Dose-response to anaesthetic induction with sufentanil: haemodynamic and electroencephalographic effects

  • Jitender Sarecn
  • Robert J. Hudson
  • Morley Rosenbloom
  • Ian R. Thomson
Reports of Investigation



To determine the effect of a five-fold variation in sufentanil dose on the haemodynamic and electroencephalo graphic (EEG) response to anaesthetic induction and tracheal intubation.


Thirty-four patients undergoing elective coronary artery bypass grafting (CABG) participated in this randomized double-blind study. Patients in Group L (n= 17) received 3 μg · kg−1 sufentanil and those in Group H (n= 17) 15 μg · kg−1. Premedication was 60 μg · kg−1 lorazepam po. Anaesthesia and neuromuscular blockade were induced by infusing sufentanil and 0.15 mg · kg−1 vecuronium iv over five minutes. Haemodynamic data and the electroencephalographic (EEG) spectral edge were acquired by computer and compared at Control, Induction and Intubation.


Sufentanil dose did not affect the haemodynamic or EEG response at end-induction. No bradyarrhythmias occurred, and the incidence of hypotension was 12% in both groups. However, during induction apparent electromyographic artifacts and a transiently greater increase in heart rate were observed in Group H. The serum sufentanil concentration at Induction was 6.1 ± 1.8 ng · ml−1 in Group L and 25.4 ± 8.8 ng · ml−1 in Group H, and did not correlate with haemodynamic changes. No patient recalled any intraoperative event.


Increasing sufentanil dose from 3 to 15 μg · kg−1 does not influence the ultimate haemodynamic response to induction. Combined with lorazepam premedication, 3 μg · kg−1 sufentanil produces near-maximal haemodynamic and EEG effects and is adequate for induction and tracheal intubation of patients undergoing CABG. Sufentanil 15 μg · kg−1 is no more efficacious, and causes transient cardiovascular stimulation.


Fentanyl Coronary Artery Bypass Grafting Mean Arterial Pressure Sufentanil Pulmonary Capillary Wedge Pressure 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.



Déterminer les effets hémodynamiques et électroencéphalographiques (EEG) d’une dose quintuple de sufentanil sur l’induction de l’anesthésie et l’intubation de la trachée.


Trente-quatre patients subissant une chirurgie de revascularisation myocardique (CRVM) non urgente participaient à cette étude aléatoire conduite à double insu. Les patients du groupe L (n= 17) recevaient sufentanil 3 μg · kg−1 et ceux du groupe H (n = 17) 15 μg · kg−1. Tous étaient prémédiqués au lorazepam 60 μg kg−1 per os. L’anesthésie et la curarisation étaient initiées en perfusant le sufentanil et le vécuronium 0,15 mg kg−1 iv en cinq minutes. Les données hémodynamiques et l’EEG spectral comprimé étaient recueillies sur ordinateur et comparées à la phase de contrôle, à l’induction et au moment de l’intubation.


Le sufentanil n’a pas eu d’effets hémodynamiques ou EEG à l’induction. On n’a pas observé de bradycardie et l’incidence d’hypotension a été de 12% pour les deux groupes. Cependant, pendant l’induction, des perturbations visibles à l’EEG et une augmentation transitoire plus importante de la fréquence cardiaque étaient observés dans le group H. La concentration sérique de sufentanil à l’induction était de 6, 1 ± 1, 8 ng ml−1 pour le groupe L et de 25, 4±8, 8 ng · ml−1 pour le groupe H et n’était pas en corrélation avec les changements hémodynamiques. Aucun des patients n’a mentionné un rappel d’événements peropératoires.


Laugmentation de la posologie du sufentanil de 3 à 15 mg kg−1 n’a pas d’unfluence sur la réponse hémodynamique en fin d’induction. Associé à une prémédication de lorazepam, le sufentanil 3 μg kg−1 produit des effets hémodynamiques et EEG presque maximaux et est adéquat pour l’induction et l’intubation de la trachée de patients subissant une CRVM. Le sufentanil 15 μg · kg−1 n’est pas plus efficace et provoque une stimulation cardiovasculaire transitoire.


  1. 1.
    Bailey PL, Stanley TH. Intravenous opioid anesthetics.In: Miller RD (Ed.). Anesthesia, 4th ed. New York: Churchill Livingstone, 1994: 291–387.Google Scholar
  2. 2.
    Starr NJ, Sethna DH, Estafanous FG. Bradycardia and asystole following the rapid administration of sufentanil with vecuronium. Anesthesiology 1986; 64: 521–3.PubMedCrossRefGoogle Scholar
  3. 3.
    Spiess BD, Sathoff RH, El-Ganzouri ARS, Ivankovich AD. High-dose sufentanil: four cases of sudden hypotension on induction. Anesth Analg 1986; 65: 703–5.PubMedCrossRefGoogle Scholar
  4. 4.
    Reitan JA, Stengert KB, Wymore ML, Martucci RW. Central vagal control of fentanyl-induced bradycardia during halothane anesthesia. Anesth Analg 1978; 57: 31–6.PubMedGoogle Scholar
  5. 5.
    Flacke JW, Davis LJ, Flacke WE, Bloor BC, Van Etten AP. Effects of fentanyl and diazepam in dogs deprived of autonomic tone. Anesth Analg 1985; 64: 1053–9.PubMedGoogle Scholar
  6. 6.
    Liu W-S, Bidwai AV, Stanley TH, Isern-Amaral J. Cardiovascular dynamics after large doses of fentanyl and fentanyl plus N2O in the dog. Anesth Analg 1976; 55: 168–72.PubMedGoogle Scholar
  7. 7.
    Arndt JO, Mikat M, Parasher C. Fentanyl’s analgesic, respiratory, and cardiovascular actions in relation to dose and plasma concentration in unanesthetized dogs. Anesthesiology 1984; 61: 355–61.PubMedCrossRefGoogle Scholar
  8. 8.
    Bovill JG, Sebel PS, Wauquier A, Rog P. Electroencephalographic effects of sufentanil anaesthesia in man. Br J Anaesth 1982; 54: 45–52.PubMedCrossRefGoogle Scholar
  9. 9.
    Scott JC, Cooke JE, Stanski DR. Electroencephalographic quantitation of opioid effect: comparative pharmacodynamics of fentanyl and sufentanil. Anesthesiology 1991; 74: 34–42.PubMedCrossRefGoogle Scholar
  10. 10.
    Bowdle TA, Ward RJ. Induction of anesthesia with small doses of sufentanil or fentanyl: dose versus EEG response, speed of onset, and thiopental requirement. Anesthesiology 1989; 70: 26–30.PubMedCrossRefGoogle Scholar
  11. 11.
    Philbin DM, Rosow CE, Schneider RC, Koski G, D’Ambra MN. Fentanyl and sufentanil anesthesia revisited: how much is enough? Anesthesiology 1990; 73: 5–11.PubMedCrossRefGoogle Scholar
  12. 12.
    Thomson IR, MucAdams CL, Hudson RJ, Rosenbloom M. Drug interactions with sufentanil. Hemodynamic effects of premedication and muscle relaxants. Anesthesiology 1992; 76: 922–9.PubMedCrossRefGoogle Scholar
  13. 13.
    Gregory TK, Pettus DC. An electroencephalographic processing algorithm specifically intended for analysis of cerebral electrical activity. J Clin Monit 1986; 2: 190–7.PubMedCrossRefGoogle Scholar
  14. 14.
    Bazaral MG, Wagner R, Abi-Nader E, Estafanous FG. Comparison of the effects of 15 and 60 μg/kg fentanyl used for induction of anesthesia in patients with coronary artery disease. Anesth Analg 1985; 64: 312–8.PubMedCrossRefGoogle Scholar
  15. 15.
    Sprigge JS, Wynands JE, Whalley DG, et al. Fentanyl infusion anesthesia for aortocoronary bypass surgery: plasma levels and hemodynamic response. Anesth Analg 1982; 61: 972–8.PubMedCrossRefGoogle Scholar
  16. 16.
    Thomson IR, Putnins CL, Friesen RM. Hyperdynamic cardiovascular responses to anesthetic induction with high-dose fentanyl. Anesth Analg 1986; 65: 91–5.PubMedCrossRefGoogle Scholar
  17. 17.
    Thomson IR, Hudson RJ, Rosenbloom M, Torchia MG. Catecholamine responses to anesthetic induction with fentanyl and sufentanil. J Cardiothorac Anesth 1988; 2: 18–22.PubMedCrossRefGoogle Scholar
  18. 18.
    Chi OZ, Sommer W, Jasaitis D. Power spectral analysis of EEG during sufentanil infusion in humans. Can J Anaesth 1991; 38: 275–80.PubMedCrossRefGoogle Scholar

Copyright information

© Canadian Anesthesiologists 1997

Authors and Affiliations

  • Jitender Sarecn
    • 1
  • Robert J. Hudson
    • 1
  • Morley Rosenbloom
    • 1
  • Ian R. Thomson
    • 1
  1. 1.Department of AnesthesiaSt. Boniface General HospitalWinnipegCanada

Personalised recommendations