Introduction

Aortic regurgitation (AR) occurs when blood flows retrograde across the aortic valve from the aorta into the left ventricle (LV) during diastole.

This abnormal backflow of blood leads to pathologic changes in the heart in order to compensate for the decreased effective cardiac output that results. These pathologic changes are highly dependant on the severity and rapidity of onset of AR. They require a significant amount of time to take place, therefore if acure AR were to occur, compensation for the increased LV volume would not be able to take place.

The small increase in left ventricular end diastolic volume (LVEDV) due to the acute AR would lead to a greatly increased left ventricular end diastolic pressure (LVEDP). This increased pressure is automatically transmitted to the pulmonary vasculature leading to severe symptoms of left heart failure including flash pulmonary edema.

However in chronic AR, the LV dilates and hypertrophies (eccentrically) slowly over time. These changes help to maintain normal LV pressures in the setting of a significantly increased LV volume. In fact, patients with severe chronic AR may have the largest LV end-diastolic volumes produced by any cardiac disease state and yet their LV end-diastolic pressures are not significantly elevated.

The stroke volume increases greatly in these patients so that despite the severe AR, a normal effective forward cardiac output can be maintained. As the AR continues to worsen, the LV can no longer dilate or hypertrophy further leading to increased LV pressures which are then transmitted to the pulmonary vasculature. Symptoms of heart failure then occur.

Also, as the AR worsens allowing larger volumes of blood to be regurgitated during diastole, the aortic diastolic pressures drop significantly. These low diastolic pressures, coupled with the increased systolic pressures produced by the hypertrophied LV to maintain cardiac output, produce a wide pulse pressure. The large stroke volume can produce signs and symptoms of a high flow state (see below) and the low diastolic pressures can significantly affect coronary perfusion pressures, since the coronary arteries fill during diastole.