How can digoxin toxicity contribute to tachyarrhythmias, and how should it be managed?

• A. Can cause atrial tachycardia with block or other tachyarrhythmias; stop digoxin and correct electrolytes; administer digoxin-specific antibody if severe
• B. Causes only bradycardia; administer atropine
• C. Causes ventricular fibrillation; immediate defibrillation
• D. Not related to tachyarrhythmias

Answer: (A)

Digoxin toxicity can provoke tachyarrhythmias because digoxin amplifies conduction abnormalities and ectopic automaticity in the heart. By inhibiting the Na+/K+ ATPase, digoxin increases intracellular calcium, which boosts contractility but also promotes depolarizations outside the normal rhythm, leading to various tachyarrhythmias. A classic pattern is atrial tachycardia with block, but other tachyarrhythmias can occur as well. The drug also enhances vagal tone, slowing AV nodal conduction, which can produce blocks or unusual rhythm disturbances in the setting of toxicity.

The best way to manage this is to stop digoxin, correct electrolyte disturbances (especially potassium and magnesium, which influence excitability and conduction), and, in severe or life-threatening cases, administer digoxin-specific antibody fragments to neutralize the circulating drug. Supportive care and careful rhythm monitoring follow, with attention to avoiding interventions that could worsen toxicity (for example, calcium administration is approached cautiously in acute toxicity). The combination of stopping the toxin, correcting electrolytes, and using the antidote in severe cases addresses both the underlying mechanism and the resulting arrhythmias.