Key result
Sugammadex administration was associated with an acute, transient second-degree Mobitz type I atrioventricular block lasting 45 seconds, implying a brief parasympathetic effect.
Why the study?
Sugammadex used to reverse neuromuscular blockade can cause marked bradycardia and rarely asystole, but the mechanism remains to be clarified.
Case Report (n=1)
Sugammadex can induce a transient, acute-onset second-degree atrioventricular block, suggesting a brief parasympathetic effect on the AV node.
Sugammadex may trigger transient Mobitz I block under sevoflurane; single case leaves open true incidence and causality.
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.
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Abdelrahim et al. (2023) conducted a case report in Atrioventricular block (n=1). Sugammadex was evaluated on Second-degree, Mobitz type I block. Sugammadex administration was associated with an acute, transient second-degree Mobitz type I atrioventricular block lasting 45 seconds, implying a brief parasympathetic effect.
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