Severe Bradycardia, Renal Failure, Atrioventricular Nodal Blockade, Shock, and Hyperkalemia (BRASH) Syndrome Successfully Managed With Transvenous Pacing and Continuous Renal Replacement Therapy.

BRASH (Bradycardia, Renal failure, Atrioventricular nodal blockade, Shock, and Hyperkalemia) syndrome is a life-threatening clinical syndrome characterized by a vicious cycle in which hyperkalemia and AV nodal blocking medications synergistically produce profound bradycardia and hemodynamic instability. A 71-year-old male with stage IIIB chronic kidney disease (CKD), heart failure with improved ejection fraction, and coronary artery disease status post coronary artery bypass grafting, on carvedilol, losartan, and torsemide, was brought to the emergency room from a rehabilitation facility for a syncopal event and unresponsiveness. He had been recently hospitalized for multifocal pneumonia and respiratory syncytial virus infection, with suspected volume depletion and ongoing AV nodal blockade contributing to the development of BRASH syndrome. He was in respiratory distress, profound shock, and bradycardia with a heart rate of 30 BPM. Labs revealed severe acute kidney injury (creatinine 6.2 mg/dL), hyperkalemia (6.9 mmol/L), and metabolic acidosis (pH 7.19). Chest radiograph demonstrated pulmonary edema. His condition rapidly progressed to airway compromise requiring intubation, cardiogenic shock requiring vasopressors, and refractory bradycardia necessitating transvenous pacing after failure of atropine, dopamine, and transcutaneous pacing. He was admitted to the intensive care unit and promptly initiated on continuous renal replacement therapy (CRRT), resulting in correction of electrolyte and acid-base abnormalities with subsequent resolution of severe bradycardia, allowing discontinuation of transvenous pacing. Infectious workup remained negative, and echocardiography demonstrated preserved left ventricular systolic function. Following stabilization, he was successfully extubated and weaned off CRRT. His subsequent hospital course was complicated by recurrent oliguric renal failure requiring initiation of intermittent hemodialysis. Upon discharge, he remained hemodynamically stable with improved mental status and was planned for long-term hemodialysis and inpatient rehabilitation. The synergistic interaction of hyperkalemia and AV nodal blockade is the central pathophysiologic mechanism underlying BRASH syndrome. Common triggers include hypovolemia and medications that promote AV nodal blockade or hyperkalemia in vulnerable patients with advanced age, CKD, and heart failure. The resulting profound bradycardia further reduces cardiac output, worsening renal perfusion and perpetuating hemodynamic instability. Prognosis depends largely on early recognition and prompt intervention. This case highlights a severe presentation of BRASH syndrome in which timely initiation of CRRT corrected the underlying metabolic derangements, and transvenous pacing provided temporary hemodynamic support, ultimately leading to clinical recovery.