History:
The natural history of AR is a slow and insidious disease process, with many patients remaining a symptomatic for decades. In a symptomatic patients, a cardiac murmur found during a routine medical examination often leads to diagnosis; however once cardiac symptoms develop, clinical deterioration is rapid.
The principal symptoms associated with severe AR are exertional dyspnea, orthopnea, and paroxysmal noctumal dyspnea. These symptoms appear when pulmonary venous pressure is elevated in association with significant cardiomegaly and myocardial dysfunction. These changes occur late in the natural history of the disease.
Angina pectoris may occur without CAD because coronary perfusion is inadequate to meet the demands of the enlarged and hypertrophic left ventricle. Less commonly, aortitis can involve the origion of the coronary arteries, leading to angina.
Palpitation is a common complaint associated with a hyperdynamic and tachycardic left ventricle in significant AR Palpitation also may be due to frequent premature ventricular contraction.
Syncope is an uncommon symptom associated with AR.
Sudden cardiac deaths have been relatively rare in asymptomatic patients with normal LV funcation ( <0.2% per Year ).
In contrast to chronic AR, symptoms of acute AR (commonly from infective endocarditis, aortic dissection, or trauma) develop rapidly and are very poorly tolerated. In acute AR, the normal sized ventricle is unable to adapt to the sudden increase in regurgitant volume, In additional to the normal left atrial inflow. Thus, patients develop pulmonary congestion associated with LV failure and, possibly cardiogenic shocks.
Physical:
Hemodynamically severe AR causes a widened pulse pressure, often greater than 100 mm Hg, associated with a low diastolic pressure, often less than 60 mm Hg.
The de Musset sign is when patients head frequently bob with each heartbeat.
The Corrigan pulse is when patients pulses are of the water hammer or collapsing type, with obrupt distention and quick collapse.
The Quincke sign is when light transmitted through the patients fingertip shows capillary pulsations.
The Hill sign is when popliteal cuff systolic pressure exceeds brachial cuff pressure by more then 60 mm Hg.
The Duroziez sign is when a systolic murmur is heard over the femoral artery when compressed proximally and when diastolic murmur is heard when the femoral artery is compress distally.
The Muller sign is systolic pulsations of the uvula.
The Traube sign (also called pistol shot sounds) refers to booming systolic and diastolic sounds heard over the femoral artery.
The apical impulse in chronic AR is diffuse, hyperdynamic, and displaced inferiorly and leftward.
S? gallop correlates with development of LV dysfunction.
The typical diastolic murmur of AR has a decrescendo shape. A high frequency early diastolic murmur often occurs in mild AR, whereas a rough holodiastolic or decrescendo diastolic murmur occurs more commonly in severe AR. The volume and velocity of blood across the incompetent aortic valve tapers off in mild to last diastole as the aortic and LV pressures equilibrate. The diastolic murmur of AR is usually best heard adjacent to the sternum in the second to fourth left intercostals space. A concomitant systolic ejection murmur is common in moderate to severe.
The murmur associated with acute AR may not be impressive. If cardiac decompensation is present, the diastolic murmur of acute AR may be very soft and surprisingly short.
Antegrade flow across the mitral valve is thought to cause an Austin Flint murmur, which is a mind and late diastolic apical low frequency murmur or rumble. The rumble occurs during rapid closure of the mitral valve as flow velocity is increasing across the valve and LV diastolic pressure is rising rapidly because of severe aortic reflux. Its presence indicates severe AR.