Critical Care Medicine-Neurologic Disorders>>>>>Valvular Heart Disease
Question 3#

A 46-year-old female with a history of hepatitis C and intravenous drug abuse presents to the emergency department with fevers, rigors, confusion, and acute shortness of breath.

The vital signs are as follows:

Chest radiograph shows diffuse pulmonary edema. Echocardiography demonstrates a vegetation on the noncoronary cusp of the aortic valve with severe aortic regurgitation. Although awaiting surgery, the patient is admitted to the cardiology ICU.

Which intervention in the most appropriate next step?

a. Nitroprusside
b. Epinephrine
c. Norepinephrine
d. Furosemide

Correct Answer is A


Correct Answer: A

Acute aortic regurgitation can lead to rapid cardiovascular and respiratory deterioration. The left ventricle cannot accommodate the acute rise in left ventricular preload, and as a result, stroke volume decreases. Left ventricular diastolic pressure rises rapidly causing premature closure of the mitral valve in diastole. Further increases in left ventricular pressure may cause a phenomenon known as diastolic mitral regurgitation, which increases the pressures in the left atrium and pulmonary circulation. Patients with acute aortic regurgitation may present with tachycardia, hypotension, and pulmonary edema. Cardiogenic shock in the setting of acute aortic regurgitation is an indication for emergent aortic valve replacement. Inotropic agents (dobutamine) and/or vasodilators (nitroprusside) may be required to temporize the hemodynamics before the procedure. Nitrodilators cause venous and arterial vasodilation resulting in decreased preload and afterload. Addition of dobutamine may also improve cardiopulmonary function by increasing inotropy and decreasing systemic vascular resistance and thus afterload. Patients with severe aortic regurgitation have wide pulse pressure due to the rapid aortic run off. Decreasing left ventricular afterload helps to decrease the gradient between the aorta and the left ventricle in diastole, thus reducing the regurgitant volume. 

Chronic aortic regurgitation, on the other hand, results in myocardial remodeling, which tolerates increased preload to a much greater extent than acute aortic regurgitation. In chronic aortic regurgitation, gradually increased left ventricular diastolic pressures result in eccentric left ventricular hypertrophy. Because of the eccentric hypertrophy, the increased preload can increase stroke volume and cause increased systolic pressures. This in turn increases left ventricular ejection time and thus decreases diastolic time resulting in decreased coronary perfusion. However, according to the law of Laplace, left ventricular dilation (increased radius) leads to increased wall tension and thus increased afterload. Thus, chronic aortic regurgitation represents a state of both increased preload and increased afterload.


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