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Anesth Analg 2006;102:1094-1102 © 2006 International Anesthesia Research Society doi: 10.1213/01.ane.0000198509.55543.d6
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Abstract |
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In this randomized, double-blind, controlled study, we tested the hypothesis that nitrous oxide (N2O) affects bispectral index (BIS) and 95% spectral edge frequency (SEF95) in response to tracheal intubation during anesthesia with isoflurane and sevoflurane. In protocol 1, we randomly allocated 90 ASA physical status I patients to 6 groups (n = 15 each). Anesthesia was induced with isoflurane or sevoflurane with 0%, 33%, or 66% N2O. The concentration of isoflurane and sevoflurane was gradually increased and end-tidal concentrations were maintained at 1.1% and 1.7%, respectively. Tracheal intubation was performed 12 min after induction of anesthesia. BIS was significantly increased 1 min after tracheal intubation compared before laryngoscopy in patients receiving only isoflurane or sevoflurane (P = 0.001 and 0.007, respectively). In patients receiving 66% N2O-isoflurane or 66% N2O-sevoflurane, both BIS and SEF95 were significantly decreased after tracheal intubation and significantly lower than in those patients receiving only isoflurane or sevoflurane, respectively (P < 0.01 for both). In protocol 2, 3 µg/kg of IV fentanyl completely abolished the decrease of BIS and SEF95 after tracheal intubation during anesthesia with 66% N2O-isoflurane and 66% N2O-sevoflurane (n = 10). We conclude that 66% N2O induced a paradoxical decrease of BIS in response to tracheal intubation during anesthesia with isoflurane and sevoflurane.
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Introduction |
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Nitrous oxide (N2O) is a frequently used adjunct to general anesthesia. It decreases the minimum alveolar concentration of volatile anesthetics and the plasma concentration of IV anesthetics required for loss of consciousness, in addition to preventing the response to surgical incision (1–3). Processed electroencephalographic (EEG) variables such as bispectral index (BIS), 95% spectral edge frequency (SEF95), and relative ß ratio have been introduced for numeric evaluation of hypnosis and sedation. Of those variables, BIS correlates well with the level of responsiveness and provides an excellent prediction of the loss of consciousness and has been most extensively used (4). A previous study has shown that N2O has no effect on BIS or SEF95 when used alone (5). It was also documented that it did not change BIS when used as an adjunct to IV anesthetics (6,7). However, these studies were focused on monitoring only BIS change whereby the effect of N2O on EEG or other processed EEG variables during anesthesia with single volatile anesthetics remains unclear.
During anesthesia, EEG changes according to the level of anesthesia and in response to noxious stimuli. ‘Paradoxical arousal’ has been defined as the condition presenting with a marked decrease of EEG frequency and subsequent decrease of BIS induced by noxious stimuli such as surgical incision (8–11). Paradoxical arousal is observed during anesthesia with volatile anesthetics, particularly in combination with N2O (8–10). Although the mechanism is unknown, N2O activates the reticular formation in the brainstem, leading to a decrease of the EEG frequency (12,13), indicating that N2O plays an important role in inducing paradoxical arousal. Noxious stimuli usually enhance sympathetic activity and increase BIS (7,14,15). However, the use of N2O may contribute to a decrease of the BIS value in the presence of noxious stimuli. Given that BIS is routinely used for evaluating the levels of consciousness during anesthesia and, in particular, the BIS value is used for titration of the dose of anesthetics (16), it is important that the possible paradoxical effect of N2O on BIS should be elucidated.
Tracheal intubation, one of the most intense noxious stimuli during anesthesia, is responsible for a marked increase of sympathetic activity. In the present study, we investigated the hypothesis that N2O may affect EEG and BIS change in response to tracheal intubation during anesthesia with a single volatile anesthetic, either isoflurane or sevoflurane. For elucidating the concentration-dependent effect of N2O on the change of BIS and SEF95, we have evaluated these variables at small (33%) and large (66%) concentrations of N2O. Also, we have examined whether fentanyl pretreatment diminishes the paradoxical EEG changes induced by N2O as well as hemodynamic changes in response to tracheal intubation.
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Methods |
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Effect of N2O Added to Isoflurane and Sevoflurane on BIS and SEF95 (Protocol 1)
After obtaining approval from the Institutional Ethics Committee, we received written informed consent from 90 ASA physical status I patients aged 20–70 yr who were scheduled to undergo elective orthopedic or gynecological surgery. The study was conducted in a double-blind fashion. Excluded from the study were patients with abnormal electrocardiogram, cardiovascular, respiratory or psychological diseases, or with predicted difficulty in tracheal intubation. Other exclusion criteria included a regular use of hypnotic medication, drug or alcohol abuse, and obesity. Patients were randomly assigned to one of the following 6 groups (15 per group) according to which anesthetic mixture they received: isoflurane in oxygen (oxygen-isoflurane group); isoflurane and 33% N2O in oxygen (33% N2O-isoflurane group); isoflurane and 66% N2O in oxygen (66% N2O-isoflurane group); sevoflurane in oxygen (oxygen-sevoflurane group); sevoflurane and 33% N2O in oxygen (33% N2O-sevoflurane group); sevoflurane and 66% N2O in oxygen (66% N2O-sevoflurane group). Random allocation to these groups was made using a computer-generated random number table. No sedatives were given before surgery. Before anesthesia, a venous catheter was inserted and acetated Ringer’s solution was infused at a rate of 10 mL · kg–1 · h–1 throughout the study. Intraoperative monitoring consisted of a five-lead electrocardiogram, noninvasive measurement of arterial blood pressure, and pulse oximetry. EEG data were continuously monitored by a monitor (Model A-2000, version 3.34; Aspect Medical Systems, Newton, MA) using BisSensor strips (Aspect Medical Systems). The impedance of each electrode was maintained at <2 kiloohms. All binary data packets, containing raw wave data as well as BIS and SEF95, were recorded on a personal computer (LB500/J2; NEC Corporation, Tokyo, Japan) using Bispectrum Analyzer for BIS developed by Hagihira et al. (11) and analyzed later. Expired gas was collected via a sampling tube connected to the facemask at a rate of 200 mL/min. Carbon dioxide tensions and the concentrations of anesthetics were measured with a gas analyzer (Capnomac Ultima; Datex Instrumentrium Corp., Helsinki, Finland).
Anesthesia was induced via a facemask and a semiclosed circle system with a total gas flow of 6 L/min. End-tidal carbon dioxide tension was maintained at 35–40 mm Hg. The concentrations of isoflurane and sevoflurane were initially 0.3% and then increased slowly until the end-tidal concentration reached 1.1% and 1.7%, respectively. The concentrations of these two anesthetics were chosen according to their minimum alveolar concentrations and our previous experiences (14,17). After loss of consciousness, 0.1 mg/kg of vecuronium was given IV. No additional drugs were given, nor were other surgical procedure performed during the study period. Induction of anesthesia and tracheal intubation were performed by one of the authors (YO), who was able to know only the end-tidal concentration of anesthetics and carbon dioxide tension but blinded as to EEG, BIS, SEF95, mean arterial blood pressure (MAP), and heart rate (HR). Twelve minutes after the induction of anesthesia, the trachea was intubated and lungs were ventilated with the same concentration of anesthetics as before tracheal intubation. MAP, HR, BIS, and SEF95 were compared before the induction of anesthesia (baseline), 5 min after induction, immediately before laryngoscopy, and every minute until 5 min after intubation. These values were recorded by other authors (IH and KN) who were blinded as to group allocation.
Effect of Fentanyl on BIS and SEF95 During Anesthesia With 66% N2O and Isoflurane, Sevoflurane (Protocol 2)
We obtained written informed consent from 40 ASA physical status I patients, aged 20 to 70 yr. Inclusion and exclusion criteria were the same as those in protocol 1. Patients were randomly assigned to one of the following 4 groups (10 per group) according to which gas mixture they received and presence or absence of fentanyl: 66% N2O and isoflurane in oxygen with/without fentanyl (i.e., N2O-isoflurane-fentanyl and N2O-isoflurane groups, respectively); 66% N2O and sevoflurane in oxygen with/without fentanyl (i.e., N2O-sevoflurane-fentanyl and N2O-sevoflurane groups, respectively). Randomization was done as described previously. Anesthesia was induced as described in protocol 1. Five minutes after the induction of anesthesia, patients in N2O-isoflurane and N2O-sevoflurane groups received 5 mL of saline, whereas patients in N2O-isoflurane-fentanyl and N2O-sevoflurane-fentanyl groups received a bolus of fentanyl 3 µg/kg in a total volume of 5 mL that was indistinguishable from saline by its description. Saline or fentanyl solutions were prepared by one of the authors (KT) who did not participate in anesthesia or data collection. Other experimental procedures were the same as described in protocol 1.
The number of patients in each group of protocol 1 was determined based on our previous study (14). In that study, BIS increased from 39 ± 5 to 54 ± 10 after tracheal intubation. Power analysis on the assumption of a type I error protection of 0.05 and a power of 0.80 to detect a 20% change in BIS after tracheal intubation showed that 14 patients were required for each of the 3 groups receiving isoflurane or sevoflurane. The number of patients in each group in protocol 2 was determined on the basis of the study results of protocol 1. Ten patients were required in each group to detect a 20% increase of BIS by fentanyl, with a type 1 error of 0.05 and a power of 0.80. Patients’ characteristics and hemodynamic data are expressed as the mean ± sd. BIS and SEF95 data are expressed as median and quartiles (25th and 75th percentiles). Statistical analysis was performed using Sigmastat 3.0 (Systat Software Inc. Richmond, CA). Differences in sex ratios among the 6 groups in protocol 1 and 4 groups in protocol 2 were examined by 
2 test. Within-group differences in MAP and HR were examined by one-way analysis of variance. On the other hand, analysis of variance for repeated measures was used to examine differences in MAP and HR among the groups in both protocols. Within-group and between-group differences in BIS and SEF95 were examined by one-way analysis of variance on ranks, followed by Student-Newman-Keuls test. Within-group differences of BIS and SEF95 were examined only with the value before laryngoscopy. Values were considered significant when P < 0.05.
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Results |
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Effect of N2O Added to Isoflurane and Sevoflurane on BIS and SEF95 (Protocol 1)
There were no differences in patient characteristics or baseline hemodynamics among the 6 groups (Tables 1 and 2). The end-tidal concentrations of isoflurane and sevoflurane were increased to 1.1% and 1.7%, respectively, within 7 min of anesthesia induction and were stable throughout the study. End-tidal carbon dioxide tensions and isoflurane or sevoflurane concentrations before and after tracheal intubation were comparable among the oxygen-isoflurane, 33% N2O-isoflurane and 66% N2O-isoflurane groups or among the oxygen-sevoflurane, 33% N2O-sevoflurane and 66% N2O-sevoflurane groups, with no differences being found in these values before laryngoscopy and after tracheal intubation (Table 3). No patients had a systolic blood pressure less than 80 mm Hg or a HR slower than 50 bpm. None complained of awareness during anesthesia when questioned postoperatively. Laryngoscopy and tracheal intubation were performed within 20 s in all patients and there were no differences in the time required for these procedures among the groups (data not shown).
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MAP and HR were stable until the time of laryngoscopy and significantly increased after tracheal intubation compared with baseline and before laryngoscopy in all groups (P < 0.01 for all); however, there were no differences in overall changes of MAP or HR among the oxygen-isoflurane, 33% N2O-isoflurane, and 66% N2O-isoflurane groups or among the oxygen-sevoflurane, 33% N2O-sevoflurane, and 66% N2O-sevoflurane groups (Table 2).
BIS was between 96 and 98 at baseline and decreased during the induction of anesthesia, reaching below 50 in all patients before laryngoscopy. Slow 
waves with high amplitude (approximately 100 µV) with a marked decrease of BIS and SEF95 appeared during induction in 4 and 5 patients in the 66% N2O-isoflurane and 66% N2O-sevoflurane groups, respectively. Those slow waves disappeared within 5 min, and there were no differences in BIS among the oxygen-isoflurane, 33% N2O-isoflurane, and 66% N2O-isoflurane groups or among the oxygen-sevoflurane, 33% N2O-sevoflurane, and 66% N2O-sevoflurane groups before laryngoscopy; exceptionally, however, BIS at 5 min after anesthesia induction in the 33% N2O- and 66% N2O-sevoflurane groups was significantly lower than those in the oxygen-sevoflurane group. One minute after tracheal intubation, BIS values were significantly increased relative to those before laryngoscopy in the oxygen-isoflurane and oxygen-sevoflurane groups (P = 0.001 and 0.007, respectively), but significantly decreased in the 66% N2O-isoflurane and 66% N2O-sevoflurane groups (P = 0.004 and 0.002, respectively) (Fig. 1). Individual BIS values increased in 13, 14, 9, and 10 patients in the oxygen-isoflurane, oxygen-sevoflurane, 33% N2O-isoflurane, and 33% N2O-sevoflurane groups, respectively. On the other hand, BIS was decreased in 11 and 12 patients in the 66% N2O-isoflurane and 66% N2O-sevoflurane groups, respectively (Fig. 2). At 1 to 5 min after tracheal intubation, BIS was significantly lower in the 66% N2O-isoflurane and 66% N2O-sevoflurane groups compared with the oxygen-isoflurane and oxygen-sevoflurane groups, respectively (P < 0.01 for both).
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P < 0.05 and 
P < 0.01 compared with oxygen-isoflurane (A) or oxygen-sevoflurane (B) group at the same time point.
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SEF95 was decreased after the induction of anesthesia. Compared with the oxygen-isoflurane and oxygen-sevoflurane groups, it was significantly lower after tracheal intubation in the 33% N2O-isoflurane and 33% N2O-sevoflurane groups, besides being significantly lower both during induction of anesthesia and after tracheal intubation in the 66% N2O-isoflurane and 66% N2O-sevoflurane groups, respectively (Fig. 3). Throughout the study period, EEG burst suppression was not observed in any patient. In patients on 66% N2O, slow waves with high amplitude, which were transiently detected during induction of anesthesia, also appeared after tracheal intubation. Those slow waves were not seen in patients receiving only isoflurane or sevoflurane or in combination with 33% N2O (Fig. 4).
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Effect of Fentanyl Added to 66% N2O-Isoflurane and 66% N2O-Sevoflurane on BIS and SEF95 (Protocol 2)
There were no differences in patients’ characteristics or baseline hemodynamics among the 4 groups (Tables 4 and 5). MAP, HR, BIS, and SEF95 in the N2O-isoflurane and N2O-sevoflurane groups were comparable to those following the same experimental procedure in protocol 1. Increase of MAP and HR in response to tracheal intubation was completely suppressed by fentanyl, and there were no differences in these values 1-5 min after tracheal intubation relative to those before laryngoscopy in the N2O-isoflurane-fentanyl and N2O-sevoflurane-fentanyl groups (Table 5). Both BIS and SEF95 significantly decreased during induction of anesthesia in all groups. However, there were no differences in BIS or SEF95 after tracheal intubation compared with the values before laryngoscopy in the N2O-isoflurane-fentanyl or N2O-sevoflurane-fentanyl groups (Figs. 5 and 6), which were significantly decreased after tracheal intubation in the N2O-isoflurane and N2O-sevoflurane groups. Individual BIS was decreased in 8, 10, 4, and 4 patients in the N2O-isoflurane, N2O-sevoflurane, N2O-isoflurane-fentanyl, and N2O-sevoflurane-fentanyl groups, respectively, 1 min after tracheal intubation compared with BIS before laryngoscopy. Slow waves with high amplitude were observed during the induction of anesthesia in 3, 4, 4, and 3 patients in the N2O-isoflurane, N2O-isoflurane-fentanyl, N2O-sevoflurane, and N2O-sevoflurane-fentanyl groups, respectively; however, it was not seen in the N2O-isoflurane-fentanyl or N2O-sevoflurane-fentanyl groups after tracheal intubation (Fig. 4).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This is the first report evaluating the effect of N2O used in combination with a single volatile anesthetic on EEG change in response to tracheal intubation. As reported previously, BIS increased after tracheal intubation in most patients receiving only isoflurane or sevoflurane (14). Although such an increase of BIS was moderately suppressed by 33% N2O combined with either isoflurane or sevoflurane, it was more interesting to note that BIS was significantly decreased after tracheal intubation by 66% N2O combined with either isoflurane or sevoflurane (Fig. 1). Our results are entirely different from previous studies on IV anesthetics documenting that N2O had no effect on BIS or hemodynamic changes in response to tracheal intubation (6,7), albeit with limited findings that those studies examined only BIS and with the effect of N2O on EEG or other processed EEG variables remaining unclear.
In contrast to BIS, tracheal intubation did not affect SEF95 in patients receiving only isoflurane or sevoflurane, suggesting that it did not exert any significant effect on the frequency of EEG, as it did on BIS without N2O (Fig. 3). In contrast, 66% N2O in combination with isoflurane or sevoflurane significantly decreased SEF95 after tracheal intubation. These differences between BIS and SEF95 changes could be attributable to the different methods used for calculating these variables. SEF95 predominantly reflects the shift of EEG frequency, but does not quantify the degree of phase coupling between different frequency components within a signal as reflected in BIS (18).
The decrease of BIS and SEF95 observed in the present study apparently suggests that N2O increased the depth of anesthesia after tracheal intubation. However, sympathetic response induced by tracheal intubation, as shown by the increase of MAP and HR, was not suppressed by N2O. An increase of cardiac output leads to an increase of cerebral blood flow and may affect the pharmacokinetics of volatile anesthetics; however, the alveolar concentrations of poorly soluble drugs such as sevoflurane are the least sensitive to cardiac output changes (19). The unchanged end-tidal concentrations of anesthetics after tracheal intubation indicate that the plasma and intracerebral concentrations of anesthetics were not changed. In protocol 2, inhibition of hemodynamic changes by fentanyl failed to affect the end-tidal concentration of anesthetics (data not shown). Of importance is the fact that fentanyl suppressed the decrease of both BIS and SEF95 after tracheal intubation (Figs. 5 and 6), which is in contrast to the usual effect of fentanyl on the EEG (20). These findings suggest that the changes of EEG associated with the decrease of BIS observed in patients on 66% N2O with isoflurane or sevoflurane can be designated as paradoxical arousal induced by tracheal intubation.
Paradoxical arousal is caused by intense noxious stimuli such as surgical incision and intraabdominal irrigation, characterized by a shift of dominant frequency of EEG to slow waves with the resultant decrease of BIS (8–11). These EEG changes were counteracted by increasing the concentration of inhaled anesthetics or the addition of analgesics (8,9,11). In the present study, 3 µg/kg of fentanyl completely suppressed the increase of MAP and HR and inhibited the decrease of BIS, which is consistent with previous studies (8,11). These findings suggest that the decrease of BIS is the outcome of paradoxical arousal.
Interestingly, paradoxical arousal is usually observed during anesthesia with isoflurane or sevoflurane with N2O (8–10) but not with IV anesthetics (6,7). In the present study, 33% N2O did not affect BIS or SEF95 in response to tracheal intubation; however, 66% N2O decreased both BIS and SEF95 (Figs. 1 and 3), suggesting that a large concentration of N2O is responsible for inducing a paradoxical decrease of BIS in response to tracheal intubation. Although the reason for this is not clear, animal studies have shown that N2O stimulates the activity of reticular neurons in the brainstem, evolving in affecting the frequency of the EEG (12,13). Slowing of EEG frequency by N2O during the induction of anesthesia without noxious stimuli observed in the present study also supports these hypotheses, although there were wide interindividual variations in EEG frequency and these slow waves disappeared several minutes later. A large concentration (>5%) of isoflurane does not inhibit the activity of reticular neurons (21), but thiopental and propofol do at clinically used concentrations (22). These findings may explain the lack of EEG changes when N2O is concomitantly used with IV anesthetics.
Paradoxical arousal is often reported in the presence of insufficient analgesia (9,10). In the present study, BIS was lower than 50 in all patients before tracheal intubation, apparently indicating that the depth of anesthesia was deep enough. However, the increase of MAP and HR in combination with the paradoxical decrease of BIS suggests that the levels of anesthesia were not deep enough to inhibit the increase of sympathetic activity at the concentrations of isoflurane and sevoflurane used in the present study (1.1% and 1.7%, respectively). Both an increase in the concentration of inhaled anesthetics and administration of IV anesthetics or analgesics would be conducive to suppressing these changes despite a significant decrease of BIS.
Hagihira et al. (11) have shown that surgical incision does not significantly affect BIS or SEF95 during anesthesia with N2O-isoflurane and N2O-sevoflurane and have suggested that BIS is not as sensitive as bicoherence to detect noxious stimuli. In the present study, tracheal intubation, another kind of noxious stimuli, triggered a significant change in EEG and BIS. These differences suggest the possibility that laryngoscopy and tracheal intubation are more intense than surgical incision, as shown by the large increase of both MAP and HR in the present study. Differential pathways for conducting the stimuli caused by surgical incision and tracheal intubation to the central nervous system may also be responsible for the difference. Paradoxical decrease should be considered when an abrupt decrease of BIS in the presence of noxious stimuli occurs during anesthesia, particularly with N2O.
A major limitation of the present study is that the effect of N2O was examined at a single concentration of isoflurane and sevoflurane. Concentrations of volatile anesthetics are comparable with previous studies (11,14). Although BIS was significantly increased in patients who did not receive N2O after tracheal intubation, intraoperative awareness did not occur. At smaller concentrations, however, tracheal intubation would induce more remarkable increases of MAP, HR, and BIS, leading to cardiovascular complications or intraoperative awareness. At larger concentrations, a decrease of sympathetic activity would prevent the development of paradoxical arousal and possible change of EEG into ‘burst and suppression’ would disturb the proper interpretation of BIS.
In summary, 66% N2O added to 1.1% isoflurane or 1.7% sevoflurane significantly decreased BIS and SEF95 after tracheal intubation but failed to suppress the hemodynamic changes in response to tracheal intubation. Because the decrease of these variables was counteracted by fentanyl, this EEG change would be the result of paradoxical arousal. Careful monitoring of EEG wave is necessary when an abrupt decrease of BIS is observed in the presence of noxious stimuli.
We thank Dr. Mitsuji Matsushita, staff anesthesiologist at Hoshigaoka Koseinenkin Hospital, Hirakata, Osaka, Japan for technical assistance for processing data.
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Footnotes |
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Accepted for publication October 31, 2005.
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