Abstract Body (Do not enter title and authors here): Case Presentation:
A 98-year-old female with hypertension, atrial fibrillation on Metoprolol succinate 100 mg daily, and stage 3a chronic kidney disease presented to the emergency department with altered mental status. On arrival, her heart rate was 30 BPM and blood pressure was 79/47 mmHg. Physical examination revealed lethargy, bradycardia, and cool extremities. An electrocardiogram showed junctional bradycardia at 36 BPM with a known right bundle branch block. Laboratory tests indicated shock with elevated lactic acid (2.6 mmol/L), creatinine (1.71 mg/dL from a baseline of ~1.20 mg/dL), transaminitis (aspartate transaminase 68 U/L, alanine transaminase 79 U/L), and hyperkalemia (potassium 6.1 mmol/L). The diagnosis of BRASH syndrome was made based on bradycardia, renal dysfunction, AV nodal blockade, shock, and hyperkalemia. Due to concerns of cardiogenic shock resulting from profound bradycardia, an intravenous dopamine infusion was initiated, and the patient was transferred to the cardiac critical care unit. She responded to medical management addressing hyperkalemia and bradycardia, and did not require renal replacement therapy or pacemaker placement. Following these interventions, her mental status, vital signs, and signs of end-organ damage rapidly improved. The patient was downgraded and subsequently discharged with close cardiology follow-up.

Discussion:
This case highlights the under-recognized diagnosis of BRASH syndrome as a cause of cardiogenic shock. BRASH syndrome, an acronym for Bradycardia, Renal failure, AV node blockers, Shock, and Hyperkalemia, is typically observed in patients on AV nodal blocking medications. The proposed pathophysiology involves an acute kidney injury, often precipitated by dehydration in elderly patients with preexisting kidney disease. The renal impairment leads to hyperkalemia and accumulation of AV nodal blocking medications like beta-blockers, which act synergistically to produce significant bradycardia. This results in substantial cardiac shock, further worsening renal perfusion and fueling a vicious cycle. Clinicians should recognize the combination of features rather than focusing solely on individual components of the syndrome. Immediate recognition and initiation of advanced measures such as inotropic support can reverse the underlying disease process and lead to a promising recovery. BRASH syndrome, though rare, is a rapidly reversible cause of cardiogenic shock if promptly identified and managed.