• M A Tooley, C L Stapleton, G L Greenslade, and C Prys-Roberts.
• Medical Physics and Bioengineering, University of Bristol, Bristol, UK. mark.a.tooley@bris.ac.uk
• Br J Anaesth. 2004 Jan 1; 92 (1): 25-32.

BackgroundPropofol has been shown to affect the mid-latency auditory evoked response (MLAER) in a dose-dependant manner. Few studies have investigated the addition of alfentanil. Myogenic responses, such as the post-auricular responses (PAR), can confound the MLAER but there has been little investigation as to which electrode site reduces this interference.MethodsWe studied the MLAER in 27 women. They received an infusion of alfentanil 15 micro g kg(-1) h(-1), followed by either a high or low infusion regimen of propofol (final infusion rates 6 and 3 mg kg(-1) h(-1)). We compared the results with those of our study using propofol alone. We collected the data from two electrode sites: vertex-inion and vertex-mastoid. We evaluated the occurrence of the PAR and the shape of the MLAER at each electrode site.ResultsThe infusion rate of propofol associated with loss of the eyelash response in 50% of subjects was 3.3 mg kg(-1) h(-1). This was significantly lower than using propofol alone (5.8 mg kg(-1) h(-1)). Nb latency was the best MLAER discriminator of unconsciousness (sensitivity 94%, specificity 88%), with a threshold of 46 ms (propofol alone was 53 ms). The addition of alfentanil did not alter the relationship between propofol infusion rate and MLAER. The vertex-inion electrode site gave the best protection against PAR in awake subjects (P=0.0003), and after 30 min of propofol infusion (P=0.06). The magnitude of the MLAER obtained from the vertex-mastoid electrodes was larger than from the other site, although the increase was not consistent throughout the waveform (brain stem 100%, Nb 14%).ConclusionsAddition of alfentanil lowers the propofol infusion rate required to produce unconsciousness and the Nb latency that predicts it. The better of the two sites to reduce the incidence of PAR is the vertex-inion electrode site.

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