BRASH syndrome—characterized by bradycardia, renal failure, atrioventricular (AV) nodal blockade, shock, and hyperkalemia—has recently been recognized as a distinct clinical entity. This syndrome is notable for its resistance to standard treatments for bradycardia and shock and poses a risk of rapid clinical deterioration [1]. The pathophysiology of BRASH syndrome likely involves a synergistic interaction between AV nodal blockade and hyperkalemia, leading to bradycardia, renal impairment, and shock [2,3].
