Abstract: TH-PO0103
BRASH: A Vicious Cycle
Session Information
- AKI: Pathogenesis and Disease Mechanisms
November 06, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 102 AKI: Clinical, Outcomes, and Trials
Authors
- Singh, Shashwat, St Vincent's Medical Center, Bridgeport, Connecticut, United States
- Pena Zapata, Oscar Yasser, St Vincent's Medical Center, Bridgeport, Connecticut, United States
Introduction
BRASH is an acronym for bradycardia, renal failure, AV node blockade, shock, and hypotension. First described in 2016, most of our information on BRASH syndrome comes from case reports.
Case Description
We describe the incidence of BRASH syndrome in a 91-year-old patient was admitted to our center twice in a span of 1 month, with hyperkalemia and severe bradycardia.
EPISODE 1: 91-year-old male with coronary artery disease with multiple stents, CKD 3b, atrial fibrillation with history of ablation was seen in ED due to fall. Blood pressure was 100s/50s and HR was less than 45 on admission. Potassium was 5 mg/dL and creatinine was elevated at 2.5 gm/dL. He was taking metoprolol succinate 25 mg daily, sacubitril-valsartan 24-26 mg twice daily and torsemide 40 mg daily which were held on admission. His blood pressure and heart rate returned to normal, and potassium and creatinine levels improved by day 3, when he was discharged and advised to avoid these medications.
EPISODE 2: He was admitted for another episode of syncope and admitted with bradycardia, hypotension, AKI and hyperkalemia. He received IV fluids and standard hyperkalemia treatment. He was taking metoprolol, sacubitril-valsartan and torsemide contrary to the advice. As his hyperkalemia and creatinine improved, so did his vital signs although he still remained bradycardic with irregular rhythm. He received permanent pacemaker implantation on the 3rd day of admission. Sacubitril-valsartan was held on discharge. Metoprolol was continued.
Discussion
The dangerous cycle of BRASH syndrome starts with any condition causing volume depletion which causes poor renal perfusion. This leads to hyperkalemia which potentiates the beta blockade caused by AV nodal blocker, resulting in poor cardiac output due to decreased heart rate. Cardiac output further worsens renal perfusion, and the cycle continues. Bradycardia in this syndrome responds to intravenous calcium instead of atropine because it is not due to increased vagal tone. This is a deviation from standard ACLS algorithm. Additionally, bradycardia occurs at lower levels of hyperkalemia and EKG does not shows typical changes of PR prolongation and eventually sine wave formation. As per a systematic review, over 50% cases had non-severe hyperkalemia (less than 6.5 mg/dL). With increasing use of beta blockers, ACE/ARBs and MRAs, the incidence of this syndrome will continue to increase and requires more awareness in the community.