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Department of Anesthesiology, Faculty of Medicine, University of Yamanashi, Yamanashi, Japan
Address correspondence and reprint requests to Tadahiko Ishiyama, MD, PhD, Department of Anesthesiology, Faculty of Medicine, University of Yamanashi, 1110 Shimokato, Tamaho, Nakakoma, Yamanashi 409–3898, Japan. Address e-mail to ishiyama{at}yamanashi.ac.jp.
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Abstract |
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Introduction |
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Two studies (6,7) reported that the bispectral index (BIS) correlates well with the level of responsiveness and the sedative and hypnotic effects of anesthetic drugs. Therefore, the BIS can quantify the degree of sedation produced by epidural anesthesia.
The purpose of the present study was to investigate whether ropivacaine epidural anesthesia reduces the BIS during the awake phase and during sevoflurane general anesthesia.
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Methods |
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Patients were premedicated with intramuscular midazolam 0.02 mg/kg 30 min before entering the operating room. Before anesthesia, a venous catheter was inserted and acetated Ringer’s solution was infused at a rate of 10 mL · kg–1 · h–1 IV throughout the study period. Intraoperative monitoring consisted of a 5-lead electrocardiogram, noninvasive measurements of arterial blood pressure (BP), and pulse oximetry (Spo2). With the patients in the lateral position and after intradermal anesthesia with 1% mepivacaine, the epidural space was identified with an 18-gauge Tuohy needle at a vertebral level between T8 and T12 using a loss-of-resistance to air technique. An epidural catheter was then inserted 5 cm cephalad into the epidural space. Thereafter, patients were turned to the supine position. Then, the BIS monitoring electrodes were applied to the forehead of each patient as recommended by the manufacturer. All electrode impedance levels were kept below 7.5 k
. The BIS value was obtained from an A-1050 monitor (Version 3.05.05; Aspect Medical Systems, Natick, MA). High pass and low pass filters for BIS calculation were at 1 and 50 Hz, respectively, with a 50 Hz notch filter. The BIS smoothing rate was set at 30 s.
The patients were randomly allocated to 2 groups receiving either 5 mL of epidural saline (group S) or the same volume of 0.75% ropivacaine (group R). Sensory block was verified by loss of sensation to cold using a glass ampoule cooled by 4°C at 5 and 20 min after the epidural injection. Motor block of the lower limb was evaluated by asking the patients to flex the knees and ankles and rated for 3 points: 0 = full motor strength; 1 = partial blockade; 2 = complete blockade. Assessments of motor block were made immediately after the evaluation of sensory block.
Two phases of the BIS measurements were performed. First, the BIS measurements were made during the awake phase. BIS values were recorded at pre-epidural injection (control) and at 7, 12, 13, 14, 22, and 23 min after the epidural saline or ropivacaine injection. Although sensory and motor assessment made this study open labeled, the BIS measurements were performed by a blinded investigator who did not know the results of sensory and motor assessments.
General anesthesia was then induced in all patients with 2 mg/kg propofol IV and 0.15 mg/kg vecuronium IV. After tracheal intubation, anesthesia was maintained with 0.75% sevoflurane (end-tidal) in an air/oxygen mixture with a fresh gas flow of 6 L/min. End-tidal sevoflurane concentration, end-tidal carbon dioxide tension (Petco2), and rectal temperature were also monitored. The patients’ lungs were mechanically ventilated to maintain Petco2 at 32 to 38 mm Hg. The fraction of inspired oxygen was adjusted to avoid Spo2 less than 97%.
In the second portion of the study, we evaluated the BIS after induction of general anesthesia. From approximately 10 min after tracheal intubation, the BIS measurements were made at 1-min intervals for 10 min.
Mean arterial BP was maintained at more than 60 mm Hg using 50–100 µg phenylephrine bolus doses, if needed. If a given patient had a BIS value more than 60, the sevoflurane concentration was increased in 0.25% increments. When the BIS decreased to less than 50 after increasing the sevoflurane concentration, the sevoflurane concentration was reduced in 0.25% decrements. Regardless of the adjustment of sevoflurane concentration, the BIS measurements were performed at a predetermined time.
Data are presented as number, mean ± sd, or median and quartiles (25th and 75th percentiles). Patients’ age, height, weight, initial BIS values, mean arterial BP, heart rate, Spo2, Petco2, and rectal temperature were compared using unpaired Student’s t-tests. Intragroup differences of sensory blockade were analyzed using Wilcoxon’s signed rank test. The Mann-Whitney U-test was used to analyze the motor blockade and for the BIS values during the awake phase and during general anesthesia. Statistical significance was assumed for P < 0.05.
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Results |
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The BIS during the awake phase in group R was significantly lower at 12, 13, and 23 min than in group S (Fig. 1) (P < 0.05). No patients in group S had the BIS lower than 90, whereas 3 patients in group R had BIS less than 80.
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The BIS during general anesthesia with sevoflurane was significantly lower in group R than in group S (Fig. 2) (P < 0.0001). Nine patients in group S had a BIS higher than 60, whereas no patient in group R had a BIS higher than 60. This difference was statistically significant (P < 0.0005). The end-tidal sevoflurane concentration had to be increased to 1.0–2.0% in 5 of 9 patients in whom the BIS was higher than 60 in group S. There were no patients in group R who required an increase of sevoflurane concentration. The sevoflurane concentration in group S at the end of the second study period was 0.93 ± 0.37% (mean ± sd), whereas the sevoflurane concentration in group R was 0.75%.
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Discussion |
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The mechanism of sedative effects caused by neuraxial anesthesia has been shown to be associated with blockade of both motor and sensory activity (8). Regarding motor afferents during the awake phase, epidural anesthesia with 5 mL of 0.75% ropivacaine did not produce neuromuscular blockade in the lower extremities although it might have caused motor blockade in the abdominal muscles. Therefore, blockade of motor afferents may have caused a minor influence on the sedative effects of epidural anesthesia during the awake phase. Then, during general anesthesia, we used vecuronium 0.15 mg/kg IV in both groups. Because an identical dose was used, muscle relaxation would have been comparable in the groups. Blockade of motor afferents could have induced little effect on the greater degree of sedation in group R during general anesthesia. Concerning sensory afferents, epidural anesthesia blocks sensory perceptions. Sensory afferents include noxious and non-noxious perceptions. Because we performed the BIS measurements before the surgical procedures, there was only the blockade of non-noxious sensory activity during the study period. Therefore, the sedative effects produced by epidural anesthesia in the present study may have been mainly associated with blockade of non-noxious sensory activity and partly associated with blockade of motor activity.
Other possible mechanisms of the sedative effects of epidural anesthesia could include circulating ropivacaine contributing to general anesthesia. Epidural administration of ropivacaine has been shown to result in a rapid rise with a peak at 12–60 minutes and gradual decline with a half-life of 3.6–5.8 hours in plasma concentration (9,10). McCartney et al. (11) reported that IV ropivacaine 45 mg did not produce any signs of effects on the central nervous system. However, IV local anesthetics such as lidocaine decreased the minimum alveolar concentration of halothane in a dose-dependent fashion (12). It could not be excluded that systemically absorbed ropivacaine acted on the brain to produce general anesthetic effects.
Although epidural anesthesia decreased the BIS during the awake phase, the median BIS in the epidural ropivacaine group was 89–92 and that in the epidural saline group was 93–94. A BIS of more than 85 indicates awake and intact memory (13). Another report suggested that the BIS between 100 and 80 may be no different in probability of a positive response (6). Therefore, awareness, recall, and cognitive function would have been maintained in the epidural ropivacaine group during the awake phase, although the BIS decreased significantly. The decreased BIS in the epidural ropivacaine group during the awake phase might have little meaning in the clinical setting.
It has been reported that sensory block extending to the high thoracic level (T2-4) resulted in increased sedation in spinal anesthesia (14). We observed in the present study that sensory block reached, on average, the fourth thoracic dermatome 20 minutes after the epidural ropivacaine injection. Times until maximum cephalad and caudad spread of sensory blockade with epidural ropivacaine were reported as 20 and 15 minutes, respectively (15). Thus, high thoracic sensory blockade was established at the times of the BIS measurements during the awake phase (22 and 23 minutes) and during general anesthesia. Nevertheless, our study showed that epidural anesthesia with high thoracic sensory blockade did not produce profound sedative effects during the awake phase. Because epidural anesthesia with similar sensory block level caused profound sedation during general anesthesia, some factors other than level of sensory blockade should have been involved in the synergistic interaction between epidural and general anesthesia. Before induction of general anesthesia, there are physical, tactile, auditory, and visual stimulation, including BP measurement by BP cuff, sound from electrocardiogram monitor, and conversation among operating room staff. It may be possible that those stimuli would counteract the sedative effects associated with epidural anesthesia during the awake phase.
Combined general and epidural anesthesia causes hypotension in a large proportion of patients. Mean arterial BP less than 50 to 55 mm Hg impairs cerebral autoregulation, and decreases cerebral blood flow. The BIS may decrease as a result of reduced cerebral perfusion pressure (16). Thus, hypotension should be avoided during the study period. We have shown in the previous study that ephedrine increased the BIS but phenylephrine did not (17). Therefore, we used phenylephrine in the present study to maintain arterial BP. In agreement with our previous study, the BIS did not alter after the phenylephrine injection in the present study.
In conclusion, epidural anesthesia decreased the BIS during the awake phase and during general anesthesia. The decrease of the BIS associated with the epidural anesthesia was more prominent during general anesthesia than during the awake phase.
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  M. Senturk, B. Gucyetmez, T. Ozkan-Seyhan, M. Karadeniz, S. Dincer, D. Akpir, T. Sengul, and T. Denkel Comparison of the effects of thoracic and lumbar epidural anaesthesia on induction and maintenance doses of propofol during total i.v. anaesthesia Br. J. Anaesth., August 1, 2008; 101(2): 255 - 260. [Abstract] [Full Text] [PDF]
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 J. Zhang, W. Zhang, and B. Li The Effect of Epidural Anesthesia with Different Concentrations of Ropivacaine on Sevoflurane Requirements Anesth. Analg., April 1, 2007; 104(4): 984 - 986. [Abstract] [Full Text] [PDF]
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P < 0.0005, 
P < 0.0001 versus group S.
