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Role of Fluid and Sodium Retention in Experimental Ventilator-Induced Lung Injury

Background: Ventilator-induced lung injury (VILI) via respiratory mechanics is deeply interwoven with hemodynamic, kidney and fluid/electrolyte changes. We aimed to assess the role of positive fluid balance in the framework of ventilation-induced lung injury. Methods:Post-hoc analysis of seventy-eig...

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Autores principales: Gattarello, Simone, Pasticci, Iacopo, Busana, Mattia, Lazzari, Stefano, Palermo, Paola, Palumbo, Maria Michela, Romitti, Federica, Steinberg, Irene, Collino, Francesca, Vassalli, Francesco, Langer, Thomas, Moerer, Onnen, Saager, Leif, Herrmann, Peter, Cadringher, Paolo, Meissner, Konrad, Quintel, Michael, Gattinoni, Luciano
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8473803/
https://www.ncbi.nlm.nih.gov/pubmed/34588999
http://dx.doi.org/10.3389/fphys.2021.743153
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author Gattarello, Simone
Pasticci, Iacopo
Busana, Mattia
Lazzari, Stefano
Palermo, Paola
Palumbo, Maria Michela
Romitti, Federica
Steinberg, Irene
Collino, Francesca
Vassalli, Francesco
Langer, Thomas
Moerer, Onnen
Saager, Leif
Herrmann, Peter
Cadringher, Paolo
Meissner, Konrad
Quintel, Michael
Gattinoni, Luciano
author_facet Gattarello, Simone
Pasticci, Iacopo
Busana, Mattia
Lazzari, Stefano
Palermo, Paola
Palumbo, Maria Michela
Romitti, Federica
Steinberg, Irene
Collino, Francesca
Vassalli, Francesco
Langer, Thomas
Moerer, Onnen
Saager, Leif
Herrmann, Peter
Cadringher, Paolo
Meissner, Konrad
Quintel, Michael
Gattinoni, Luciano
author_sort Gattarello, Simone
collection PubMed
description Background: Ventilator-induced lung injury (VILI) via respiratory mechanics is deeply interwoven with hemodynamic, kidney and fluid/electrolyte changes. We aimed to assess the role of positive fluid balance in the framework of ventilation-induced lung injury. Methods:Post-hoc analysis of seventy-eight pigs invasively ventilated for 48 h with mechanical power ranging from 18 to 137 J/min and divided into two groups: high vs. low pleural pressure (10.0 ± 2.8 vs. 4.4 ± 1.5 cmH(2)O; p < 0.01). Respiratory mechanics, hemodynamics, fluid, sodium and osmotic balances, were assessed at 0, 6, 12, 24, 48 h. Sodium distribution between intracellular, extracellular and non-osmotic sodium storage compartments was estimated assuming osmotic equilibrium. Lung weight, wet-to-dry ratios of lung, kidney, liver, bowel and muscle were measured at the end of the experiment. Results: High pleural pressure group had significant higher cardiac output (2.96 ± 0.92 vs. 3.41 ± 1.68 L/min; p < 0.01), use of norepinephrine/epinephrine (1.76 ± 3.31 vs. 5.79 ± 9.69 mcg/kg; p < 0.01) and total fluid infusions (3.06 ± 2.32 vs. 4.04 ± 3.04 L; p < 0.01). This hemodynamic status was associated with significantly increased sodium and fluid retention (at 48 h, respectively, 601.3 ± 334.7 vs. 1073.2 ± 525.9 mmol, p < 0.01; and 2.99 ± 2.54 vs. 6.66 ± 3.87 L, p < 0.01). Ten percent of the infused sodium was stored in an osmotically inactive compartment. Increasing fluid and sodium retention was positively associated with lung-weight (R(2) = 0.43, p < 0.01; R(2) = 0.48, p < 0.01) and with wet-to-dry ratio of the lungs (R(2) = 0.14, p < 0.01; R(2) = 0.18, p < 0.01) and kidneys (R(2) = 0.11, p = 0.02; R(2) = 0.12, p = 0.01). Conclusion: Increased mechanical power and pleural pressures dictated an increase in hemodynamic support resulting in proportionally increased sodium and fluid retention and pulmonary edema.
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spelling pubmed-84738032021-09-28 Role of Fluid and Sodium Retention in Experimental Ventilator-Induced Lung Injury Gattarello, Simone Pasticci, Iacopo Busana, Mattia Lazzari, Stefano Palermo, Paola Palumbo, Maria Michela Romitti, Federica Steinberg, Irene Collino, Francesca Vassalli, Francesco Langer, Thomas Moerer, Onnen Saager, Leif Herrmann, Peter Cadringher, Paolo Meissner, Konrad Quintel, Michael Gattinoni, Luciano Front Physiol Physiology Background: Ventilator-induced lung injury (VILI) via respiratory mechanics is deeply interwoven with hemodynamic, kidney and fluid/electrolyte changes. We aimed to assess the role of positive fluid balance in the framework of ventilation-induced lung injury. Methods:Post-hoc analysis of seventy-eight pigs invasively ventilated for 48 h with mechanical power ranging from 18 to 137 J/min and divided into two groups: high vs. low pleural pressure (10.0 ± 2.8 vs. 4.4 ± 1.5 cmH(2)O; p < 0.01). Respiratory mechanics, hemodynamics, fluid, sodium and osmotic balances, were assessed at 0, 6, 12, 24, 48 h. Sodium distribution between intracellular, extracellular and non-osmotic sodium storage compartments was estimated assuming osmotic equilibrium. Lung weight, wet-to-dry ratios of lung, kidney, liver, bowel and muscle were measured at the end of the experiment. Results: High pleural pressure group had significant higher cardiac output (2.96 ± 0.92 vs. 3.41 ± 1.68 L/min; p < 0.01), use of norepinephrine/epinephrine (1.76 ± 3.31 vs. 5.79 ± 9.69 mcg/kg; p < 0.01) and total fluid infusions (3.06 ± 2.32 vs. 4.04 ± 3.04 L; p < 0.01). This hemodynamic status was associated with significantly increased sodium and fluid retention (at 48 h, respectively, 601.3 ± 334.7 vs. 1073.2 ± 525.9 mmol, p < 0.01; and 2.99 ± 2.54 vs. 6.66 ± 3.87 L, p < 0.01). Ten percent of the infused sodium was stored in an osmotically inactive compartment. Increasing fluid and sodium retention was positively associated with lung-weight (R(2) = 0.43, p < 0.01; R(2) = 0.48, p < 0.01) and with wet-to-dry ratio of the lungs (R(2) = 0.14, p < 0.01; R(2) = 0.18, p < 0.01) and kidneys (R(2) = 0.11, p = 0.02; R(2) = 0.12, p = 0.01). Conclusion: Increased mechanical power and pleural pressures dictated an increase in hemodynamic support resulting in proportionally increased sodium and fluid retention and pulmonary edema. Frontiers Media S.A. 2021-09-13 /pmc/articles/PMC8473803/ /pubmed/34588999 http://dx.doi.org/10.3389/fphys.2021.743153 Text en Copyright © 2021 Gattarello, Pasticci, Busana, Lazzari, Palermo, Palumbo, Romitti, Steinberg, Collino, Vassalli, Langer, Moerer, Saager, Herrmann, Cadringher, Meissner, Quintel and Gattinoni. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Physiology
Gattarello, Simone
Pasticci, Iacopo
Busana, Mattia
Lazzari, Stefano
Palermo, Paola
Palumbo, Maria Michela
Romitti, Federica
Steinberg, Irene
Collino, Francesca
Vassalli, Francesco
Langer, Thomas
Moerer, Onnen
Saager, Leif
Herrmann, Peter
Cadringher, Paolo
Meissner, Konrad
Quintel, Michael
Gattinoni, Luciano
Role of Fluid and Sodium Retention in Experimental Ventilator-Induced Lung Injury
title Role of Fluid and Sodium Retention in Experimental Ventilator-Induced Lung Injury
title_full Role of Fluid and Sodium Retention in Experimental Ventilator-Induced Lung Injury
title_fullStr Role of Fluid and Sodium Retention in Experimental Ventilator-Induced Lung Injury
title_full_unstemmed Role of Fluid and Sodium Retention in Experimental Ventilator-Induced Lung Injury
title_short Role of Fluid and Sodium Retention in Experimental Ventilator-Induced Lung Injury
title_sort role of fluid and sodium retention in experimental ventilator-induced lung injury
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8473803/
https://www.ncbi.nlm.nih.gov/pubmed/34588999
http://dx.doi.org/10.3389/fphys.2021.743153
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