Hemodynamic responses during induction: comparison of Marsh and Schnider pharmacokinetic models.

Abstract

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. 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. 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). 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.