Aortic Regurgitation

Overview of Aortic Regurgitation


Chronic aortic regurgitation, which is more common than acute, is most often due to rheumatic disease or a bicuspid valve, but can also be due to connective tissue disorders. It normally manifests as congestive heart failure when regurgitant volume approaches ~ 40% of SV, and is considered “severe” at 60% of SV. Acute regurgitation is usually due to dissection, trauma, or infective endocarditis. Unlike aortic stenosis, aortic regurgitation rarely leads to sudden death. While rarely fatal, a rapid decrease in forward flow with no compensatory ventricular changes can lead to acute pulmonary congestion and hypotension.

Medical and Surgical Treatment

Chronic AR usually takes 10-20 years to become symptomatic, but at that point survival is ~ 5 years without valve replacement. Afterload reduction (ACE inhibitors), diuretics, and digitalis are typically used. The AV should be replaced before irreversible ventricular changes occur. Acute AR, by contrast, often requires inotropic support (dopamine or dobutamine) and more substantial afterload reduction, ex. with vasodilators such as nitroprusside, followed by early surgery (medical management alone carries a high mortality rate).

Effect on cardiac anatomy

Left ventricle gradually becomes eccentrically hypertrophic (has to contract more in order to get the same net forward flow, as part of each cardiac cycle is ejected backwards) and dilates (“cor bovinum”), as it has to maintain a supranormal stroke volume. Massively-enlarged LV is less compliant, and small changes in filling pressures can lead to large changes in preload / cardiac output. Incompetent valve lowers DBP, which can reduce coronary flow even in the absence of CAD. The body compensates by lowering SVR. Regurgitant flow only occurs during diastole, thus low heart rates increase the regurgitant fraction. At end stage, as ventricular function deteriorates, the EF declines and LEDP will start to increase. Large LVEDV can lead to MR. Note that because of compensatory mechanisms, in patients with chronic AI the clinical history will be fairly useless (i.e. these patients are asymptomatic until end-stage nears).

Aortic Regurgitation in Non-Cardiac Surgery


Pulmonary artery catheterization is indicated in all acute AR cases, as well as in severe chronic AR (> 60% regurgitant fraction) and in anyone who receives nitroprusside. Note that MR may be present as well (large v wave) and LVEDP may be artificially elevated. The arterial pressure wave has a wide pulse pressure, and a bisferiens pulse may also be present. Doppler TEE can quantify the severity of regurgitation and guide therapeutic interventions. Reversal of blood flow is present in the aorta during all of diastole (holodiastolic) with severe aortic regurgitation, the further down the more severe the regurgitation.


Maintain HR 80-100 (minimizes regurgitant flow, although optimal HR is controversial) and reduce afterload to encourage forward flow. While preload must be maintained (these patients are dependent on it), keep in mind that excessive LV volume can lead to pulmonary edema.

When general anesthesia is required, patients with depressed ventricular function should receive an opiate-based anesthetic. Those with normal function can probably tolerate desflurane, which may be ideal because of its vasodilatory effects. Pancuronium helps achieve a HR of 80-100. Afterload reduction with nitroprusside requires full hemodynamic monitoring. Ephedrine is the preferred first-line vasopressor, although small doses of phenylephrine (25–50 ucg) can be attempted.

Cardiopulmonary bypass introduces several important considerations – first, the LV may distend with initiation of CPB. Second, moderate/severe AI may affect the surgeon’s approach to CPB, with an incompetent aortic valve preventing delivery of anterograde cardioplegia (which must then be injected into the ostia)

Most patients tolerate spinal and epidural anesthesia (provided intravascular volume is maintained), although epidural may be preferred.

Aortic Regurgitation in Cardiac Surgery

Post-Repair / Bypass

Echocardiographic Assessment of Aortic Regurgitation

The ASE recommends assessing jet width (measured within 1 cm of the AV, otherwise the width expands unpredictably) and vena contracta in the TEE assessment of aortic regurgitation. Additional measurements (such as regurgitant fraction by PW doppler or AI jet velocity) may be unreliable in TEE if the ultrasound beam is not aligned properly.

ASE Parameters for AI Quantification 1. Jet Width (> 65% is severe) 2. Vena Contracta (> 0.6 cm is severe)

For complete recommendations and commentary, see the ASE Guidelines.