BRASH Syndrome Unmasked: Digoxin Toxicity in the Setting of Cardiogenic Shock and Multiorgan Dysfunction

Digoxin, a cardiac glycoside historically used for rate control in atrial arrhythmias and symptom relief in chronic heart failure, possesses a narrow therapeutic index and is highly susceptible to pharmacokinetic and pharmacodynamic disruption in critically ill patients. Its use in acute decompensated heart failure and cardiogenic shock is therefore controversial. We present the case of a 75-year-old woman with chronic heart failure with reduced ejection fraction who developed progressive bradycardia and cardiogenic shock after treatment with digoxin and amiodarone for 2:1 atrial flutter. Her hospital course was complicated by acute kidney injury, severe hyperkalemia, ischemic hepatitis, and persistent bradycardia following electrical cardioversion. Serum digoxin levels were supratherapeutic early in the intensive care unit course and subsequently normalized, though bradyarrhythmias persisted. The patient's presentation and clinical trajectory were consistent with BRASH (bradycardia, renal failure, AV-nodal blockade, shock, and hyperkalemia) syndrome , with amiodarone-digoxin interaction and systemic hypoperfusion likely amplifying myocardial digoxin sensitivity. She improved with supportive therapy, correction of metabolic derangements, withdrawal of AV-nodal-blocking agents, and cardioversion, without administration of digoxin-specific antibody fragments. This case highlights the importance of early recognition of BRASH physiology, cautious use of AV-nodal blockers in low-output states, and prioritization of underlying physiologic correction over reliance on serum drug levels alone in critically ill patients.