TY - JOUR
T1 - The effect of propofol on haemodynamics: cardiac output, venous return, mean systemic filling pressure, and vascular resistances
AU - de Wit, F.
AU - van Vliet, A. L.
AU - de Wilde, R. B.
AU - Jansen, J. R.
AU - Vuyk, J.
AU - Aarts, L. P.
AU - de Jonge, E.
AU - Veelo, D. P.
AU - Geerts, B. F.
PY - 2016
Y1 - 2016
N2 - Background: Although arterial hypotension occurs frequently with propofol use in humans, its effects on intravascular volume and vascular capacitance are uncertain. We hypothesized that propofol decreases vascular capacitance and therefore decreases stressed volume. Methods: Cardiac output (CO) was measured using Modelflow(R) in 17 adult subjects after upper abdominal surgery. Mean systemic filling pressure (MSFP) and vascular resistances were calculated using venous return curves constructed by measuring steady-state arterial and venous pressures and CO during inspiratory hold manoeuvres at increasing plateau pressures. Measurements were performed at three incremental levels of targeted blood propofol concentrations. Results: Mean blood propofol concentrations for the three targeted levels were 3.0, 4.5, and 6.5 mu g ml(-1). Mean arterial pressure, central venous pressure, MSFP, venous return pressure, Rv, systemic arterial resistance, and resistance of the systemic circulation decreased, stroke volume variation increased, and CO was not significantly different as propofol concentration increased. Conclusions: An increase in propofol concentration within the therapeutic range causes a decrease in vascular stressed volume without a change in CO. The absence of an effect of propofol on CO can be explained by the balance between the decrease ineffective, or stressed, volume (as determined by MSFP), the decrease in resistance for venous return, and slightly improved heart function. Clinical trial registration: Netherlands Trial Register: NTR2486
AB - Background: Although arterial hypotension occurs frequently with propofol use in humans, its effects on intravascular volume and vascular capacitance are uncertain. We hypothesized that propofol decreases vascular capacitance and therefore decreases stressed volume. Methods: Cardiac output (CO) was measured using Modelflow(R) in 17 adult subjects after upper abdominal surgery. Mean systemic filling pressure (MSFP) and vascular resistances were calculated using venous return curves constructed by measuring steady-state arterial and venous pressures and CO during inspiratory hold manoeuvres at increasing plateau pressures. Measurements were performed at three incremental levels of targeted blood propofol concentrations. Results: Mean blood propofol concentrations for the three targeted levels were 3.0, 4.5, and 6.5 mu g ml(-1). Mean arterial pressure, central venous pressure, MSFP, venous return pressure, Rv, systemic arterial resistance, and resistance of the systemic circulation decreased, stroke volume variation increased, and CO was not significantly different as propofol concentration increased. Conclusions: An increase in propofol concentration within the therapeutic range causes a decrease in vascular stressed volume without a change in CO. The absence of an effect of propofol on CO can be explained by the balance between the decrease ineffective, or stressed, volume (as determined by MSFP), the decrease in resistance for venous return, and slightly improved heart function. Clinical trial registration: Netherlands Trial Register: NTR2486
U2 - https://doi.org/10.1093/bja/aew126
DO - https://doi.org/10.1093/bja/aew126
M3 - Article
C2 - 27199311
SN - 0007-0912
VL - 116
SP - 784
EP - 789
JO - British Journal of Anaesthesia
JF - British Journal of Anaesthesia
IS - 6
ER -