BACKGROUND: Hyperventilation during sevoflurane-N2O-O2 mask induction in adults is associated with a hyperdynamic circulatory response and epileptiform electroencephalogram (EEG). We tested the hypothesis that delaying onset of hyperventilation will prevent severe (periodic) epileptiform EEG and hyperdynamic response. METHODS:Thirty patients were randomized to receive either delayed (group D, n=15) or immediate (group I, n=15) onset of hyperventilation during sevoflurane (8% in N2O 50%) mask inhalation induction with single-breath method for unconsciousness. Fifteen patients were allowed to breathe spontaneously for 2 min after loss of consciousness and controlled hyperventilation (ETCO2 <4%) was started thereafter. In 15 patients controlled hyperventilation was started immediately after loss of consciousness. EEG was recorded, and mean arterial pressure (MAP) and heart rate (HR) registered. RESULTS:Epileptiform EEG patterns were seen in 13 patients in group I and in 9 patients in group D (n.s.). Periodic epileptiform discharges (PED) tended to occur more often in group I (P=0.07). Heart rate and MAP were higher in group I than in group D from 2 min to 3 min (P < 0.05), and both HR and MAP rose significantly from the baseline in group I. In group D, HR but not MAP rose significantly from baseline. CONCLUSION: Regardless of its timing, hyperventilation at a high sevoflurane concentration produced severe epileptiform EEG with a hyperdynamic response. PED tended to occur more often with immediate onset of hyperventilation.
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BACKGROUND: Hyperventilation during sevoflurane-N2O-O2 mask induction in adults is associated with a hyperdynamic circulatory response and epileptiform electroencephalogram (EEG). We tested the hypothesis that delaying onset of hyperventilation will prevent severe (periodic) epileptiform EEG and hyperdynamic response. METHODS: Thirty patients were randomized to receive either delayed (group D, n=15) or immediate (group I, n=15) onset of hyperventilation during sevoflurane (8% in N2O 50%) mask inhalation induction with single-breath method for unconsciousness. Fifteen patients were allowed to breathe spontaneously for 2 min after loss of consciousness and controlled hyperventilation (ETCO2 <4%) was started thereafter. In 15 patients controlled hyperventilation was started immediately after loss of consciousness. EEG was recorded, and mean arterial pressure (MAP) and heart rate (HR) registered. RESULTS:Epileptiform EEG patterns were seen in 13 patients in group I and in 9 patients in group D (n.s.). Periodic epileptiform discharges (PED) tended to occur more often in group I (P=0.07). Heart rate and MAP were higher in group I than in group D from 2 min to 3 min (P < 0.05), and both HR and MAP rose significantly from the baseline in group I. In group D, HR but not MAP rose significantly from baseline. CONCLUSION: Regardless of its timing, hyperventilation at a high sevoflurane concentration produced severe epileptiform EEG with a hyperdynamic response. PED tended to occur more often with immediate onset of hyperventilation.
Authors: Barbara Schultz; Christian Otto; Arthur Schultz; Wilhelm Alexander Osthaus; Terence Krauss; Thorben Dieck; Björn Sander; Niels Rahe-Meyer; Konstantinos Raymondos Journal: PLoS One Date: 2012-07-19 Impact factor: 3.240
Authors: Markus Abt; Theo Dinklo; Andreas Rothfuss; Elisabeth Husar; Robert Dannecker; Katja Kallivroussis; Richard Peck; Lucette Doessegger; Christoph Wandel Journal: Clin Pharmacol Ther Date: 2019-05-31 Impact factor: 6.875