A patient with an untreated large arteriovenous fistula (AV fistula) in the thigh develops high-output cardiac failure. The primary physiological reason is:

• A High-pressure arterial blood injures the tricuspid valve, causing regurgitation and right heart failure
• B The AV fistula provides a low-resistance shunt that increases venous return, chronically elevating cardiac output; over time, ventricular dilation and dysfunction develop ✓
• C Shunting of oxygenated blood away from tissues triggers polycythaemia, increasing blood viscosity and afterload
• D The fistula creates turbulence that activates the coagulation cascade, causing recurrent pulmonary emboli

Explanation

An AV fistula bypasses the high-resistance arteriolar bed, creating a low-resistance pathway that diverts blood from arteries directly to veins. This causes a fall in peripheral vascular resistance (afterload) and a marked increase in venous return (preload). The heart responds acutely by increasing cardiac output via the Frank-Starling mechanism. Chronically, sustained volume overload leads to cardiac chamber dilation, eccentric hypertrophy, and eventually systolic dysfunction — high-output cardiac failure. Branham's sign (bradycardia on manual AV fistula compression) is a clinical correlate. Options B–D are not the primary mechanisms of high-output failure.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.