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Editorial
This letter highlights that type IA antiarrhythmics like disopyramide are notorious for causing QT prolongation and torsade de pointes, offering an alternative explanation for a previously reported case attributed to sevoflurane.
To the Editor: Abe et al. [1] present a case of intraoperative torsade de pointes and ventricular fibrillation, which they ascribe to the use of sevoflurane. However, there are other likely explanations for the arrhythmias in this case. Notably, torsade de pointes did not develop until after the administration of disopyramide, a type IA antiarrythmic. Type IA agents, particularly quinidine, but including disopyramide and procainamide, are notorious for their association with prolongation of the QT interval and torsade de pointes [2,3]. It is surprising that the authors did not comment on this relationship in their article. The authors ascribe some importance to the observation that arrhythmias resolved after the discontinuation of sevoflurane; however, torsade de pointes is self-limiting in a high percentage of cases [3]. Finally, there is no mention of the postoperative electrocardiogram. The presence of new QT prolongation after discontinuation of sevoflurane would have helped to confirm the contribution of disopyramide to the observed arrhythmias. A likely scenario in this case is that the initial arrhythmia (atrial fibrillation) developed as a result of increased sympathetic tone during repeat laryngoscopy, with torsade de pointes resulting as a complication of the attempted treatment. It should be noted that the suggested dose of magnesium sulfate for treatment of torsade de pointes is 1-2 g IV, rather than the 0.5 g administered in this case [3,4].
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Steven Deem (1998) studied this question.
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