Department of Anesthesiology, Hospital São João, EPE, Porto, Portugal.
Eur J Anaesthesiol. 2012 Oct;29(10):477-83. doi: 10.1097/EJA.0b013e3283542421.
Haemodynamic stability during induction is a cornerstone of cardiac anaesthesia. The evaluation of pharmacokinetic models for propofol during induction is lacking.
To compare haemodynamics during cardiac anaesthesia induction with two pharmacokinetic models.
Randomised controlled trial.
Department of Cardiothoracic Surgery, São João Hospital; July to December 2010.
Ninety consecutive elective adult cardiac surgical patients.
Random assignment to effect-site target-controlled infusion by Marsh (n = 45) or Schnider (n = 45) pharmacokinetic models with an equilibration constant of 1.2 min(-1) adapted to Marsh's model. Invasive blood pressure measurements, propofol dose, and bispectral index (BIS) were recorded. After an initial target concentration of 1.5 μg ml(-1), concentrations were upward-titrated in 0.5 μg ml(-1) increments until the BIS was <50.
No differences were observed between Marsh and Schnider models in required propofol dose (0.99 ± 0.26 vs. 0.93 ± 0.31 mg kg(-1), P = 0.322), decrease in mean blood pressure (25 ± 13 vs. 22 ± 14%, P = 0.192) or the need for vasopressors (20 vs. 24%, P = 0.800), but the use of the Marsh model resulted in a lower predicted effect-site concentration (2.3 ± 0.4 vs. 2.7 ± 0.6 μg ml(-1), P = 0.006) and shorter time to induction (296 ± 59 vs. 338 ± 87 s, P = 0.024). There was a greater decrease in mean blood pressure in older patients (>60 years; 29 ± 10 vs. 22 ± 11%, P = 0.004) irrespective of model, but obese (BMI ≥30 kg m(-2)) and nonobese patients did not differ.
Decrease in mean blood pressure.
In effect-site targeting with a 1.2 min(-1) equilibration constant, Marsh's model is comparable to Schnider's during induction of anaesthesia.
诱导期间的血流动力学稳定性是心脏麻醉的基石。丙泊酚在诱导期间的药代动力学模型的评估是缺乏的。
比较两种药代动力学模型在心脏麻醉诱导期间的血液动力学。
随机对照试验。
圣若昂医院心胸外科；2010 年 7 月至 12 月。
90 例连续的择期成年心脏手术患者。
随机分配到效应部位靶控输注由 Marsh（n = 45）或 Schnider（n = 45）药代动力学模型与 1.2 min（-1）平衡常数适应 Marsh 的模型。记录有创血压测量、丙泊酚剂量和脑电双频指数（BIS）。初始目标浓度为 1.5 μg ml（-1）后，浓度以 0.5 μg ml（-1）的增量递增，直至 BIS < 50。
Marsh 和 Schnider 模型在所需丙泊酚剂量（0.99 ± 0.26 与 0.93 ± 0.31 mg kg（-1），P = 0.322）、平均血压下降（25 ± 13 与 22 ± 14%，P = 0.192）或血管加压药的需要（20 与 24%，P = 0.800）方面无差异，但 Marsh 模型导致较低的预测效应部位浓度（2.3 ± 0.4 与 2.7 ± 0.6 μg ml（-1），P = 0.006）和诱导时间更短（296 ± 59 与 338 ± 87 s，P = 0.024）。在年龄较大的患者（> 60 岁；29 ± 10 与 22 ± 11%，P = 0.004）中，平均血压下降更大，但肥胖（BMI ≥ 30 kg m（-2））和非肥胖患者没有差异。
平均血压下降。
在 1.2 min（-1）平衡常数的效应部位靶向中，Marsh 模型在麻醉诱导期间与 Schnider 模型相当。
