A Case Report of Acute Onset and Rapid Resolution of Atrioventricular Block After Sugammadex: Is the Autonomic System Involved?

Abstract

Administering sugammadex to reverse neuromuscular blockade can cause marked bradycardia and rarely asystole. In this case, a rapid onset, biphasic heart rate response; slowing then speeding, after administering sugammadex was noted while at steady state, 1.3% end-tidal sevoflurane. On review of the electrocardiogram (ECG), the heart rate slowing coincided with the onset of a second-degree, Mobitz type I block that lasted 45 seconds. No other events, drugs, or stimuli coincided with the event. The acute onset and transient nature of the atrioventricular block without evidence of ischemia implies a brief parasympathetic effect on the atrioventricular node after sugammadex administration.

Clarifying the grey space of sugammadex induced bradycardia

“…The document also comments on the postmarketing experience with bradycardia pointing out that ''cases of marked bradycardia and bradycardia with cardiac arrest have been observed within minutes after administration of sugammadex.'' Case reports from around the world confirm this postmarketing experience as they report sugammadex-induced bradycardia with various outcomes [2][3][4][5][6][7]. With such widespread use, the described 1% incidence of sugammadex-inducedand-likely-clinically-inconsequential bradycardia is perhaps not useful when understanding the risk of marked bradycardia with cardiac arrest.…”