Nunes Rogean Rodrigues, Cavalcante Sara Lúcia
Serviço de Anestesiologia do São Lucas, Hospital de Cirurgia e Anestesia, Fortaleza, CE.
Rev Bras Anestesiol. 2002 Apr;52(2):133-45.
Dexmedetomidine, an alpha2-adrenergic agonist, has been described as being able to decrease the demand for both venous and inhalational agents. This study aimed at evaluating the influence of Dexmedetomidine upon sevoflurane end-expiratory concentration (EC) with monitoring the depth of anesthesia.
Participated in this study 40 female adult patients, physical status ASA I, submitted to gynecological laparoscopy under general anesthesia maintained with sevoflurane, who were randomly divided in two groups: Group I (n=20), without dexmedetomidine; and Group II (n=20), with dexmedetomidine, in continuous infusion, as follows: Rapid phase (1 microg kg(-1) in 10 min(-1)) 10 minutes before anesthesia induction, followed by a maintenance phase (0.4 microg kg(-1) h(-1)) throughout the surgery. The following parameters were analyzed: BP, HR, BIS, SEF 95%, delta%, suppression rate (SR), rSO2, CE, SpO2 and P(ET)CO2, in the following moments: M1 - before dexmedetomidine or 0.9% saline infusion; M2 - prior to intubation; M3 - following intubation; M4 - before incision; M5 - following incision; M6 - before CO2 inflation; M7 - following CO2 inflation; M8 - 10 min after CO2 inflation; M9 - 10 min after M8; M10 - 20 min after M8; M11 - 30 min after M8; M12 - 40 min after M8; and M13 - at emergence. Time for emergence and hospital discharge were also recorded.
Dexmedetomidine has decreased sevoflurane end-expiratory concentration from M4 to M13 (p<0.05) when comparing Group I and Group II. No clinically significant changes were observed in hemodynamic parameters. Time for emergence in Groups I and II was 11 +/- 0.91 min. and 6.35 +/- 0.93 min., respectively (p < 0.05). Time for hospital discharge was 7.45 +/- 0.69 h in Group I and 8.37 +/- 0.88 h in Group II (p < 0.05).
Dexmedetomidine was effective in decreasing sevoflurane end-expiratory concentration while maintaining hemodynamic stability without impairing time for hospital discharge, in addition to promoting an earlier emergence.
右美托咪定是一种α2肾上腺素能激动剂，已被描述为能够减少静脉和吸入性麻醉剂的用量。本研究旨在通过监测麻醉深度来评估右美托咪定对七氟醚呼气末浓度（EC）的影响。
40例ASA I级成年女性患者参与本研究，她们在七氟醚维持的全身麻醉下行妇科腹腔镜手术，并被随机分为两组：I组（n = 20），未使用右美托咪定；II组（n = 20），持续输注右美托咪定，具体如下：麻醉诱导前10分钟快速输注阶段（1微克/千克，10分钟内输注完毕），随后在整个手术过程中维持输注阶段（0.4微克/千克·小时）。分析以下参数：血压（BP）、心率（HR）、脑电双频指数（BIS）、95%频谱边缘频率（SEF 95%）、δ指数（delta%）、抑制率（SR）、局部脑血氧饱和度（rSO2）、呼气末浓度（CE）、脉搏血氧饱和度（SpO2）和呼气末二氧化碳分压（P(ET)CO2），在以下时刻进行测量：M1 - 右美托咪定或0.9%生理盐水输注前；M2 - 气管插管前；M3 - 气管插管后；M4 - 手术切口前；M5 - 手术切口后；M6 - CO2气腹前；M7 - CO2气腹后；M8 - CO2气腹后10分钟；M9 - M8后10分钟；M10 - M8后20分钟；M11 - M8后30分钟；M12 - M8后40分钟；以及M13 - 苏醒时。记录苏醒时间和出院时间。
比较I组和II组时，右美托咪定使七氟醚呼气末浓度从M4至M13降低（p < 0.05）。血流动力学参数未观察到具有临床意义的变化。I组和II组的苏醒时间分别为11 ± 0.91分钟和6.35 ± 0.93分钟（p < 0.05）。I组的出院时间为7.45 ± 0.69小时，II组为8.37 ± 0.88小时（p < 0.05）。
右美托咪定在维持血流动力学稳定的同时，有效降低了七氟醚呼气末浓度，且不影响出院时间，此外还促进了更早的苏醒。
