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From the Department of Anesthesiology, Shanghai Jiaotong University Affiliated Shanghai First People’Hospital, Shanghai, China.
Address correspondence to: Sheng-Jin Ge, Department of Anesthesiology, Shanghai First People’s Hospital, Shanghai 200080, China. E-mail: steeroncn{at}yahoo.com.cn
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Abstract |
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Methods: Forty adult patients undergoing elective surgery were studied. After tracheal intubation, anesthesia was maintained with an end-tidal isoflurane concentration (FETISO) of 1.0% for 20 min, then a 10-mL dose of either vecuronium 0.05 mg•kg-1, 0.1 mg•kg-1, 0.2 mg•kg-1 or saline was administered in a randomized, double-blind design. The AAI and bispectral index (BIhx) were monitored throughout the study and analyzed off-line.
Results: BIhx was unaltered after the administration of saline or vecuronium. The mean of the averaged (per patient) AAI values recorded from two minutes to ten minutes after the administration of saline or vecuronium 0.05 mg•kg-1 did not differ significantly from the corresponding mean recorded from 15 min to 20 min after FETISO maintained 1.0% (P = 0.678, 0.169), however after the administration of vecuronium 0.1 mg•kg-1 or 0.2 mg•kg-1, AAI was reduced from 18.3, 18.0 to 14.8, 13.4 (P = 0.016, 0.017).
Conclusions: Neuromuscular block with vecuronium reduces AAI in patients during steady state anesthesia without surgical stimuli, while BIhx is unaltered. The cut-off values of AAI for events should be determined according to the level of neuromuscular blockade when monitoring the depth of anesthesia/sedation.
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Introduction |
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Richmond et al.8 reported that neuromuscular block with vecuronium 0.05 mg•kg-1 did not affect depth of anesthesia as measured by the AEP waveform (Pa and Nb), the primary components of MLAEP. Greif et al.9 showed, in a recent study, that BIS® (Aspect Medical Systems, Newton, MA, USA) was unaltered by mivacurium administration during propofol anesthesia. However, during clinical monitoring, we observed that vecuronium administration appeared to reduce AAI. The present study aimed to verify this phenomenon.
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Methods |
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Patients were fasted for at least eight hours and were pre-medicated with atropine 0.5 mg and phenobarbital 0.1 g intramuscularly. In the operating room, electrocardiogram, heart rate, invasive arterial pressure, respiration, pulse oximetry and temperature with continuous recording were commenced via a Cardiocap/5 monitor (Datex-Ohmeda, Helsinki, Finland). In our preliminary observations, blood pressure cuff inflation seemed to increase AAI in one patient, so invasive arterial pressure was employed.
During the study, 500 mL Ringer’s solution and 500 mL gelatin solution - Gelofusine® (Shengyang B. Braun, Heilongjiang, China) were infused in order to keep an appropriate circulating blood volume.
AAI was recorded using the A-line monitor (software version 1.5; Danmeter A/S, Odense, Denmark). The AEP were elicited with a bilateral click stimulus of 65dB intensity, 2 msec duration, and repetition rate of 9 Hz (one click each 110 msec) from three silver-silver chloride electrodes (Neuroline, Medicotest A/S, Oelstykke, Denmark) positioned at mid-forehead (+), left forehead (reference) and left mastoid (-). The AEP analysis window had an 80 msec duration and the pre-processing of the electroencephalogram (EEG) sweeps consisted of artifact rejection and 25 to 65 Hz finite impulse response 170th order band-pass filtering. The monitor was based on a short moving time average together with an ARX model. This technology facilitated fast extraction of the AEP. Figure 1
shows a flow chart of the signal processing.
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All of the electrodes were positioned after the skin was cleaned with alcohol to remove surface oils and abraded with gauze to remove dead epidermal cells. Skin preparation was repeated if the impedance was greater than 5000 Ohms. In order to minimize artifacts, the patients were asked to close their eyes and relax after the electrodes were attached.
AAI and BIhx values were generated every second and ten seconds, respectively, stored automatically and analyzed subsequently.
BIhx and AAI have sophisticated artifact rejection algorithms and the auditory clicks generate signals 100 times smaller than the remainder of the EEG, so there is no interference between devices when used simultaneously.2,7
We induced general anesthesia with fentanyl 3 µg•kg-1, propofol 2 mg•kg-1 and succinylcholine 1.5 mg•kg-1 intravenously. After tracheal intubation, mechanical ventilation was commenced with 100% oxygen and the end-tidal carbon dioxide tension was adjusted to 34 to 38 mmHg. The end-tidal isoflurane concentration (FETISO) was maintained at 1.0% for 20 min before a 10-mL dose of the study drug was administered in approximately 20 sec in a blinded fashion. The study ended ten minutes later.
The 10-mL study drug was prepared by a designated investigator, with sealed envelopes insuring randomization to vecuronium 0.05 mg•kg-1, vecuronium 0.1 mg•kg-1, vecuronium 0.2 mg•kg-1 or saline.
Statistical analysis
AAI and BIhx values were recorded from 15 min after FETISO stabilized at 1.0% to ten minutes after the injection of vecuronium or saline.
The means of averaged AAI or BIhx values during five minutes before and from two minutes to ten minutes after the study drug injection were compared using Wilcoxon signed ranks test.
The mean percentages of decrease of AAI and BIhx were calculated and compared using one-way analysis of variance.
Probability values below 0.05 were considered statistically significant.
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Results |
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) were similar.
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).
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). The mean of averaged AAI values recorded during two to ten minutes after the administration of saline or vecuronium 0.05 mg•kg-1 did not differ from the corresponding mean prior to injection (P = 0.678, 0.169). Averaged AAI values decreased after the administration of vecuronium 0.1 mg•kg-1 or 0.2 mg•kg-1 (P = 0.016, 0.017; Table II). The mean percentages of decrease of AAI in the saline and vecuronium 0.05 mg•kg-1, 0.1 mg•kg-1 and 0.2 mg•kg-1 groups were 0.3%, 10.1%, 16.3% and 21.6%, respectively. Decreases in the vecuronium 0.1 mg•kg-1 and 0.2 mg•kg-1 groups were greater (P = 0.016, 0.010) than in the saline group (Table II). The mean percentages of the decrease of AAI did not differ significantly (P = 0.533) in the vecuronium groups.
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Discussion |
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The ARX model is a new model to evaluate the MLAEP index that can extract the information much faster than the classic model, the moving time average model.1,3,6 Recently, the ARX model AEP index (AAI) has been proposed as a promising method to monitor the depth of anesthesia.1–7 However, the effect of neuromuscular blocking agents on AAI remains unclear.
Similar to previous clinical observations, AAI fluctuated much more obviously than BIhx in this study. The total update delay of BIhx (30 sec) is longer than that of AAI (less than six seconds), and the BIhx value generated much slower (per ten seconds) than the AAI value (per second), therefore rapid changes might not be detected by BIhx with a result of less fluctuation. However, other differences in technologies might also contribute to this observed difference.
In the present study, we found that neuromuscular blockade with vecuronium did not alter BIhx, as in the study by Greif et al.9 However, vecuronium in doses of 0.1 and 0.2 mg•kg-1 reduced AAI significantly.
There are two reasons why neuromuscular blockade with vecuronium may affect AAI and BIhx (BIS®):
1. The frequency composition of electromyographic (EMG) activity overlaps that of AAI and BIhx and simple filtering will not completely remove EMG artifact from the recordings. Then the EMG signal from the frontalis, temporoparietalis, and mastoid muscles may interfere with the analysis and extraction of AAI and BIhx. Moreover, EMG contamination can mimic the EEG and AEP of waking patients, thus falsely increasing BIhx and AAI. Paralysis may therefore reduce BIhx and AAI by alleviating artifact from muscles lying near the electrodes;
2. The "afferent muscle spindle theory" states that signals from muscle stretch receptors stimulate arousal centres in the brain.9,11 Paralysis may also reduce signals from muscle stretch receptors that normally contribute to arousal.
But, why were BIhx and BIS® not altered in this study and that of Greif et al.,9 while AAI was reduced with neuromuscular blockade? Maybe this is because of the different algorithms and technologies used by BIhx (BIS®) and AAI. BIhx (BIS®) is largely derived from the spectrum of the spontaneous EEG, while AAI is calculated from the auditory evoked responses. Evoked responses have two advantages over the spontaneous EEG in the study of the depth of anesthesia: 1) evoked responses are an indication of the responsiveness of the central nervous system, whereas spontaneous EEG reflects the resting level;3 2) evoked responses have anatomical significance, each peak reflecting a specific anatomical structure.3,12 BIhx (BIS®) was developed based on a database of prior recordings and the expert opinion of anesthesiologists. It may more properly be regarded as an "expert system" rather than just a monitor. Thus, it is possible that EMG activity affected AAI greatly while it changed BIhx (BIS®) little, or that neuromuscular blockade did effectively result in cortical depression, but BIhx (BIS®) could not detect it while AAI could.
Since larger doses of vecuronium reduce AAI more, we hypothesize that AAI may be lower at deeper levels of neuromuscular block during steady state anesthesia. However, we could not monitor neuromuscular block (since it is a stimulus) simultaneously in this study. The EMG shown on the A-line device is the facial EMG. The way the EMG is calculated is by taking the energy in the 65 to 85 Hz range of the spectrum of the recorded data. It is only an estimation of the total energy of the EMG. AAI and BIhx were calculated with 25 to 65 and 0.5 to 60 Hz band-pass filtering, respectively, so the EMG (65–85 Hz) activity may not represent the true information regarding interference with AAI and BIhx. Consequently we did not use the EMG data shown on the A-line device.
EMG activity and the signal from muscle stretch receptors will be greater in patients under surgery, so it is possible that AAI will be reduced more after the administration of vecuronium. Nevertheless, we chose to perform this trial in anesthetized patients without surgical stimuli, which are highly variable in intensity.
Because AAI has been introduced into clinical monitoring, it will be important to take into consideration that AAI can be affected by neuromuscular blockade. If this is because of the EMG activity, which we think is likely, the technology to extract and calculate AAI needs to be improved. However, it is almost impossible to extract the AEP from the EMG background activity without any EMG interference. If, on the other hand, this is because of reduced signals from muscle stretch receptors, AAI can be assumed to be more sensitive than BIhx for measuring the hypnotic level. Whatever the reason(s), the cut-off values of AAI for determining events should be determined according to the level of neuromuscular blockade when monitoring the depth of anesthesia/sedation.
We conclude that AAI is reduced by vecuronium during steady state anesthesia in patients without surgical stimuli, while BIhx is unaltered.
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Footnotes |
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Financial support was received from the Department of Anesthesiology, Shanghai First People’s Hospital.
There are no commercial or non-commercial affiliations that are or may be perceived to be a conflict of interest with this work.
Accepted for publication May 12, 2003. Revision accepted September 10, 2003.
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References |
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2 Struys MM, Jensen EW, Smith W, et al. Performance of the ARX-derived auditory evoked potential index as an indicator of anesthetic depth. A comparison with bispectral index and hemodynamic measures during propofol administration. Anesthesiology 2002; 96: 803–16.[Medline]
3 Urhonen E, Jensen EW, Lund J. Changes in rapidly extracted auditory evoked potentials during tracheal intubation. Acta Anaesthesiol Scand 2000; 44: 743–8.[Medline]
4 Alpiger S, Helbo-Hansen HS, Jensen EW. Effect of sevoflurane on the mid-latency auditory evoked potentials measured by a new fast extracting monitor. Acta Anaesthesiol Scand 2002; 46: 252–6.[Medline]
5 Litvan H, Jensen EW, Revuelta M, et al. Comparison of auditory evoked potentials and the A-line ARX index for monitoring the hypnotic level during sevoflurane and propofol induction. Acta Anaesthesiol Scand 2002; 46: 245–51.[Medline]
6 Litvan H, Jensen EW, Galan J, et al. Comparison of conventional averaged and rapid averaged, autoregressive-based extracted auditory evoked potentials for monitoring the hypnotic level during propofol induction. Anesthesiology 2002; 97: 351–8.[Medline]
7 Ge SJ, Zhuang XL, Wang YT, Wang ZD, Li HT. Changes in the rapidly extracted auditory evoked potentials index and the bispectral index during sedation induced by propofol or midazolam under epidural block. Br J Anaesth 2002; 89: 260–4.
8 Richmond CE, Matson A, Thornton C, Dore CJ, Newton DE. Effect of neuromuscular block on depth of anaesthesia as measured by the auditory evoked response. Br J Anaesth 1996; 76: 446–8.
9 Greif R, Greenwald S, Schweitzer E, et al. Muscle relaxation does not alter hypnotic level during propofol anesthesia. Anesth Analg 2002; 94: 604–8.
10 Stanski DR. Monitoring depth of anesthesia. In: Miller RD (Ed.). Anesthesia, 5th ed. Beijing: Science Press; 2001: 1087–116.
11 Lanier WL, Iaizzo PA, Milde JH, Sharbrough FW. The cerebral and systemic effects of movement in response to a noxious stimulus in lightly anesthetized dogs. Possible modulation of cerebral function by muscle afferents. Anesthesiology 1994; 80: 392–401.[Medline]
12 Thornton C, Sharpe RM. Evoked responses in anaesthesia. Br J Anaesth 1998; 81: 771–81.
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