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Paroxystic systemic hypertension during inhalation induction with sevoflurane 8%

Limoges, France

To the Editor:

The depth of anesthesia may be difficult to evaluate during mask induction with sevoflurane 8%. This may have major consequences in hypertensive patients. A paroxystic systemic hypertension was observed during single breath vital capacity induction of anesthesia with sevoflurane in a previously equilibrated hypertensive patient. This hypertension occurred despite two and a half minutes of inhalation of sevoflurane 8% in N₂O 50% (Figure 1A). Just before this hypertensive crisis, bispectral index value reached 65 and end-tidal concentration of sevoflurane 5.7%. Hypertension occurred at the time of insertion of a Guedel airway and lasted 3.5 min (peak arterial pressure: 337/201 min Hg) (Figures 1B-C). This was controlled by 20 µgkg^–1 alfentanil but was followed by hypotension and hypoxemia related to vasogenic pulmonary edema. The exact causes of such a hypertensive crisis remains to be elucidated. An increase in sympathetic reactivity in hypertensive patients as well as a nociceptive stimulus during light anesthesia may have triggered this hypertension already observed during anesthesia with sevoflurane.^1–3 A transient increase in sympathetic reactivity during induction with high concentrations of sevoflurane has been suggested by previous studies whereas a decrease in sympathetic reactivity has been measured during a progressive increase in sevoflurane up to 3% after propofol induction.^4–7 This adverse effect questions the use of sevoflurane inhalation without opioids for induction of anesthesia in hypertensive patients when considering the poor value of the bispectral index, of end-tidal concentration of sevoflurane or its duration of administration in predicting the depth of anesthesia and the hemodynamic reaction to nociceptive stimuli.

View larger version (59K): [in this window] [in a new window]   FIGURE 1 Continuous recording of arterial pressure and heart rate at the start of hypertensive crisis (Figure 1A), at its maximum (Figure 1B) and at the beginning of its decline when alfentanil was injected (Figure 1C).

References

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