The increase of vasomotor tone avoids the ability of the dynamic preload indicators to estimate fluid responsiveness

Abstract

Abstract Background The use of vasoconstrictor can affect the dynamic indices to predict fluid responsiveness. We investigate the effects of an increase of vascular tone on dynamic variables of fluid responsiveness in a rabbit model of hemorrhage, and to examine the ability of the arterial pressure surrogates dynamic indices to track systolic volume variation (SVV) during hypovolemia under increased vasomotor tone. Methods Eighteen anesthetized and mechanically ventilated rabbits were studied during normovolemia (BL) and after blood progressive removal (15 mL/kg, BW). Other two sets of data were obtained during PHE infusion with normovolemia (BL + PHE) and during hypovolemia (BW + PHE). We measured central venous and left ventricular (LV) pressures and infra diaphragmatic aortic blood flow (AoF) and pressure. Pulse pressure variation (PPV), systolic pressure variation (SPV) and SVV were estimated manually by the variation of beat-to-beat PP, SP and SV, respectively. We also calculated PPVapnea as 100 × (PPmax-PPmin)/PP during apnea. The vasomotor tone was estimated by total peripheral resistance (TPR = mean aortic pressure/mean AoF), dynamic arterial elastance (Eadyn = PPV/SVV) and arterial compliance (C = SV/PP). We assessed LV preload by LV end-diastolic pressure (LVEDP). We compared the trending abilities between SVV and pressure surrogate indices using four-quadrant plots and polar plots. Results Baseline PPV, SPV, PPVapnea, and SVV increased significantly during hemorrhage, with a decrease of AoF (P < 0.05). PHE induced significant TPR and Eadyn increase and C decrease in bled animals, and a further decrease in AoF with a significant decrease of all dynamic indices. There was a significant correlation between SVV and PPV, PPVapnea and SPV in normal vasomotor tone (r2 ≥ 0.5). The concordance rate was 91%, 95% and 76% between SVV and PPV, PPVapnea and SPV, respectively, in accordance with the polar plot analysis. During PHE infusion, there was no correlation between SVV and its surrogates, and both four-quadrant plot and polar plot showed poor trending. Conclusion In this animal model of hemorrhage and increased vasomotor tone induced by phenylephrine the ability of dynamic indices to predict fluid responsiveness seems to be impaired, masking the true fluid loss. Moreover, the arterial pressure surrogates have not the reliable trending ability against SVV.