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| ===Hemodynamic Consequences of Aortic Insufficiency===
| | #redirect[[Aortic insufficiency natural history]] |
| ====Acute aortic insufficiency====
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| Acute aortic insufficiency is often secondary to either trauma or [[infective endocarditis]]. While the heart can accommodate the changes of chronic aortic insufficiency over time, the acute changes of acute aortic insufficiency are not well accommodated by the [[left ventricle]].
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| The rapid rise in left ventricular pressure causes the [[mitral valve]] to close earlier during diastole. This early closure fortunately prevents backwards flow of blood into the pulmonary vascular bed. The very high left ventricular end diastolic pressure often keeps the aortic diastolic pressure from falling too low and thus there is often not a wide pulse pressure. Indeed absence of a wide [[pulse pressure]] in the patient with acute aortic insufficiency should alert the clinician to potential failure of the [[left ventricle]].
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| ====Chronic Aortic Regurgitation====
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| The hemodynamic impact of aortic regurgitation is to cause progressive dilation and hypertrophy of the [[left ventricle]]. The [[mitral valve]] ring may also dilate which may lead in turn to [[mitral regurgitation]]. The left atrium may dilate as a result of the [[mitral regurgitation]].
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| It has been said that '[[aortic regurgitation]] begets [[aortic regurgitation]]'. The high oscillatory shear associated with [[aortic regurgitation]] may lead to further dilation of the [[aorta]], which in turn may lead to further [[aortic regurgitation]].
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| Volume overload associated with [[aortic regurgitation]] leads to left ventricular hypertrophy. The sarcomers replicate in series and there is elongation of the [[myocyte]]s and myocardial fibrils. As a result of this hypertrophy the ratio of the ventricular wall thickness to cavity radius remains normal and therefore wall stress is normal. In [[aortic regurgitation]] there is eccentric hypertrophy where as in [[aortic stenosis]] there is concentric hypertrophy where there is replication of the sarcomers in parallel. Once wall thickening fails to keep up with the hemodynamic load, end systolic wall stress rises and at this point the left ventricle fails. The dramatic enlargement of the heart that is seen with [[aortic regurgitation]] is called [[cor bovinum]]. Over time the left ventricle will decompensate and there will be increasing interstitial fibrosis and a stiffening or a reduction in the compliance of the left ventricular wall. At this point the patient will experience a rise in the end diastolic pressure and volume. The first decline is seen with exercise and then the patient begins to have a reduction in forward output at rest.
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| Patients with chronic aortic insufficiency may also develop [[myocardial ischemia]]. This is due to the fact that they have an increase in demand due to an increased thickness of the LV and also a reduction in the supply due to a lower perfusion pressure during diastole.
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| ==References==
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| {{Reflist|2}}
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| [[Category:Cardiology]]
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| {{WH}}
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| {{WS}}
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