Weiskopf R B, Cahalan M K, Eger E I, Yasuda N, Rampil I J, Ionescu P, Lockhart S H, Johnson B H, Freire B, Kelley S
Department of Anesthesia, University of California, San Francisco 94143-0648.
Anesth Analg. 1991 Aug;73(2):143-56.
The cardiovascular actions of three concentrations of desflurane (formerly I-653), a new inhalation anesthetic, were examined in 12 unmedicated normocapnic, normothermic male volunteers. We compared the effects of 0.83, 1.24, and 1.66 MAC desflurane with measurements obtained while the same men were conscious. Desflurane caused a dose-dependent increase in right-heart filling pressure and a decrease in systemic vascular resistance and mean systemic arterial blood pressure. As measured by echocardiography, left ventricular end-diastolic area did not change except for a small increase at 1.66 MAC desflurane, and systolic wall stress was less at all concentrations of desflurane than during the conscious state. Desflurane did not change cardiac index or left ventricular ejection fraction. Heart rate did not change at 0.83 MAC, but progressively increased with deeper desflurane anesthesia. Stroke volume index was less at all concentrations of desflurane than while the men were conscious, but desflurane did not alter the velocity of ventricular circumferential fiber shortening. Mixed venous blood PO2 and oxyhemoglobin saturation were higher during all concentrations of desflurane anesthesia than during the conscious state. No volunteer developed a metabolic acidosis. We conclude that desflurane with controlled ventilation and constant PaCO2 causes cardiovascular depression, as indicated by the increased cardiac filling pressure and decreased stroke volume index and by no change in the velocity of circumferential fiber shortening in the presence of decreased systolic wall stress. However, cardiac output is well maintained, and heart rate does not increase at light levels of anesthesia. The cardiovascular actions of 0.83 and 1.66 MAC desflurane were also reexamined in 6 of the 12 men during the seventh hour of anesthesia. Prolonged desflurane anesthesia resulted in lesser cardiovascular depression than was evidenced during the first 90 min. The measures of cardiac filling (central venous pressure and left ventricular end-diastolic cross-sectional area) did not differ between the early and late periods of anesthesia. Systemic vascular resistance decreased further during the late period, but systolic wall stress did not differ between the two time periods. During the seventh hour of desflurane anesthesia, heart rate and cardiac index were higher at both anesthetic concentrations than during the first 90 min of anesthesia. Left ventricular ejection fraction and velocity of fiber shortening did not change with duration of desflurane anesthesia. Oxygen consumption, oxygen transport, the ratio of the two, mixed venous PO2, and mixed venous oxyhemoglobin saturation (SO2) increased late in the anesthetic in comparison with the first 90 min.
在12名未用药、正常碳酸血症、体温正常的男性志愿者身上，研究了新型吸入麻醉药地氟烷（原I-653）三种浓度的心血管作用。我们将0.83、1.24和1.66MAC地氟烷的作用与这些男性清醒时的测量结果进行了比较。地氟烷使右心充盈压呈剂量依赖性增加，全身血管阻力和平均体动脉血压降低。通过超声心动图测量，除在1.66MAC地氟烷时有小幅度增加外，左心室舒张末期面积未改变，且在所有地氟烷浓度下，收缩期壁应力均低于清醒状态时。地氟烷未改变心脏指数或左心室射血分数。在0.83MAC时心率未改变，但随着地氟烷麻醉加深心率逐渐增加。在所有地氟烷浓度下，每搏量指数均低于男性清醒时，但地氟烷未改变心室圆周纤维缩短速度。在所有地氟烷麻醉浓度下，混合静脉血氧分压和氧合血红蛋白饱和度均高于清醒状态。没有志愿者出现代谢性酸中毒。我们得出结论，在控制通气和恒定PaCO2的情况下，地氟烷会导致心血管抑制，表现为心脏充盈压升高、每搏量指数降低，以及在收缩期壁应力降低的情况下圆周纤维缩短速度未改变。然而，心输出量维持良好，在浅麻醉水平时心率不增加。在12名男性中的6名麻醉第7小时时，再次检查了0.83和1.66MAC地氟烷的心血管作用。长时间地氟烷麻醉导致的心血管抑制程度低于最初90分钟时。心脏充盈指标（中心静脉压和左心室舒张末期横截面积）在麻醉早期和晚期无差异。在后期全身血管阻力进一步降低，但两个时间段的收缩期壁应力无差异。在地氟烷麻醉第7小时时，两个麻醉浓度下的心率和心脏指数均高于麻醉最初90分钟时。左心室射血分数和纤维缩短速度不随地氟烷麻醉持续时间而改变。与最初90分钟相比，麻醉后期氧耗、氧运输、两者的比值、混合静脉血氧分压和混合静脉氧合血红蛋白饱和度（SO2）均增加。
