A 70-year-old man is on digoxin for AF rate control. He presents with bradycardia (HR 38 bpm), nausea, and confusion. ECG shows regularised slow ventricular rate with junctional rhythm. Serum digoxin is 3.8 ng/mL. Potassium is 5.8 mmol/L. The mechanism of digoxin toxicity causing this ECG pattern is:
- A Excessive beta-1 receptor blockade reducing sinus rate and AV conduction
- B Inhibition of Na+/K+-ATPase leading to excess intracellular calcium causing increased vagal tone and triggered automaticity ✓
- C Direct sodium channel blockade causing QRS prolongation and bradycardia
- D Potassium channel blockade causing QT prolongation and AV block
Explanation
Digoxin inhibits the Na+/K+-ATPase pump, causing intracellular Na+ accumulation, which reduces the Na+/Ca2+ exchanger's ability to extrude Ca2+, resulting in intracellular Ca2+ excess. This causes two main electrophysiological effects: (1) Enhanced vagal tone (direct and via sensitisation of baroreceptors) causing sinus bradycardia and AV block — explaining the regularised junctional escape rhythm in AF, and (2) Triggered automaticity from delayed afterdepolarisations (DAD) causing ectopic rhythms. Hyperkalaemia potentiates toxicity by impairing Na+/K+-ATPase further. Digoxin does not block Na+ channels or K+ channels directly. Beta-blockade is a different mechanism.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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Written and medically reviewed by the StethoPrep medical team.