Due to copyright issues, an electronic copy of the thesis must be ordered from the faculty. For the faculty to have time to process the order, the order must be received by the faculty at the latest 2 days before the public defence. Orders received later than 2 days before the defence will not be processed. After the public defence, please address any inquiries regarding the thesis to the candidate.
Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Professor Michelle S. Chew, Karolinska Institutet
- Second opponent: Professor Nils Kristian Skjærvold, Norwegian University of Science and Technology
- Third member and chair of the evaluation committee: Professor II Signe Søvik, University of Oslo
Chair of the Defence
Professor II Per Steinar Halvorsen, University of Oslo
Principal Supervisor
Eldrid Langesæter, Oslo University Hospital
Summary
This thesis in anaesthesiology investigated haemodynamic instability during induction of general anaesthesia, with particular focus on postinduction hypotension and preventive vasopressor treatment.
Postinduction hypotension is common and has been associated with increased risk of myocardial injury, renal injury, and postoperative morbidity. However, evidence regarding the haemodynamic effects of different induction doses of propofol and remifentanil, and the effectiveness of prophylactic vasopressor administration, remains limited.
Three randomised clinical studies were conducted at Haugesund Hospital, Norway, including otherwise healthy women undergoing elective gynaecological surgery. Anaesthesia was induced using target-controlled infusions of propofol and remifentanil. Continuous beat-to-beat invasive haemodynamic monitoring was performed using the LiDCO™plus system.
Studies 1 and 2 examined the haemodynamic effects of different induction doses of propofol and remifentanil. Lower doses did not reduce the marked decreases in systolic arterial pressure, cardiac output, and heart rate observed during induction. Increasing the remifentanil dose within clinically relevant ranges did not further worsen haemodynamic depression.
Study 3 evaluated prophylactic bolus administration of norepinephrine, phenylephrine, and ephedrine. Norepinephrine and phenylephrine temporarily delayed the reduction in blood pressure but were associated with substantial decreases in heart rate and cardiac output. Ephedrine provided superior short-term haemodynamic stability and maintained blood pressure, heart rate, and cardiac output more effectively.
Across all studies, induction with propofol and remifentanil consistently caused profound haemodynamic depression. Early reductions in heart rate were strongly associated with reduced cardiac output, suggesting that bradycardia may serve as an early marker of haemodynamic compromise.
Additional information
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