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López A, Grignola JC, Angulo M, et al. Effects of early hemodynamic resuscitation on left ventricular performance and microcirculatory function during endotoxic shock. Intensive Care Med Exp. 2015;3(1):49doi: 10.1186/s40635-015-0049-y.
López, A., Grignola, J. C., Angulo, M., Alvez, I., Nin, N., Lacuesta, G., Baz, M., Cardinal, P., Prestes, I., Bouchacourt, J. P., Riva, J., Ince, C., & Hurtado, F. J. (2015). Effects of early hemodynamic resuscitation on left ventricular performance and microcirculatory function during endotoxic shock. Intensive care medicine experimental, 3(1), 49. https://doi.org/10.1186/s40635-015-0049-y
López, Alejandra, et al. "Effects of early hemodynamic resuscitation on left ventricular performance and microcirculatory function during endotoxic shock." Intensive care medicine experimental vol. 3,1 (2015): 49. doi: https://doi.org/10.1186/s40635-015-0049-y
López A, Grignola JC, Angulo M, Alvez I, Nin N, Lacuesta G, Baz M, Cardinal P, Prestes I, Bouchacourt JP, Riva J, Ince C, Hurtado FJ. Effects of early hemodynamic resuscitation on left ventricular performance and microcirculatory function during endotoxic shock. Intensive Care Med Exp. 2015 Dec;3(1):49. doi: 10.1186/s40635-015-0049-y. Epub 2015 May 08. PMID: 26215813; PMCID: PMC4513023.
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Intensive Care Med Exp. 2015 Dec;3(1):49. doi: 10.1186/s40635-015-0049-y. Epub 2015 May 08.

Effects of early hemodynamic resuscitation on left ventricular performance and microcirculatory function during endotoxic shock.

Intensive care medicine experimental

Alejandra López, Juan Carlos Grignola, Martín Angulo, Ignacio Alvez, Nicolás Nin, Gonzalo Lacuesta, Manuel Baz, Pablo Cardinal, Ivana Prestes, Juan P Bouchacourt, Juan Riva, Can Ince, Francisco Javier Hurtado

Affiliations

  1. Pathophysiology Department, University Hospital, School of Medicine, Universidad de la República, Av. Italia 2870, 15th Floor, CP 11600, Montevideo, Uruguay, [email protected].

PMID: 26215813 PMCID: PMC4513023 DOI: 10.1186/s40635-015-0049-y

Abstract

BACKGROUND: Microcirculation 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.

METHODS: Twenty-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.

RESULTS: LPS 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 (R (2) = 0.63).

CONCLUSIONS: Early 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.

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