Complete heart block of multifactorial aetiology following sugammadex administration.

Abstract

Sugammadex-induced bradycardia is well known and the incidence is quoted to be around 0.6–1%. 1,2 While the mechanism is unknown, sugammadex-induced bradycardia can be resistant to the administration of anti-cholinergics 3 and may degenerate to pulseless electrical activity 4 or asystole, 5 warranting management with vasopressors and inotropes alongside standard cardio-pulmonary resuscitation (CPR) measures. We report a patient who developed asystole immediately after administration of 200 mg (2.7 mg/kg) of sugammadex, which then evolved into complete heart block (CHB) requiring temporary transvenous pacing over 24 h. An 84-year-old male weighing 73 kg with features of acute acalculous cholecystitis was scheduled for an emergency laparoscopic cholecystectomy. Significant past medical history included hypertension, hypercho-lesterolaemia, ischaemic heart disease with moderate systolic dysfunction (ejection fraction 37%), stable angina and chronic kidney disease with an estimated glomerular filtration rate of 45 ml/min/1.72 m 2 . He was independent with his activities of daily living; however, he described New York Heart Association Class 2 dyspnoea. His medications included isosorbide mononitrate, candesartan, aspirin, atorvastatin and pantoprazole. His baseline troponin level during this admission was elevated to 66 ng/l, a change from 43 ng/l (reference range (cid:1) 16 ng/l) measured three weeks prior, and this was attributed to his gallbladder inflammation and renal dysfunction. A preoperative electrocardiogram (ECG) showed sinus rhythm with a heart rate (HR) of 66/min and left bundle branch block.