HAEMODYNAMIC EFFECTS OF PROPOFOL: INDUCTION WITH 2.5 MG KG−1

• Published in: British journal of anaesthesia : BJA Vol. 67; no. 5; pp. 618 - 620
• Main Authors: FAIRFIELD, J.E., DRITSAS, A., BEALE, R.J.
• Format: Journal Article
• Language: English
• Published: Oxford Elsevier Ltd 01.11.1991; Oxford University Press
• Subjects: Adult; Anaesthetics; Anesthesia, Dental; Anesthesia, Intravenous; Anesthetics. Neuromuscular blocking agents; Biological and medical sciences; Blood Pressure - drug effects; Body Weight; Cardiac Output - drug effects; echocardio-graphy; Female; Heart Rate - drug effects; Hemodynamics - drug effects; Humans; intravenous: propofol; Male; Measurement techniques: Doppler ultrasound; Medical sciences; Neuropharmacology; Pharmacology. Drug treatments; Propofol - pharmacology; Vascular Resistance - drug effects; intravenous: propofol; echocardio-graphy; Measurement techniques: Doppler ultrasound; Anaesthetics; Human; General anesthesia; Intravenous administration; Hemodynamics; General anesthetic; Induction
• ISSN: 0007-0912; 1471-6771
• DOI: 10.1093/bja/67.5.618

Serial measurements of haemodynamic variables were performed at 1-min intervals in nine ASA I, unpremedicated patients before and for 5 min after induction of anaesthesia with propofol 2.5 mg kg−1. End-tidal carbon dioxide concentration was maintained within the normal range. Stroke volume and left ventricular function were measured by Doppler and cross-sectional echo-cardiography at the aortic valve. Systemic arterial pressure was measured by automated oscillotonometry and heart rate by electrocardiograph. Stroke volume, cardiac output, systemic vascular resistance, left ventricular stroke work and rate-pressure product were calculated. There was a decrease at all time points in systolic, mean and diastolic arterial pressure. There was an initial increase in heart rate and cardiac output, with a subsequent decrease to less than baseline. There was an initial decrease in systemic vascular resistance followed by partial recovery, and a delayed decrease in left ventricular function as measured by peak aortic blood flow velocity and acceleration.