Nathan N, Vial G, Benrhaiem M, Peyclit A, Feiss P
Department of Anaesthesia and Intensive Care, CHRU Dupuytren, 2 Ave Martin Luther King, 87042, Limoges cédex, France.
Anaesthesia. 2001 Mar;56(3):251-7. doi: 10.1046/j.1365-2044.2001.01717-2.x.
Haemodynamic parameters during an inhalation induction with 8% sevoflurane were compared with those obtained with a target-controlled infusion of propofol in 50 hypertensive patients in a prospective randomised study. Heart rate and arterial pressure were recorded continuously. End-tidal sevoflurane and nitrous oxide concentration, SpO2 and bispectral index (BIS) were also collected from the beginning of anaesthesia until 8 min after tracheal intubation. Patients either received 4 mg.l-1 target-concentration propofol or performed a vital capacity inhalation of 8% sevoflurane in a high flow of oxygen (8 l.min-1) supplemented with 50% nitrous oxide at loss of consciousness. As soon as BIS was < 60, 20 microg.kg-1 alfentanil and 0.6 mg.kg-1 rocuronium were injected and orotracheal intubation was then performed 1 min later. Thereafter, the end-tidal concentration of sevoflurane was reduced to 1.3 minimum alveolar concentration (MAC). Hypotension was defined as a 30% decrease in arterial pressure and was treated with repeated 3-mg boluses of ephedrine. When 12 mg ephedrine was unable to correct hypotension, the concentration of propofol was reduced by 1 mg.l-1 and that of sevoflurane by 0.5%. Hypotension occurred in 22 patients in the sevoflurane group and 21 in the propofol group, and hypertension occurred in two and three patients in each group, respectively. The maximal reduction in mean (SD) arterial pressure was similar in the sevoflurane (45 (4) mmHg) and propofol (41.3 (2.6) mmHg) groups, as were the ephedrine requirements (9.6 (1.1) vs. 9.1 (1.1) mg, sevoflurane vs. propofol, p > 0.05), the duration of hypotension (276 (37) vs. 292 (38) s, sevoflurane vs. propofol, p > 0.05), and the number of hypotensive episodes or anaesthetic changes and depth of anaesthesia. Nevertheless, heart rate was lower during the 8 min following tracheal intubation in the sevoflurane group. In both groups, the duration of hypotension was easily controlled either by ephedrine or by adjusting the anaesthetic concentrations. Overall, haemodynamic tolerance appears to be similar in the two techniques. Because hypotension occurred after alfentanil in most patients, this study questioned which is the best opioid dose, if any, to associate with propofol or sevoflurane for the induction in hypertensive patients.
在一项前瞻性随机研究中,对50例高血压患者吸入8%七氟醚诱导麻醉期间的血流动力学参数与靶控输注丙泊酚时获得的参数进行了比较。持续记录心率和动脉压。从麻醉开始至气管插管后8分钟,还收集了呼气末七氟醚和氧化亚氮浓度、SpO₂及脑电双频指数(BIS)。患者在意识消失时,要么接受4mg·L⁻¹的靶浓度丙泊酚,要么在高流量氧气(8L·min⁻¹)并补充50%氧化亚氮的情况下进行8%七氟醚的肺活量吸入。一旦BIS<60,即注射20μg·kg⁻¹阿芬太尼和0.6mg·kg⁻¹罗库溴铵,1分钟后进行经口气管插管。此后,将七氟醚的呼气末浓度降至1.3最低肺泡有效浓度(MAC)。低血压定义为动脉压下降30%,用3mg麻黄碱重复推注治疗。当12mg麻黄碱无法纠正低血压时,将丙泊酚浓度降低1mg·L⁻¹,七氟醚浓度降低0.5%。七氟醚组22例患者出现低血压,丙泊酚组21例,两组分别有2例和3例患者出现高血压。七氟醚组(45(4)mmHg)和丙泊酚组(41.3(2.6)mmHg)平均(标准差)动脉压的最大降幅相似,麻黄碱需求量(七氟醚组9.6(1.1)mg,丙泊酚组9.1(1.1)mg,p>0.05)、低血压持续时间(七氟醚组276(37)秒,丙泊酚组292(38)秒,p>0.05)以及低血压发作次数或麻醉调整和麻醉深度也相似。然而,七氟醚组气管插管后8分钟内心率较低。在两组中,低血压持续时间均可通过麻黄碱或调整麻醉浓度轻松控制。总体而言,两种技术的血流动力学耐受性似乎相似。由于大多数患者在阿芬太尼后出现低血压,本研究质疑在高血压患者诱导麻醉时,与丙泊酚或七氟醚联合使用的最佳阿片类药物剂量(若有的话)是多少。