An 82-year-old man is evaluated for a heart murmur. He states that he feels healthy. On review of systems, he has had no chest pain, dyspnea, lightheadedness, syncope, or lower extremity swelling. The patient walks several miles per day. He has a history of hypertension treated with amlodipine. He is a lifetime nonsmoker. Blood pressure is 145/60 mm Hg and pulse is 72/min and regular. The lungs are clear on auscultation. Echocardiogram reveals a calcified aortic valve without stenosis but with severe aortic regurgitation. The left ventricle is dilated with an ejection fraction of 63%. No other valvular abnormalities are noted. Which of the following compensatory mechanisms best explains why this patient is asymptomatic with the existing pathology?

Question

An 82-year-old man is evaluated for a heart murmur.  He states that he feels healthy.  On review of systems, he has had no chest pain, dyspnea, lightheadedness, syncope, or lower extremity swelling.  The patient walks several miles per day.  He has a history of hypertension treated with amlodipine.  He is a lifetime nonsmoker.  Blood pressure is 145/60 mm Hg and pulse is 72/min and regular.  The lungs are clear on auscultation.  Echocardiogram reveals a calcified aortic valve without stenosis but with severe aortic regurgitation.  The left ventricle is dilated with an ejection fraction of 63%.  No other valvular abnormalities are noted.  Which of the following compensatory mechanisms best explains why this patient is asymptomatic with the existing pathology?

Quizplus · Accepted Answer

11ec25c8_d330_cbf6_bc81_b52953523cb3_MD0003_00 Aortic regurgitation (AR) involves leakage of blood from the aorta back into the left ventricle during diastole. In severe AR, regurgitant volume can be up to 50% of total stroke volume, causing significant volume overload of the left ventricle. The left ventricle initially adapts via the Frank-Starling mechanism, with left ventricular (LV) stretch allowing for an increase in stroke volume to help maintain cardiac output. As the volume overload becomes chronic, the left ventricle further adapts via eccentric hypertrophy, which involves the addition of myocardial fibers in series. This allows for both increased LV compliance to accommodate additional LV volume and increased LV contractility to sustain increased stroke volume and maintain cardiac output. series In the short term, eccentric hypertrophy is beneficial because it allows for an initial asymptomatic period in the setting of severe chronic AR. However, in the long term, eccentric hypertrophy is maladaptive because it causes increased LV wall stress, which eventually leads to LV contractile dysfunction and decompensated heart failure. (Choices A and C) Severe AR causes an increase (rather than decrease) in LV preload as the left ventricle receives diastolic blood from both the left atrium and the aorta through the regurgitant aortic valve. Initially via the Frank-Starling mechanism, and later via eccentric hypertrophy, the left ventricle responds to the increased preload with increased (rather than decreased) stroke volume. (Choice B) Eccentric hypertrophy involves a temporary increase in LV contractility to maintain stroke volume during the compensated, asymptomatic period of severe chronic AR. The eventual decrease in LV contractility is indicated by clinical decompensation and the onset of heart failure symptoms (eg, dyspnea, peripheral edema). (Choice E) Because cardiac output is sustained, total peripheral resistance (TPR) remains largely unchanged throughout the compensated period of severe chronic AR. Once symptomatic decompensation with reduced cardiac output sets in, TPR increases (via peripheral vasoconstriction) to help maintain organ and tissue perfusion. Educational objective: In severe, chronic aortic regurgitation, the left ventricle responds to volume overload with eccentric hypertrophy to increase both left ventricular compliance and contractility, allowing for an increase in stroke volume to maintain cardiac output. This allows for a temporary asymptomatic period. However, overwhelming wall stress eventually leads to symptomatic, decompensated heart failure.

An 82-Year-Old Man Is Evaluated for a Heart Murmur