Contractility in humans after coronary artery surgery - Echocardiographic assessment with preload-adjusted maximal power

Citation
C. Schmidt et al., Contractility in humans after coronary artery surgery - Echocardiographic assessment with preload-adjusted maximal power, ANESTHESIOL, 91(1), 1999, pp. 58-70
Citations number
45
Categorie Soggetti
Aneshtesia & Intensive Care","Medical Research Diagnosis & Treatment
Journal title
ANESTHESIOLOGY
ISSN journal
00033022 → ACNP
Volume
91
Issue
1
Year of publication
1999
Pages
58 - 70
Database
ISI
SICI code
0003-3022(199907)91:1<58:CIHACA>2.0.ZU;2-N
Abstract
Background Propofol's unique pharmacokinetic profile offers advantages for titration and rapid emergence in patients after coronary artery bypass graf t (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) contractil ity by means of a single-beat contractile index based on LV maximal power ( PWRmax). Methods: The study was conducted in 30 patients after CABG surgery. Immedia tely after admission to the intensive care unit (ICU), four different plasm a concentrations of propofol 0.65, 1.30, 1.95, and 2.60 mu g/ml were establ ished At each concentration level, the cardiac and vascular effects of prop ofol were studied by combining echocardiographic data with invasively deriv ed aortic root pressure. Preload was characterized by LV end-diastolic dime nsions. Afterload was Indicated in terms of indexed systemic vascular resis tance (SVRI), LV end-systolic meridional wad stress (LV-ESWS), and arterial elastance (E-a). Quantification of effects on contractility was achieved b y preload-adjusted PWRmax. Results: Myocardial contractility did not change during a fourfold increase in propofol plasma concentration. Preload-adjusted PWRmax amounted to 3.90 +/- 1.75 W.ml(-2).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. Conclusions: The current results strongly suggest that propofol lacks direc t cardiac depressant effects. Nevertheless, meaningful vascular actions of propofol could be demonstrated Significant decreases in ventricular lending conditions accounted for a marked decrease in arterial blood pressure and supported the concept that propofol in clinically relevant concentration is a vasodilator.