Anesth Analg 2006;103:902-907
© 2006 International Anesthesia Research Society
doi: 10.1213/01.ane.0000237282.76394.6b
TECHNOLOGY, COMPUTING, AND SIMULATION
The Contribution of Remifentanil to Middle Latency Auditory Evoked Potentials During Induction of Propofol Anesthesia
Stefan Schraag, MD, PhD*,
Joachim Flaschar, Dipl-Ing (FH) ,
Manuela Schleyer, MD ,
Michael Georgieff, MD, PhD , and
Gavin N.C. Kenny, MD, BSc(Hons), FRCA, FANZCA
From the *Department of Perioperative Medicine, Golden Jubilee National Hospital, Clydebank, UK; Department of Anesthesiology, University of Ulm, Germany; and Department of Anesthesia, Glasgow Royal Infirmary, Glasgow, UK.
Address correspondence and reprint requests to Stefan Schraag, MD PhD, Department of Perioperative Medicine, Golden Jubilee National Hospital, Clydebank G81 4HX, Scotland, UK. Address e-mail to stefanschraag{at}btinternet.com.
There is a debate regarding whether opioids, as a component of general anesthesia, are adequately reflected in the assessment of anesthesia based on derivatives of the electroencephalogram. To test the hypothesis of a possible quantitative contribution of remifentanil on middle latency auditory evoked potentials, we studied its interaction with propofol anesthesia in 45 unpremedicated male patients undergoing elective lower limb orthopedic surgery. They were allocated randomly to three groups. The first two groups received remifentanil either with a high (8 ng mL1) or a low (3 ng mL1 target concentration using target-controlled infusion (TCI). The third group received spinal anesthesia instead of remifentanil. Anesthesia was induced by a stepwise increase in propofol concentration using TCI. The auditory evoked potential index (AEPex) and calculated propofol effect site concentrations were determined at loss of consciousness and the reaction to laryngeal mask airway insertion was noted. The propofol infusion was then converted to a closed-loop TCI using an AEPex value of 40 as the target. We found no significant contribution of remifentanil alone on the auditory evoked response, whereas increasing concentrations of remifentanil led to a significant decrease of the calculated propofol effect site concentrations (P = 0.023) necessary for unconsciousness. Prediction probability for AEPex was inversely related to the remifentanil concentration and was best for the control group, which received propofol alone. These results support previous findings of a quantitative interaction between remifentanil and propofol for loss of consciousness but question the specific contribution of remifentanil to auditory evoked potentials.
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