CARDIOPULMONARY BYPASS-INDUCED CHANGES IN PLASMA-CONCENTRATIONS OF PROPOFOL AND IN AUDITORY-EVOKED POTENTIALS

Citation
E. Hammaren et al., CARDIOPULMONARY BYPASS-INDUCED CHANGES IN PLASMA-CONCENTRATIONS OF PROPOFOL AND IN AUDITORY-EVOKED POTENTIALS, British Journal of Anaesthesia, 77(3), 1996, pp. 360-364
Citations number
17
Categorie Soggetti
Anesthesiology
ISSN journal
00070912
Volume
77
Issue
3
Year of publication
1996
Pages
360 - 364
Database
ISI
SICI code
0007-0912(1996)77:3<360:CBCIPO>2.0.ZU;2-B
Abstract
Unbound, rather than total, plasma concentrations may be related to th e anaesthetic action of propofol. Therefore, we measured plasma concen trations of propofol and recorded Nb wave latencies of auditory evoked potentials (AEP) during continuous infusion of propofol in 15 patient s undergoing coronary artery bypass grafting (CABG) surgery. After ind uction of anaesthesia with fentanyl, propofol was infused continuously at a rate of 10 mg kg(-1) h(-1) for 20 min, and then the rate was red uced to 3 mg kg(-1) h(-1). Administration of heparin before cardiopulm onary bypass (CPB) did not affect total or unbound propofol concentrat ion. Initiation of CPB decreased mean total propofol concentration fro m 2.6 to 1.7 mu g ml(-1) (P < 0.01). Simultaneously, mean unbound prop ofol concentration remained at 0.06 mu g ml(-1) because of a slight in crease in the mean free fraction of plasma propofol (from 2.3 to 3.5%; P > 0.05). During hypothermic CPB, mean total propofol concentration increased to concentrations measured before bypass (to 2.1 mu g ml(-1) ; P > 0.05 vs value before CPB) and the mean unbound propofol concentr ation was at its highest (0.07 mu g ml(-1); P < 0.05 vs value before h eparin). After CPB and administration of protamine, the mean total pro pofol concentration remained lowered (1.7 mu g ml(-1); P < 0.05 vs val ue before heparin) and th mean unbound propofol concentration returned to the level measured before heparin (P < 0.001 vs value during hypot hermia). The latency of the Nb wave from recordings of AEP increased a fter induction of anaesthesia, reached its maximum during hypothermia and was prolonged during the subsequent phases of the study. The laten cy of the Nb wave did not correlate with total or unbound propofol con centration. We conclude that the changes in total and unbound concentr ations of plasma propofol were not parallel in patients undergoing CAB G. During CPB or at any other time during the CABG procedure, the unbo und propofol concentration did not decrease and Nb wave latency was pr olonged compared with baseline values measured after induction of anae sthesia before the start of CPB.