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Workshop Three Appraisal Guide
5.) Describe aortic regurgitation, mitral regurgitation, tricuspid regurgitation, aortic stenosis and mitral stenosis.
Aortic regurgitation is caused by an acute or chronic lesion of rheumatic fever, bacterial endocarditis, syphilis, hypertension, connective tissue disorders, or atherosclerosis. The heomdynamic repercussions depend on the size of the leak. During systole, blood is ejected from the left ventricle into the aorta. If the aortic semilunar valve is affected, some of the ejected blood flows back into the left ventricle. Volume overload occurs in the ventricle because it receives blood from the left atrium during diastole and blood from the aorta during systole. Over time the end diastolic volume of the left ventricle increases and myocardial fibers stretch to accommodate the extra fluid. Ventricular dilation and hypertrophy eventually cannot compensate for the aortic incompetence and heart failure develops. Clinical manifestations include widened pulse pressure resulting from increased stroke volume and back flow. Turbulence across the aortic valve during diastole produces a characteristic murmur. Large stroke volume and rapid runoff of blood from the aorta cause prominent carotid pulsations and throbbing peripheral pulses. Dysrhythnias and endocarditis are common complications of aortic regurgitation.
Mitral regurgitation permits backflow of blood from the left ventricle into the left atrium during ventricular systole, giving rise to a loud pansystolic (through out systole) murmur that radiates into the back and axilla. It has various causes mitral valve prolapse, rheumatic heart disease, infective endocarditis, CAD, connective tissue disease (Marfan Syndrome) and congestive cardiomyopathty. In mitral regurgitation the left ventricle becomes dilated and hypertrophied to maintain adequate cardiac output, despite increase volume from the left atrium. The volume of backflow reentering the left atrium gradually increases,...