This letter highlights the importance of considering alternative causes, such as proarrhythmic drugs and electrolyte imbalances, before attributing torsade de pointes to sevoflurane anesthesia.
To the Editor: We read with interest the report by Abe et al. [1] of torsade de pointes ventricular tachycardia (VT) during sevoflurane anesthesia. Although the authors state that this arrhythmia was induced by sevoflurane, other explanations are equally or more plausible. For example, the disopyramide that was used to treat atrial fibrillation may prolong the QT interval and produce torsade de pointes VT [2]. Administration by the IV route, plus the presence of hypokalemia, may have been further contributing factors. In addition, perhaps the patient actually had ischemia-induced polymorphic VT [3], which may be difficult to differentiate from torsade de pointes. Unfortunately, no heart rate or ST segment data are given, and only one blood pressure value was reported. The latter was certainly low, and hypotension may have also occurred during the atrial fibrillation and/or after the administration of disopyramide, a potent myocardial depressant. Likewise, tachycardia may have been associated with the atrial fibrillation, especially after the administration of disopyramide, which has a vagolytic effect on the AV node [4]. The implication that the torsade de pointes VT ended because the sevoflurane was discontinued is also poorly substantiated. Standard therapy for this arrhythmia was not given: there was no use of potassium, isoproterenol, or overdrive pacing, and only 0.5 g of magnesium was administered. For torsade de pointes VT, >1 g of magnesium may be necessary [3]. Although the torsade eventually subsided after the sevoflurane was discontinued, other events occurred at this time, as well. The fraction of inspired oxygen was increased to 100%, and the patient awakened from general anesthesia, which probably increased her blood pressure. Both of these events may have improved myocardial oxygen delivery, thereby terminating ischemia-induced polymorphic VT, if present. The absence of problems during a subsequent operation avoiding sevoflurane has little relevance because many other aspects of the second anesthetic differed from the first. Only by the administration of sevoflurane in a controlled manner, without the influences of proarrhythmic drugs, hypokalemia and ischemia, can one appropriately examine the potential causative effects of sevoflurane in the development of torsade de pointes VT. M. Denise Daley, MD, FRCPC, DABA Peter H.
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Daley et al. (1998) studied this question.
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