An elderly alcoholic with dyspnea and edema; which is the most likely cause of high-output heart failure?

An elderly alcoholic with dyspnea and edema; which is the most likely cause of high-output heart failure?

• A. Uncontrolled hypertension
• B. Beriberi
• C. Mitral regurgitation
• D. Aortic stenosis

Answer: (B)

High-output heart failure occurs when tissues demand or receive more blood flow than the heart can sustain, often due to decreased systemic vascular resistance or widespread vasodilation. In wet beriberi, thiamine (vitamin B1) deficiency—common in alcohol misuse and malnutrition—impairs energy production in the heart and peripheral tissues. The lack of thiamine reduces activity of key enzymes (like pyruvate dehydrogenase), leading to reduced ATP, myocardial weakness, and dilatation. At the same time, systemic vasodilation lowers afterload, so the body reflexively increases heart rate and stroke volume to meet tissue perfusion. The combination of a dilated, energetic heart trying to pump against low resistance results in a high cardiac output that eventually becomes inefficient, producing dyspnea and edema characteristic of high-output heart failure. Uncontrolled hypertension raises afterload and favors pressure overload with a tendency toward heart failure with reduced exercise tolerance, not the classic high-output state. Mitral regurgitation causes volume overload and increased preload, which can produce heart failure symptoms but does not typify the high-output mechanism driven by systemic vasodilation seen in beriberi. Aortic stenosis directly limits forward output, causing low-output heart failure rather than high-output. So, in an elderly alcoholic with dyspnea and edema, beriberi is the most likely cause of high-output heart failure due to thiamine deficiency leading to vasodilation and increased cardiac workload.

High-output heart failure occurs when tissues demand or receive more blood flow than the heart can sustain, often due to decreased systemic vascular resistance or widespread vasodilation.

In wet beriberi, thiamine (vitamin B1) deficiency—common in alcohol misuse and malnutrition—impairs energy production in the heart and peripheral tissues. The lack of thiamine reduces activity of key enzymes (like pyruvate dehydrogenase), leading to reduced ATP, myocardial weakness, and dilatation. At the same time, systemic vasodilation lowers afterload, so the body reflexively increases heart rate and stroke volume to meet tissue perfusion. The combination of a dilated, energetic heart trying to pump against low resistance results in a high cardiac output that eventually becomes inefficient, producing dyspnea and edema characteristic of high-output heart failure.

Uncontrolled hypertension raises afterload and favors pressure overload with a tendency toward heart failure with reduced exercise tolerance, not the classic high-output state. Mitral regurgitation causes volume overload and increased preload, which can produce heart failure symptoms but does not typify the high-output mechanism driven by systemic vasodilation seen in beriberi. Aortic stenosis directly limits forward output, causing low-output heart failure rather than high-output.

So, in an elderly alcoholic with dyspnea and edema, beriberi is the most likely cause of high-output heart failure due to thiamine deficiency leading to vasodilation and increased cardiac workload.