Abstract

It is generally accepted that a neuraxial blockade strengthens the sedative effects of propofol. Deafferentation caused by neuraxial blockade is thought to play a key role. The objective is to determine whether epidural blockade affects the bispectral index (BIS) of propofol and two other pharmacodynamic endpoints, mean arterial pressure (MAP) and cardiac output (CO). Randomised, placebo-controlled study. University hospital. Patients scheduled for surgery needing epidural analgesia. 28 ASA one or two patients received 0, 50, 100 or 150 mg of epidural ropivacaine. After stabilisation of the epidural blockade, propofol was given by target-controlled infusion. The propofol plasma target concentrations were increased at 6-min intervals from 0 to 1, 2.5, 4 and 6 μg ml-1. The study was performed before surgery. Three endpoints, BIS, mean arterial blood pressure and CO were measured from baseline (prior to the administration of epidural ropivacaine) until 2 h after the start of propofol infusion. The propofol concentration-effect data were analysed to determine the interaction between epidural blockade and propofol sedation. In the absence of propofol, the increase in number of epidural blocked segments from 0 to 15.5 (range 6 to 21) reduced the MAP by 30%, without affecting BIS or CO. In the absence of epidural blockade, the increase in propofol concentration to 6 μg ml-1 reduced BIS, MAP and CO. When combined, epidural anaesthesia and intravenous propofol exhibited no pharmacodynamic interaction on any of the three endpoints. In addition, epidural blockade did not affect the propofol effect-site equilibration half-life for its haemodynamic effects (11.5 ± 0.5 min) or for its effects on the BIS (4.6 ± 0.4 min). Epidural blockade reduces the propofol requirements for sedative end points. This is not the result of a pharmacodynamic interaction. Dutch trial register CCMO, Central Committee on Research Involving Human Subjects, trial number NL 32295.058.10.

Full Text
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