[Hemodynamic effects of the induction of general anesthesia after low thoracic epidural anesthesia].

Sixteen ASA 1 or 2 patients scheduled for abdominal surgery were included in the study after they had given their informed consent. Thirty minutes after starting a low-thoracic epidural anaesthesia (median level of sensitivity loss: T5), the patients were randomly given an intravenous bolus injection of either thiopentone (4 mg.kg-1, n = 8) or etomidate (0.5 mg.-1, n = 8), associated with succinylcholine 1 mg.kg-1. One minute after induction of general anaesthesia, the patients were intubated and mechanically ventilated (V(T) 8 ml.kg-1, rate 12 c.min-1). Mean arterial blood pressure (MAP) (oscillometric method), cardiac output (CO) (transthoracic bioimpedance) and heart rate were recorded semi-continuously. Total peripheral resistances (TPR) were calculated using the formula TPR = (MA/CO)*80. There were no differences between the groups in patient age, height, weight, and cardiovascular consequences of epidural anaesthesia. After anaesthetic induction and before endotracheal intubation, there was a slight decrease in CO in both groups, without any change in MAP. After intubation, MAP increased in both groups through peripheral vasoconstriction, whereas CO did not increase further. A significant tachycardia was occurred only seen in the thiopentone group, before and after tracheal intubation. This study showed that thiopentone and etomidate were suitable drugs for anaesthetic induction in a patient under epidural blockade. However, the absence of tachycardia following etomidate may be beneficial in cardiac patients. The monitoring of cardiac output determinants during thiopentone and etomidate anaesthesia require further invasive investigations.