Abstract 4367824: The Dual Threat: BRASH Syndrome Triggered by Beta Blockers and Calcium Channel Blockers

Case Description: BRASH syndrome is characterized by the following: bradycardia, renal failure, atrioventricular blockade, shock, and hyperkalemia. Due to its overlapping features, it is often under-reported and misdiagnosed as isolated hyperkalemia. This case involves a 53-year-old male who presented with palpitations following a hemodialysis session. Upon arrival, the patient was tachycardic and found to be in atrial flutter (Figure 1). Initial treatment with diltiazem effectively controlled his heart rate. However, the following day, the patient received additional beta-blockers and developed hypotension (72/50 mmHg), bradycardia (39 bpm) (Figure 2), and hyperkalemia (K 7.3). Upon being upgraded to the cardiac care unit (CCU), his management included atropine, epinephrine, glucagon, and calcium gluconate. Ultimately, the patient was stabilized with urgent dialysis. Discussion: BRASH syndrome is a cyclical condition that includes the amalgamation of the following: bradycardia, renal failure, atrioventricular (AV) nodal blockade, shock, and hyperkalemia. Carries an in-hospital mortality of 5.7%. It is often underreported and mistaken for isolated hyperkalemia or AV blocker toxicity. One reason for this underreporting is the subtlety of its presentation, which can easily be confused with hyperkalemia alone, especially when patients present primarily with bradycardia and renal dysfunction. Unlike typical hyperkalemia, which generally needs to be severe to induce bradycardia, BRASH syndrome can cause significant bradycardia even with moderate potassium elevations due to the synergistic effect of AV nodal blockers and renal failure. This case of BRASH syndrome, triggered by both beta-blockers and calcium channel blockers, is rare. The combined use of both agents compounds the effects on AV node conduction and can severely depress heart rate, especially when renal impairment leads to reduced drug clearance. Management of BRASH syndrome requires addressing all components of the syndrome. Initial treatment often includes correction of hyperkalemia with calcium gluconate and insulin. Bradycardia may be managed with atropine, epinephrine, or pacing. Additionally, medications contributing to AV node blockade should be held, and hemodynamic support with vasopressors may be necessary if hypotension persists. In some cases, such as ours, dialysis may be required to manage hyperkalemia and improve renal clearance of medications.