Aortic insufficiency: Hemodynamic treatment

Clinical - Cardiovascular

Aortic insufficiency (AI) or regurgitation (AR) may be acute or chronic in nature. Infective endocarditis involving the aortic valve, trauma to the aortic valve and acute aortic dissection are well-described causes of acute AR. The etiologies of chronic AR include connective tissue diseases such as Marfan syndrome and Ehlers-Danlos syndrome, bicuspid aortic valve, and other inflammatory diseases of the aorta. These lesions predispose patients to developing aortic aneurysms and dissection, and aortic root dilation that disrupt the normal architecture of the aortic valve cusps and leaflets and thus cause AR.

Aortic regurgitation is a volume overload lesion of the left ventricle and the amount of regurgitation depends on the pressure gradient between the aorta and the left ventricle in diastole, the time available for regurgitation in diastole and the effective orifice area.

Chronic AR results in long-term volume overloading of the left ventricle and over time compensatory eccentric hypertrophy develops. Both left ventricular end systolic volume (ESV) and end diastolic volume (EDV) increase, but the EDV increases more. Stroke volume increases and the ventricular radius increases which increases ventricular wall tension. Some concentric hypertrophy occurs as compensation but wall stress remains elevated in both systole and diastole. Most patients tolerate chronic AR for a long period of time until ventricular function declines and congestive heart failure develops.

In situations of acute AR, there is not enough time for eccentric hypertrophy to develop and diastolic compliance remains normal (not elevated as in chronic AR). Thus the regurgitant volume causes very high left ventricular end diastolic pressure, the left ventricle may acutely dilate and acute mitral regurgitation occurs which is poorly tolerated. There is increased left atrial pressure that is transmitted to the pulmonary vasculature. Pulmonary edema and right ventricular failure quickly result.

Hemodynamic goals for AR:

Maintain sinus rhythm with heart rate slightly fast (80’s) to reduce time in diastole for regurgitation to occur. Treat bradycardia aggressively. Reduce afterload to reduce aortic diastolic pressure and regurgitation Maintain preload volume in order to maintain adequate LVEDP and forward stroke volume Maintain contractility to encourage forward stroke volume with dilated left ventricle

Management of AR:  

Hypotension should not be treated with pure vasoconstrictor medications because arterial vasoconstriction will increase afterload and increase the regurgitant fraction. Avoid medications such as phenylephrine which cause increased afterload and reflex bradycardia both of which contribute to increased AR. Hypotension should be treated with augmentation of heart rate, preload and contractility.


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