BackgroundThe 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.MethodsEighteen 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.ResultsBaseline 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.ConclusionIn 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.
BackgroundMicrocirculation and macrohemodynamics are severely compromised during septic shock. However, the relationship between these two compartments needs to be further investigated. We hypothesized that early resuscitation restores left ventricular (LV) performance and microcirculatory function but fails to prevent metabolic disorders. We studied the effects of an early resuscitation protocol (ERP) on LV pressure/volume loops-derived parameters, sublingual microcirculation, and metabolic alterations during endotoxic shock.MethodsTwenty-five pigs were randomized into three groups: LPS group: Escherichia coli lipopolysaccharide (LPS); ERP group: LPS + ERP based on volume expansion, dobutamine, and noradrenaline infusion; Sham group. LV pressure/volume-derived parameters, systemic hemodynamics, sublingual microcirculation, and metabolic profile were assessed at baseline and after completing the resuscitation protocol.ResultsLPS significantly decreased LV end-diastolic volume, myocardial contractility, stroke work, and cardiac index (CI). Early resuscitation preserved preload, and myocardial contractility, increased CI and heart rate (p < .05). LPS severely diminished sublingual microvascular flow index (MFI), perfused vascular density (PVD), and the proportion of perfused vessels (PPV), while increased the heterogeneity flow index (HFI) (p < .05). Despite MFI was relatively preserved, MVD, PVD, and HFI were significantly impaired after resuscitation (p < .05). The macro- and microcirculatory changes were associated with increased lactic acidosis and mixed venous O2 saturation when compared to baseline values (p < .05). The scatter plot between mean arterial pressure (MAP) and MFI showed a biphasic relationship, suggesting that the values were within the limits of microvascular autoregulation when MAP was above 71 ± 6 mm Hg (R2 = 0.63).ConclusionsEarly hemodynamic resuscitation was effective to restore macrohemodynamia and myocardial contractility. Despite MAP and MFI were relatively preserved, the persistent microvascular dysfunction could explain metabolic disorders. The relationship between micro- and systemic hemodynamia and their impact on cellular function and metabolism needs to be further studied during endotoxic shock.Electronic supplementary materialThe online version of this article (doi:10.1186/s40635-015-0049-y) contains supplementary material, which is available to authorized users.
BackgroundPulse pressure (PPV) and stroke volume (SVV) variations may not be reliable in the setting of pulmonary hypertension and/or right ventricular (RV) failure. We hypothesized that RV afterload increase attenuates SVV and PPV during hypovolemia in a rabbit model of pulmonary embolism (PE) secondary to RV dysfunction.MethodsSeven anesthetized and mechanically ventilated rabbits were studied during four experimental conditions: normovolemia, blood withdrawal, pulmonary embolism and fluid loading of a colloidal solution. Central venous, RV and left ventricular (LV) pressures, and infra-diaphragmatic aortic blood flow (AoF) and pressure were measured. SV was estimated by the integral of systolic AoF. We analyzed RV and LV function through stroke work output curves. PPV and SVV were obtained by the variation of beat-to-beat PP and SV, respectively. We assessed RV and LV diastolic and systolic function by the time rate of relaxation (tau) and the ratio of the first derivative of ventricular pressure and the highest isovolumic developed pressure (dP/dt/DP), respectively. The vasomotor tone was estimated by the dynamic arterial elastance (Eadyn = PPV/SVV).ResultsPPV and SVV increased significantly during hemorrhage and returned to baseline values after PE which was associated to biventricular right-downward of the stroke work curves and a decrease of AoF and SV (P < 0.05). RV systo-diastolic function and LV systolic function were impaired. All the animals were nonresponders after volume expansion. Eadyn did not show any significant change during the different experimental conditions.ConclusionsThe dynamic preload indicators (SVV and PPV) were significantly reduced after a normotensive PE in hypovolemic animals, mainly by the systo-diastolic dysfunction of the RV associated with LV systolic impairment, which makes the animals nonresponsive to volume loading. This normalization of dynamic preload indices may prevent the detrimental consequence of fluid loading.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.