Saito S, Miyoshi S, Yoshikawa D, Shimada H, Morita T, Kitani Y
Department of Anesthesiology and Reanimatology, Gunma University School of Medicine, Maebashi, Japan.
Anesth Analg. 1996 Oct;83(4):726-30. doi: 10.1097/00000539-199610000-00011.
Electroconvulsive therapy (ECT) increases neuronal energy consumption and alters systemic hemodynamics. We examined the effects of ECT on regional cerebral oxygen saturation (rSo2) using a near-infrared spectro-photometer. Heart rate (HR), mean arterial blood pressure (MAP), and rSo2 were continuously monitored throughout ECT under general anesthesia in 43 patients. In all subjects, rSo2 changed in a consistent pattern during ECT, initially decreasing (-9.4% +/- 0.9%) just after application of the electrical current and subsequent increasing (8.7% +/- 0.9%) beyond the pre-ECT value. A close correlation was demonstrated between the increase in rSo2 and the mean blood pressure after the electrical shock (r2 = 0.832, P < 0.0001). We conclude that ECT initially may increase cerebral metabolic rate of oxygen more than cerebral blood flow and that rapidly increasing blood pressure transiently may overwhelm cerebral pressure autoregulation.
电休克疗法(ECT)会增加神经元能量消耗并改变全身血流动力学。我们使用近红外分光光度计研究了ECT对局部脑氧饱和度(rSo2)的影响。在全身麻醉下,对43例患者在ECT全过程中持续监测心率(HR)、平均动脉血压(MAP)和rSo2。在所有受试者中,ECT期间rSo2呈一致模式变化,在施加电流后最初下降(-9.4%±0.9%),随后升高(8.7%±0.9%)超过ECT前的值。电击后rSo2的升高与平均血压之间存在密切相关性(r2 = 0.832,P < 0.0001)。我们得出结论,ECT最初可能使脑氧代谢率的增加超过脑血流量,并且血压的快速短暂升高可能会使脑压力自动调节功能不堪重负。