Background BRASH syndrome, characterized by bradycardia, renal failure, atrioventricular nodal blockade, shock, and hyperkalemia, is a recently described clinical entity that remains underrecognized. Current evidence is limited to case reports and small case series, and the pharmacological patterns underlying this syndrome have not been systematically evaluated. Methods We conducted a retrospective pharmacovigilance study using the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS) from January 2004 to March 2025. Individual case safety reports explicitly coded as BRASH syndrome were identified and deduplicated. Associations between BRASH syndrome and individual drugs were assessed using Reporting Odds Ratios (RORs) and Information Components (ICs) with 95% confidence intervals. Drugs showing positive disproportionality signals were categorized according to their presumed role in the BRASH pathophysiological cascade. Results A total of 1,081 reports were included. The median age of patients was 74 years (interquartile range, 64,82); 45.5% were female, 38.7% were male, and sex was not reported in 15.8% of cases. All cases were classified as serious adverse drug reactions, including 7.1% fatal and 34.4% life-threatening events. Strong disproportionality signals were observed for atrioventricular nodal blocking agents, including metoprolol (ROR, 58.6; 95% CI, 52.0,66.1), verapamil (ROR, 52.5; 95% CI, 43.4,63.3), and carvedilol (ROR, 28.7; 95% CI, 24.4,33.6). Additional signals involved drugs plausibly contributing to renal dysfunction or hyperkalemia. Multiple pharmacologically relevant drugs were frequently reported within individual cases. Conclusions BRASH syndrome is associated with combinations of cardiovascular and renal-active medications rather than single-drug exposure, supporting its interpretation as a polypharmacy-driven clinical syndrome in vulnerable patients.