D.BASEM ELSAID ENANYLECTURER OF CARDIOLOGY

AINSHAMS UNIVERSITY

Acute Aortic regurge

ETIOLOGY

-Usually a medical emergency cardiogenic shock (no compensatory mechanisms)-Endocarditis:valve destruction, leaflet perforationaortic perivalvular abscess may rupture into the left ventricle, resulting in AR, or into the left atrium or right ventricular outflow tract, with a clinical presentation that mimics acute aortic regurgitation. -Aortic dissection:Mechanisms:Dilation of the sinuses with incomplete coaptation of the leaflets at the center of the valveinvolvement of a valve commissure resulting in inadequate leaflet supportDirect extension of the dissection into the base of a leaflet, resulting in a flail valve leafletProlapse of the dissection flap across the aortic valve into the left ventricular outflow tract in diastole impeding leaflet closure. -Rupture of a congenitally fenestrated cusp-Traumatic rupture of the valve leaflets -Iatrogenic : aortic balloon valvotomy or a failed surgical valve repair-Acute mechanical valve regurgitation can be caused by valve thrombosis, IEC

PATHOPHYSIOLOGY

--Acute increase in left ventricular diastolic pressure and a fall in forward cardiac output exacerbated by a shortening of diastolic filling time {early closure of the mitral valve (due to high end diastolic pressures) + tachycardia (caused by a decrease in forward flow and cardiac output)}. The net effect is often profound hypotension and cardiogenic shock.--Elevated left ventricular end-diastolic pressure leads to elevated left atrial and pulmonary venous pressures, which can lead to pulmonary edema

CLINICAL PRESENTATION

--Sudden cardiovascular collapse. --Other presenting symptoms are related to the cause of acute AR (eg, signs and symptoms of endocarditis or aortic dissection)

Physical examination

--Manifestations of cardiogenic shock profound hypotension, pallor, diaphoresis, occasional cyanosis, and other signs of peripheral vasoconstriction. --The pulse pressure is normal or may be reduced, but the pulse is usually weak, thready, and rapid.--If aortic dissection inequality of pulses and blood pressure between the left and right arms may be observed {may not be appreciated in the setting of profound hypotension}. --The cardiac apex is generally not displaced and is not hyperdynamic.--peripheral manifestations of chronic AR are less apparent or may be entirely absent (no wide pulse pressure)

Cardiac auscultation

--The early closure of the mitral valve generally produces a soft or absent S1--The aortic component of S2 is often soft, while P2 is usually increased, reflecting pulmonary hypertension.--An S3 is frequently heard but an S4 is absent.--In contrast to the high pitched holodiastolic decrescendo murmur of chronic AR, the murmur with acute AR is a low pitched early diastolic murmur beginning after S2, may not be heard, especially when the diastolic gradient between the aorta and left ventricle lessens.--A systolic murmur resulting from the increased volume of blood crossing the aortic valve may be heard, but is usually not loud.--The combination of a soft systolic and a low-pitched diastolic murmur often produces a "to-and-fro" murmur at the cardiac base in acute AR.

Electrocardiogram

--No specific electrocardiographic changes.--Nonspecific ST and T wave abnormalities are common due to the markedly elevated left ventricular pressures. --If acute AR is due to aortic dissection, involvement of the right coronary artery can result in ECG findings of acute myocardial infarction

Chest radiograph

-Pulmonary edema redistribution of blood flow to the upper lobes and an increase in size and amount of the pulmonary vasculature-The cardiac silhouette may be markedly enlarged due to pericardial effusion-Widened mediastinum may result from aortic root dilation

Echocardiography

--Diagnostic in acute AR.{TOE more benefits}--The cause of aortic regurgitation can be determined aortic valve endocarditis or aortic dissection--Severe acute AR is based upon the following findings:-A vena contracta width (narrowest segment of the color flow jet) >6 mm.-For central severe jets, the jet width in the left ventricular outflow tract is large (≥65 percent of the outflow tract width).-For severe eccentric jets, the visualized jet width is variable.-A dense continuous wave Doppler signal with a steep diastolic slope (pressure half-time <200 msec).{rapid equalization of pressure Ao.,LV}-The presence of holodiastolic flow reversal in the descending thoracic and proximal abdominal aorta.--EF, pericardial effusion

Other imaging modalities

--CT imaging may help delineate the anatomy by identifying the intimal flap, as well as the site and extent of dissection and the possible involvement of major branch arteries.--Usually no time to perform cardiac catheterization or contrast angiography. Emergency valve surgery should not be delayed for coronary angiography if there is severe acute AR with hemodynamic instability

TREATMENT

--Emergency aortic valve replacement or repair--If delay temporary stabilization : intravenous vasodilators, such as nitroprusside, and possibly inotropic agents such as dopamine or dobutamine in an attempt to enhance forward flow and lower left ventricular end-diastolic pressure. --An intraaortic balloon pump is contraindicated because inflation of the balloon in diastole will worsen the severity of AR.

Acute mild or moderate AR

--Due to an aortic dissection aortic valve resuspension along with graft replacement of the ascending aorta often allows preservation of the native valve with resolution of valve incompetence. --Due to endocarditis, antibiotic therapy alone may be sufficient unless the patient has another indication for valve replacement

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