Aortic Insufficiency Acute and Chronic The etiology, pathophysiology, and clinical manifestations of chronic and acute insufficiency are different, as is the therapy

Aortic Regurgitation Etiology In the past rheumatic fever and syphilis were major causes of aortic regurgitation, but these diseases have diminished in frequency in recent years due to the availability of antibiotics. As these two infectious diseases have diminished, diseases of the connective tissue and anatomic abnormalities of the valve have become more frequent causes.

Chronic Aortic Regurgitation Congenital Etiology Aortic Valve Prolapse - myxomatous valve Bicuspid Aortic Valve Coarctation of the Aorta – dilation of the aorta Connective Tissue Disorders – loss of structural support Marfan’s Syndrome, Ehlers-Danlos Syndrome etc. Idiopathic Cystic Medial Necrosis Ventricular Septal Defect – loss of cusp support

Chronic Aortic Regurgitation Acquired Etiology Rheumatic Heart Disease – fibrosis and retraction Syphilitic Aortitis – dilation of the aorta Dissecting Aneurysm – disruption of support Bacterial Endocarditis Systemic Lupus Traumatic Aortic Insufficiency Hypertension – dilation of the aorta

Acute Aortic Insufficiency Infective Endocarditis Dissecting Aneurysm Rupture of the Aortic Leaflets trauma myxomatous valve

Dilated Aortic Root

Aortic Dissection

Valvular Abnormalities Nodular Rheumatic Disease Aortic Root Dilation Endocarditis

Aortic Regurgitation Pathophysiology Chronic Aortic Regurgitation Represents a volume overload(AS=pressure overload) The LV responds by dilating(SV LVEDV but LVEDP =) Eccentric hypertrophy occurs (sarcomeres replicate in series). In AS concentric LVH occurs as the sarcomeres replicate in parallel In the late stages of AR as LV failure occurs the ventricle continues to dilate LVEDP

Aortic Regurgitation Pathophysiology

Aortic Regurgitation Pathophysiology

Aortic Regurgitation Pathophysiology Acute Aortic Insufficiency The volume overload will be suddenly imposed on a left ventricle unable to dilate acutely As a result, marked elevation of the left ventricular end-diastolic pressure occurs Such sudden hemodynamic changes produce pulmonary venous hypertension and acute pulmonary edema

Aortic Regurgitation Clinical Manifestations History Chronic Aortic Regurgitation Dyspnea (orthopnea, PND, exertional dyspnea) Angina when it occurs is usually nocturnal (due to the bradycardia and low diastolic blood pressure) Acute Aortic Regurgitation There is sudden cardiovascular collapse, with congestive heart failure and hypotension

Aortic Regurgitation Clinical Manifestations Physical Examination Chronic AR Acute AR Systolic BP Systolic BP = Diastolic BP Diastolic BP = Aortic Pulse Pressure Aortic Pulse Pressure = Heart Rate = Heart Rate S1 = (in CHF ) S1 S2 = S2 S3 absent(except CHF) S3 present S4 usually not present S4 never present

Aortic Regurgitation Clinical Manifestations Physical Examination (Auscultation) The AR murmur is a diastolic murmur that begins after A2 It is a decrescendo murmur heard best with the patient sitting up and leaning forward The severity of the murmur correlates better with the duration than with the intensity of the murmur In acute AR the murmur is also a decrescendo murmur but is of short duration since the LVEDP is elevated and pressure equalizes rapidly between LV and the aorta

Murmur of Aortic Regurgitation S 2 S 1

Aortic Regurgitation Clinical Manifestations Physical Examination Austin Flint Murmur occurs in severe AR. Created by rapid outflow across a partially closed MV. The MV is normal but partially closed due to rising LVDP. Corrigan’s Pulse (water hammer pulse) pulse that rapidly rises and falls de Musset’s Sign – bobbing of the head Traube’s Sign – booming systolic and diastolic sounds over the femoral artery

Aortic Regurgitation Clinical Manifestations Physical Examination Muller’s Sign – systolic pulsations of the uvula Durozier’s Sign – systolic murmur over the femoral artery when compressed proximally, and a diastolic murmur when it is compressed distally Quicke’s Sign – flushing and blanching of the nail beds when lightly compressed

Aortic Regurgitation Laboratory Evaluation

Aortic Regurgitation Laboratory Evaluation Chronic Acute Normal size LV with pulmonary vascular congestion LVE with normal pulmonary vasculature

Aortic Regurgitation Echocardiography

Aortic Regurgitation Echocardiography

Aortic Regurgitation Cardiac Catheterization

Aortic Regurgitation Natural History Chronic AR Mortality increases with onset of symptoms 4 year survival with angina, 2 years with CHF It is imperative to intervene before irreversible LV dysfunction occurs Acute AR These patients suffer early death if they do not undergo emergent surgical intervention

Aortic Regurgitation Management Medical Management SBE prophylaxis is important Afterload reduction will reduce the regurgitant volume Avoidance of atrial fibrillation and bradycardia are important as these are poorly tolerated Serial echocardiographic follow-up to monitor LV function

Aortic Regurgitation Management Surgical Management Not indicated in asymptomatic patients with good exercise tolerance and good LV function Surgical treatment is advised in patients with severe AR who are symptomatic and who have impaired LV function Long term results reveal 80-90% three year survival in patients with preserved LV function, and 40-60% three year survival in patients with poor LV function Every effort should be made to operate on patients before irreversible LV dysfunction occurs