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* From the Department of Anesthesiology, Chang Gung Memorial Hospital;
the Department of Public Health, Chang Gung University, Taoyuan; and
the Department of Electronic Engineering, National Penghu Institute of Technology; Penghu, Taiwan, ROC.
Address correspondence to: Dr. Ching-Yue Yang, Department of Anesthesiology, Chang Gung Memorial Hospital, No. 5 Fu-Shing Street, Kweishan, Taoyuan, Taiwan 333, R.O.C. Phone: 886-3-3281200, ext. 3621; Fax: 886-3-3281200 ext, 2793; E-mail 1: yangcy{at}adm.cgmh.org.tw; E-mail 2: yangcy88{at}seed.net.tw
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Abstract |
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Methods: 40 patients scheduled for a laminectomy, posterior spinal fusion, vertebroplasty, or total hip replacement, ASA physical status I or II and aged over 50 yr, were randomly divided into two groups. Thiopental 5 mg·kg–1 iv, fentanyl 2.5 µg·kg–1 iv, and rocuronium 0.7 mg·kg–1 iv were used in the thiopental group (n = 20) for anesthetic induction; the same protocol was used in the propofol group (n = 20) except that 2 mg·kg–1 propofol iv was given instead of thiopental. The AAI, non-invasive blood pressure, and heart rate were measured every minute before induction for three minutes, at 1.5 min post-induction, and then each minute post-intubation for eight minutes.
Results: The AAI increased significantly at one and two minutes after intubation in the thiopental group (to 56.5 ± 18.6 at 1 min and 44.7 ± 18.7 at 2 min after intubation vs 19.9 ± 7.5 at 1.5 min after induction; P < 0.05). Thereafter, AAI values gradually decreased three minutes after intubation. The AAI was inhibited continuously after intubation in the propofol group, and no significant elevation was seen.
Conclusion: Our results, using the AAI to monitor anesthetic depth during induction and tracheal intubation, suggest that at equipotent doses propofol provided a more stable level of anesthesia than did thiopental.
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Introduction |
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Our previous study reported that endotracheal intubation after a thiopental induction in elderly patients may induce temporary hypertension and tachycardia even in the amnesic phase.9 Because the extent of the blood pressure increase is so high, it may increase morbidity due to cardiac and neurological adverse effects. If we use propofol for intubation in elderly patients, there is significantly less post-intubation hypertension and tachycardia. How does anesthetic depth change when using these agents for anesthetic induction and intubation, and how does the anesthetic depth correlate with post-intubation hypertension and tachycardia? The answers are not clear at present. We hypothesized that propofol induces deeper anesthesia than does thiopental, so propofol should produce less hypertension and tachycardia. The objective of this study was to compare the anesthetic depth during induction of anesthesia with either propofol or thiopental for patients aged over 50 yr. The anesthetic depth was assessed with the AAI.
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Methods |
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Data analysis
Data are presented as the mean and standard deviation (SD). Two-way analysis of variance (ANOVA) with repeated measures was used to examine how continuous variables (such as AAI, MBP, and HR) differed within the study period between the two study groups. Interactions between time and study groups were examined first. Tukey’s HSD multiple comparisons were made to locate where differences existed. The mean square error was used for multiple comparisons. Computations were carried out in the ANOVA model with the main effect and interactions according to Hines’s report.10 All P values presented were two-sided, and the significance level was 0.05.
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Results |
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Response to anesthetic induction
Before anesthetic induction, MBP, AAI, and HR were similar in the thiopental and propofol groups (Figures 1
and 2). The AAI decreased in all groups 1.5 min after thiopental or propofol induction (83.2 ± 8.7 vs 19.9 ± 7.5 in the thiopental group and 82.4 ± 11 vs 10.8 ± 4.6 in the propofol group, P < 0.05 respectively, Figure 1). As for MBP and HR, only MBP in the propofol group was significantly reduced after iv induction (P < 0.05, Figure 2). There was no significant change in MBP in the thiopental group or HR in either group after anesthetic induction.
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). Thereafter, AAI values gradually decreased in the thiopental group (Figure 1). However, AAI values remained low after intubation in the propofol group (Figure 1). Intubation was not associated with an increase in MBP in the propofol group (P > 0.05, Figure 2). In the thiopental group, intubation produced a significant elevation in blood pressure one minute after intubation when compared with control (P < 0.05, Figure 2). MBP in the thiopental group was also higher than that in the propofol group from one to four minutes after intubation (P < 0.05, Figure 2). Intubation was not associated with any change in HR in the propofol group when compared with control (P > 0.05, Figure 2). However, HR was significantly elevated in the thiopental group one minute after intubation when compared with the control (P < 0.05, Figure 2). There was no difference in the HR after intubation between groups. |
Discussion |
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Recently, the AAI was developed to assess the depth of anesthesia.6 Recent articles report that the AAI is an accurate indicator of the level of anesthetic depth and may be more valuable when monitoring depth of sedation than the bispectral index.7,8 We chose this technique for continuous monitoring of anesthetic depth after induction of anesthesia and intubation.
Propofol and thiopental are both popular anesthetic induction agents.11,12 We previously reported that tracheal intubation induced less hypertension and tachycardia when propofol was used for induction. Thiopental did not inhibit hypertension or tachycardia induced by tracheal intubation.9 Although cardiac inhibition and vasodilation from propofol may produce hypotension and bradycardia,11–13 other commonly used general anesthetics, including thiopental, are similar.11,14,15 For example, Mouren et al. reported that propofol did not inhibit the myocardial performance of a blood-perfused isolated heart, but that thiopental did.16 Therefore, cardiac inhibition or vasodilation might not be the only factor in the inhibition of hypertension and tachycardia which can be found during tracheal intubation with propofol anesthesia. Inhibition of those actions by propofol may also originate in the central nervous system. Articles have reported that propofol is a good amnesic sedative and centrally inhibits the cardiovascular system especially in the cardiovascular control center, the medulla.17,18 Our results show that the AAI decreased rapidly after propofol or thiopental induction. However, the AAI increased in response to intubation in patients receiving thiopental. It appeared to be a reaction reflecting insufficient anesthetic depth, although patients did not completely regain consciousness. This reaction was not observed in the propofol group where the AAI remained low. Changes in blood pressure and heart rate paralleled changes in the AAI, suggesting that anesthetic depth is closely related to changes in BP and HR. However there is no evidence that the mechanisms by which noxious stimulation increase the AAI and MBP/HR are the same.
In summary, we used the AAI to monitor anesthetic depth during induction of anesthesia and tracheal intubation, and demonstrated that propofol 2 mg·kg–1 iv provides a more stable anesthetic depth than does thiopental 5 mg·kg–1 iv in patients > 50 yr. Propofol is also associated with less hypertension and tachycardia in response to tracheal intubation.
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Footnotes |
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References |
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2 Gajraj RJ, Doi M, Mantzaridis H, Kenny GN. Analysis of the EEG bispectrum, auditory evoked potentials and the EEG power spectrum during repeated transitions from consciousness to unconsciousness. Br J Anaesth 1998; 80: 46–52.
3 Gajraj RJ, Doi M, Mantzaridis H, Kenny GN. Comparison of bispectral EEG analysis and auditory evoked potentials for monitoring depth of anaesthesia during propofol anaesthesia. Br J Anaesth 1999; 82: 672–8.
4 Sebel PS, Heneghan CP, Ingram DA. Evoked responses-a neurophysiological indicator of depth of anaesthesia (Editorial). Br J Anaesth 1985; 57: 841–2.
5 Iselin-Chaves IA, Moalem HE, Gan TJ, Ginsberg B, Glass PS. Changes in the auditory evoked potentials and the bispectral index following propofol or propofol and alfentanil. Anesthesiology 2000; 92: 1300–10.[Medline]
6 Jensen EW, Nygaard M, Henneberg SW. On-line analysis of middle latency auditory evoked potentials (MLAEP) for monitoring depth of anaesthesia in laboratory rats. Med Eng Phys 1998; 20: 722–8.[Medline]
7 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]
8 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.
9 Yang CY, Hsu JC, Lin CM, Huang SJ, Chung HS, Shyr MH. Hemodynamic responses of thiopental and propofol in different-aged patients during endotracheal intubation. Chang Gung Med J 2001; 24: 376–82.[Medline]
10 Hines WG. Pragmatics of pooling in ANOVA tables. Am Statist 1996; 50: 127–39.
11 Vohra A, Thomas AN, Harper NJ, Pollard BJ. Non-invasive measurement of cardiac output during induction of anaesthesia and tracheal intubation: thiopentone and propofol compared. Br J Anaesth 1991; 67: 64–8.
12 Sellgren J, Ejnell H, Elam M, Ponten J, Wallin BG. Sympathetic muscle nerve activity, peripheral blood flows, and baroreceptor reflexes in humans during propofol anesthesia and surgery. Anesthesiology 1994; 80: 534–44.[Medline]
13 Park WK, Lynch III C. Propofol and thiopental depression of myocardial contractility. A comparative study of mechanical and electrophysiologic effects in isolated guinea pig ventricular muscle. Anesth Analg 1992; 74: 395–405.
14 Lindgren L, Yli-Hankala A, Randell T, Kirvela M, Scheinin M, Neuvonen PJ. Hemodynamic and cate-cholamine responses to induction of anaesthesia and tracheal intubation: comparison between propofol and thiopentone. Br J Anaesth 1993; 70: 306–10.
15 GinT, O’Meara ME, Kan AF, Leung RK, Tan P, Yau G. Plasma catecholamines and neonatal condition after induction of anaesthesia with propofol or thiopentone at caesarean section. Br J Anaesth 1993; 70: 311–6.
16 Mouren S, Baron JF, Albo C, Szekely B, Arthaud M, Viars P. Effects of propofol and thiopental on coronary blood flow and myocardial performance in an isolated rabbit heart. Anesthesiology 1994; 80: 634–41.[Medline]
17 Yang CY, Luk HN, Chen SY, Wu Chai CY. Propofol inhibits medullary pressor mechanisms in cats. Can J Anaesth 1997; 44: 775–81.
18 Krassioukov AV, Gelb AW, Weaver LC. Action of propofol on central sympathetic mechanisms controlling blood pressure. Can J Anaesth 1993; 40: 761–9.
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