A 34-year-old woman comes to the office due to exertional dyspnea. The patient has a history of IgA nephropathy; she received hemodialysis for 2 years before undergoing kidney transplantation last month. Chest x-ray reveals cardiomegaly and pulmonary congestion. Further evaluation determines that her symptoms are likely due to persistence of the arteriovenous fistula that was used for hemodialysis. Which of the following physiologic changes are most likely present in this patient due to the fistula?

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11ec160b_3c8a_2366_9249_55697c0f3c1d_MD0001_00 This patient with dyspnea and chest x-ray showing an enlarged heart and pulmonary edema likely has high-output heart failure due to excessive flow through her arteriovenous fistula. A surgically created arteriovenous fistula forms an enlarged vein that serves as an access point for hemodialysis (which requires a vessel with high blood flow rates); however, if the fistula becomes too large, it can lead to hemodynamic complications. A large arteriovenous fistula allows a high proportion of blood flow to bypass the resistance of the systemic arterioles, causing markedly decreased systemic vascular resistance (SVR) (ie, reduced afterload). Blood passing through the low peripheral resistance returns to the right atrium quickly and easily, resulting in increased venous return (ie, increased preload). Both the reduced afterload and increased preload facilitate increased stroke volume (ie, increased cardiac output). A baroreceptor reflex-mediated increase in contractility and heart rate in response to hypotension may also contribute to increased cardiac output. With excessively large fistulas, the left ventricle becomes unable to keep up with the increased venous return despite a persistent increase in cardiac output; left ventricular diastolic pressure gradually increases, and decompensated heart failure develops. Other common causes of high-output heart failure also involve decreased SVR as the initial disturbance. (Choice A) Hypovolemia (eg, severe dehydration) involves a marked reduction in blood volume. Venous return is decreased, leading to reduced cardiac output and a compensatory increase in SVR. (Choice B) Low-output heart failure (the typical cause of cardiogenic shock) involves left ventricular dysfunction as the initial disturbance, which leads to decreased cardiac output and a compensatory increase in SVR. Increased pressure is transmitted backward from the left ventricle, causing elevated central venous pressure (ie, increased venous return [preload]). (Choice C) The pathophysiology of sepsis is similar to high-output heart failure in that reduced SVR is the initial disturbance and is followed by a compensatory increase in cardiac output. However, in sepsis the leaky vasculature reduces intravascular volume to decrease venous return, preventing volume overload of the left ventricle. (Choice E) Stimulation of both alpha-1 and beta-1 adrenergic receptors (eg, with norepinephrine) causes arteriolar constriction to increase SVR, venoconstriction to increase venous return, and increased heart rate and contractility to increase cardiac output. Educational objective: High-output heart failure results from markedly decreased systemic vascular resistance (eg, large arteriovenous fistula) that leads to increased venous return and increased cardiac output. Despite a sustained increase in cardiac output, the left ventricle is unable to keep up with the increased venous return, and decompensated heart failure develops. __________ References: High-output cardiac failure. (http://www.ncbi.nlm.nih.gov/pubmed/30020709)

A 34-Year-Old Woman Comes to the Office Due to Exertional