Aortic regurgitation is the flow of blood back into the left ven-tricle from the aorta during diastole. It may be caused by in-flammatory lesions that deform the leaflets of the aortic valve, preventing them from completely closing the aortic valve orifice. This valvular defect also may result from endocarditis, congenital abnormalities, diseases such as syphilis, a dissecting aneurysm that causes dilation or tearing of the ascending aorta, or deterioration of an aortic valve replacement.
In aortic regurgitation, blood from the aorta returns to the left ventricle during diastole in addition to the blood normally deliv-ered by the left atrium. The left ventricle dilates, trying to ac-commodate the increased volume of blood. It also hypertrophies, trying to increase muscle strength to expel more blood with above-normal force—raising systolic blood pressure. The arteries attempt to compensate for the higher pressures by reflex vasodilation; the peripheral arterioles relax, reducing peripheral resistance and diastolic blood pressure.
Aortic insufficiency develops without symptoms in most patients. Some patients are aware of a forceful heartbeat, especially in the head or neck. There may be marked arterial pulsations that are visible or palpable at the carotid or temporal arteries. This is a re-sult of the increased force and volume of the blood ejected from the hypertrophied left ventricle. Exertional dyspnea and fatigue follow. Progressive signs and symptoms of left ventricular failure include breathing difficulties (eg, orthopnea, paroxysmal noctur-nal dyspnea), especially at night.
A diastolic murmur is heard as a high-pitched, blowing sound at the third or fourth intercostal space at the left sternal border. The pulse pressure (ie, difference between systolic and diastolic pres-sures) is considerably widened in patients with aortic regurgita-tion. One characteristic sign of the disease is the water-hammer pulse, in which the pulse strikes the palpating finger with a quick, sharp stroke and then suddenly collapses. Diagnosis may be con-firmed by echocardiogram, radionuclide imaging, ECG, magnetic resonance imaging, and cardiac catheterization.
Before the patient undergoes invasive or dental procedures, anti-biotic prophylaxis is needed to prevent endocarditis. Aortic valvuloplasty or valve replacement is the treatment of choice, preferably performed before left ventricular failure. Surgery is recommended for any patient with left ventricular hypertrophy, regardless of the presence or absence of symptoms.
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