Key result
The Marsh pharmacokinetic model for propofol was comparable to the Schnider model during induction of cardiac anaesthesia, with no significant difference in mean blood pressure decrease (25% vs 22%, P=0.192).
Why the study?
Does the Marsh pharmacokinetic model compared to the Schnider model improve hemodynamic stability (decrease in mean blood pressure) during propofol induction in adult patients undergoing elective cardiac surgery?
RCT (n=90)
Random assignment
No
Does the Marsh pharmacokinetic model compared to the Schnider model improve hemodynamic stability (decrease in mean blood pressure) during propofol induction in adult patients undergoing elective cardiac surgery?
Absolute Event Rate: 25% vs 22%
p-value: p=0.192
The Marsh and Schnider pharmacokinetic models for propofol target-controlled infusion provide comparable hemodynamic stability during induction of anesthesia in cardiac surgery.
Either model may be used for propofol TCI without differential hypotension risk; confirms their equivalence in cardiac surgery induction.
CONTEXT: Haemodynamic stability during induction is a cornerstone of cardiac anaesthesia. The evaluation of pharmacokinetic models for propofol during induction is lacking. OBJECTIVE: To compare haemodynamics during cardiac anaesthesia induction with two pharmacokinetic models. DESIGN: Randomised controlled trial. SETTING: Department of Cardiothoracic Surgery, São João Hospital; July to December 2010. PATIENTS: Ninety consecutive elective adult cardiac surgical patients. INTERVENTION: 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. RESULTS: 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. MAIN OUTCOME MEASURES: Decrease in mean blood pressure. CONCLUSION: In effect-site targeting with a 1.2 min(-1) equilibration constant, Marsh's model is comparable to Schnider's during induction of anaesthesia.
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Viterbo et al. (2012) conducted an RCT in Elective cardiac surgery (n=90). Marsh pharmacokinetic model for propofol vs. Schnider pharmacokinetic model for propofol was evaluated on Decrease in mean blood pressure (p=0.192). The Marsh pharmacokinetic model for propofol was comparable to the Schnider model during induction of cardiac anaesthesia, with no significant difference in mean blood pressure decrease (25% vs 22%, P=0.192).
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