Digoxin toxicity in a patient with atrial fibrillation is worsened by hypokalaemia. The mechanism involves:

• A Low K+ decreases renal tubular secretion of digoxin, raising plasma levels
• B Low K+ enhances digoxin binding to Na+/K+-ATPase (both compete for same site on the alpha subunit) ✓
• C Low K+ increases sympathetic tone, which synergises with digoxin's vagomimetic effect
• D Low K+ causes rhabdomyolysis, releasing digoxin from skeletal muscle stores

Explanation

Potassium and digoxin bind to overlapping sites on the extracellular alpha-subunit of Na+/K+-ATPase. In hypokalaemia, reduced extracellular K+ competes less effectively with digoxin, increasing digoxin's affinity and inhibitory effect on the pump—leading to greater intracellular Na+ accumulation, increased Na+/Ca2+ exchange, elevated intracellular Ca2+, and enhanced cardiac automaticity and triggered arrhythmias. Correcting hypokalaemia is therefore a cornerstone of managing digoxin toxicity.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.