Aortic regurgitation

Keep them filled, keep the heart rate fast, vasodilate them and given them dobutamine.

Physiological consequences of aortic regurgitation

The diastolic return of blood back into the ventricle via the aortic valve contributes to preload. The ventricle distends, and there is a compensatory increase in stroke volume. The normal sympathetic response to acute aortic regurgitation is excitatory - heart rate, contractility and stroke volume all increase.

Aortic regurgitation is classified by the approximate fraction of the stroke volume which is returned to the LV with each contraction.

Mild aortic regurgitation is usually well compensated. The compensation manifests as an eccentric LV hypertrophy and an increase in the LV chamber volume. No significant increase in myocardial oxygen consumption occurs in this scenario because volume work is less expensive metabolically than pressure work.

Moderate aortic regurgitation (regurgitated fraction more than 60% of stroke volume) is usually associated with some degree of congestive heart failure. The left ventricle dilates and thickens to such an extent that its contractility becomes impaired, and pulmonary vessels experience an increase in pressure as a result. That feature makes these people especially prone to pulmonary oedema in response to fluid boluses.

Severe aortic regurgitation is a rather rapid self-amplifying spiral. Once the LV failure is well established, cardiac output begins to suffer. Once the cardiac output begins to suffer, diastolic filling of the coronary arteries decreases, contributing to worsening LV failure. And on top of that, in response to the hypotension of reduced cardiac output, the sympathetic nervous system stupidly vasoconstricts the peripheral vessels, thereby increasing afterload and thus increasing the regurgitated fraction.

Strategies to compensate for the physiological consequences of aortic stenosis


Forward flow relies on adequate preload. The left ventricle needs to be well filled in order to produce enough cardiac output to overcome the fact that a significant proportion of it will slosh back through the aortic valve. GTN is to be avoided because the reduction in preload will totally cripple left ventricular systolic function.


Aortic regurgitation is a diastolic murmur; the regurgitant flow occurs in diastole. Thus, it stands to reason that the shorter the diastole, the less time there is for regurgitation. These people do better with rapid heart rates, and some who are symptomatic at rest will demonstrate a marked improvement in symptoms with some exercise.

In short, keep the heart rate high. The textbook number to aim for is about 90 beats per minute.


Strangely, it is relatively unimportant to maintain sinus rhythm. These patients seem to cope well with atrial fibrillation.


Contractility needs to be high. The LV needs to work harder in order to produce the same cardiac output. Thus, contractility-reducing agents such as beta-blockers are going to be counterproductive here.

In fact some extra beta-1 effects might be useful here; Dobutamine comes to mind.


In these people, the afterload cannot be allowed to rise. The higher the afterload, the more blood is pushed back into the ventricle through the regurgitant valve. Thus, it is important to keep the afterload as low as diastolic coronary filling will permit.

Agents which are specific to the arterial circulation may be used. Sodium nitroprusside has historically been the favourite; however it also decreases preload, so it would only be of real benefit in end-stage decompensated LV failure where there is significant LV dilatation. If there is no decompensated CCF, calcium channel blockers are probably a better choice.


Moore and Martin's chapter on valvular disease in "A Practical Approach to Cardiac Anaesthesia" is a must-read

(in general, that book is awesome)