{"title":"Failure of Implantable Cardioverter-defibrillator Pacing Capture in BRASH Syndrome with Severe Hyperkalemia.","authors":"Stephen Roche, Michael Kanan, Deana Mikhalkova","doi":"10.19102/icrm.2026.17071","DOIUrl":null,"url":null,"abstract":"<p><p>This case report describes a 54-year-old woman with end-stage renal disease and heart failure who presented with BRASH syndrome: a synergistic cycle of bradycardia, renal failure, atrioventricular nodal blockade, shock, and hyperkalemia. The patient, who was adherent to metoprolol and amiodarone, presented with a profound ventricular escape rhythm of 16 bpm and hemodynamic instability after missing 4 days of hemodialysis. An interesting complication was the failure of her implantable cardioverter-defibrillator (ICD) to achieve pacing capture, a phenomenon likely driven by a potassium level of 7.8 mEq/L causing myocardial inexcitability. Additionally, the recent uptitration of a carotid sinus nerve stimulator for baroreflex activation therapy may have contributed to the bradycardic cycle. Immediate medical management of hyperkalemia with calcium, insulin, and dextrose successfully restored ICD capture, followed by emergent dialysis, which normalized her rhythm. This case emphasizes that BRASH syndrome should be considered in undifferentiated bradycardia, particularly when refractory to atropine, and highlights that correcting the underlying metabolic derangement is essential to restoring cardiac excitability and device function.</p>","PeriodicalId":36299,"journal":{"name":"Journal of Innovations in Cardiac Rhythm Management","volume":"17 7","pages":"6784-6787"},"PeriodicalIF":0.0000,"publicationDate":"2026-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13679920/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Innovations in Cardiac Rhythm Management","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.19102/icrm.2026.17071","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/7/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
引用次数: 0
Abstract
This case report describes a 54-year-old woman with end-stage renal disease and heart failure who presented with BRASH syndrome: a synergistic cycle of bradycardia, renal failure, atrioventricular nodal blockade, shock, and hyperkalemia. The patient, who was adherent to metoprolol and amiodarone, presented with a profound ventricular escape rhythm of 16 bpm and hemodynamic instability after missing 4 days of hemodialysis. An interesting complication was the failure of her implantable cardioverter-defibrillator (ICD) to achieve pacing capture, a phenomenon likely driven by a potassium level of 7.8 mEq/L causing myocardial inexcitability. Additionally, the recent uptitration of a carotid sinus nerve stimulator for baroreflex activation therapy may have contributed to the bradycardic cycle. Immediate medical management of hyperkalemia with calcium, insulin, and dextrose successfully restored ICD capture, followed by emergent dialysis, which normalized her rhythm. This case emphasizes that BRASH syndrome should be considered in undifferentiated bradycardia, particularly when refractory to atropine, and highlights that correcting the underlying metabolic derangement is essential to restoring cardiac excitability and device function.