A 44-year-old man with a history of intravenous drug use came to the emergency department due to fever and chills. Multiple blood culture sets were positive for Staphylococcus aureus, and the patient was diagnosed with infective endocarditis. He was successfully treated with a long course of antibiotics. Six months later, he returns to the clinic for a follow-up evaluation. The patient has no symptoms and reports good exercise tolerance. He is afebrile, blood pressure is 140/62 mm Hg, pulse is 82/min, and respirations are 16/min. Chest auscultation reveals a decrescendo diastolic murmur over the third intercostal space along the left sternal border. Echocardiogram shows severe aortic regurgitation, likely as a sequela to the prior infection. Which of the following changes is most responsible for maintaining cardiac output in the setting of this valvular abnormality?
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This patient has developed chronic aortic regurgitation (AR) as a consequence of infective endocarditis. Incomplete closure of the aortic valve during diastole allows a portion of left ventricular stroke volume to leak back into the left ventricle; in severe AR this regurgitant flow volume may be up to 50% of total forward stroke volume. Left ventricular dilation caused by the increase in left ventricular end-diastolic volume (LVEDV) (volume overload) triggers eccentric hypertrophy, which involves ventricular wall lengthening due to the addition of myocardial contractile fibrils organized in series. This compensatory response causes an increase in stroke volume that is able to maintain cardiac output, and allows for a relatively long asymptomatic period (eg, several years) in most patients with chronic AR.
However, the compensatory eccentric hypertrophy in chronic AR is overall maladaptive. Over time, progressive left ventricular dilation leads to overwhelming wall stress with decreased stroke volume and eventual left ventricular failure.
(Choice A) Concentric hypertrophy occurs due to conditions that create ventricular pressure overload (eg, hypertension, aortic stenosis); it involves ventricular wall thickening due to the addition of myocardial contractile fibrils in parallel. Although some concentric hypertrophy may occur in AR, eccentric hypertrophy due to volume overload is the predominant change.
(Choice B) In AR, left ventricular preload or LVEDV is increased, rather than decreased. This helps the ventricle maintain cardiac output via the Frank-Starling mechanism. Decreased preload would cause a reduction in cardiac output.
(Choice C) Increased aortic elasticity (ie, decreased compliance or increased aortic stiffening) occurs with aging and results in higher systolic blood pressure, widened pulse pressure, and reduced cardiac output.
(Choice D) In chronic AR, there is an effective increase in left ventricular afterload due to the enlarged chamber size (increases wall stress) and high peak systolic pressures. This increases left ventricular work, making it more difficult to maintain cardiac output and eventually leads to heart failure.
(Choice F) Because cardiac output is maintained by an increase in stroke volume, there is typically minimal increase in heart rate in chronic AR. However, in acute AR, eccentric hypertrophy does not have time to develop and the capacity to increase stroke volume is limited. The resulting decrease in cardiac output triggers a reflexive increase in heart rate, but this response is typically insufficient and most patients develop severe cardiogenic shock with pulmonary edema.
Educational objective:
In chronic aortic regurgitation, persistent left ventricular volume overload triggers eccentric hypertrophy, which causes a compensatory increase in stroke volume to maintain cardiac output. This compensatory mechanism allows for a relatively long asymptomatic period in most patients; however, left ventricular dysfunction eventually occurs, leading to heart failure.