Crashing BRASH Syndrome: NavigatingThe Storm Of Cardiovascular Chaos
Presenter
Muhammad Abdullah, MD, Shaikh Zayed Hospital, Lahore, Punjab, Pakistan
Noman Khalid, MD1, Muhammad Abdullah, MD2, Muhammad Adil Afzal, MD1, Furqan Bhullar, MD1, Michael Alexander Pelidis, MD1, Ameer Muhammad, MD1, Safee Ullah Haider, MD2, Sherif Elkattawy, MD1, Rahul Vasudev, MD1 and Fayez E. Shamoon, M.D.3, (1)St. Joseph's Health, Paterson, NJ, (2)Shaikh Zayed Hospital, Lahore, Punjab, Pakistan, (3)RWJBarnabas Health, Newark, NJ
Title:
Crashing BRASH Syndrome: Navigating The Storm Of Cardiovascular Chaos
Introduction:
BRASH syndrome is a rare clinical entity characterized by bradycardia resulting from AV-blockade, accompanied by hyperkalemia, hypotension, and renal failure. Effectively managing BRASH syndrome can be challenging, particularly as it occasionally proves resistant to medication-based interventions. In this case, we present the unfortunate outcome of an elderly female patient with BRASH syndrome who, despite receiving aggressive management, did not survive.
Clinical Case:
A 90-year-old female with HFpEF, hypertension and paroxysmal atrial fibrillation (on carvedilol and dronedarone) was admitted for multifocal pneumonia. The hospital course was complicated by symptomatic bradycardia with a heart rate (HR) of 35 BPM, BP 90/60 mmHg, SpO2 95% on BiPAP, and blood glucose of 58 mg/dL. EKG showed a HR of 38 with no ST or T wave changes. Labs showed potassium of 6.3 mmol/L, creatinine of 2.42 mg/dL, TSH of 2.150 ulU/ml, and a lactic acid of 5.7 mmol/L. Antihypertensives and beta blockers were held. Potassium-lowering agents and vasopressors (Dopamine drip 3 mg/kg/min) were administered. Temporary transcutaneous pacing was placed to reverse persistent bradycardia with hemodynamic instability. Unfortunately, due to the patient’s goals of care, central line placement for the purpose of temporary transvenous pacing was not possible. Another round of potassium-lowering agents was administered for refractory hyperkalemia, but the patient’s bradycardia and blood pressure continued to deteriorate and the patient passed away.
Discussion:
In our case, hyperkalemia likely secondary to dronedarone caused bradycardia. This led to a decreased cardiac output and renal hypoperfusion, which in turn worsened renal function and subsequently impaired excretion of the beta-blockers. This vicious cycle led to BRASH syndrome causing the patient’s demise. Early recognition and prompt management are critical to reduce mortality.