Key result
Plasma target-controlled infusion of propofol using Marsh's model induced sedation faster than Schnider's model (1.51 vs 2.8 minutes; P<0.001), with no significant difference in hemodynamics.
Why the study?
Does the Marsh pharmacokinetic model improve hemodynamic stability compared to the Schnider model during induction of anesthesia in patients undergoing elective surgery?
RCT (n=60)
randomly assigned
Does the Marsh pharmacokinetic model improve hemodynamic stability compared to the Schnider model during induction of anesthesia in patients undergoing elective surgery?
The Marsh pharmacokinetic model for propofol target-controlled infusion induces sedation faster than the Schnider model, with similar hemodynamic profiles during anesthesia induction.
Marsh model enables faster sedation without hemodynamic differences; supports its selection over Schnider for propofol TCI in elective surgery.
BACKGROUND: Hemodynamic stability is one of the most critical concerns during induction of anesthesia. Whether the pharmacokinetic model by Marsh or the one by Schnider will produce better hemodynamic stability remains unclear. This study compared hemodynamic changes during induction between the two models. METHODS: 60 patients who underwent elective surgery were randomly assigned to plasma target-controlled infusion by Marsh's (n = 30) or Schnider's (n = 30) model with an initial target concentration of 4 μg×mL-1. The target was then reset and gradually titrated to a sedation level with a narcotrend index (NI) below 64. Stroke volume, cardiac output, systemic vascular resistance, arterial pressure, target, and effect site concentration, and dose of propofol infused were recorded every minute during the first 25 minutes of infusion. RESULTS: Throughout the first 25 minutes, stroke volume index and cardiac index were decreased significantly in both Marsh and Schnider groups, but no statistical difference was detected between the groups (p > 0.05). Central venous pressure (CVP), systemic vascular resistance index (SVRI), and heart rate (HR) did not significantly change during induction (p > 0.05). Time to loss of responsiveness (LOR), and time for NI to decrease to 64 was faster in Marsh than in Schnider (1.51 ± 0.8 minutes vs. 2.8 ± 1.2 min, p < 0.001; 3.3 ± 2.0 minutes vs. 5.2 ± 2.3 minutes, p < 0.01, respectively). CONCLUSIONS: When target concentrations are titrated according to NI during induction of anesthesia, Marsh's model could induce sedation faster than Schnider's. Meanwhile, hemodynamic changes were not observed to be statistically different between the two models. Hypotension induced by plasma target-controlled infusion of propofol could mainly be attributed to decreased stroke volume instead of vascular dilation.
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Yang et al. (2014) conducted an RCT in elective surgery requiring induction of anesthesia (n=60). Plasma target-controlled infusion by Marsh's model vs. Schnider's model was evaluated on Time to loss of responsiveness (LOR) (p=<0.001). Plasma target-controlled infusion of propofol using Marsh's model induced sedation faster than Schnider's model (1.51 vs 2.8 minutes; P<0.001), with no significant difference in hemodynamics.
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