Irita K, Kai Y, Takahashi S
Department of Anesthesiology and Critical Care Medicine, Faculty of Medicine Kyushu University, Fukuoka, Japan.
Fukuoka Igaku Zasshi. 1999 Jan;90(1):14-22.
Little attention has been paid to oxygen demand/supply balance during the cooling phase of cardiopulmonary bypass (CPB). We examined the changes in systemic oxygen utilization caused by the initiation of deep hypothermic CPB.
We calculated the changes in systemic oxygen consumption (VO2) and its related parameters in 5 patients who underwent reconstruction of the aortic arch using deep hypothermic CPB. Rectal temperature was decreased to 18 centigrade on average.
VO2 decreased immediately after the initiation of hypothermic CPB. VO2 decreased by an average of 50% and 64%, while rectal temperatures decreased from 35 to 34 and 32 centigrade, respectively. Hemoglobin-bound oxygen accounted for 68% of VO2 just before CPB and 28% after the rectal temperature decreased to 32 centigrade. This decrease in VO2 correlated with the maximum temperature gradient between the venous and the arterial blood during the cooling phase. The abrupt decrease in VO2 by initiating CPB was associated with an increase in mixed venous oxygen saturation and a decrease in oxygen extraction ratio. VO2 values during the cooling phase were much lower than those during the rewarming phase at any given rectal temperatures. VO2 values at rectal temperatures of 34 and 32 centigrade during the cooling phase of CPB were 40% and 29% of those during the rewarming phase of CPB, respectively. This difference was caused by the changes in VO2 derived from hemoglobin-bound oxygen, and VO2 derived from dissolved oxygen did not show any significant changes during the cooling and the rewarming phase. Hysteresis of VO2 was also observed as a function of the nasopharyngeal temperature. The arterial lactate concentration showed an insignificant but gradual increase during the cooling phase.
These observations suggested that an immediate decrease in VO2 and the following low values of VO2 caused by the initiation of deep hypothermic CPB could not be simply due to a decrease in the metabolic rate for oxygen but rather due to disturbances in oxygen utilization, one of which seemed to be caused by the impaired oxygen release from hemoglobin. It was also suggested that an increase in mixed venous oxygen saturation by initiating hypothermic CPB did not necessarily indicate an adequate oxygen/demand supply balance.
在体外循环（CPB）降温阶段，对氧供需平衡的关注较少。我们研究了深低温CPB启动后引起的全身氧利用变化。
我们计算了5例接受深低温CPB下主动脉弓重建患者的全身氧耗量（VO2）及其相关参数的变化。直肠温度平均降至18摄氏度。
低温CPB启动后VO2立即下降。当直肠温度分别从35降至34和32摄氏度时，VO2平均下降50%和64%。CPB前血红蛋白结合氧占VO2的68%，直肠温度降至32摄氏度后占28%。VO2的这种下降与降温阶段静脉血和动脉血之间的最大温度梯度相关。启动CPB后VO2的突然下降与混合静脉血氧饱和度增加和氧摄取率降低有关。在任何给定的直肠温度下，降温阶段的VO2值均远低于复温阶段。CPB降温阶段直肠温度为34和32摄氏度时的VO2值分别为CPB复温阶段的40%和29%。这种差异是由血红蛋白结合氧产生的VO2变化引起的，而溶解氧产生的VO2在降温和复温阶段均未显示出任何显著变化。VO2还表现为鼻咽温度的函数滞后现象。降温阶段动脉血乳酸浓度呈无显著意义但逐渐升高。
这些观察结果表明，深低温CPB启动后VO2立即下降以及随后的低VO2值并非仅仅由于氧代谢率降低，而是由于氧利用紊乱，其中之一似乎是由于血红蛋白氧释放受损所致。还表明，启动低温CPB后混合静脉血氧饱和度增加并不一定表明氧供需平衡充足。
