Triaging the Clinical Dilemma of a Suicidal Attempt With Sotalol Overdose Presenting With Ventricular Tachycardia, Asystole, and Torsades de Pointes

TL;DR

A patient overdosed on sotalol, causing severe heart rhythm issues, and was successfully treated with hemodialysis despite normal kidney function.

Contribution

This case highlights the successful use of hemodialysis for sotalol overdose in a patient with normal renal function.

Findings

The patient developed life-threatening arrhythmias including torsades de pointes and asystole after sotalol overdose.

Hemodialysis was effective in resolving arrhythmias and correcting QTc prolongation despite normal kidney function.

Standard therapies like glucagon and magnesium sulfate were insufficient, emphasizing the need for aggressive interventions.

Abstract

Sotalol overdose presents a significant clinical challenge due to its dual properties as a nonselective beta-blocker and potassium channel blocker, leading to life-threatening arrhythmias such as ventricular tachycardia, torsades de pointes, and asystole. The combined negative chronotropic and QT-prolonging effects of sotalol increase the risk of malignant arrhythmias, particularly in cases of overdose. We report the case of a 59-year-old female who ingested a large dose of sotalol in a suicide attempt and presented with a cascade of arrhythmias, including ventricular tachycardia, asystole, and torsades de pointes. On arrival, she was bradycardic with a heart rate (HR) of 59 beats per minute (bpm) and normotensive with blood pressure (BP) of 128/76 mmHg. However, within 24 hours, the patient deteriorated and presented with worsening bradycardia (HR: 52 bpm) and inciting hypotension (BP: 57/32 mmHg, mean arterial pressure: <60 mmHg). Despite initial resuscitative measures, including calcium gluconate, atropine, glucagon, and transcutaneous pacing, the patient progressed to asystole, requiring cardiopulmonary resuscitation and advanced cardiac life support. Given sotalol’s beta-blocking effects and potassium channel blockade, ventricular arrhythmias persisted despite the administration of amiodarone, magnesium sulfate, and dopamine for hemodynamic support. QTc prolongations of 329 ms and 463 ms were noted on telemetry, raising concern for recurrent torsades de pointes. The refractory nature of the arrhythmias necessitated emergent hemodialysis to enhance sotalol clearance despite the patient having normal renal function. Ultimately, emergent hemodialysis was initiated to enhance the clearance of sotalol. The patient’s arrhythmias resolved, and QTc prolongations were no longer noted on telemetry observation. She was subsequently discharged to a psychiatric facility without lasting cardiac or neurological deficits. This case underscores the importance of early recognition and aggressive management of beta-blocker overdose, particularly when initial therapies fail. Conventional treatments such as glucagon and magnesium sulfate were insufficient in resolving arrhythmias, likely due to sotalol’s prolonged pharmacodynamic effects and persistent QT prolongation. We highlight the successful use of hemodialysis as a definitive intervention in a patient with normal renal function, demonstrating its role in rapidly removing sotalol and preventing further toxicity. However, the availability of hemodialysis and its applicability in similar cases warrant further validation. This case provides a framework for clinicians managing severe sotalol overdose when arrhythmias persist despite standard therapies.

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