From the Department of Anaesthesiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands (MP, TWLS, MIVDV, PLB, MMRFS, AFK), Department of Anesthesia and Critical Care Medicine, Maria Middelares Hospital (SA, AFK); and Department of Anesthesia, Ghent University, Ghent, Belgium (MMRFS).
Eur J Anaesthesiol. 2017 Oct;34(10):695-701. doi: 10.1097/EJA.0000000000000639.
Induction of anaesthesia with propofol and remifentanil often induces unwanted bradycardia and hypotension, raising concerns regarding tissue oxygenation. The electrophysiological cardiac effects of remifentanil can be reversed by atropine.
To investigate if prophylactic administration of atropine can attenuate the negative haemodynamic effects of propofol and a high dose of remifentanil during induction of anaesthesia.
A double-blind, randomised controlled trial.
Single-centre, University Medical Center Groningen, The Netherlands.
Sixty euvolaemic patients scheduled for surgery under general anaesthesia.
Anaesthesia was induced and maintained with a target-controlled infusion of propofol with a target effect-site concentration (Ce) of 2.5 μg ml, remifentanil (target-controlled infusion), (Ce 8 ng ml) and cis-atracurium. Methylatropine (500 μg) or 0.9% saline was administered at immediately before induction of anaesthesia.
The changes (Δ) in mean arterial pressure (MAP), heart rate (HR), cardiac index (CI), rate pressure product, cerebral tissue oxygenation and peripheral tissue oxygenation between induction of anaesthesia (T0) and 10 min later (T10).
Atropine significantly attenuated the changes in the outcome measures between T0 and T10. Median (inter-quartile range) changes were MAP, Δ = -24 (-40 to -21) vs. Δ = -37 mmHg (-41 to -31) (P = 0.02); HR, Δ = 0 ± 13 vs. -19 ± 11 bpm (P < 0.01); CI, Δ = -0.4 ± 0.7 vs. -0.9 ± 0.6l min m (P < 0.01) and rate pressure product, Δ = -3241 (-5015 to -613) vs. Δ = -5712 mmHg min (-6715 to -3917) (P < 0.01). Cerebral tissue oxygenation and peripheral tissue oxygenation did not change in either group. Maximum HR after atropine was 102 (86 to 116) vs. 85 bpm (76 to 95).
Administration of atropine, before induction of anaesthesia with propofol and high-dose remifentanil, can significantly reduce the decreases in HR, MAP and CI.
Clinicaltrials.gov identifier: NCT01871922.
异丙酚和瑞芬太尼诱导麻醉常引起意外的心动过缓和低血压，这引发了对组织氧合的担忧。瑞芬太尼的电生理心脏效应可以被阿托品逆转。
研究在麻醉诱导期间预防性给予阿托品是否可以减轻异丙酚和高剂量瑞芬太尼的负性血液动力学效应。
双盲、随机对照试验。
荷兰格罗宁根大学医学中心的单中心。
计划在全身麻醉下接受手术的 60 名等容患者。
麻醉诱导和维持采用异丙酚的靶控输注，靶效应室浓度（Ce）为 2.5μg/ml，瑞芬太尼（靶控输注），（Ce 8ng/ml）和顺式阿曲库铵。在麻醉诱导前立即给予甲基阿托品（500μg）或 0.9%生理盐水。
麻醉诱导（T0）与 10 分钟后（T10）之间平均动脉压（MAP）、心率（HR）、心指数（CI）、心率血压乘积、脑氧合和外周组织氧合的变化（Δ）。
阿托品显著减轻了 T0 和 T10 之间的结局测量的变化。中位数（四分位数范围）的变化为 MAP，Δ=-24（-40 至-21）vs.Δ=-37mmHg（-41 至-31）（P=0.02）；HR，Δ=0±13 vs.-19±11bpm（P<0.01）；CI，Δ=-0.4±0.7 vs.-0.9±0.6l/min/m（P<0.01）和心率血压乘积，Δ=-3241（-5015 至-613）vs.Δ=-5712mmHg·min（-6715 至-3917）（P<0.01）。两组脑氧合和外周组织氧合均无变化。阿托品后最大 HR 为 102（86 至 116）比 85bpm（76 至 95）。
在异丙酚和高剂量瑞芬太尼诱导麻醉前给予阿托品可显著降低 HR、MAP 和 CI 的降低。
Clinicaltrials.gov 标识符：NCT01871922。
