Hahn R G
Department of Anaesthesiology, Huddinge University Hospital, Sweden.
Acta Anaesthesiol Scand. 1993 May;37(4):357-60. doi: 10.1111/j.1399-6576.1993.tb03728.x.
This study examined whether the increased haemodilution from fluid loading in patients who develop hypotension at the onset of epidural anaesthesia (EDA) can be explained by high-level blockade or by stress-induced elevation of the blood glucose concentration. In 20 men aged between 53 and 87, crystalloid volume loading was carried out with 10 ml.kg-1 b.w. and EDA was induced with mepivacaine 2% and adrenaline 1:200,000. Irrespective of the blood pressure reaction to the blockade, there was no change in blood glucose level. A strong linear correlation between haemodilution and arterial pressure was found, in spite of unchanged blood glucose levels, in 10 patients in whom EDA was induced with bupivacaine 0.5%, and in 10 patients who received spinal anaesthesia with tetracaine 1%. There was no correlation between the haemodilution and the extent of sensory analgesia. These results support the view that low arterial pressure alone triggers the increased haemodilution observed during EDA-induced hypotension.
本研究探讨了在硬膜外麻醉（EDA）开始时出现低血压的患者中，因液体负荷导致的血液稀释增加是由高位阻滞还是应激诱导的血糖浓度升高所引起。对20名年龄在53至87岁之间的男性患者，按10 ml.kg-1体重进行晶体液负荷，并使用2%甲哌卡因和1:200,000肾上腺素诱导EDA。无论血压对阻滞的反应如何，血糖水平均无变化。在10例用0.5%布比卡因诱导EDA的患者以及10例用1%丁卡因进行脊髓麻醉的患者中，尽管血糖水平未变，但发现血液稀释与动脉压之间存在强烈的线性相关性。血液稀释与感觉镇痛程度之间无相关性。这些结果支持以下观点，即仅动脉压降低就会引发在EDA诱导的低血压期间观察到的血液稀释增加。
