Effect of propofol on heart rate, arterial pressure and digital plethysmograph variability

• Published in: British Journal of Anaesthesia Vol. 73; no. 2; pp. 167 - 173
• Main Authors: ROBINSON, B.J., BUYCK, H.C.E., GALLETLY, D.C.
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Oxford Elsevier Ltd 01.08.1994; Oxford University Press
• Subjects: Adult; Anaesthetics; Anaesthetics, i.v.: propofol; Anesthetics. Neuromuscular blocking agents; Biological and medical sciences; Blood Pressure - drug effects; Fingers - blood supply; Heart; heart rate; Heart Rate - drug effects; Heart, heart rate; Humans; i.v.: propofol; Male; Measurement techniques: plethysmography; Measurement techniques: spectral analysis; Medical sciences; Middle Aged; Neuropharmacology; Pharmacology. Drug treatments; Plethysmography; Propofol - pharmacology; Regional Blood Flow - drug effects; Respiration - drug effects; Stimulation, Chemical; Anaesthetics, i.v.: propofol; Heart, heart rate; Measurement techniques: spectral analysis; Measurement techniques: plethysmography; Human; Heart rate; Intravenous administration; General anesthetic; General anesthesia; Hemodynamics; Normal; Plethysmography
• ISSN: 0007-0912; 1471-6771
• DOI: 10.1093/bja/73.2.167

We have investigated the effects of propofol on beat-to-beat fluctuations in heart rate, arterial pressure (continuous arterial tonometry) and infrared finger plethysmography in 10 healthy male patients undergoing elective surgery. Administration of Diprivan (propofol 10mg ml−1) 0.2 ml kg−1 followed by an infusion of 1 ml/kg−1 h−1 was associated with transient tachycardia and a reduction in arterial pressure that preceded an increase in plethysmograph amplitude. The temporal sequence of these cardiovascular changes suggests that the initial tachycardia was not a reflex response to hypotension and that cutaneous changes in adrenergic tone were not responsible for the decrease in arterial pressure. The observation that the hypotensive action of propofol preceded the increase in plethysmographic amplitude suggests that multiple mechanisms were implicated in the hypotensive action of propofol and the relative importance of these mechanisms may vary according to the time of measurement. Compared with preanaesthetic control values, spectral analysis of heart rate variability, arterial pressure and plethysmograph variability showed reduction in variability and total spectral power. Spectral power in low (<0.08 Hz) and mid (0.08–0.15Hz) frequency bands decreased for each variable, while high (>0.15 Hz) frequency “ventilatory” power decreased for heart rate and possibly diastolic pressure and increased for systolic pressure and plethysmograph variability. The complex pattern of change in cardiovascular variability was possibly caused by: (a) initial, transient vagolysis, (b) initial hypotension caused either by intrathoracic pooling of blood, direct myocardial depression or vasodilatation in non-cutaneous beds, (c) peripheral alpha-adrenergic sympatholysis, (d) resetting of the baroreflex mechanism, (e) decreased ventilatory amplitude and (f) increase in venous capacitance that augmented ventilation-induced fluctuations in arterial pressure.