A 72-year-old woman on chronic digoxin and furosemide presents with nausea, xanthopsia (yellow-green vision), and a heart rate of 42 with frequent premature ventricular beats. Serum potassium is 3.0 mEq/L. Which statement best explains the arrhythmogenic mechanism of her toxicity?

• A Digoxin inhibits potassium channels directly, prolonging repolarization
• B Furosemide competitively blocks renal digoxin secretion, raising tissue levels
• C Digoxin increases vagal tone, causing re-entry at the AV node
• D Hypokalemia displaces digoxin from Na+/K+-ATPase, enhancing its inhibitory effect ✓

Explanation

Digoxin inhibits Na+/K+-ATPase, and potassium competes with digoxin for binding at this pump. Hypokalemia therefore potentiates digoxin toxicity even at 'therapeutic' serum concentrations, producing enhanced automaticity and delayed afterdepolarizations via intracellular calcium overload. This is why potassium repletion is the first step in mild digoxin toxicity with hypokalemia. Option A is wrong because digoxin does not block potassium channels; option B is incorrect because furosemide has no such interaction.

Reference: Katzung's Basic and Clinical Pharmacology, 16th ed.

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Written and medically reviewed by the StethoPrep medical team.