Department of Anesthesia/Critical Care Medicine, Tsuchiura Kyodo General Hospital, 11-7 Manabeshinmachi, 300, Tsuchiura, Ibaraki, Japan.
J Anesth. 1997 Jun;11(2):88-93. doi: 10.1007/BF02480067.
Clonidine premedication has been increasingly used in clinical anesthesia. Though clonidine was found to alter pressor responses to various sympathomimetics, its effect on epidural test dose efficacy to detect intravascular injection has never been evaluated. Eighty healthy patients were randomly assigned to one of four groups, each of which was anesthetized with 1% end-tidal isoflurane and 67% nitrous oxide in oxygen after endotracheal intubation. The control-epinephrine group (n=20) given no clonidine premedication received 3 ml of 1.5% lidocain with 15 μg epinephrine (1:200000) intravenously to simulate an intravenously administered epidural test dose. The control-saline group (n=20) given no clonidine premedication received 3 ml of normal saline intravenously. The clonidine-epinephrine and clonidine-saline groups (n=20 each) were identical to the control groups, but were premedicated with oral clonidine, approximately 5 μg·kg(-1), 90 min before induction of general anesthesia. Heart rate (HR) and systolic blood pressure (SBP) were measured by a blinded observer at 20-s intervals for 4 min after intravenous injections of the test dose or saline. Following intravenous test dose injection, there were no significant diferences between the control-epinephrine and the clonidine-epinephrine groups in mean maximum increments of both HR (28±3vs 30±3 bpm, [mean±standard error], respectively) and SBP (46±6vs 45±4 mmHg, respectively). Six patients in the control-epinephrine and 4 in the clonidine-epinephrine group developed negative HR responses (HR increment <20 bpm). Since HR and SBP were essentially unchanged in the two groups receiving saline, sensitivities (negative predictive values) based on the HR criterion (positive if ≥20 bpm increase in HR) were 80% and 70% (83% and 77%) with and without clonidine premedication, respectively (P>0.05 between groups). However, when a modified HR criterion (positive if ≥10 bpm increase in HR) was used, sensitivities, specificities, and positive and negative predictive values were all 100% with or without clonidine. On the other hand, all of 20 patients in the control-epinephrine and the clonidine-epinephrine groups exhibited positive SBP responses (SBP increment ≥15 mmHg). Therefore, based on the SBP criterion, sensitivities, specificities, and positive and negative predictive values were all found to be 100% regardless of the presence of clonidine. We conclude that oral clonidine 5μg·kg(-1) premedication alters neither (a) hemodynamic responses to the intravenously administered epidural test dose containing 15 μg epinephrine, nor (b) the efficacy for detecting intravascular injection based on either criterion in adult patients under stable isoflurane anesthesia.
可乐定预处理在临床麻醉中越来越多地被使用。尽管可乐定被发现改变了对各种拟交感神经药的升压反应,但它对硬膜外试验剂量检测血管内注射的效果从未被评估过。80 名健康患者被随机分配到四组中的一组,每组在气管插管后用 1%呼气末异氟烷和 67%氧化亚氮麻醉。对照组(肾上腺素组)(n=20)未给予可乐定预处理,静脉给予 3ml 1.5%利多卡因加 15μg 肾上腺素(1:200000),模拟静脉给予硬膜外试验剂量。对照组(生理盐水组)(n=20)未给予可乐定预处理,静脉给予 3ml 生理盐水。氯定-肾上腺素组和氯定-生理盐水组(每组 n=20)与对照组相同,但在全麻诱导前 90 分钟口服约 5μg·kg(-1)的可乐定。静脉注射试验剂量或生理盐水后 4 分钟内,由盲法观察者以 20 秒的间隔测量心率(HR)和收缩压(SBP)。静脉注射试验剂量后,对照组(肾上腺素组)和氯定-肾上腺素组之间的 HR 和 SBP 最大增量的平均最大值无显著差异(分别为 28±3bpm 和 45±4mmHg)。对照组(肾上腺素组)中有 6 例患者和氯定-肾上腺素组中有 4 例患者出现 HR 负反应(HR 增量<20bpm)。由于两组接受生理盐水的 HR 和 SBP 基本不变,基于 HR 标准(如果 HR 增加≥20bpm 则为阳性)的敏感性(阴性预测值)分别为 80%和 70%(分别为 83%和 77%),有或没有可乐定预处理(组间无显著差异)。然而,当使用改良的 HR 标准(如果 HR 增加≥10bpm 则为阳性)时,无论有无可乐定,敏感性、特异性和阳性及阴性预测值均为 100%。另一方面,对照组(肾上腺素组)和氯定-肾上腺素组的 20 例患者均出现 SBP 阳性反应(SBP 增量≥15mmHg)。因此,基于 SBP 标准,无论是否存在可乐定,敏感性、特异性、阳性和阴性预测值均为 100%。我们得出结论,在稳定的异氟烷麻醉下,成人患者口服 5μg·kg(-1)可乐定预处理既不会改变静脉给予含有 15μg 肾上腺素的硬膜外试验剂量的血流动力学反应,也不会改变基于任何标准检测血管内注射的效果。