective tissue disorders. Acute aortic insufficiency most commonly follows infec-tive endocarditis, trauma, or aortic dissection.
Regardless of the cause, aortic regurgitation produces volume overload of the left ventricle. The effective forward SV is reduced because of backward (regur-gitant) flow of blood into the lef t ventricle during diastole. Systemic arterial diastolic pressure and SVR are typically low. The decrease in cardiac afterload helps facilitate ventricular ejection. Total SV is the sum of the effective stroke volume and the regurgi-tant volume. The regurgitant volume depends on the heart rate (diastolic time) and the diastolic pressure gradient across the aortic valve (diastolic aortic pres-sure minus left ventricular end-diastolic pressure). Slow heart rates increase regurgitation because of the associated disproportionate increase in diastolic time, whereas increases in diastolic arterial pressure favor regurgitant volume by increasing the pressure gradient for backward flow.
With chronic aortic regurgitation, the left ven-tricle progressively dilates and undergoes eccentric hypertrophy. Patients with severe aortic regurgita-tion have the largest end-diastolic volumes of any heart disease. The resulting increase in end-diastolic volume maintains an effective SV. Any increase in the regurgitant volume is compensated by an increase in end-diastolic volume. Left ventricular end-diastolic pressure is usually normal or only slightly elevated, because ventricular compliance initially increases. Eventually, as ventricular function deteriorates, the ejection fraction declines, and impaired ventricular emptying is manifested as gradual increases in left ventricular end-diastolic pressure and end-systolic volume.
Sudden incompetence of the aortic valve does not allow compensatory dilatation 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 left ventricular end-diastolic pres-sure is transmitted back to the pulmonary circula-tion and causes acute pulmonary venous congestion.
Acute aortic regurgitation typically presents as the sudden onset of pulmonary edema and hypoten-sion, whereas chronic regurgitation usually presents insidiously as congestive heart failure. Symptoms are generally minimal (in the chronic form) when the regurgitant volume remains under 40% of SV, but become severe when it exceeds 60%. Angina can occur even in the absence of coronary disease. The myocardial oxygen demand is increased from muscle hypertrophy and dilatation, whereas the myocardial blood supply is reduced by low diastolic pressures in the aorta as a result of the regurgitation.
As with mitral regurgitation, RSV and RF for aortic regurgitation can be estimated by pulsed Doppler echocardiography. Stroke volume is measured at the left ventricular outflow tract (LVOT) and at the mitral valve (MV). The stroke volume ejected at the LVOT includes both the stroke volume that entered the left ventricle through the mitral valve and the volume of blood that entered the left ventricle through the leaky aortic valve.
RSVaortic regurgitation =(ALOVT ×TVILVOT)
− (AMV × TVIMV)
RF = RSV/SV
Pressure half-time (T1/2, see the section on mitral stenosis above) of the regurgitant jet is another useful echocardiographic parameter for clinically assessing the severity of aortic regurgitation. The shorter the half-time, the more severe the regurgitation; severe regurgitation rapidly raises left ventricular diastolic pressure and results in more rapid pressure equili-bration. Unfortunately, T1/2 is affected not only by the regurgitant orifice area, but also by aortic and ventric-ular pressure. An aortic regurgitation jet with a T1/2 less than 240 msec is associated with severe regurgitation.
Most patients with chronic aortic regurgitation remain asymptomatic for 10–20 years. Once signifi-cant symptoms develop, the expected survival time is about 5 years without valve replacement. Diuretics and afterload reduction, particularly with ACE inhibitors, generally benefit patients with advanced chronic aortic regurgitation. The decrease in arte-rial blood pressure reduces the diastolic gradient for regurgitation. Patients with chronic aortic regurgi-tation should receive valve replacement before irre-versible ventricular dysfunction occurs.
Patients with acute aortic regurgitation typi-cally require intravenous inotropic and vasodilator therapy. Early intervention is indicated in patients with acute aortic regurgitation: medical manage-ment alone is associated with a high mortality rate.
The heart rate should be maintained toward the upper limits of normal (80–100 beats/min).Bradycardia and increases in SVR increase the regurgitant volume in patients with aorticregurgitation, whereas tachycardia can contribute to myocardial ischemia. Excessive myocardial depres-sion should also be avoided. The compensatoryincrease in cardiac preload should be maintained, but overzealous fluid replacement can readily result in pulmonary edema.
Invasive hemodynamic monitoring should be employed in patients with acute aortic regurgita-tion and in those with severe chronic regurgita-tion. Premature closure of the mitral valve often occurs during acute aortic regurgitation and may cause pulmonary capillary wedge pressure to give a falsely high estimate of left ventricular end-diastolic pressure. The appearance of a large v wave suggests mitral regurgitation secondary to dilatation of the left ventricle. The arterial pressure wave in patients with aortic regurgitation characteristically has a very wide pulse pressure. Pulsus bisferiens may also be present in patients with moderate to severe aor-tic insufficiency and is thought to result from the rapid ejection of a large SV. Color-flow Doppler TEE can be invaluable in quantitating the severity of the regurgitation and guiding therapeutic interventions. By definition, some reversal of blood flow is pres-ent in the aorta during all of diastole (holodiastolic) with severe aortic regurgitation; moreover, the more distal the detection of holodiastolic flow reversal is in the aorta, the more severe the regurgitation.
C. Choice of Agents
Most aortic insufficiency patients tolerate spinal and epidural anesthesia well, provided intravascu-lar volume is maintained. When general anesthesia is required, inhalational agents may be ideal because of the associated vasodilatation. Phenylephrine (25–50 mcg) can be used to treat hypotension second-ary to anesthetic-induced vasodilatation. Large doses of phenylephrine increase SVR (and arterial diastolic pressure) and may exacerbate the regurgitation.