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脑血管循环的计算机模拟:麻醉诱导期间颅内血流动力学评估

Computer simulation of cerebrovascular circulation: assessment of intracranial hemodynamics during induction of anesthesia.

作者信息

Bekker A, Wolk S, Turndorf H, Kristol D, Ritter A

机构信息

Department of Anesthesiology, New York University Medical Center, New York 10016, USA.

出版信息

J Clin Monit. 1996 Nov;12(6):433-44. doi: 10.1007/BF02199704.

Abstract

OBJECTIVE

The purpose of this project was to develop a computer model of cerebrovascular hemodynamics interacting with a pharmacokinetic drug model to examine the effects of various stimuli on cerebral blood flow and intracranial pressure during anesthesia.

METHODS

The mathematical model of intracranial hemodynamics is a seven-compartment, constant-volume system. A series of resistance relate blood and cerebrospinal fluid fluxes to pressure gradients between compartments. Arterial, venous, and tissue compliance are also included. Autoregulation is modeled by transmural pressure-dependent, arterial-arteriolar resistance. The effect of a drug (thiopental) on cerebrovascular circulation was simulated by a variable arteriolar-capillary resistance. Thiopental concentration was predicted by a three-compartment, pharmacokinetic model. The effect site compartment was included to account for a disequilibrium between drug plasma and biophase concentrations. The model was validated by comparing simulation results with available experimental observations. The simulation program is written in VisSim dynamic simulation language for an IBM-compatible PC.

RESULTS

The model developed was used to calculate the cerebral blood flow and intracranial pressure changes that occur during the induction phase of general anesthesia. Responses to laryngoscopy and intubation were predicted for simulated patients with elevated intracranial pressure and non-autoregulated cerebral circulation. Simulation shows that the induction dose of thiopental reduces intracranial pressure up to 15%. The duration of this effect is limited to less than 3 minutes by rapid redistribution of thiopental and cerebral autoregulation. Subsequent laryngoscopy causes acute intracranial hypertension, exceeding the initial intracranial pressure. Further simulation predicts that this untoward effect can be minimized by an additional dose of thiopental administered immediately prior to intubation.

CONCLUSION

The presented simulation allows comparison of various drug administration schedules to control intracranial pressure and preserve cerebral blood flow during induction of anesthesia. The model developed can be extended to analyze more complex intraoperative events by adding new submodels.

摘要

目的

本项目旨在开发一种脑血管血液动力学与药代动力学药物模型相互作用的计算机模型,以研究麻醉期间各种刺激对脑血流量和颅内压的影响。

方法

颅内血液动力学的数学模型是一个七室恒容系统。一系列阻力将血液和脑脊液流量与各室之间的压力梯度相关联。还包括动脉、静脉和组织顺应性。通过跨壁压力依赖性动脉 - 小动脉阻力对自动调节进行建模。通过可变的小动脉 - 毛细血管阻力模拟药物(硫喷妥钠)对脑血管循环的影响。硫喷妥钠浓度由三室药代动力学模型预测。加入效应室以解释药物血浆浓度与生物相浓度之间的不平衡。通过将模拟结果与可用的实验观察结果进行比较来验证该模型。模拟程序用VisSim动态模拟语言编写,用于IBM兼容个人计算机。

结果

所开发的模型用于计算全身麻醉诱导期期间发生的脑血流量和颅内压变化。对颅内压升高和脑循环无自动调节的模拟患者预测了喉镜检查和插管的反应。模拟表明,硫喷妥钠的诱导剂量可使颅内压降低高达15%。由于硫喷妥钠的快速再分布和脑自动调节,这种效应的持续时间限制在不到3分钟。随后的喉镜检查会导致急性颅内高压,超过初始颅内压。进一步的模拟预测,在插管前立即给予额外剂量的硫喷妥钠可将这种不良效应降至最低。

结论

所呈现的模拟允许比较各种给药方案,以在麻醉诱导期间控制颅内压并维持脑血流量。所开发的模型可以通过添加新的子模型扩展以分析更复杂的术中事件。

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