The Influence of Remifentanil on the Dynamic Relationship between Sevoflurane and Surrogate Anesthetic Effect Measures Derived from the EEG

The Influence of Remifentanil on the Dynamic Relationship between Sevoflurane and Surrogate Anesthetic Effect Measures Derived from the EEG
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瑞芬太尼对七氟醚与脑电图替代麻醉效果测量之间动态关系的影响

DOI:
10.1097/00000542-200203000-00009
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发表时间:
2002
期刊:
影响因子:
8.8
通讯作者:
A. Dahan
A. Dahan
中科院分区:
医学1区
文献类型:
--
作者:
E. Olofsen;J. Sleigh;A. Dahan

文献摘要

被引文献

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作者使用来自脑电图的三个参数:95%频谱边缘频率(SEF)、典型单变量参数(CUP)和脑电双频指数(BIS),模拟瑞芬太尼对七氟烷动力学的影响。方法36例美国麻醉医师协会评定为I级或II级的患者,瑞芬太尼靶浓度分别为0 ng/ml、2 ng/ml、4 ng/ml和8 ng/ml,其中12例患者的瑞芬太尼靶浓度为0 ng/ml,8例患者的瑞芬太尼靶浓度为2 ng/ml,8例患者的瑞芬太尼靶浓度为4 ng/ml,8例患者的瑞芬太尼靶浓度为8 ng/ml。接下来(手术前),对呼气末七氟烷浓度(FET,sevo)进行了几次逐步改变。数据采集系统同时记录FET、sevo、原始脑电图、BIS和SEF。作者使用效应室和抑制性S形EMAX模型的组合来描述FET、sevo与BIS、SEF和CUP之间的关系。使用群体数据分析程序NONMEM估计模型参数(t1/2ke 0、EMAX、EMIN、C50、CUP权重因子)。测定了显著的瑞芬太尼模型参数依赖性(P < 0.01)。结果根据SEF测定,瑞芬太尼对t1/2ke 0(1.91 ± 0.26 min [平均值±标准误差])没有影响,但引起C50增加(基线= 1.48 ± 0.12%; 8 ng/ml时增加80%)和EMIN降低(基线= 10.8 ± 0.6 Hz; 8 ng/ml时降低80%)。根据CUP测定,瑞芬太尼导致t1/2ke 0呈剂量依赖性降低(基线= 4.31 ± 1.00 min; 8 ng/ml时降低60%),对C50无影响(基线= 0.88 ± 0.13%)。根据BIS测定,瑞芬太尼导致t1/2ke 0呈剂量依赖性降低(基线值= 3.11 ± 0.32 min; 8 ng/ml时降低40%),而不影响C50(基线值= 1.12 ± 0.05%)。合并数据集的中位R2值分别为SEF 0.815、CUP 0.933(P < 0.01 vs. SEF)和BIS 0.952(P < 0.01 vs. SEF和CUP)。瑞芬太尼的加入仅增加了CUP的R2值。结论瑞芬太尼可促进七氟醚的血脑平衡,而不影响BIS和CUP测定的催眠效力。在R2方面,作者的药效学模型最好地描述了麻醉-BIS关系。
Background The authors modeled the influence of remifentanil on the dynamics of sevoflurane using three parameters derived from the electroencephalogram: 95% spectral edge frequency (SEF), canonical univariate parameter (CUP), and Bispectral Index (BIS). Methods Thirty-six patients with American Society of Anesthesiologists physical status class I or II were recruited, of which 12 received a target remifentanil concentration of 0 ng/ml, eight 2 ng/ml, eight 4 ng/ml, and another eight 8 ng/ml. Next (before surgery), several step-wise changes in the end-tidal sevoflurane concentration (FET,sevo) were performed. A data acquisition system simultaneously recorded FET,sevo, the raw electroencephalogram, BIS, and SEF. The authors used a combination of an effect compartment and an inhibitory sigmoid EMAX model to describe the relation between FET,sevo and BIS, SEF, and CUP. Model parameters (t1/2ke0, EMAX, EMIN, C50, &ggr;, CUP weight factors) were estimated using the population data analysis program NONMEM. Significant remifentanil model parameter dependencies (P < 0.01) were determined. Results Determined from SEF, remifentanil had no effect on t1/2ke0 (1.91 ± 0.26 min [mean ± standard error]) but caused an increase in C50 (baseline = 1.48 ± 0.12%; 80% increase at 8 ng/ml) and decrease in EMIN (baseline = 10.8 ± 0.6 Hz; 80% reduction at 8 ng/ml). Determined from CUP, remifentanil caused a dose-dependent decrease in t1/2ke0 (baseline = 4.31 ± 1.00 min; 60% decrease at 8 ng/ml), with no effect on C50 (baseline = 0.88 ± 0.13%). Determined from BIS, remifentanil caused a dose-dependent decrease in t1/2ke0 (baseline value = 3.11 ± 0.32 min; 40% decrease at 8 ng/ml), without affecting C50 (baseline = 1.12 ± 0.05%). Median R2 values of the pooled data set were 0.815 for SEF, 0.933 for CUP (P < 0.01 vs. SEF), and 0.952 for BIS (P < 0.01 vs. SEF and CUP). Addition of remifentanil increased the R2 values for CUP only. Conclusions Remifentanil accelerates sevoflurane blood–brain equilibration without affecting its hypnotic potency as determined from BIS and CUP. In terms of R2, the authors’ pharmacodynamic model describes the anesthetic–BIS relation best.