Pathophysiology

The pathophysiology of acute and chronic AR is different.

In acute AR, there is a sudden increase in the volume of blood in the LV during diastole. The left ventricle volume can only increase marginally in response to this acute change so left ventricular end diastolic pressure rises sharply. LA and pulmonary venous pressure rises and results in acute heart failure.

Acute AR presentation

In acute aortic regurgitation (acute AR), the clinical presentation will depend on the underlying cause. If the regurgitation is mild the predominant symptoms may relate to the underlying cause; for example acute tearing chest pain radiating to the back suggests aortic dissection, or the peripheral signs and symptoms of sepsis in infective endocarditis. AR associated with aortic dissection means that the dissection involves the ascending aorta down to the annulus.

Learning bite

If aortic regurgitation is sudden and severe the patient will present in acute pulmonary oedema or cardiogenic shock.

In chronic AR, there is time for compensation and the LV progressively dilates and hypertrophies to maintain the ejection fraction. Tachycardia decreases the diastolic filling time and so reduces the regurgitant volume. During early stages of the disease, the heart is able to respond to exertion with an appropriate increase in cardiac output. As a result, AR can be tolerated for years.

Chronic AR presentation

With chronic aortic regurgitation (chronic AR), patients may be asymptomatic for years although a murmur may have been previously noted.

Common symptoms:

• Awareness of the heart beat /palpitations especially at rest (because of the hyperactive dilated LV)
• Chest pain
• Fatigue

As the disease progresses:

• Heart failure
• Angina (as in AS this can occur despite normal coronary arteries)