A case report presented at the American College of Chest Physicians conference detailed an instance of BRASH syndrome, characterized by bradycardia, renal insufficiency, atrioventricular nodal blockade, shock, and hyperkalemia.
The report described a 66-year-old female patient with diabetes, hypertension, and atrial fibrillation who presented with vomiting, diarrhea, and generalized weakness for 1 week. The patient was on apixaban, flecainide, and metoprolol. Initial vital signs showed hypotension (81/42 mmHg), bradycardia (41 bpm), and a respiratory rate of 18. Laboratory findings revealed hyperkalemia (5.8 mmol/L), acute kidney injury (creatinine 6.4 mg/dL, baseline 0.8 mg/dL), BUN 82 mg/dL, metabolic acidosis (CO2 12 mmol/L, anion gap 17), lactic acid 3.5 mmol/L, and troponin 36 ng/L.
Electrocardiogram demonstrated sinus bradycardia with trifascicular block and prolonged QTc, without signs of ischemia. Imaging studies revealed acute colitis, and an echocardiogram showed a preserved ejection fraction (60%) with mild left atrial dilation. The patient’s telemetry also detected atrial fibrillation, with heart rates in the 30s.
The patient's condition was complicated by hypovolemic shock, necessitating fluid resuscitation and brief vasopressor support to maintain a mean arterial pressure (MAP) of 65 mmHg. Treatment included discontinuation of atrioventricular (AV) nodal-blocking drugs, initiation of oral amiodarone with a heparin drip, and management of hyperkalemia with a treatment cocktail. As a result of worsening renal failure and acidosis, renal replacement therapy was initiated. The patient's heart rate improved, and she was discharged in stable condition after discontinuing flecainide and metoprolol, with close cardiology follow-up.
BRASH syndrome occurs when renal insufficiency leads to the accumulation of AV nodal-blocking agents, resulting in bradycardia and shock. Common triggers include hypovolemia, medication overdose, and infections. The pathophysiological mechanism likely involves the synergistic effects of AV-nodal block and hyperkalemia, leading to pronounced bradycardia, reduced cardiac output, and further renal impairment.
Diagnosis of BRASH syndrome is primarily clinical, with presentations ranging from asymptomatic bradycardia to cardiac arrest. The treatment goals include managing hyperkalemia, providing hemodynamic support for hypovolemia, and discontinuing AV nodal-blocking agents while addressing the underlying triggers, such as dehydration.
First described in 2016, BRASH syndrome remains an emerging clinical entity, particularly important given the widespread use of AV nodal blockers in hypertension and arrhythmia management.
The authors declared no competing interests.
