A chronic alcoholic man presents with warm, flushed extremities, tachycardia, wide pulse pressure, and biventricular failure with pulmonary congestion. There is no evidence of coronary disease. Which mechanism best explains his cardiac failure?

• A Impaired pyruvate dehydrogenase activity causing high-output failure from peripheral vasodilatation ✓
• B Direct ethanol toxicity producing irreversible loss of contractile myofibrils
• C Deposition of immunoglobulin light chains in the ventricular wall
• D Iron-mediated oxidative injury of cardiac myocytes

Explanation

Wet beriberi results from thiamine (vitamin B1) deficiency. Thiamine is a cofactor for pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase, so deficiency impairs aerobic metabolism and produces peripheral vasodilatation with arteriovenous shunting, driving a high-output state that fails the ventricles. It responds dramatically to parenteral thiamine. Alcoholic dilated cardiomyopathy is a separate low-output entity, while light chain deposition and iron overload describe amyloidosis and hemochromatosis respectively.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.