Effects of halothane, enflurane, and isoflurane on somatosensory evoked potentials during nitrous oxide anesthesia

The effects of 0.5, 0.75, and 1 MAC of halothane, enflurane, and isoflurane in 60% nitrous oxide on somatosensory cortical evoked potentials were studied in 30 patients undergoing corrective surgery for scoliosis. The evoked potentials were averaged at the scalp from the electroencephalogram following repeated bilateral posterior tibial nerve stimulation at the ankle. Latencies and amplitudes of the resulting potentials were measured and compared with the post-induction control values. Graded increase in latencies and graded decrease in amplitudes were found with increasing concentrations of all the three agents (P less than 0.05), confirming that the effects were dose related. Reductions in amplitudes were more marked than increase in latencies. The authors conclude that, during nitrous oxide-based anesthesia, enflurane, and isoflurane resulted in less alteration of somatosensory cortical evoked potentials than halothane. In conjunction with 60% nitrous oxide, 0.5 and 0.75 MAC of halothane, 0.5, 0.75, and 1.0 MAC of isoflurane and enflurane, respectively, were found to be compatible with the generation of waves adequate for evaluation.     

DIFFERENTIAL EFFECTS OF PROPOFOL AND NITROUS OXIDE ON POSTERIOR TIBIAL NERVE SOMATOSENSORY CORTICAL EVOKED POTENTIALS DURING ALFENTANIL ANAESTHESIA

We have studied differential effects of propofol and nitrousoxide on posterior tibial nerve somatosensory evoked potentials(PTN-SEP) during a continuous infusion of alfentanil. In study1, 14 patients received initially 66% nitrous oxide in oxygen,which was replaced 90 min after incision by propofol 6 mg kg^–1h^–1. This substitution resulted in a significant increasein mean P1N1 amplitude from 1.01 (SD 1.14) µV to 2.61(2.17) µV (P < 0.01), while amplitudes of later peakswere unaffected. Latencies of peaks N1, P2 and N2 increasedafter the substitution. In study 2, 30 patients undergoing spinalsurgery received either alfentanil-nitrous oxide anaesthesia(group l, n = 15) or alfentanil-propofol anaesthesia (groupll, n = 15). P1N1 amplitude was significantly greater in groupll (3.24 (1.08) µV) than in group l (1.64 (0.97) µV)(P < 0.01). Latencies of peaks P2 and N2 were of significantlygreater duration in group II than in group I. Because earlycortical PTN-SEP peaks were preserved better during alfentanil-propofolanaesthesia we conclude that this combination may be a suitablealternative to alfentanil-nitrous oxide anaesthesia, when spinalcord function monitoring with PTN-SEP is indicated.     

DEPRESSION OF CORTICAL SOMATOSENSORY EVOKED POTENTIALS BY NITROUS OXIDE

The effects of the inhalation of50% nitrous oxide on somatosensoryevoked potentials during a fentanyf-oxygen anaesthetic techniquefor central nervous system surgery were evaluated. The latencyand amplitude of the first cortical wave were obtained usingconventional somatosensory techniques with median or posteriortibialnerve stimulation. Data were collected before and afterthe inhalation of 50% nitrous oxide in oxygen introduced atthe conclusion of the surgical procedure. The addition of nitrousoxide was associated with consistent decreases in the amplitudeof somatosensory evoked potentials, but with no significantchanges in latency. Since no electrical, physiological, or surgicalevent was associated with these changes, the results suggestthat they were attributable to nitrous oxide per se.     

The effect of nitrous oxide on the inhibition of somatosensory evoked potentials by sevoflurane in children

Inhalational anaesthetics inhibit somatosensory evoked potentials. The present study examined the effect of nitrous oxide in anaesthetic mixture with sevoflurane on the somatosensory evoked potential in children. Forty-five patients aged between 6 months and 6 years undergoing club foot surgery were studied to verify the influence of sevoflurane alone (21 patients) and sevoflurane with nitrous oxide (24 patients) on the somatosensory evoked potential. Fractional inspired concentration of nitrous oxide and fractional end-tidal (alveolar) sevoflurane were measured to estimate the multiples and submultiples of the minimal alveolar concentration (age corrected). The somatosensory evoked potential signals were obtained by stimulation of the median nerve. Nitrous oxide (FI = 0.63 +/- 2.5) with sevoflurane caused more reduction in the amplitude of somatosensory evoked potential waves and a greater increase in the latency of somatosensory evoked potential waves in comparison with sevoflurane alone. The results show that it is possible to obtain the inhibition of somatosensory evoked potential with smaller concentrations of sevoflurane, when it is used with nitrous oxide.     

SOMATOSENSORY AND AUDITORY EVOKED RESPONSES RECORDED SIMULTANEOUSLY: DIFFERENTIAL EFFECTS OF NITROUS OXIDE AND TSOFLURANE

Auditory (AER) and somatosensory evoked responses (SSER) wererecorded simultaneously in eight patients under anaesthesiabefore surgery. We studied the effects of equi-MAC end-expiratoryconcentrations of isoflurane (0.65–0.75%) and nitrousoxide (60–65%). The anaesthetics were changed at randomin three consecutive 10-min periods so that each patient receivedboth drugs. From the AER recorded from the vertex and inion.Pa and Nb latency and amplitude were measured. N13, P20 latencyand N13 amplitude were measured from SSER recordings from theneck and P15, N20. P25, N35, P45 latency and P15-N20, N20-P25,P25-N35 and N35-P45 amplitude from the scalp over the hand areaof the sensory cortex. Compared with nitrous oxide, isofluranesignificantly increased the latencies of the AER waves Pa (P= 0.02) andNb (P = 0.02), and the SSER waves N20 (P = 0.001)and P25 (P = 0.04). We were unable to demonstrate significantdifferences in Pa and Nb amplitude between isoflurane and nitrousoxide that we had seen previusly. However, the amplitude ofthe SSER wave N20 was reduced significantly by nitrous oxidecompared with isoflurane (P = 0.0004). This wave (N20) is thoughtto emanate from the thalamo-cortical radiations, and our findingsmay be explained by an analgesic effect of nitrous oxide mediatedby endogenous opioids. ^*Present address: Department of Anaesthesia, Royal Free Hospital,Pond Street, London NW3.     

BLOOD CONCENTRATIONS OF NITROUS OXIDE IN THEATRE PERSONNEL

Blood concentrations of nitrous oxide were measured in anaesthetists,surgeons and theatre nursus. Comparison of anaesthetists andsurgeons working in the same theatre showed that in ENT surgeonsconcentrations were greater (p<<0.01), while in generalsurgeons they were smaller (P<<0.003). Blood concentrationsof nitrous oxide in the "circulating" nurses were low; withscavenging they were unmeasurable. Atmogpheric concentrationsin the breathing zones were usually greater than the correspondmgblood concentrations, but this was not always true. However,a positive correlation between blood and atmospheric concentrationswas obrained (r = 0.82). Meticulous use of scavenging devicesproduced a mean reduction in blood nitrous oxide concentranonsof 86% for all groups. The mean blood concentration of nitrousoxide in anaesthetists when scavenging was used was 45 p.p.m.(1.9 µmol litre^–1).This figure should be taken intoaccount in establishing maximum permitted exposure to nitrousoxide.     

Effects of ketamine on somatosensory evoked potentials during nitrous oxide anesthesia in humans

The effects of ketamine with 60% nitrous oxide were studied on subcortical sensory evoked potentials recorded at Erb's point (N9), neck (N13) and on cortical potentials recorded at the scalp (N20) following median nerve stimulations in 7 neurologically normal patients. Latencies and amplitudes of the potentials were measured and compared with postinduction control values taken during inhalation of 60% nitrous oxide. Ketamine 2 mg.kg-1 (iv) was administered initially and incremental dose was 50 micrograms.kg-1.min-1. N20 latency decreased at 15, 30 minutes after ketamine administration from a control value of 18.7 +/- 0.9 msec to 18.2 +/- 1.1, 18.2 +/- 1.1 msec respectively, and N13-N20 interpeak latency decreased from 6.0 +/- 0.4 msec to 5.5 +/- 0.7, 5.4 +/- 0.7 msec (mean +/- SD). The author concluded that during nitrous oxide-based anesthesia, ketamine did not inhibit specific thalamoneocortical pathways.     

EFFECTS OF NITROUS OXIDE ON AUDITORY CORTICAL EVOKED POTENTIALS AND SUBJECTIVE THRESHOLDS

This study has examined the effects of inhaled nitrous oxideon the N1 and P2 components of the cortical auditory evokedpotentials (AEP) in the latency interval 80–300 ms afterthe stimulus. The amplitudes, latencies and thresholds of theAEP were measured at a range of end-tidal nitrous oxide concentrations(0%, 10%, 20%, 40%) in 10 subjects with normal hearing. Systematicdecreases in amplitude and latency were observed with an increasein threshold. A study of the effect of stimulus intensity onAEP amplitude showed that the amplitude change with nitrousoxide was accounted for largely by systematic increase in evokedpotential threshold. Subjective pure tone thresholds were notaffected by the concentrations of nitrous oxide used, indicatingthat the AEP changes were independent of subjective hearinglevel. ^*Present address: St Thomas' Hospital, Lambeth Palace Road,London SE1 7EH.     

Median nerve evoked responses and explicit memory during recovery from isoflurane/nitrous oxide anesthesia

PURPOSE: To evaluate median nerve somatosensory evoked responses during recovery from anesthesia in relation to clinical findings. METHODS: Twenty-two gynecologic patients received isoflurane in nitrous oxide for anesthesia. Midlatency somatosensory evoked responses (N20, P25, N35, P45, N50) were recorded the day before surgery (AWAKE), during steady state anesthesia (STABLE), and every five minutes after discontinuation of anesthesia until the patients were able to name a shown object correctly (RECOVERY). Next day the patients were questioned with a structured interview about their explicit memory of the immediate recovery period and classified into groups: No-MEM (no memory) and MEM (memory). Multivariate analysis of variance compared electrophysiological parameters at the different time points and between the two memory groups. RESULTS: During STABLE isoflurane/N2O anesthesia, all cortical amplitudes were reduced (P< or =0.003) and all latencies were prolonged compared with AWAKE (P<0.001). At RECOVERY the latencies N35, P45, N50 remained prolonged (P< or =0.001), while the amplitudes N20P25 and P45N50 were reduced in comparison to AWAKE (P< or =0.02). The latencies P45 (48+/-8 vs. 61+/-9 msec) and N50 (67+/-12 vs. 81+/-10 msec) were shorter in the patients of the group MEM (P< or =0.03) at RECOVERY. CONCLUSION: The reversibility of anesthetic induced changes in amplitudes and latencies of median nerve somatosensory evoked responses reflected clinical awakening during emergence from isoflurane/nitrous oxide anesthesia. In the patients who had recall for the immediate recovery period, the reversibility of anesthetic induced changes of components P45 and N50 was faster than in patients without recall.     

Variability of somatosensory cortical evoked potentials during spinal surgery. Effects of anesthetic technique and high-pass digital filtering

The effects of anesthetic technique (nitrous oxide or propofol) and high-pass digital filtering on within-patient variability of posterior tibial nerve somatosensory cortical evoked potentials (PTN-SCEP) were compared prospectively in two groups of 20 patients undergoing spinal surgery. Average P1N1 amplitude was significantly higher and P1N1 amplitude variability lower during propofol/alfentanil anesthesia than during nitrous oxide/alfentanil anesthesia. Off-line 30-Hz high-pass digital filtering significantly reduced P1N1 amplitude variability without decreasing P1N1 amplitude. In 93 patients studied retrospectively, a significant negative logarithmic correlation (r = -0.77) was observed between P1N1 amplitude and P1N1 amplitude variability. This study shows the importance of maintaining the highest possible PTN-SCEP amplitudes during spinal surgery. Propofol/opioid anesthesia may be an alternative anesthetic technique to nitrous oxide/opioid anesthesia during spinal cord function monitoring.     

EFFECT OF HALOTHANE AND NITROUS OXIDE ANAESTHESIA ON NATURAL KILLER LYMPHOCYTES FROM PATIENTS WITH BENIGN AND MALIGNANT BREAST DISEASE

The effect of halothane and nitrous oxide on the capacity ofnatural killer (NK) lymphocytes from female patients with benignand malignant breast disease to kill the tumour cell line K562,was studied in vitro. There was no depression of activity ofNK lymphocytes when exposed to 2 % halothane and 66% nitrousoxide either alone or in combination. However, NK lymphocyteactivity was depressed at higher concentrations of halothaneand the decrease in activity was significant (P < 0.01) when4% halothane was used. These findings suggest that exposureto clinically-used concentrations of halothane and nitrous oxidedoes not interfere with the NK lymphocyte response of the host.     

Nitrous oxide in neuroanaesthesia: an appraisal

A handful of recent publications have brought relevant contributions to the ongoing debate over the use of nitrous oxide in neuroanaesthesia. The present article reviews these publications. The question of whether nitrous oxide can be safely used in patients with reduced cerebral compliance and the relationship between hypocapnic vasoconstriction and nitrous oxide are discussed. The implications of the use of nitrous oxide during evoked potentials recording (motor evoked potentials and somatosensory evoked potentials) are discussed. The possible harmful effect of nitrous oxide in cerebral ischaemia is debated.     

Reappraisal of the role of motor and somatosensory evoked potentials during open distal aortic repair

ObjectiveIntraoperative motor and somatosensory evoked potentials have been applied to monitor spinal cord ischemia during repair. However, their predictive values remain controversial. The purpose of this study was to evaluate the impact of motor evoked potentials and somatosensory evoked potentials on spinal cord ischemia during open distal aortic repair.MethodsOur group began routine use of both somatosensory evoked potentials and motor evoked potentials at the end of 2004. This study used a historical cohort design, using risk factor and outcome data from our department's prospective registry. Univariate and multivariable statistics for risk-adjusted effects of motor evoked potentials and somatosensory evoked potentials on neurologic outcome and model discrimination were assessed with receiver operating characteristic curves.ResultsBoth somatosensory evoked potentials and motor evoked potentials were measured in 822 patients undergoing open distal aortic repair between December 2004 and December 2019. Both motor evoked potentials and somatosensory evoked potentials were intact for the duration of surgery in 348 patients (42%). Isolated motor evoked potential loss was observed in 283 patients (34%), isolated somatosensory evoked potential loss was observed in 18 patients (3%), and both motor evoked potential and somatosensory evoked potential loss were observed in 173 patients (21%). No spinal cord ischemia occurred in the 18 cases with isolated somatosensory evoked potential loss. When both signals were lost, signal loss happened in the order of motor evoked potentials and then somatosensory evoked potentials. Immediate spinal cord ischemia occurred in none of those without signal loss, 4 of 283 (1%) with isolated motor evoked potential loss, and 15 of 173 (9%) with motor evoked potential plus somatosensory evoked potential loss. Delayed spinal cord ischemia occurred in 12 of 348 patients (3%) with intact evoked potentials, 24 of 283 patients (8%) with isolated motor evoked potentials loss, and 27 of 173 patients (15%) with motor evoked potentials + somatosensory evoked potentials loss (P < .001). Motor evoked potentials and somatosensory evoked potentials loss were each independently associated with spinal cord ischemia. For immediate spinal cord ischemia, no return of motor evoked potential signals at the conclusion of the surgery had the highest odds ratio of 15.87, with a receiver operating characteristic area under the curve of 0.936, whereas motor evoked potential loss had the highest odds ratio of 3.72 with an area under the curve of 0.638 for delayed spinal cord ischemia.ConclusionsSomatosensory evoked potentials and motor evoked potentials are both important monitoring measures to predict and prevent spinal cord ischemia during and after open distal aortic repairs. Intraoperative motor evoked potential loss is a risk for immediate and delayed spinal cord ischemia after open distal aortic repair, and somatosensory evoked potential loss further adds predictive value to the motor evoked potential.     

Visual evoked potentials and nitrous oxide-induced neuronal depression: role for benzodiazepine receptors

We have examined the role of benzodiazepine receptors in nitrous oxide- induced neuronal depression in rats. The changes in neuronal excitability induced by nitrous oxide and the benzodiazepine inverse agonist, Ro15-4513, were monitored by measurement of visual evoked potentials (VEP). Administration of Ro15-4513 10 mg kg-1 i.p., in rats breathing air, did not affect the amplitude or latency of VEP. However, the same concentrations of Ro15-4513 antagonized nitrous oxide-induced depression of VEP amplitudes. We conclude that antagonism of nitrous oxide-induced depression by Ro15-4513 indicates that at least part of the decreased neuronal excitability caused by nitrous oxide could be ascribed to interactions with the GABAA receptor complex.      

Nitrous oxide has different effects on the EEG and somatosensory evoked potentials during isoflurane anaesthesia in patients

Background: Electroencephalogram (EEG) and somatosensory evoked potentials (SEPs) are altered by inhalation anaesthesia. Nitrous oxide is commonly used in combination with volatile anaesthetics. We have studied the effects of nitrous oxide on both EEG and SEPs simultaneously during isoflurane burst-suppression anaesthesia.
Methods: Twelve ASA I-II patients undergoing abdominal or orthopaedic surgery were anaesthetized with isoflurane by mask. After intubation and relaxation the isoflurane concentration was increased to a level at which an EEG burst-suppression pattern occurred (mean isoflurane end-tidal concentration 1.9 (SD 0.2) %. With a stable isoflurane concentration, the patients received isoflurane-air-oxygen and isoflurane-nitrous oxide-oxygen (FiO₂ 0.4) in a randomized cross-over manner. EEG and SEPs were simultaneously recorded before, and after wash-out or wash-in periods for nitrous oxide. The proportion of EEG suppressions as well as SEP amplitudes for cortical N₂₀ were calculated.
Results: The proportion of EEG suppressions decreased from 53.5% to 34% ( P < 0.05) when air was replaced by nitrous oxide. At the same time, the cortical N₂₀ amplitude was reduced by 69% ( P < 0.01).
Conclusion: The results suggest that during isoflurane anaesthesia, nitrous oxide has a different effect on EEG and cortical SEP at the same time. The effects of nitrous oxide may be mediated by cortical and subcortical generators.     

Differential effects of nitrous oxide and propofol on myogenic transcranial motor evoked responses during sufentanil anaesthesia

We have compared the effects of 50% nitrous oxide and propofol, each administered concurrently with sufentanil, on the amplitudes and latencies of the compound muscle action potential (CMAP) response to transcranial electrical stimulation. Using a crossover design, 12 patients undergoing spinal surgery were exposed to both 50% nitrous oxide and propofol, the latter in a bolus-infusion regimen. Six patients received nitrous oxide first and six received propofol first. CMAP were recorded from the tibialis anterior muscle in response to both single and paired transcranial electrical stimuli. With single pulse stimulation, median CMAP amplitude was significantly greater during administration of nitrous oxide than propofol (nitrous oxide 335 (10th-90th percentiles 35-849) microV; propofol 36 (0-251) microV) (P < 0.01). With paired stimulation, there was no significant difference in CMAP amplitude during the two regimens (nitrous oxide 1031 (296-1939) microV; propofol 655 (0-1867) microV). The results indicate that propofol caused more depression of transcranial electrical motor evoked responses than 50% nitrous oxide but that the difference was probably clinically unimportant when a paired stimulation paradigm was used.      

Etidocaine and extradural somatosensory evoked potentials after posterior tibial nerve stimulation

We have examined the effects of lumbar extradural administrationof 1% etidocaine 10 ml on somatosensory evoked potentials toposterior tibial nerve stimulation measured in the cervicalextradural space. Eight patients, anaesthetized with propofoland nitrous oxide, were studied before hysterectomy and a controlgroup received a similar anaesthetic and 0.9% sodium chloridesolution 10 ml in the lumbar extradural space. Etidocaine decreasedsignificantly overall amplitude of the evoked potentials andthe amplitudes of all peaks, between 30 and 50 min after extraduralinjection. The effects of etidocaine on spinal cord conductionwere greater than those found previously for lignocaine andbupivacaine, suggesting that it is the local analgesic of choicefor inhibiting afferent conduction.     

Evoked potentials following diazepam or fentanyl

The effects of fentanyl or diazepam on somatosensory, visual and brainstem auditory evoked potentials were studied in 13 healthy patients scheduled for elective surgery. Following control recordings of evoked potentials, either diazepam 20 mg or fentanyl 200 micrograms was administered intravenously. Evoked potentials were then recorded twice in the subsequent hour. No significant changes occurred in the latency or amplitude of somatosensory, visual or brainstem auditory evoked potentials. Although dose-related changes in evoked potential latencies and amplitudes have been demonstrated with both the inhalational and intravenous anaesthetics, these changes did not occur with diazepam or fentanyl used alone. An anaesthetic technique based on these two drugs would be suitable when intra-operative evoked potential monitoring is required to assess ischaemia and preservation of evoked responses.     

Effects of halothane, enflurane, and isoflurane in nitrous oxide on multilevel somatosensory evoked potentials

The effects of halothane, enflurane, and isoflurane were studied at 0.5, 0.75, and 1 MAC in 60% N2O on subcortical sensory evoked potentials recorded at the popliteal fossa (PF), the spine (L-3, C-6) and on cortical potentials recorded at the scalp (SC) following bilateral posterior tibial nerve stimulations at the ankle in 28 patients undergoing scoliosis surgery. Latencies and amplitudes of the resulting potentials at each level were compared with postinduction control values. With increasing MAC, latency and amplitude changes seen at C6 (subcortical) were also compared with those at SC (cortical). Increasing the concentrations of each agent resulted in a graded increase in latency and a graded decrease in amplitude, at all levels. At SC each increase in MAC with each agent resulted in an increase in latency (P less than 0.05) and a decrease in amplitude (P less than 0.005), respectively. The increases in SC latency at 0.75, 1 MAC were larger than the increase in latency at C-6 (P less than 0.005) and the decreases in SC amplitudes at 0.5, 0.75 and 1 MAC were greater than the decrease in amplitude at C-6 (P less than 0.01). Halothane, enflurane, and isoflurane in 60% N2O altered subcortical potentials less than cortical potentials. Enflurane and isoflurane at 0.5, 0.75, and 1 MAC, and halothane at 0.5, 0.75 MAC maintained subcortical and cortical potentials that were adequate for evaluation. However, 1 MAC of halothane suppressed cortical potentials but maintained subcortical potentials. Subcortical C-6 potential may serve as an additional monitor.     

Effect of fentanyl and enflurane on sensory evoked potentials in the human in basic flunitrazepam/N2O anesthesia

The use of evoked potential recording is commonly employed for monitoring peripheral and central sensory functions during neurosurgical procedures. However, the neuronal structures studied must not be changed by the anesthetic agents used. In this connection, the influence of two anesthetics, fentanyl and enflurane, on evoked potentials was investigated under basic anesthesia. A total of 60 patients undergoing lumbar disc removal were included in the study. Somatosensory (SEP), auditory (AEP), and visual (VEP) evoked potentials were each recorded in 20 patients the day before operation. Basic anesthesia was induced with flunitrazepam, nitrous oxide, and pancuronium bromide. Following induction, recordings of evoked potentials were again made. One half of each group of 20 patients received increasing doses of fentanyl (1.8, 3.6, and 7.2 micrograms/kg in the somatosensory and auditory groups; 4.0 and 8.0 micrograms/kg in the visual group). The other half was given increasing inspiratory concentrations of enflurane (0.5, 1.0, and 1.5 vol.%). At each level of anesthesia, SEPs, AEPs or VEPs were recorded. As compared with preoperative recordings, post-stimulus latencies were virtually unaffected by the basic anesthesia. Fentanyl caused little increase in the latencies of middle-latency-SEPs and of peak P2 of the VEPs. With enflurane, however, the latencies of the SEPs were dose-dependently prolonged, in particular those of the later components (P25 to N55). The same was true for the peak P2 in the VEPs. AEPs were not changed at all. From the results it can be concluded that enflurane, but not fentanyl, impairs impulse conduction in central synaptic pathways.(ABSTRACT TRUNCATED AT 250 WORDS)