A 68-year-old man with chronic atrial fibrillation and heart failure presents to the emergency department with severe nausea, visual disturbances (yellow-green halos around lights), and palpitations. His ECG shows the pattern marked **A** — sagging "reverse tick" ST depression with bidirectional ventricular tachycardia. Serum potassium is 5.8 mmol/L (normal 3.5–5.0). He has been on digoxin 250 μg daily for 2 years; his creatinine is 1.8 mg/dL (eGFR ~35 mL/min/1.73m²). Which of the following is the most appropriate immediate management?

Explanation

## Why Digoxin-specific Fab fragments (Digibind) after correction of hypokalemia is right The ECG pattern marked **A** — sagging "reverse tick" ST depression combined with **bidirectional ventricular tachycardia** — is the pathognomonic ECG hallmark of severe digoxin toxicity. This patient has classic acute digoxin toxicity: visual disturbances (xanthopsia), severe nausea, bidirectional VT, and hyperkalemia (K 5.8 mmol/L). According to Goodman & Gilman 14e and KD Tripathi 8e, bidirectional VT is highly specific for digoxin toxicity and arises from delayed afterdepolarizations caused by digoxin-induced intracellular calcium overload and Na+/K+-ATPase inhibition. The serum K >5.5 mmol/L in acute toxicity is a life-threatening finding (historically 100% fatal before Fab fragments). Management requires: (1) STOP digoxin immediately; (2) CORRECT hypokalemia/hyperkalemia cautiously — in this case K is elevated, so potassium supplementation is contraindicated; instead, IV magnesium should be given; (3) **DIGOXIN-SPECIFIC FAB FRAGMENTS** are the definitive antidote — indicated for life-threatening arrhythmias (VT/VF), K >5.5 mmol/L, or hemodynamic instability. Fab fragments bind free digoxin and are renally excreted, rapidly reversing toxicity within 30 minutes. The correct sequence is: stop digoxin, correct magnesium (and avoid potassium given the hyperkalemia), and administer Digibind. The answer reflects the standard guideline that Fab fragments are the cornerstone of severe digoxin toxicity management. ## Why each distractor is wrong - **Intravenous potassium chloride 20 mEq over 30 minutes**: This is contraindicated. The patient already has hyperkalemia (K 5.8 mmol/L). Potassium supplementation would worsen hyperkalemia and increase the risk of fatal arrhythmia. IV potassium is only given if K <3.5 mmol/L in digoxin toxicity (to reduce toxicity risk); here it would be harmful. - **Immediate transvenous pacing for symptomatic bradycardia and IV amiodarone for VT suppression**: Transvenous pacing is contraindicated in digoxin toxicity — the irritable myocardium is prone to provocation of ventricular fibrillation by the pacing wire. Amiodarone increases serum digoxin levels (CYP3A4 and P-glycoprotein inhibition) and would worsen toxicity. The definitive treatment is Fab fragments, not antiarrhythmic drugs. - **Intravenous calcium gluconate 10% to antagonize hyperkalemia and restore cardiac membrane stability**: Although calcium is used in hyperkalemia from other causes, it is explicitly AVOIDED in acute digoxin toxicity (theoretical risk of "stone heart" from intracellular calcium overload, though evidence is debated). The standard teaching is to avoid calcium in digoxin toxicity and instead use Fab fragments to remove the offending drug. **High-Yield:** Bidirectional VT + hyperkalemia + xanthopsia in a digoxin patient = severe toxicity → **STOP digoxin, correct Mg, give Digibind Fab fragments**; avoid K supplementation and calcium; avoid transvenous pacing. [cite: Goodman & Gilman 14e Ch 31; KD Tripathi 8e Ch 37; Harrison 21e Ch 257]