Voltage-gated sodium channels mediating conduction in vagal motor fibers innervating the esophageal striated muscle.

BACKGROUND BRASH syndrome is a newly recognized clinical entity characterized by bradycardia, renal failure, atrioventricular blockade, shock, and hyperkalemia. Patients with BRASH syndrome often have severe bradycardia that is refractory to antidotes and chronotropic medications. In these situations, transvenous pacemaker and renal replacement therapy may be necessary. Therefore, rapid diagnosis and correct management of this entity are crucial to reduce mortality. We report a case and the management of BRASH syndrome in the Emergency Department. CASE REPORT A 76-year-old man with chronic kidney disease stage 3, essential hypertension and psoriasis, and receiving atenolol presented to the Emergency Department with lethargy and weakness that started 3 days ago, with rapid deterioration into shock. His initial laboratory tests revealed hyperkalemia, metabolic acidosis, and acute kidney injury. His initial electrocardiogram was remarkable for sinus bradycardia with junctional escape rhythm with ventricular rate of 26 bpm. A chest X-ray was normal. Transthoracic echocardiogram showed normal systolic and diastolic function. Atenolol was immediately held. He was treated with potassium-lowering agents and vasoactive drugs. Due to the persistence of bradycardia, even after reversal of hyperkalemia, a temporary transvenous pacemaker was placed. Renal replacement therapy was not required. Renal function improved and heart rate stabilized at 80 bpm. The patient was discharged and advised to avoid atrioventricular-blocking agents, with Cardiology follow-up. CONCLUSIONS BRASH syndrome is a serious complication due to a combination of hyperkalemia, hypotension, and bradycardia in the setting of kidney dysfunction and medications that block the atrioventricular node. Hemodynamic support and temporary pacemaker use may be needed to manage this entity.