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Research Snapshot Theater: Cardiovascular/Renal, Adult

BRASH Syndrome: A Rare but Critical Cause of Bradycardia and Shock in the Elderly

Tuesday, March 24, 2026
11:15 AM - 12:15 PM Central Time
Location: Connections Central - RST 02

  • Bidhan B. Shah, MD

    Maryland

    Disclosure(s): No relevant financial relationship(s) to disclose.

  • AG

    Ashok Gaire, MD

    Internal Medicine Resident
    Anne Arundel Medical Center

    Disclosure information not submitted.

  • Hasan Kamal, MD (he/him/his)

    Anne Arundel Medical Center, Maryland

    Disclosure(s): No relevant financial relationship(s) to disclose.

  • AM

    Adrien Mazer, MD

    Critical Care Medicine Physician
    Anne Arundel Medical Center

    Disclosure information not submitted.

Introduction: BRASH syndrome, characterized by bradycardia, renal failure, AV nodal blockade, shock, and hyperkalemia, is a condition that can lead to life-threatening instability. It represents a vicious cycle in which each component exacerbates the others, often triggered by a mild insult in patients on AV nodal blockers.


Description: A 72-year-old woman with hypertension and type 2 diabetes presented with nausea, vomiting, and hyperglycemia (glucose: 335 mg/dL). In the ED, she was bradycardic (HR: 28 bpm), hypotensive with blood pressure (BP) of 95/52 mm Hg, and normoxic. Home medications included metoprolol succinate and diltiazem. Labs showed hyperkalemia (K⁺: 7.5 mmol/L), acute kidney injury (BUN/Cr: 32/2.3 mg/dL), high anion gap metabolic acidosis (bicarbonate: 11 mmol/L, gap: 19), and lactate of 11 mmol/L. Electrocardiogram (EKG) revealed a junctional rhythm with narrow QRS complexes and no typical hyperkalemic changes.

With bradycardia, hypotension, renal dysfunction, hyperkalemia, and AV nodal blocker use, BRASH syndrome was suspected. She received two 0.5 mg intravenous (IV) atropine doses with modest heart rate improvement. Hyperkalemia was treated with IV calcium gluconate, insulin with dextrose, albuterol, and furosemide. She did not require dialysis. Renal function and blood pressure improved with IV fluids.

A transthoracic echocardiogram showed preserved ejection fraction (70%) with grade I diastolic dysfunction. Renal ultrasound was negative for obstruction. A1c was 7.1%, and urine protein-to-creatinine ratio was elevated, consistent with diabetic kidney disease. Diltiazem was discontinued; metoprolol was cautiously resumed without recurrent bradycardia. She was discharged in stable condition with a plan for outpatient cardiology follow-up.


Discussion: Differentiating BRASH syndrome from isolated hyperkalemia and AV nodal blocker overdose is clinically relevant. BRASH typically involves moderate hyperkalemia, bradycardia, and therapeutic levels of AV nodal blockers, unlike overdose cases. Patients are usually medication-compliant, and symptoms arise from synergy between hyperkalemia and AV nodal blockade. This distinction can guide targeted management. Conclusions were developed with AI assistance.