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The future of mechanical ventilation: lessons from the present and the past

The adverse effects of mechanical ventilation in acute respiratory distress syndrome (ARDS) arise from two main causes: unphysiological increases of transpulmonary pressure and unphysiological increases/decreases of pleural pressure during positive or negative pressure ventilation. The transpulmonar...

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Autores principales: Gattinoni, Luciano, Marini, John J., Collino, Francesca, Maiolo, Giorgia, Rapetti, Francesca, Tonetti, Tommaso, Vasques, Francesco, Quintel, Michael
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5508674/
https://www.ncbi.nlm.nih.gov/pubmed/28701178
http://dx.doi.org/10.1186/s13054-017-1750-x
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author Gattinoni, Luciano
Marini, John J.
Collino, Francesca
Maiolo, Giorgia
Rapetti, Francesca
Tonetti, Tommaso
Vasques, Francesco
Quintel, Michael
author_facet Gattinoni, Luciano
Marini, John J.
Collino, Francesca
Maiolo, Giorgia
Rapetti, Francesca
Tonetti, Tommaso
Vasques, Francesco
Quintel, Michael
author_sort Gattinoni, Luciano
collection PubMed
description The adverse effects of mechanical ventilation in acute respiratory distress syndrome (ARDS) arise from two main causes: unphysiological increases of transpulmonary pressure and unphysiological increases/decreases of pleural pressure during positive or negative pressure ventilation. The transpulmonary pressure-related side effects primarily account for ventilator-induced lung injury (VILI) while the pleural pressure-related side effects primarily account for hemodynamic alterations. The changes of transpulmonary pressure and pleural pressure resulting from a given applied driving pressure depend on the relative elastances of the lung and chest wall. The term ‘volutrauma’ should refer to excessive strain, while ‘barotrauma’ should refer to excessive stress. Strains exceeding 1.5, corresponding to a stress above ~20 cmH(2)O in humans, are severely damaging in experimental animals. Apart from high tidal volumes and high transpulmonary pressures, the respiratory rate and inspiratory flow may also play roles in the genesis of VILI. We do not know which fraction of mortality is attributable to VILI with ventilation comparable to that reported in recent clinical practice surveys (tidal volume ~7.5 ml/kg, positive end-expiratory pressure (PEEP) ~8 cmH(2)O, rate ~20 bpm, associated mortality ~35%). Therefore, a more complete and individually personalized understanding of ARDS lung mechanics and its interaction with the ventilator is needed to improve future care. Knowledge of functional lung size would allow the quantitative estimation of strain. The determination of lung inhomogeneity/stress raisers would help assess local stresses; the measurement of lung recruitability would guide PEEP selection to optimize lung size and homogeneity. Finding a safety threshold for mechanical power, normalized to functional lung volume and tissue heterogeneity, may help precisely define the safety limits of ventilating the individual in question. When a mechanical ventilation set cannot be found to avoid an excessive risk of VILI, alternative methods (such as the artificial lung) should be considered.
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spelling pubmed-55086742017-07-17 The future of mechanical ventilation: lessons from the present and the past Gattinoni, Luciano Marini, John J. Collino, Francesca Maiolo, Giorgia Rapetti, Francesca Tonetti, Tommaso Vasques, Francesco Quintel, Michael Crit Care Review The adverse effects of mechanical ventilation in acute respiratory distress syndrome (ARDS) arise from two main causes: unphysiological increases of transpulmonary pressure and unphysiological increases/decreases of pleural pressure during positive or negative pressure ventilation. The transpulmonary pressure-related side effects primarily account for ventilator-induced lung injury (VILI) while the pleural pressure-related side effects primarily account for hemodynamic alterations. The changes of transpulmonary pressure and pleural pressure resulting from a given applied driving pressure depend on the relative elastances of the lung and chest wall. The term ‘volutrauma’ should refer to excessive strain, while ‘barotrauma’ should refer to excessive stress. Strains exceeding 1.5, corresponding to a stress above ~20 cmH(2)O in humans, are severely damaging in experimental animals. Apart from high tidal volumes and high transpulmonary pressures, the respiratory rate and inspiratory flow may also play roles in the genesis of VILI. We do not know which fraction of mortality is attributable to VILI with ventilation comparable to that reported in recent clinical practice surveys (tidal volume ~7.5 ml/kg, positive end-expiratory pressure (PEEP) ~8 cmH(2)O, rate ~20 bpm, associated mortality ~35%). Therefore, a more complete and individually personalized understanding of ARDS lung mechanics and its interaction with the ventilator is needed to improve future care. Knowledge of functional lung size would allow the quantitative estimation of strain. The determination of lung inhomogeneity/stress raisers would help assess local stresses; the measurement of lung recruitability would guide PEEP selection to optimize lung size and homogeneity. Finding a safety threshold for mechanical power, normalized to functional lung volume and tissue heterogeneity, may help precisely define the safety limits of ventilating the individual in question. When a mechanical ventilation set cannot be found to avoid an excessive risk of VILI, alternative methods (such as the artificial lung) should be considered. BioMed Central 2017-07-12 /pmc/articles/PMC5508674/ /pubmed/28701178 http://dx.doi.org/10.1186/s13054-017-1750-x Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Review
Gattinoni, Luciano
Marini, John J.
Collino, Francesca
Maiolo, Giorgia
Rapetti, Francesca
Tonetti, Tommaso
Vasques, Francesco
Quintel, Michael
The future of mechanical ventilation: lessons from the present and the past
title The future of mechanical ventilation: lessons from the present and the past
title_full The future of mechanical ventilation: lessons from the present and the past
title_fullStr The future of mechanical ventilation: lessons from the present and the past
title_full_unstemmed The future of mechanical ventilation: lessons from the present and the past
title_short The future of mechanical ventilation: lessons from the present and the past
title_sort future of mechanical ventilation: lessons from the present and the past
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5508674/
https://www.ncbi.nlm.nih.gov/pubmed/28701178
http://dx.doi.org/10.1186/s13054-017-1750-x
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