A 72-year-old male with BRASH syndrome and hyperkalemia (6.9) who suffered cardiac arrest was successfully stabilized with pacing, epinephrine, and continuous renal replacement therapy.
Case Report (n=1)
This case highlights the presentation and multifaceted management of BRASH syndrome, emphasizing the dangerous synergistic relationship between AV nodal blockers and renal impairment.
Abstract BRASH syndrome represents a constellation of symptoms which make up the acronym: bradycardia, renal failure, atrioventricular nodal block, shock, and hyperkalemia. Although the relationship between AV nodal blockers and renal dysfunction have been known for decades, the ‘BRASH’ moniker is a relatively recent establishment and the syndrome as a whole is thought to remain under recognized 1. A 72 year-old male presented for evaluation of altered mental status. His medical history was significant for diastolic heart failure, cerebrovascular accident, chronic kidney disease (IIIb), atrial fibrillation on apixaban, intracerebral vascular aneurysm s/p surgical clipping, and hypertension. Profound bradycardia, specifically sinus bradycardia with frequent premature atrial complexes (Figure 1), with mild hypotension was noted on arrival to the emergency department which was refractory to the administration of atropine. While undergoing a computed tomography scan, the patient suffered a cardiac arrest with pulseless electrical activity. Resuscitation attempts achieved return of spontaneous circulation, and the patient was placed on transcutaneous pacer pads with an epinephrine drip before transport to the medical intensive care unit for further management. Lab work demonstrated hyperkalemia (6.9), anemia (Hgb 4.5), lactic acidosis, and elevated creatinine. A temporary transvenous pacemaker wire and a temporary dialysis catheter were placed. While the patient did initially demonstrate increasing vasopressor requirements, his blood pressure and heart rate did normalize with continuous renal replacement therapy. The synergistic relationship between atrioventricular nodal-blocking agents and renal impairment has been well established in medical literature for over half a century 2. Iatrogenic depression of intrinsic AV nodal function produces a state of diminished cardiac output from bradycardia. As cardiac output drops, blood flow is shunted away from the kidneys resulting in decreased glomerular filtration and potassium excretion at the distal convoluted tubule. The ensuing hyperkalemia may result in worsening bradycardia, and patients may decompensate into shock or cardiac arrest as the process continues. As BRASH syndrome represents a constellation of symptoms without a singular underlying cause, management likewise takes a multifaceted approach. Cardiac membrane stabilization with calcium chloride or calcium gluconate is an important initial step. The use of positive inotropes such as epinephrine or isoproterenol is indicated in refractory bradycardia, as well as consideration for temporary pacing should the patient remain unstable. Hyperkalemia may be addressed by promoting intracellular shift or excretion: insulin with dextrose, albuterol nebulizers (which provides the added benefit of positive inotropy), and loop diuretics are all useful tools for rapid correction. This abstract is funded by: None
Mckinney et al. (2026) conducted a case report in BRASH syndrome (n=1). Multifaceted management (pacing, epinephrine, continuous renal replacement therapy) was evaluated. A 72-year-old male with BRASH syndrome and hyperkalemia (6.9) who suffered cardiac arrest was successfully stabilized with pacing, epinephrine, and continuous renal replacement therapy.