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*Department of Anesthesiology, Technical University, Munich, Germany;
Department of Anesthesiology, Academic Hospital University of Amsterdam, The Netherlands;
Northwick Park Hospital, St. Mary's Medical School, London, United Kingdom;
§Eppendorf Hospital, Hamburg, Germany;
||Academic Hospital and Departments of
¶Medical Technology and
**Informatics, Technical University Duisburg, Germany
Address correspondence and reprint requests to Cor J. Kalkman, MD, Department of Anesthesiology H1-116, Academic Hospital University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands. Address e-mail to c.j.kalkman{at}amc.uva.nl
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Abstract |
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Implications: Reliable estimation of anesthetic adequacy remains a challenge. Changes in spontaneous or auditory evoked brain activity after a brief electrical stimulus at the wrist could not be used to predict whether anesthetized patients would subsequently move at the time of surgical incision.
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Introduction |
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In addition to detecting intraoperative awareness, it would be useful if a monitor were able to predict the need for additional anesthetics or analgesics to prevent movement or laryngospasm (in patients with a laryngeal mask airway in place) in response to noxious stimuli. The electroencephalogram (EEG) represents spontaneous electrical activity in the superficial cortical layer of pyramidal cells. Although marked EEG changes occur during the transition from the awake to the anesthetized state, these changes are biphasic; that is, two anesthetic levels may have similar EEG profiles (1). Accordingly, attempts to use EEG spectral variables to predict inadequate levels of anesthesia in individuals have been remarkably unsuccessful (2). The early cortical (mid-latency) auditory evoked response (MLAER) represents signal transmission and processing in the acoustic pathway from the cochlea to the primary auditory cortex. This evoked signal changes predictably in response to both increases in the anesthetic concentration (3–8) and to surgical stimulation (9,10). It may be unrealistic to expect either signal (EEG or MLAER) in an unstimulated patient to predict movement when surgery starts. However, the response of these signals to a lesser noxious stimulus might be predictive of what would happen with surgical incision.
A multicenter clinical study allowed us to test whether changes in the EEG or MLAER variables after tetanic stimulation at the wrist could be used to predict subsequent movement after skin incision in patients anesthetized with 1 MAC isoflurane in N2O, in a large group of patients. In addition, we investigated whether the EEG or MLAER variables before noxious stimulation (tetanus and skin incision) could differentiate between patients who subsequently moved (movers) and those who did not (nonmovers).
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Methods |
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Midazolam 7.5 mg was given orally 1 h before anesthesia. Anesthesia was induced with propofol 2.0–2.5 mg/kg IV. Tracheal intubation was facilitated with succinylcholine 1 mg/kg. Using overpressure ventilation, patients were rapidly equilibrated to 0.6% end-expiratory isoflurane in 50% N2O (1 MAC). Heart rate and noninvasive blood pressure were recorded every 2 min during the study. After the end-tidal isoflurane concentration had been maintained for at least 15 min at 0.6%, a 5-s tetanic stimulus (40 mA, 50 Hz) was applied to the ulnar nerve at the wrist. If the patient moved during the period between tetanic stimulus and skin incision, rescue medication was given (propofol and fentanyl), and all subsequent data (posttetanus and pre- and postskin incision) from this particular patient were excluded from later analysis. Skin incision was performed at least 5 min after application of the tetanic stimulus, and the presence or absence of movement was recorded. Movement in response to a stimulus was recorded if the patient made purposeful withdrawal responses or when the head or legs moved within 2 min after the tetanic stimulus or skin incision.
The EEG/auditory evoked response (AER) data acquisition system was custom-designed for this project. It consisted of a small (148 x 78 x 29 mm) battery-powered amplifier and stimulator unit placed in close proximity to the patient's head. The main feature that distinguishes this system from commercially available equipment is that interference by diathermy noise and "common mode" line interference (line frequency in Europe 50 Hz) is efficiently eliminated, thus allowing continuous acquisition of EEG/AER data in the proximity of poorly shielded devices, such as heating apparatus and infusion pumps, as well as during frequent use of electrocautery (11). A single-channel EEG was recorded from Ag-AgCl electrodes placed on the forehead and left mastoid, with the right mastoid as common. Electrode impedance was checked automatically and maintained <5 k
. Binaural auditory stimulation was performed at 6.1 Hz with rarefaction clicks (70 dB above hearing level) using insert earphones. The raw EEG data were sampled at a rate of 1 kHz and stored on a computer for off-line analysis. The exact position of each click was marked in the raw datafile, allowing off-line AER averaging using various filter settings and averaging paradigms. To allow estimation of signal quality during the study period, the raw EEG data and a moving AER average were continuously displayed on the monitor screen.
For the present study, we used normal ensemble averaging, in which every datapoint in the AER waveform represents the arithmetic mean of all sweeps over the respective recording periods. The data were filtered using an analog 400-Hz low-pass filter, digitally filtered with a 25-Hz high-pass filter, and three-point smoothing was applied. Waveforms consisting of 1024 averaged sweeps of 100 ms duration, equivalent to 2.6 min of recording, were used in the analysis. These were obtained immediately before and immediately after tetanic stimulation and incision (four periods). One experienced observer (CT) blinded to clinical center and study period identified peaks Pa and Nb in the MLAER waveform. Latencies and absolute and interpeak MLAER amplitudes were determined.
The raw signal for the four study periods was subjected to power spectral analysis using 2-s EEG epochs (EEG bandwidth 0.5–30 Hz, electromyogram (EMG) bandwidth 30.5–400 Hz). The following variables were calculated: total power; absolute and relative power in the delta (0.5–3.0 Hz), theta (3.5–8.0 Hz), alpha (8.5–12.0 Hz), and beta (12.5–30.0 Hz) bands; median frequency and 95% edge frequency; and EMG power in two bands: EMG 1 (30–70 Hz) and EMG 2 (70–250 Hz).
The EEG and MLAER variables were log-transformed, as untransformed these variables are not normally distributed. Data are presented as geometric means with their respective confidence intervals. Two sample t-tests were performed to test whether: 1) the post- versus pretetanus differences were different in movers at incision compared with nonmovers, after excluding patients who moved at tetanus; 2) the pretetanus values were different in movers and nonmovers to tetanic stimulation; 3) the preincision values were different in movers and nonmovers to incision after excluding patients who moved at tetany.
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Results |
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Reproducible auditory evoked brainstem potentials, as evidenced by the presence of a characteristic peak V of the brainstem auditory response (latency 6–7 ms) could be recorded in every patient during anesthesia with 1 MAC isoflurane in N2O. At 1 MAC isoflurane in N2O, the mid-latency segment of the AER waveform, representing the early cortical response, was severely depressed (Fig. 1). Peak-to-peak amplitude PA/Nb was <0.5 µV in 62% of patients.
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The hemodynamic variables were similarly unable to predict whether patients would move to surgical incision. The post- versus pretetanus differences were not significantly different in movers at incision compared with nonmovers. Pretetanus values were not different in movers and nonmovers to tetanic stimulation. The preincision values were not different in movers and nonmovers to incision. Table 2 shows the geometric means and confidence intervals for systolic blood pressure and heart rate before and after the application of a 5-s tetanus and before and after skin incision. The post- versus preincision differences were also not significantly different between movers and nonmovers, although it approached significance (P = 0.07) for systolic blood pressure. There was a greater increase in systolic blood pressure increase in movers compared with nonmovers.
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Discussion |
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One explanation for the fact that EEG and MLAER data were unable to distinguish movers from nonmovers is that anesthetic depression of the auditory pathway and cortical signal processing areas may not parallel anesthetic depression of the afferent-efferent nociceptive reflex pathway and the autonomic nervous system. If, at a given anesthetic concentration, cortical auditory areas are more depressed than the spinal nociceptive reflex-mediating areas, then the present data support the concept proposed by Rampil et al. (12) and Rampil (13) that MAC represents primarily the level of depression of a spinal antinociceptive reflex. To establish whether the level of anesthesia is sufficient to prevent movement of unparalyzed patients in response to a surgical incision, one would have to assess either the level of analgesia and/or the level of depression of the motor neuron pool, for example, by recording retrograde activation of motor neurons after peripheral motor nerve stimulation (F-waves) (14).
Another explanation is that anesthesia was too deep or the tetanic stimulus not intense or prolonged enough. Although we assessed the MLAER only at 1 MAC, it is likely that the dose-response MAC curve for MLAER is shifted to the left compared with the curve for the classical MAC end point of movement on incision. As a result, MLAER may be more susceptible to inhaled anesthetics. Our data suggest that MLAER are nearly completely suppressed at isoflurane concentrations that are compatible with a 50% proportion of movers. Although the purpose of this study was not to compare depression of MLAER at 1.0 MAC isoflurane with awake baseline responses, our data are in agreement with previous reports showing that 1.0 MAC isoflurane in N2O produces profound depression of the MLAER amplitude. Schwender et al. (15) observed nearly complete suppression of MLAER in patients undergoing heart surgery with 1.0% isoflurane in O2. The awake amplitudes were 1.0–2.0 µV. Newton et al. (16) found that 0.4% end-tidal isoflurane in oxygen administered to anesthetist volunteers decreased Pa amplitude from 0.70 to 0.29 µV; Nb latency increased from 44.9 to 53.9 ms. Tetanic stimulation failed to produce a significant change in either hemodynamic or MLAER or EEG variables. However, ethical and technical (if the patient moved grossly, then rescue medication had to be administered, and the study was ended) considerations prohibited us from applying a more powerful tetanic stimulus or using a lighter level of anesthesia.
Several studies from participants of our group and others have suggested that MLAER may indicate the potential of intraoperative wakefulness and thus might be used clinically to prevent awareness with recall (16–18). Even in the absence of N2O, MLAER are severely suppressed at 0.4%–0.8% end-tidal isoflurane or sevoflurane concentrations (7,19). At these anesthetic concentrations, there was a low incidence of motor signs of wakefulness (coughing, limb movement, or facial movement). In contrast, during N2O/opioid/benzodiazepine anesthesia, MLAER amplitudes were 3 times higher, and there was fivefold higher incidence of movement. The authors (19) concluded that primary processing of sensory stimuli in the primary sensory cortex was blocked during isoflurane/N2O anesthesia and that this was reflected in the changes in the MLAER.
In conclusion, although the MLAER and EEG variables may find clinical applications as alarms for possible intraoperative wakefulness with the attendant possibility of recall, it is unlikely that this evoked signal or the EEG (as it was processed in the present study) can be of practical use in titrating anesthesia to prevent movement to noxious stimulation.
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Acknowledgments |
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We thank Mrs. M. Porsius (Amsterdam), Mrs. D. Droese (Munich), Mr. A. Meyer (Hamburg), and Dr. U. Richter (Luebeck) for their valuable help in collecting or analyzing the EEG and evoked potentials data.
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Footnotes |
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