Walker L K, Short B L, Gleason C A, Jones M D, Traystman R J
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, MD.
Crit Care Med. 1994 Feb;22(2):291-8. doi: 10.1097/00003246-199402000-00021.
To determine if the institution of extracorporeal membrane oxygenation (ECMO) alters the cerebrovascular response to changes in PaCO2.
Prospective, randomized, controlled animal trial.
Anesthetized 1- to 7-day-old lambs of mixed breed (n = 16).
University research laboratory.
The experimental group was placed on ECMO. Both experimental and control groups (n = 8) were exposed to three concentrations of PaCO2 (hypocarbia, normocarbia, and hypercarbia) by varying mechanical ventilation and by adding carbon dioxide to the ventilator gases.
Cerebral blood flow was measured by the radiolabeled microsphere method. Arterial blood gases and sagittal sinus blood gases were drawn at the time of cerebral blood flow measurement so that cerebral metabolism, cerebral oxygen transport, and extraction could be calculated. In the control group, as PaCO2 increased from 34 +/- 2 (SD) to 53 +/- 4 torr (4.5 +/- 0.3 to 7.1 +/- 0.5 kPa), cerebral blood flow increased from 53 +/- 12 to 147 +/- 50 mL/min/100 g. This increase in cerebral blood flow was not different from that of the ECMO group, where PaCO2 increased from 33 +/- 2 to 56 +/- 3 torr (4.4 +/- 0.3 to 7.5 +/- 0.4 kPa) and cerebral blood flow increased from 48 +/- 17 to 106 +/- 38 mL/min/100 g. As PaCO2 decreased from 34 +/- 2 to 19 +/- 2 torr (4.5 +/- 0.27 to 2.5 +/- 0.27 kPa), cerebral blood flow decreased from 53 +/- 12 to 43 +/- 8 mL/min/100 g in the control group. This decrease was not different from that of the ECMO group, where cerebral blood flow decreased from 48 +/- 17 to 39 +/- 10 mL/min/100 g as PaCO2 decreased from 33 +/- 2 to 22 +/- 3 torr (4.4 +/- 0.3 to 2.9 +/- 0.4 kPa). When regional cerebral blood flow was analyzed, no regional differences in the cerebrovascular responses to PaCO2 between ECMO and control groups were found. The cerebral metabolic rate was not different between ECMO and control groups at any level of PaCO2, nor was the cerebral metabolic rate affected by changes in PaCO2. Oxygen extraction increased with hypocarbia and decreased with hypercarbia in a similar fashion in both ECMO and control groups.
The cerebrovascular response to changes in PaCO2 was unaffected by ECMO.
确定体外膜肺氧合(ECMO)的应用是否会改变脑血管对动脉血二氧化碳分压(PaCO2)变化的反应。
前瞻性、随机、对照动物试验。
1至7日龄的杂种麻醉羔羊(n = 16)。
大学研究实验室。
将实验组置于ECMO支持下。实验组和对照组(n = 8)通过改变机械通气并向通气气体中添加二氧化碳,使其暴露于三种PaCO2浓度(低碳酸血症、正常碳酸血症和高碳酸血症)环境中。
采用放射性微球法测量脑血流量。在测量脑血流量时采集动脉血气和矢状窦血气,以便计算脑代谢、脑氧输送和氧摄取情况。在对照组中,当PaCO2从34±2(标准差)升至53±4托(4.5±0.3至7.1±0.5千帕)时,脑血流量从53±12增至147±50毫升/分钟/100克。脑血流量的这种增加与ECMO组并无差异,在ECMO组中,PaCO2从33±2升至56±3托(4.4±0.3至7.5±0.4千帕),脑血流量从48±17增至106±38毫升/分钟/100克。当PaCO2从34±2降至19±2托(4.5±0.27至2.5±0.27千帕)时,对照组脑血流量从53±12降至43±8毫升/分钟/100克。这种减少与ECMO组并无差异,在ECMO组中,随着PaCO2从33±2降至22±3托(4.4±0.3至2.9±0.4千帕),脑血流量从48±17降至39±10毫升/分钟/100克。分析局部脑血流量时,未发现ECMO组与对照组在脑血管对PaCO2的反应上存在局部差异。在任何PaCO2水平下,ECMO组与对照组的脑代谢率均无差异,且脑代谢率也不受PaCO2变化的影响。在ECMO组和对照组中,低碳酸血症时氧摄取增加,高碳酸血症时氧摄取减少,二者变化方式相似。
ECMO未影响脑血管对PaCO2变化的反应。