Pathophysiology
Aortic insufficiency will introduce a volume overload on the left ventricle. The heart must consequently pump more volume of blood to maintain a normal forward cardiac output.  If the left ventricle receives half of what is initially put out back (50% regurgitant fraction), the ventricle must double its volume output to provide sufficient amounts of oxygen to the body. Increased volume load on the ventricle will cause the ventricle to dilate.

The regurgitant flow is greatest immediately following the aortic valve closure. It declines throughout diastole as the pressure in the aortic root is reduced.

The increase in size of the left ventricle demands more oxygen to the myocardium, exposing the patient to increased risk for ischemia and angina pectoris, even without coronary narrowing.

In acute AR, such as with acute bacterial endocarditis or aortic aneurysms, the left ventricle is “caught off guard” and cannot accommodate the increased volume load. The result is a quick rise in diastolic pressure which will transplant backwards into the pulmonary capillary bed resulting in prompt pulmonary edema.