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Autonomic circulatory and cerebrocortical responses during increasing depth of propofol sedation/hypnosis in humans

Gina Lafreniere, MSc, Brian Milne, MD FRCPC^*,, Donald G. Brunet, MD FRCPC, Michael A. Adams, PhD and Joel L. Parlow, MD FRCPC^*,

^* From the Departments of Anesthesiology, Pharmacology,
and Medicine,
Queen's University, Kingston, Ontario.

Address Correspondence to: Dr. Joel L. Parlow, Department of Anesthesiology, Kingston General Hospital, 76 Stuart Street, Kingston, Ontario, K7L 2V7 Canada. Phone: 613-548-7827; Fax: 613-548-1375; E-mail: parlowj{at}post.queensu.ca

Purpose: To describe the relative effects of graded central nervous system (CNS) depression, using increasing propofol infusion rates, on neurovegetative brainstem-mediated circulatory control mechanisms and higher cortical activity in healthy humans.

Methods: Propofol was administered using an infusion scheme designed to achieve three target blood concentrations in ten healthy volunteers. Blood propofol concentrations and sedation scores were determined at baseline, during the three propofol infusion levels, and 30 min into the recovery period. Electroencephalographic (EEG) power was measured in three frequency bands to quantify cortical activity, and autonomic heart rate control was quantified using spontaneous baroreflex assessment and power spectral analysis of pulse interval.

Results: Sedation scores closely paralleled propofol blood concentrations (0, 0.53 ± 0.34, 1.24 ± 0.21, 3.11 ± 0.80, and 0.96 ± 0.42 µg•mL^–1 at baseline, three infusion levels and recovery respectively), and all subjects were unconscious at the deepest level. Indices of autonomic heart rate control were decreased only at the deepest levels of CNS depression, while EEG effects were apparent at all propofol infusion rates. These EEG effects were frequency specific, with power in the beta band being affected at light levels of sedation, and alpha and delta power altered at deeper levels.

Conclusions: The results of this study support a relative preservation of neurovegetative circulatory control mechanisms during the early stages of CNS depression using gradually increasing rates of infusion of propofol. Indices of circulatory control did not reliably reflect depth of sedation.