Bruder N, Stordeur J M, Ravussin P, Valli M, Dufour H, Bruguerolle B, Francois G
Département d'Anesthésie-Réanimation, Hôpital Timone, Marseille, France.
Anesth Analg. 1999 Sep;89(3):674-8. doi: 10.1097/00000539-199909000-00027.
Delayed recovery has been advocated to limit the postoperative stress linked to awakening from anesthesia, but data on this subject are lacking. In this study, we measured oxygen consumption (V(O2)) and plasma catecholamine concentrations as markers of postoperative stress. We tested the hypothesis that delayed recovery and extubation would attenuate metabolic changes after intracranial surgery. Thirty patients were included in a prospective, open study and were randomized into two groups. In Group I, the patients were tracheally extubated as soon as possible after surgery. In Group II, the patients were sedated with propofol for 2 h after surgery. V(O2), catecholamine concentration, mean arterial pressure (MAP), and heart rate (HR) were measured during anesthesia, at extubation, and 30 min after extubation. V(O2) and noradrenaline on extubation and mean V(O2) during recovery were significantly higher in Group II than in Group I (V(O2) for Group I: preextubation 215 +/- 46 mL/min, recovery 198 +/- 38 mL/min; for Group II: preextubation 320 +/- 75 mL/min, recovery 268 +/- 49 mL/min; noradrenaline on extubation for Group I: 207 +/- 76 pg/mL, for Group II: 374 +/- 236 pg/ mL). Extubation induced a significant increase in MAP. MAP, HR, and adrenaline values were not statistically different between groups. In conclusion, delayed recovery after neurosurgery cannot be recommended as a mechanism of limiting the metabolic and hemodynamic consequences from emergence from general anesthesia.
In this study, we tested the hypothesis that delayed recovery after neurosurgery would attenuate the consequences of recovery from general anesthesia. As markers of stress, oxygen consumption and noradrenaline blood levels were higher after delayed versus early recovery. Thus, delayed recovery cannot be recommended as a mechanism of limiting the metabolic and hemodynamic consequences from emergence after neurosurgery.
延迟苏醒被认为可限制与麻醉苏醒相关的术后应激，但关于这一主题的数据尚缺。在本研究中，我们测量了氧耗（V(O2)）和血浆儿茶酚胺浓度作为术后应激的标志物。我们检验了延迟苏醒和拔管会减轻颅内手术后代谢变化这一假设。30例患者纳入一项前瞻性开放性研究，并随机分为两组。第一组患者术后尽快气管拔管。第二组患者术后用丙泊酚镇静2小时。在麻醉期间、拔管时以及拔管后30分钟测量V(O2)、儿茶酚胺浓度、平均动脉压（MAP）和心率（HR）。第二组拔管时的V(O2)和去甲肾上腺素以及恢复期间的平均V(O2)显著高于第一组（第一组V(O2)：拔管前215±46 mL/分钟，恢复时198±38 mL/分钟；第二组：拔管前320±75 mL/分钟，恢复时268±49 mL/分钟；第一组拔管时去甲肾上腺素：207±76 pg/mL，第二组：374±236 pg/mL）。拔管导致MAP显著升高。两组之间MAP、HR和肾上腺素值无统计学差异。总之，神经外科手术后延迟苏醒不能作为限制全身麻醉苏醒引起的代谢和血流动力学后果的一种机制被推荐。
在本研究中，我们检验了神经外科手术后延迟苏醒会减轻全身麻醉苏醒后果这一假设。作为应激标志物，延迟苏醒后的氧耗和去甲肾上腺素血水平高于早期苏醒。因此，延迟苏醒不能作为限制神经外科手术后苏醒引起的代谢和血流动力学后果的一种机制被推荐。
