BRASH syndrome (bradycardia, renal failure, AV nodal blockade, shock, and hyperkalemia) involves the synergistic effect of AV nodal blockade and hyperkalemia resulting in severe bradycardia. The resulting reduction in cardiac output, in turn, leads to poor renal perfusion, therefore, worsening the acute kidney injury as well as the degree of hyperkalemia. While severe hyperkalemia alone can cause bradycardia, in BRASH syndrome profound bradycardia can occur even in the setting of mild hyperkalemia due to the synergistic effect. Renally cleared AV nodal blockers, such as metoprolol and amlodipine, impose a greater risk as the concentration in the renal tubules inversely increases as the GFR decreases. If undiagnosed, this can progress to multisystem organ failure requiring transvenous pacing and hemodialysis. This vicious cycle is often initiated by a recent illness or medication changes. One of the most common causes is hypovolemia resulting from dehydration and a subsequent pre-renal acute kidney injury. Other common triggers include up-titration of medications that alter the cardiac output or renal perfusion, and the initiation of nephrotoxic agents or potassium-sparing diuretics. While estimates of this syndrome’s prevalence are unclear, it is likely under-recognized in general so it may be something to consider in such cases.
References: BRASH Syndrome: Bradycardia, Renal Failure, AV Blockade, Shock, and Hyperkalemia