Iatrogenic Hypokalemia and Hypomagnesemia: A cause of Torsades de Pointes

Patients in heart failure (HF) are prone to electrolyte imbalance and consequent potentially lethal arrhythmias. Case: 47-year-old male with cardiomyopathy and LV dysfunction, and prophylactic implanted cardioverter-defibrillator (ICD), hospitalized with dizziness and one episode of ICD discharge; denied prior similar episodes. Medications: furosemide 80 mg BID, aspirin and carvedilol. BP 119/73, pulse 98, respiratory rate 17. No clinical evidence for HF. Chest x ray: cardiomegaly, mild pulmonary congestion. Electrocardiogram: NSR, diffuse ST-T flattening, QTc interval 541 msec, LVH. ICD interrogation: torsades de pointes (TdP). Echocardiogram confirmed LV systolic dysfunction. Lab: digoxin < 0.1 ng/mL, K 2.6 mEq/L, Mg 1.0 mEq/L, Cl 86 mEq/L, bicarb 30 mEq/L, Na 129 mEq/L. Intravenous potassium and magnessium replacement improved the QTc interval, with no recurrence of TdP. Discussion Torsades de Pointes (TdP) is a distinctive form of polymorphic ventricular tachycardia (VT) associated with a prolonged QT interval. Hypokalemia induced prolonged QT with ‘early after depolarization (EAD)’ may trigger TdP, which may terminate spontaneously or degenerate into ventricular fibrillation. Treatment includes correction of electrolyte imbalance; magnesium is the drug of choice for suppressing EAD and terminating the arrhythmia. If TdP degenerates into ventricular fibrillation, it requires direct current (DC) defibrillation. Lessons: The case illustrates the importance of prompt recognition and correction of electrolyte imbalance in prevention of torsades. Judicious use of diuretics and appropriate follow up minimizes development of hypokalemia and hypomagnesemia, common basis for arrhythmias.