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Background Sevoflurane may induce epileptiform electroencephalographic activity leading to unstable Bispectral Index numbers, underestimating the hypnotic depth of anesthesia. The authors developed a method for the quantification of epileptiform electroencephalographic activity during sevoflurane anesthesia. Methods Electroencephalographic data from 60 patients under sevoflurane mask induction were used in the analysis. Electroencephalographic data were visually classified. A novel electroencephalogram-derived quantity, wavelet subband entropy (WSE), was developed. WSE variables were calculated from different frequency bands. Performance of the WSE in detection and quantification of epileptiform electroencephalographic activity and the ability of the WSE to recognize misleading Bispectral Index readings caused by epileptiform activity were evaluated. Results Two WSE variables were found to be sufficient for the quantification of epileptiform activity: WSE from the frequency bands 4-16 and 16-32 Hz. The lower frequency band was used for monophasic pattern monitoring, and the higher frequency band was used for spike activity monitoring. WSE values of the lower and higher bands followed the time evolution of epileptiform activity with prediction probabilities of 0.809 (SE, 0.007) and 0.804 (SE, 0.007), respectively. In deep anesthesia with epileptiform activity, WSE detected electroencephalographic patterns causing Bispectral Index readings greater than 60, with event sensitivity of 97.1%. Conclusions The developed method proved useful in detection and quantification of epileptiform electroencephalographic activity during sevoflurane anesthesia. In the future, it may improve the understanding of electroencephalogram-derived information by assisting in recognizing misleading readings of depth-of-anesthesia monitors. The method also may assist in minimizing the occurrence of epileptiform activity and seizures during sevoflurane anesthesia.

Background This multicenter study evaluated the effect of a new depth of anesthesia-monitoring device based on time-frequency-balanced spectral entropy of electroencephalogram monitoring (GE Healthcare Finland, Helsinki, Finland) on consumption of anesthetic drugs and recovery times after anesthesia. Methods The study was a prospective, randomized, single-blind study performed in six hospitals in Finland, Sweden, and Norway. After institutional review board approval and written informed consent from each patient, the patients were randomly allocated to anesthesia with entropy values either shown (entropy group) or not shown (control group). Anesthesia was maintained with propofol, nitrous oxide, and alfentanil. In the entropy group, propofol was given to keep the state entropy value between 45 and 65, and alfentanil was given to keep the state entropy-response entropy difference below 10 units and heart rate and blood pressure within +/-20% of the baseline values. The control group patients were anesthetized to keep heart rate and blood pressure within +/-20% of the baseline values. Statistical methods included Mann-Whitney U test and unpaired t tests. Results A total of 368 patients were studied. In the entropy group, entropy values were higher during the whole operation and especially during the last 15 min (P < 0.001). Consequently, propofol consumption was smaller in the entropy group during the whole anesthesia period (P < 0.001) and especially during the last 15 min (P < 0.001). This shortened the time delay in the early recovery parameters in the entropy group. Conclusion Entropy monitoring assisted titration of propofol, especially during the last part of the procedures, as indicated by higher entropy values, decreased consumption of propofol, and shorter recovery times in the entropy group.

Ventilation of the lungs with isoflurane in nitrous oxide and oxygen has been shown to increase the plasma concentration of norepinephrine. Whether this increase is related to the tachycardia and increased arterial blood pressures, seen following a sudden increase in the concentration of isoflurane, was tested in humans.Twenty-two healthy patients in whom the trachea was intubated were given 15 min of stable isoflurane-O2-air anesthesia [end-tidal concentration of isoflurane (ETIso) of 1.3%] (baseline). Patients were then randomly allocated to one of two groups. For 13 "IsoHigh" patients, the inspired concentration of isoflurane was increased abruptly. In those patients, the ETIso was kept at 2.6% for 10 min, i.e., until the end of the study, after which the depth of anesthesia was reduced. For nine "IsoLow" control patients, the ETIso level of 1.3% was continued until the end of the study. Heart rate, arterial pressures, catecholamine levels, and end-tidal concentration of CO2 were recorded at baseline and at 1, 1.5, 2, 4, 6, and 10 min after increase in isoflurane.IsoHigh patients showed significant increases in heart rate (40% from 84.6 to 118.1 beats/min), systolic arterial pressure (SAP, 23%, from 96.4 to 118.3 mmHg), and diastolic arterial pressure (DAP, 30%, from 53.9 to 70.0 mmHg); all three variables peaked at 2 min. Significant increases occurred also in norepinephrine levels (80%, from 0.342 to 0.615 ng/ml) and in end-tidal concentration of CO2 (from 4.22% to 4.43%), both of which peaked at 4 min. Epinephrine levels did not increase significantly, although significant differences were seen between IsoHigh and IsoLow patients during the trial. IsoLow patients had no changes in these variables.A sudden increase in isoflurane concentration is associated with a transient but clinically significant increase in heart rate, arterial pressures, and norepinephrine concentration.

Cardiovascular collapse following intravascular bupivacaine may be resistant to treatment. The effect of amrinone on recovery from bupivacaine-induced severe cardiovascular depression was evaluated in 20 pigs (13-26 kg) in a placebo-controlled randomized double-blind study. Under 0.7% isoflurane anesthesia at FIO2 0.21, 0.5% bupivacaine 2 mg.kg-1.min-1 was infused until mean arterial pressure was 40% of the baseline. Cardiac output and heart rate decreased 75% and 50% from the baseline, respectively. The total dose of bupivacaine was 17 +/- 6 (SD) mg.kg-1 in the control and 19 +/- 5 mg.kg-1 in the amrinone group, resulting in mean plasma concentrations of 42 +/- 6 and 53 +/- 19 micrograms.ml-1, respectively. A bolus of amrinone 4 mg.kg-1 (n = 10) was given immediately after cardiovascular depression, followed by an infusion of 0.6 mg.kg-1.min-1. The control animals received corresponding volumes of physiologic saline (n = 10). After cardiovascular depression, the lungs were ventilated with FIO2 1.0 without anaesthetics or sympathomimetic support. Electric activity of the heart ceased in all control animals in 3.9 +/- 2 min after cardiovascular depression despite atropine and external cardiac compression. All animals in the control group and 5 of 10 animals in the amrinone group were given atropine (P less than 0.01). The animals receiving amrinone survived without cardiac compression (P less than 0.0001). During bupivacaine infusion, all animals developed burst suppression in the electroencephalogram. At the time of cardiovascular depression, in 8 of 10 control and in 6 of 10 amrinone animals, the electroencephalogram was isoelectric.(ABSTRACT TRUNCATED AT 250 WORDS)

Background Sevoflurane is suggested as a suitable anesthetic agent for mask induction in adults. The authors recently found that hyperventilation during sevoflurane-nitrous oxide-oxygen mask induction is associated with cardiovascular hyperdynamic response. We tested the hypothesis that the hyperdynamic response can be explained by electroencephalography (EEG) findings. Methods Thirty women were randomly allocated to receive sevoflurane-nitrous oxygen-oxygen mask induction using a single-breath method, followed by either spontaneous breathing (n = 15) or controlled hyperventilation (n = 15) for 6 min. EEG was recorded. Blood pressure and heart rate were recorded at 1-min intervals. Results Epileptiform EEG activity (spikes or polyspikes) was seen in all patients with controlled hyperventilation, and in seven patients with spontaneous breathing (P < 0.01). Jerking movements were seen in three patients with controlled hyperventilation. In the controlled hyperventilation group, heart rate increased 54% from baseline at 4 min after induction (P < 0.001). Mean arterial pressure increased 17% (P < 0.05), peaking at 3 min. In the spontaneous breathing group, heart rate showed no change, and mean arterial pressure decreased by 14% (P < 0.01) at 6 min. Heart rate and mean arterial pressure differed significantly between the groups from 2 min after beginning of the induction to the end of the trial. An increase in heart rate of more than 30% from baseline always was associated with epileptiform EEG activity. Conclusions Sevoflurane mask induction elicits epileptiform EEG patterns. These are associated with an increase in heart rate in patients with controlled hyperventilation and also during spontaneous breathing of sevoflurane.