Systemic lidocaine and human somatosensoryevoked potentials during sufentanil-isoflurane anaesthesia

The effect of systemically administered lidocaine on somatosensory evoked potentials (SSEPs) during general anaesthesia has not been widely reported. Knowledge of the influence of anaesthetic agents on evoked potentials assists in interpreting evoked potential waveforms. Accordingly, we studied the behaviour of cortical and subcortical (recorded at the second cervical vertebra) SSEPs after administration of intravenous lidocaine (3 mg.kg-1 bolus followed by infusion at 4 mg.kg-1.hr-1) during a sufentanil-based anaesthetic regimen in 16 patients undergoing abdominal or orthopaedic surgery. When compared to awake baseline recordings, the sufentanil-nitrous oxide, low-dose isoflurane anaesthetic depressed N1 amplitude by approximately 40% and prolonged latency by 10%. Fifteen minutes after establishment of this anaesthetic, the amplitude and latency of N1 were 1.13 +/- 0.56 microV and 19.81 +/- 1.63 msec, respectively. Within five minutes of adding lidocaine, amplitude decreased further to 0.84 +/- 0.39 microV (P = 0.001), while latency was extended to 20.44 +/- 1.48 msec (P = 0.01). Lidocaine did not affect cervical amplitude and prolonged latency only minimally. Despite the observed effects on amplitude and latency, SSEP waveforms were preserved and interpretable. Plasma lidocaine levels obtained at 5, 20, and 40 minutes after lidocaine were 5.17 +/- 1.33, 3.76 +/- 1.14, and 3.66 +/- 0.9 micrograms.dl-1, respectively. Our results indicate that systemically administered lidocaine at therapeutic plasma levels acts synergistically with a sufentanil-based anaesthetic to depress the amplitude and prolong the latency of SSEPs.     

Hypothermia Does Not Alter Somatosensory Evoked Potential Amplitude and Global Cerebral Oxygen Extraction during Marked Sodium Nitroprusside-induced Arterial Hypotension

Background: To prevent neurologic damage, monitoring cerebral function by somatosensory evoked potentials is used in selected settings. Excision of intraocular melanoma provides a unique opportunity to assess independently during anesthesia the effects on median nerve somatosensory evoked potentials (MN-SSEPs) and cerebral oxygen extraction of sodium nitroprusside-evoked arterial hypotension with and without hypothermia.

Methods: Median nerve somatosensory evoked potentials, arterial pressure, jugular venous bulb oxygen saturation (Sjo2) and lactate concentration, and arterial-jugular bulb oxygen content difference were assessed during propofol-remifentanil anesthesia under sodium nitroprusside-evoked arterial hypotension (mean arterial pressure, 40 mmHg) with and without surface hypothermia (32[degrees]C) in 11 otherwise healthy patients undergoing resection of choroidal melanoma.

Results: Hypothermia alone did not affect peak-to-peak amplitude of N20/P25 but prolonged cortical latency of N20 (22.6 +/- 2.2 vs. 25.9 +/- 2.5 ms, P < 0.05), cervical latency of N13 (14.3 +/- 1.2 vs. 15.7 +/- 1.6 ms, P < 0.05), and central conduction time (8.3 +/- 1.4 vs. 10.2 +/- 1.6 ms, P < 0.05). Evoked arterial hypotension did not depress MN-SSEP N20/P25 amplitude either with or without hypothermia (-0.31 vs. -0.28 [mu]V, P > 0.05) or alter latency (0.08 vs. 0.1 ms, P > 0.05). Furthermore, hypotension with or without hypothermia did not change Sjo2, arterial-jugular bulb oxygen content difference, or lactate concentration.     

Hypothermia does not alter somatosensory evoked potential amplitude and global cerebral oxygen extraction during marked sodium nitroprusside-induced arterial hypotension

BACKGROUND: To prevent neurologic damage, monitoring cerebral function by somatosensory evoked potentials is used in selected settings. Excision of intraocular melanoma provides a unique opportunity to assess independently during anesthesia the effects on median nerve somatosensory evoked potentials (MN-SSEPs) and cerebral oxygen extraction of sodium nitroprusside-evoked arterial hypotension with and without hypothermia. METHODS: Median nerve somatosensory evoked potentials, arterial pressure, jugular venous bulb oxygen saturation (Sjo(2)) and lactate concentration, and arterial-jugular bulb oxygen content difference were assessed during propofol-remifentanil anesthesia under sodium nitroprusside-evoked arterial hypotension (mean arterial pressure, 40 mmHg) with and without surface hypothermia (32 degrees C) in 11 otherwise healthy patients undergoing resection of choroidal melanoma. RESULTS: Hypothermia alone did not affect peak-to-peak amplitude of N20/P25 but prolonged cortical latency of N20 (22.6 +/- 2.2 vs. 25.9 +/- 2.5 ms, P < 0.05), cervical latency of N13 (14.3 +/- 1.2 vs. 15.7 +/- 1.6 ms, P < 0.05), and central conduction time (8.3 +/- 1.4 vs. 10.2 +/- 1.6 ms, P < 0.05). Evoked arterial hypotension did not depress MN-SSEP N20/P25 amplitude either with or without hypothermia (-0.31 vs. -0.28 microV, P > 0.05) or alter latency (0.08 vs. 0.1 ms, P > 0.05). Furthermore, hypotension with or without hypothermia did not change Sjo(2), arterial-jugular bulb oxygen content difference, or lactate concentration. CONCLUSIONS: Thus, hypothermia to 32 degrees C does not alter MN-SSEP amplitude and global cerebral oxygen extraction during marked sodium nitroprusside-induced arterial hypotension with a mean arterial pressure of 40 mmHg but prolongs MN-SSEP latencies during propofol-remifentanil anesthesia in individuals without cerebrovascular disease.     

Comparison of propofol with thiopental and isoflurane for induction and maintenance of general anesthesia

Propofol, a phenol compound with a short elimination half-life, was compared with thiopental and isoflurane for induction and maintenance of general anesthesia in 60 consenting ASA I, II, and III patients. The study was randomized and open label in design. Hemodynamically, the propofol patients showed a mean +/- SEM decrease in systolic blood pressure in comparison with the thiopental/isoflurane group at 2 (115.1 +/- 4.9 vs. 136.6 +/- 6.0 mmHg), 3 (125.7 +/- 5.1 vs. 149.4 +/- 5.6 mmHg), and 5 min (126.6 +/- 3.8 vs. 144.4 +/- 6.1 mmHg) postinduction and at intubation (135.2 +/- 4.7 vs. 157.8 +/- 6.0 mmHg) (p less than 0.05). The heart rate was lower in the propofol group throughout the induction period (p less than 0.05). Patients who received propofol were ready for discharge from the recovery room sooner (67.9 +/- 4.0 vs. 80.0 +/- 3.6 min) than the thiopental/isoflurane-treated patients (p less than 0.05). Propofol is as safe and effective for induction and maintenance of general anesthesia as thiopental and isoflurane.     

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.     

Changes of latency and amplitude of short latency somatosensory evoked potentials during slow induction of anesthesia with sevoflurane

In the present study, changes of latency and amplitude of short latency somatosensory evoked potentials (SSEPs) were evaluated continuously during slow induction of anesthesia from sevoflurane awake to deep levels of anesthesia in eight scheduled surgical patients. Not consistent with other previous investigations, the latency of N20 was significantly shortened with sevoflurane after 25 minutes from the beginning of inhalation compared with the awake control levels. No increase of latency was observed. The amplitudes of N20 were decreased with sevoflurane anesthesia in relation to duration of anesthesia. These results suggest that sevoflurane alone might have no marked pharmacological properties to change the latency of SSEPs even in the deep level of anesthesia.     

Effect of time and dose on scalp-recorded somatosensory evoked potential wave augmentation by etomidate

Bolus etomidate transiently increases the amplitude of scalprecorded somatosensory evoked potentials (SSEPs). The reproducibility of this augmentation and its dose-response relationship are unknown. In unpremedicated patients, we studied the effect on the SSEP of repetitive administration of single doses of etomidate (0.1 mg/kg i.v. bolus) in six patients and increasing doses of etomidate in six additional patients. Anesthesia was induced with fentanyl (15-20 microg/kg i.v.) plus thiopental (1-2 mg/kg i.v.) and maintannined with 0.4-0.8% isoflurane in oxygen, and the surgical incision was infiltrated with bupivicaine (0.5% without epinephrine). Etomidate administration was delayed for 30 min following anesthesia induction. In group 1, 0.1 mg/kg etomidate was administered intravenously as a bolus three times at 30-min intervals. In group 2, 0.05, 0.1, or 0.2 mg/kg was administered at 30-min intervals in random order in each patient. SSEPs were measured immediately before and once each minute for 5 min after etomidate administration following nondominant median nerve stimulation. In group 1, administration of 0.1 mg/kg etomidate (three trials) increased latency of an early negative wave (N20; latency approximately 20 ms) and a positive wave following N20 (P23; latency approximately 23 ms) by 1.0-1.4 and 1.3-2.6 ms, respectively (p < 0.05). P15N20 amplitude was increased by approximately 50% (range 36-76%; p < 0.05) and N20P23 amplitude was increased to 174% of control (range 173-178%; p < 0.05) and the amplitude increase was similar during the three etomidate administrations for both P15N20 and N20P23. Latency remained elevated by approximately 1.5 ms and amplitude remained elevated (P15N20 = 138%; N20P23 = 150%) 5 min following injection. Mean arterial blood pressure was unchanged by 0.1 mg/kg etomidate. In group 2, 0.05 mg/kg etomidate altered neither amplitude nor latency. However, 0.1 and 0.2 mg/kg increased N20P23 amplitude to 161 +/- 33 and 230 +/- 10% of control (p < 0.05), respectively. N20 and P23 latency were increased by 0.1 mg/kg etomidate by approximately 1.0 ms, while 0.2 mg/kg increased N20 latency by 1.0 ms and P23 latency by 1.5 ms. Bolus administration of etomidate (0.1 mg/kg) reproducibly increased SSEP amplitude and a larger dose (0.2 mg/kg) further increased amplitude augmentation. Thus, intermittent injection of etomidate can be used to augment small SSEP waves with reproducible increases in wave amplitude.     

Effects of adenosine triphosphate (ATP) on somatosensory evoked potentials in humans anesthetized with isoflurane and nitrous oxide

In order to examine the usefulness of adenosine triphosphate (ATP) as an adjuvant to anesthesia for surgery requiring intraoperative somatosensory evoked potential (SSEP) monitoring, we have studied the effects of ATP on SSEPs in patients anesthetized with isoflurane and nitrous oxide (N₂O). A control recording of SSEP was performed while anesthesia was maintained with 0.5% end-tidal concentration of isoflurane in 60% N₂O. The recordings were repeated after an ATP infusion had been added to this basal anesthesia at the rates of 100 μgkg bw^-1 min^-1 and 200 μg kg bw^-1 min^-1. SSEP was also studied when end-tidal isoflurane concentration was increased to 1.5% after cessation of ATP infusion. An infusion of ATP combined with 0.5% isoflurane and 60% N₂O effectively inhibited an increase in blood pressure during surgery. The amplitude of the cortical component of SSEP was lowered by 1.5% isoflurane, which also increased both cortical and spinal latencies as well as central conduction time (CCT). In contrast ATP infusions at both rates induced no significant changes in latencies, amplitude and CCT. The results indicate that ATP infusion combined with 0.5% isoflurane in 60% N₂O can be a useful anesthetic technique for intraoperative SSEP monitoring because adequate anesthetic depth can be maintained by a low concentration of anesthetics without further suppression of SSEPs.     

The Effect of Isoflurane, Halothane, Sevoflurane, and Thiopental/Nitrous Oxide on Respiratory System Resistance after Tracheal Intubation

Background: After tracheal intubation, lung resistance and therefore respiratory system resistance (Rrs) routinely increase, sometimes to the point of clinical bronchospasm. Volatile anesthetics generally have been considered to be effective bronchodilators, although there are few human data comparing the efficacy of available agents. This study compared the bronchodilating efficacy of four anesthetic maintenance regimens: 1.1 minimum alveolar concentration (MAC) end-tidal sevoflurane, isoflurane or halothane, and thiopental/nitrous oxide.

Methods: Sixty-six patients underwent tracheal intubation after administration of 2 micro gram/kg fentanyl, 5 mg/kg thiopental, and 1 mg/kg succinylcholine. Vecuronium or pancuronium (0.1 mg/kg) was then given to ensure paralysis during the rest of the study. Postintubation R sub rs was measured using the isovolume technique. Maintenance anesthesia was then randomized to thiopental 0.25 mg [center dot] kg sup -1 [center dot] min sup -1 plus 50% nitrous oxide, or 1.1 MAC end-tidal isoflurane, halothane, or sevoflurane. The Rrs was measured after 5 and 10 min of maintenance anesthesia. Data were expressed as means +/- SD.

Results: Maintenance with thiopental/nitrous oxide failed to decrease Rrs, whereas all three volatile anesthetics significantly decreased Rrs at 5 min with little further improvement at 10 min. Sevoflurane decreased Rrs more than either halothane or isoflurane (P < 0.05; 58 +/- 14% of the postintubation Rrs vs. 69 +/- 20% and 75 +/- 13%, respectively).     

Midlatency auditory evoked potentials do not allow the prediction of recovery from general anesthesia with isoflurane

PURPOSE: To investigate midlatency auditory evoked potentials (MLAEP) waveforms during recovery from anesthesia. The hypothesis was that MLAEP are sensitive variables to discriminate between states of consciousness and unconsciousness during emergence from anesthesia. METHODS: MLAEP were recorded in the awake state and during the wake-up phase from isoflurane anesthesia in 22 female patients undergoing ophthalmologic surgery. During emergence from anesthesia the changes in latency and amplitude of MLAEP components Na, Pa and Nb were compared with the awake level. The next day the patients were asked for explicit memory for the recovery period. RESULTS: In 72% of the patients the MLAEP waveforms were completely suppressed during isoflurane anesthesia. When the patients responded and opened their eyes spontaneously 38 +/- 12 min after anesthesia, the latencies of Na (18.3 +/- 1.2 vs 17.6 +/- 1.3; P = 0.013) and Nb (47.4 vs 7.1 vs 44.7 +/- 7.8; P = 0.048) remained prolonged compared with awake values. In contrast, the amplitudes NaPa and PaNb had regained baseline level. Nine patients had explicit memory for the immediate recovery period. However, there was no difference for any MLAEP component between patients with and without memory at any time. CONCLUSIONS: The persistent changes of MLAEP latency components Na and Nb indicated impaired auditory signal processing 38 min after isoflurane anesthesia. There was a marked intra- and inter-individual variability during reversal of the anesthetic induced MLAEP changes. This limits the prediction of recovery of consciousness in the individual patient during emergence from anesthesia.     

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.     

Characteristics and distribution of somatosensory evoked potentials in the subthalamic region

OBJECT: The aim of the present study is to evaluate the topographical distribution of somatosensory evoked potentials (SSEPs) in the subthalamic area, including the zona incerta (ZI). Determination of this distribution may help in the correct placement of deep brain stimulation (DBS) leads. METHODS: Intraoperative SSEPs were recorded from contacts of DBS electrodes at 221 sites in 41 patients: three patients with essential tremor and 38 with Parkinson disease who underwent implantation of DBS electrodes for the relief of severe tremor or parkinsonism. RESULTS: Two distinct SSEPs were recorded in the subthalamic area. One was a monophasic positive wave with a mean latency of 15.8 +/- 0.9 msec, which the authors designated subthalamic P16. Using both cephalic and noncephalic references, subthalamic P16 was only recorded in the ventral part of the ZI (mean 6.6 +/- 1.3 mm posterior to the midcommissure point, 4.8 +/- 1.2 mm inferior to the anterior commissure-posterior commissure line, and 9.7 +/- 0.6 mm lateral to the midline). When bipolar recordings were made, the traces showed a phase reversal at the caudal part of the ZI. The second potential is a positive-negative SSEP recorded throughout the entire subthalamic area. The mean latencies of the initial positive peak and the major negative peak were 13.6 +/- 1.1 msec and 16.4 +/- 1.1 msec, respectively. Several small notches were superimposed on the peaks, and their amplitudes were largest at the contact close to the medial lemniscus. CONCLUSIONS: The results indicate that intraoperative SSEPs from DBS electrodes are helpful in refining stereotactic targets in the thalamus and subthalamic areas.     

Transcranial magnetic motor evoked potentials (tcMMEP) for functional monitoring of motor pathways during scoliosis surgery

Transcranial magnetic motor evoked potentials (tcMMEP) were used to assess the functional integrity of the descending motor pathways. The tcMMEP, recorded bilaterally from anterior tibialis muscles, were evoked by an electric current induced in the motor cortex by a high-intensity transient magnetic field applied to the scalp surface. Potentials were recorded from ten of 12 volunteer subjects and preoperatively in 11 of 11 scoliotic patients. Group mean latency in the volunteers (32.0 +/- 2.1 msec) did not differ from that of the scoliotics (28.6 +/- 5.0 msec), but values in the latter group were more variable. During nitrous oxide-narcotic anesthesia, tcMMEP with reproducible latencies were obtained in 9 of 11 (82%) cases. A small, but statistically significant, increase in latency occurred during anesthesia. Compared with preoperative values (523 +/- 490 microV), individual tcMMEP amplitudes were significantly decreased intraoperatively (163 +/- 153 microV). Although the absolute amplitudes varied widely, the minimum recorded value was over 20 microV. Thus, intraoperative tcMMEP waveforms were readily discriminable from background electrical noise. These results demonstrate the technical feasibility of intraoperative tcMMEP monitoring. Combined somatosensory evoked potential and tcMMEP monitoring may provide a more complete picture of spinal cord function, intraoperatively.     

The effect of high dose sodium thiopental on brain stem auditory and median nerve somatosensory evoked responses in humans

Median nerve somatosensory evoked potentials (MnSSEPs), brain stem auditory evoked responses (BAERs), and the cortical electro-encephalogram (EEG) were recorded in six patients during a 62-min infusion of sodium thiopental (STP) at a rate of 1.25 mg X kg-1 X min-1 (total dose, 77.5 mg/kg). The EEG became isoelectric after 22 +/- 8 (SD) min of STP infusion. Dose-related changes in the latencies and amplitudes of various evoked response wave forms were observed. However, in no instance was any component of either the MnSSEP or the BAER rendered unobtainable by STP administration. For the MnSSEP, progressive increases in the central conduction time (5.33 +/- 0.41 ms preinduction vs. 7.46 +/- 1.2 ms at t = 60 min) and in the latency of the cortical primary specific complex were observed simultaneously with significant reductions in the amplitude of the latter (2.10 +/- 0.85 muV preinduction vs. 0.85 +/- 0.55 muV at t = 60 min). Changes in the latency and amplitude of the response recorded over the upper cervical spine (C2) were not statistically significant in this small population. For the BAER, progressive and significant increases in the latencies of Waves I, III, V (e.g., Wave V latency: 6.16 +/- 0.24 vs. 6.87 +/- 0.31 ms) and in the I-III, III-V, and the I-V interwave latencies were observed. The amplitudes of the BAER components were not significantly altered. The authors conclude that the administration of a dose of STP in excess of twice that required to produce EEG isoelectricity can be compatible with effective monitoring of MnSSEPs and BAERs. However, STP produces dose-related changes in both evoked response wave forms, which must be considered in the interpretation of responses elicited during STP anesthesia.     

The effect of acute hypocapnia on human median nerve somatosensory evoked responses

This study was undertaken to define the effect of acute hypocapnia on intraoperatively recorded somatosensory evoked potentials (SSEPs). Median nerve SSEPs were studied in ten anesthetized neurologically normal adult patients undergoing elective nonneurologic surgery. End-tidal carbon dioxide tension (ETCO2) was allowed to stabilize for 15 min before SSEP recordings were obtained during normocapnia (N) (ETCO2 = 39.9 +/- 1.45 mm Hg), hypocapnia (H) (ETCO2 = 20.6 +/- 1.07 mm Hg), and after return to normocapnia (NR). Although a trend toward a reduction in the latencies of all SSEP components was evident, only the cervical (CII), and cortical (N1 and P1) latencies decreased significantly with H when compared to N. Mean latencies for CII, N1, and P1 (+/- SD) were, respectively, 14.80 +/- 1.14, 20.93 +/- 1.50, and 25.17 +/- 2.88 msec during N, and 14.50 +/- 1.13, 20.25 +/- 1.49, and 24.23 +/- 2.52 msec during H. On return to normocapnia, latencies were unchanged from N. Cortical latencies were affected to a greater extent than subcortical ones. Aside from a small but statistically significant increase in CII amplitude at H (2.05 +/- 0.55 microV vs 1.83 +/- 0.49 microV at N), SSEP amplitudes were unaffected by hypocapnia. The authors conclude that acute hypocapnia in neurologically normal patients results in a small reduction of SSEP latencies. The magnitude of the change is such that it is unlikely to interfere with recording or interpretation of intraoperative SSEPs.     

Rocuronium pharmacokinetic-pharmacodynamic relationship under stable propofol or isoflurane anesthesia

PURPOSE: To compare the pharmacokinetics, pharmacodynamics and the concentration-effect relationship of rocuronium in patients under stable propofol or isoflurane anesthesia. METHODS: Ten patients were randomized to receive fentanyl, propofol and nitrous oxide (60%) or fentanyl, thiopental, isoflurane (1.2% end-tidal concentration) and nitrous oxide (60%). To obtain good intubation conditions and maintain adequate muscle relaxation during surgery, patients received two bolus doses of rocuronium: 0.5 mg x kg(-1) (1.7 x ED95) at induction followed one hour later by 0.3 mg x kg(-1) (1 x ED95). Arterial blood samples were obtained over six hours after the second bolus dose. Plasma concentrations of rocuronium were measured using high pressure liquid chromatography. Muscle twitch tension was monitored by mechanomyography for the two doses. Pharmacokinetic and pharmacodynamic parameters were determined. RESULTS: No differences in rocuronium pharmacokinetic parameters were observed between both groups. After the second bolus, clinical duration was 20 +/- 6 min in the propofol group vs 39 +/- 8 min in the isoflurane group (P <0.05). The effect compartment concentration corresponding to 50% block, EC50, was higher under propofol anesthesia: 1008 vs 592 microg x L(-1) (P <0.05). CONCLUSION: Rocuronium body disposition is similar under stable propofol or isoflurane anesthesia. In contrast to isoflurane, propofol does not prolong the neuromuscular block. Therefore, the potentiating effect of isoflurane is of pharmacodynamic origin only, as explained by an increased sensitivity at the neuromuscular junction. In contrast with isoflurane anesthesia where the dose of rocuronium has to be decreased under stable conditions, no dose adjustment is required under propofol anesthesia.     

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

The effects of nitrous oxide, enflurane, and isoflurane on cortical somatosensory evoked potentials (SEPs) were studied in 29 patients undergoing intracranial or spinal operations. Anesthesia was induced with fentanyl (25 micrograms/kg, iv) plus thiopental (0.5-1.0 mg/kg, iv). In one group of patients (n = 12), nitrous oxide (50%) was compared with enflurane (0.25-1.0%), and in another group (n = 12) nitrous oxide (50%) was compared with isoflurane (0.25-1.0%). In a third group of patients (n = 5) with preexisting neurologic deficits, nitrous oxide (50%) was compared with enflurane (0.25-1.0%). In all three groups, one gas was administered for 30 min, and then the alternate gas was administered for 30 min; then the cycle was repeated for a total of two administrations of each of the two anesthetics. SEPs were determined before and after induction of anesthesia and at the end of each 30-min study period. The latencies and amplitudes of the early cortical components of the upper- and lower-extremity SEP were examined. Induction of anesthesia resulted in increases of latency in both upper- and lower-extremity SEPs without any alteration of amplitude. Nitrous oxide, enflurane, and isoflurane each decreased the amplitude of the upper-extremity SEPs compared with the postinduction value. The amplitude of the upper-extremity SEPs was less during nitrous oxide than with either enflurane or isoflurane. Nitrous oxide decreased the amplitude of lower-extremity SEPs below postinduction value, while enflurane and isoflurane had no effect. Isoflurane and enflurane increased the latency of both upper- and lower-extremity SEPs slightly, while nitrous oxide had no effect.(ABSTRACT TRUNCATED AT 250 WORDS)     

脑干听觉诱发电位与异氟醚麻醉浓度定性及定量关系的研究

对１０例患者研究了脑干听觉诱发电位（ＢＡＥＰ）潜伏期与异氟醚麻醉浓度定性及定量关系。全麻诱导采用２．５％硫喷妥钠（３～５ｍｇ／ｋｇ），阿曲库铵（０．６ｍｇ／ｋｇ）。气管插管后麻醉维持采用１．１５％、１．７３．％、２．３０％异氟醚及６０％Ｎ２Ｏ，肌松维持用阿曲库铵。记录麻醉前、诱导后，１．１５％、１．７３％、２．３０％及减至１．１５％异氟醚时ＢＡＥＰ峰潜期（ＰＬ）和峰间潜伏期（ＩＰＬ）值。结果表明，ＢＡＥＰ波ＶＰＬ能稳定反映异氟醚麻醉浓度变化，具有等级性并呈正相关关系，ＢＡＥＰＰＬ、各波正常值似可作为判断异氟醚麻醉深度的参考标准。     

Anesthesia for craniotomy: total intravenous anesthesia with propofol and alfentanil compared to anesthesia with thiopental sodium, isoflurane, fentanyl, and nitrous oxide

STUDY OBJECTIVE: To compare a total intravenous (IV) anesthetic technique based on propofol and alfentanil with a commonly used anesthetic technique for craniotomy. DESIGN: Open-label, randomized, clinical study. SETTING: Neurosurgical clinic at a university hospital. PATIENTS: Forty patients, aged 18 to 55 years, scheduled for brain tumor surgery. INTERVENTIONS: In 20 patients, anesthesia was induced with fentanyl and thiopental sodium and maintained with fentanyl, dehydrobenzperidol, isoflurane, nitrous oxide (N2O), and a thiopental sodium infusion. Twenty patients were anesthetized with a propofol loading infusion followed by a maintenance infusion at a fixed rate. In addition, alfentanil was administered as a loading bolus, followed by a variable-rate infusion, with additional doses as necessary to maintain hemodynamic stability. MEASUREMENTS AND MAIN RESULTS: A decrease in blood pressure (BP) after induction with thiopental sodium was followed by a significant increase in BP and heart rate (HR) during intubation. BP and HR did not change during the propofol loading infusion. However, the administration of alfentanil was followed by a similar decrease in BP with a return to baseline values during the intubation period. Return of normal orientation (7 +/- 5 minutes vs 27 +/- 23 minutes) and concentration (12 +/- 12 minutes vs 35 +/- 37 minutes) was shorter and more predictable for the propofol-alfentanil-treated patients than for the thiopental sodium patients. Maintenance propofol concentration (nine patients) was between 3 +/- 0.69 micrograms/ml and 3.36 +/- 1.17 micrograms/ml, while the concentration at awakening was 1.09 microgram/ml. Alfentanil concentration at extubation (nine patients) was 79 +/- 34 ng/ml. CONCLUSION: A total IV anesthetic technique with propofol and alfentanil is a valuable alternative to a more commonly used technique based on thiopental sodium, N2O, fentanyl, and isoflurane.     

Anesthesia and hypertension: the effect of clonidine on perioperative hemodynamics and isoflurane requirements

Thirty patients (ASA physical status II-III) with a history of arterial hypertension, whose blood pressure (BP) control varied from normotension to moderate hypertension (diastolic BP less than 110 mmHg), scheduled for elective surgery under general anesthesia, were randomly assigned to two groups. Group 1 was premedicated 90-120 min prior to induction with diazepam 0.15 mg X kg-1 po; group 2, in addition, received clonidine 5 micrograms X kg-1 po. Anesthetic depth was assessed by on-line aperiodic analysis of the electroencephalogram. Following lidocaine 1 mg X kg-1 and fentanyl 2 micrograms X kg-1 (group 1 only), anesthesia was induced with thiopental 3-4 mg X kg-1 and vecuronium 0.1 mg X kg-1 was used to facilitate endotracheal intubation. Anesthesia was maintained with isoflurane in N2O/O2 and supplemented by fentanyl. In group 2, clonidine produced a rapid preoperative control of systolic and diastolic BP from 166 +/- 32/95 +/- 14 to 136 +/- 80 +/- 11 (P less than 0.01), was more effective in blunting the reflex tachycardia associated with laryngoscopy and endotracheal intubation than lidocaine-fentanyl pretreatment. It significantly reduced the intraoperative lability (coefficient of variation) of systolic (P less than 0.01) and diastolic BP and heart rate (HR) (P less than 0.05), and resulted in significantly slower HR during recovery (P less than 0.01). Anesthetic requirements for isoflurane were reduced 40% (P less than 0.01) in group 2; narcotic supplementation was also significantly reduced (P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)