-Pathophysiology: the diastolic regurgitant flow from the aorta into the left ventricle=> increase left ventricle-end-diastolic volume & pressure =>hypertrophied & dilated LV. In acute AR, the chronic compensatory mechanisms aren’t active => increase LVEDP=> severe HF and cardiogenic shock.
-Symptom:
+ Corrigan’s pulse: is a rapidly rising "water-hammer" pulse, which collapses suddenly as arterial pressure falls rapidly during late systole and diastole.
+ Quincke’s pulse: alternate flushing and paling of the skin at the root of the nail while pressure is applied to the tip of the nail.
+ Traube’s sign: A booming "pistol-shot" sound can be heard over the femoral arteries, and a to-and-fro murmur (Duroziez’s sign) is audible if the femoral artery is lightly compressed with a stethoscope.
+ The arterial pulse pressure is widened.
+ Palpation: a diastolic thrill is often palpable along the left sternal border, and a prominent systolic thrill may be palpable in the suprasternal notch and transmitted upward along the carotid arteries.
+ Auscultation: The murmur of chronic AR is typically a high-pitched, blowing, decrescendo diastolic murmur, heard best in the third intercostal space along the left sternal border. In acute severe AR, the elevation of LVEDP may lead to early closure of the MV, an associated mid-diastolic sound, a soft or absent S1, a pulse pressure that is not particularly wide, and a soft, short diastolic murmur of AR.
-Treatment:
+ Medical: avoid exercise and physical activity, fluid and salt restriction, prophylaxis for endocarditis, diuretics, nitrates and other vasodilators. In acute severe AR: intravenous diuretics and vasodilators, then operation is indicated urgently after treatment with antibiotics.
+ Surgery: AVR considered when LV dilation (end-systolic dimension >55 mm or end-diastolic dimension >75 mm) or LV systolic dysfunction develops.
*Cardiac Catheterization and Angiography: are performed routinely in appropriate patients prior to surgery