Contractility in humans after coronary artery surgery

• Published in: Anesthesiology (Philadelphia) 1999-07, Vol.91 (1), p.58-70
• Main Authors: Schmidt, C, Roosens, C, Struys, M, Deryck, Y L, Van Nooten, G, Colardyn, F, Van Aken, H, Poelaert, J I
• Format: Article
• Language: English
• Subjects: Coronary Artery Bypass; Dose-Response Relationship, Drug; Echocardiography, Transesophageal; Humans; Hypnotics and Sedatives - pharmacology; Myocardial Contraction - drug effects; Propofol - blood; Propofol - pharmacology; Ventricular Function, Left - drug effects
• ISSN: 0003-3022
• DOI: 10.1097/00000542-199907000-00012

Propofol's unique pharmacokinetic profile offers advantages for titration and rapid emergence in patients after coronary artery bypass graft (CABG) surgery, but concern for negative inotropic properties potentially limits its use in these patients. The current study analyzed the effect of various propofol plasma concentrations on left ventricular (LV) contractility by means of a single-beat contractile index based on LV maximal power (PWR(max)). The study was conducted in 30 patients after CABG surgery. Immediately after admission to the intensive care unit (ICU), four different plasma concentrations of propofol 0.65, 1.30, 1.95, and 2.60 microg/ml were established. At each concentration level, the cardiac and vascular effects of propofol were studied by combining echocardiographic data with invasively derived aortic root pressure. Preload was characterized by LV end-diastolic dimensions. Afterload was indicated in terms of indexed systemic vascular resistance (SVRI), LV end-systolic meridional wall stress (LV-ESWS), and arterial elastance (Ea). Quantification of effects on contractility was achieved by preload-adjusted PWRmax. Myocardial contractility did not change during a fourfold increase in propofol plasma concentration. Preload-adjusted PWRmax amounted to 3.90+/-1.75 W x ml(-2) x 10(4), 3.98+/-1.69, 3.94+/-1.70, and 3.88+/-1.72, respectively (mean+/-SD). With respect to ventricular loading conditions, propofol caused a significant reduction in both pre- and afterload. The current results strongly suggest that propofol lacks direct cardiac depressant effects. Nevertheless, meaningful vascular actions of propofol could be demonstrated. Significant decreases in ventricular loading conditions accounted for a marked decrease in arterial blood pressure and supported the concept that propofol in clinically relevant concentration is a vasodilator.