Pathophysiology

Regurgitation of blood from the aorta into the left ventricle (LV) leads to:

• Increased systolic blood pressure and decreased diastolic pressure

• Widened pulse pressure → water hammer pulse

Because LV cannot sufficiently dilate in response to regurgitant blood, LV end-diastolic pressure increases rapidly → pressure transmits backwards into pulmonary circulation → pulmonary edema and dyspnea

Decreased cardiac output if severe → cardiogenic shock and myocardial ischemia

Initially, a compensatory increase in stroke volume can maintain adequate cardiac output despite regurgitation (compensated heart failure)

Over time, increased left ventricular end-diastolic volume → LV enlargement and eccentric hypertrophy of myocardium → left ventricular systolic dysfunction → decompensated heart failure