The future of mechanical ventilation: lessons from the present and the past
Abstract 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 tran...
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doaj-6f5fb3a5a014459e8ae9657474a2805c2020-11-25T00:20:52ZengBMCCritical Care1364-85352017-07-0121111110.1186/s13054-017-1750-xThe future of mechanical ventilation: lessons from the present and the pastLuciano Gattinoni0John J. Marini1Francesca Collino2Giorgia Maiolo3Francesca Rapetti4Tommaso Tonetti5Francesco Vasques6Michael Quintel7Department of Anesthesiology, Emergency and Intensive Care Medicine, University of GöttingenUniversity of MinnesotaDepartment of Anesthesiology, Emergency and Intensive Care Medicine, University of GöttingenDepartment of Anesthesiology, Emergency and Intensive Care Medicine, University of GöttingenDepartment of Anesthesiology, Emergency and Intensive Care Medicine, University of GöttingenDepartment of Anesthesiology, Emergency and Intensive Care Medicine, University of GöttingenDepartment of Anesthesiology, Emergency and Intensive Care Medicine, University of GöttingenDepartment of Anesthesiology, Emergency and Intensive Care Medicine, University of GöttingenAbstract 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 cmH2O 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 cmH2O, 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.http://link.springer.com/article/10.1186/s13054-017-1750-xMechanical ventilationAcute respiratory distress syndromeVentilator-induced lung injuryMechanical powerExtracorporeal membrane oxygenation |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Luciano Gattinoni John J. Marini Francesca Collino Giorgia Maiolo Francesca Rapetti Tommaso Tonetti Francesco Vasques Michael Quintel |
spellingShingle |
Luciano Gattinoni John J. Marini Francesca Collino Giorgia Maiolo Francesca Rapetti Tommaso Tonetti Francesco Vasques Michael Quintel The future of mechanical ventilation: lessons from the present and the past Critical Care Mechanical ventilation Acute respiratory distress syndrome Ventilator-induced lung injury Mechanical power Extracorporeal membrane oxygenation |
author_facet |
Luciano Gattinoni John J. Marini Francesca Collino Giorgia Maiolo Francesca Rapetti Tommaso Tonetti Francesco Vasques Michael Quintel |
author_sort |
Luciano Gattinoni |
title |
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_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_sort |
future of mechanical ventilation: lessons from the present and the past |
publisher |
BMC |
series |
Critical Care |
issn |
1364-8535 |
publishDate |
2017-07-01 |
description |
Abstract 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 cmH2O 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 cmH2O, 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. |
topic |
Mechanical ventilation Acute respiratory distress syndrome Ventilator-induced lung injury Mechanical power Extracorporeal membrane oxygenation |
url |
http://link.springer.com/article/10.1186/s13054-017-1750-x |
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