Anesthesia for craniotomy with intraoperative awakening: how to avoid respiratory depression and hypertension?

The letter from Dr. Venkatesan (1) correctly notes that several months before publishing our article (2) in Anesthesia & Analgesia, Yildirim et al. (3) had published an article regarding the influence of desflurane on some variables of cardiac ventricular repolarization. Yildirim et al.’s paper was published after our manuscript had been submitted to Anesthesia & Analgesia, and we had no knowledge of their work at the time our work was submitted. However, in our opinion the patients in the Yildirim et al. study may not have received the equivalent of 1 MAC of anesthesia. Patients in that study ranged from 16 to 50 yr of age. Rampil et al. (4) determined 1 MAC of desflurane in 100% oxygen as 7.25 0.0 vol% in the 18–30-yr age range and 6.0 0.29 vol% in the 31–65-yr age group. This suggests that some patients in the Yildirim et al. study received 1 MAC of desflurane. Dr. Venkatesan suggested two mechanisms connected with use of volatile anesthetics that may prolong the QTc interval and induce arrhythmia: reduction of IK current for sevoflurane and an increase in transmural dispersion of repolarization for halothane. The first mechanism was also described for isoflurane and halothane (5). There was no increase in transmural dispersion of repolarization for sevoflurane in children (6). We are not familiar with any data on the mechanism of QTc prolongation with desflurane. It seems probable that the prolongation might be caused by the influence of desflurane on IK current, similar to that induced by sevoflurane and isoflurane. Moreover, transient increases in sympathetic activity from desflurane might further prolong the QTc interval. As suggested by Yildirim et al., potential arrhythmogenic effects of desflurane may be caused by increased dispersion of the QTc interval. Further research is required to fully understand the mechanisms of QTc prolongation with inhaled anesthetics.