The acute respiratory distress syndrome (ARDS) is a predominantly inflammatory lung disease that develops in consequence of a wide spectrum of pulmonary and extrapulmonary conditions. Its biological hallmarks are the production of proinflammatory cytokines, increased vascular and alveolar permeability, alveolar edema, and infiltration with polymorphonucleate cells. The syndrome has wide inter-individual variability, and recent research has underlined the existence of at least two different phenotypes, one presenting with significantly increased inflammation features. Mechanical ventilation is the main supportive therapy for ARDS, but it can cause, depending on the intensity of its application, different levels of lung damage, from gross lung parenchyma ruptures (nowadays very rare) to minor lesions at the cellular level, to release of more inflammatory mediators, which can enhance the already present inflammatory reaction. These processes are mediated by complex mechanisms of transduction of physical forces into biological signals. Moreover, due to the increased intercellular permeability and the lack of compartmentalization, inflammatory mediators can spread in the organism and favor the development of multisystem organ failure. Although “protective” mechanical ventilation settings are now widely implemented, mortality due to ARDS and ventilator-induced lung injury is still high. The concept of modulating the inflammatory response seems rational and promising, but the results to date are disappointing, since none of the therapies aimed at reducing or controlling the lung inflammatory response have showed any benefit in terms of outcome. Innovative approaches to inflammation modulation (such as the infusion of mesenchymal stromal cells) are still under evaluation and could deliver results in the next years.

Cardiopulmonary Monitoring in the Patient with an Inflamed Lung

Tonetti T.;Ranieri V. M.
2021

Abstract

The acute respiratory distress syndrome (ARDS) is a predominantly inflammatory lung disease that develops in consequence of a wide spectrum of pulmonary and extrapulmonary conditions. Its biological hallmarks are the production of proinflammatory cytokines, increased vascular and alveolar permeability, alveolar edema, and infiltration with polymorphonucleate cells. The syndrome has wide inter-individual variability, and recent research has underlined the existence of at least two different phenotypes, one presenting with significantly increased inflammation features. Mechanical ventilation is the main supportive therapy for ARDS, but it can cause, depending on the intensity of its application, different levels of lung damage, from gross lung parenchyma ruptures (nowadays very rare) to minor lesions at the cellular level, to release of more inflammatory mediators, which can enhance the already present inflammatory reaction. These processes are mediated by complex mechanisms of transduction of physical forces into biological signals. Moreover, due to the increased intercellular permeability and the lack of compartmentalization, inflammatory mediators can spread in the organism and favor the development of multisystem organ failure. Although “protective” mechanical ventilation settings are now widely implemented, mortality due to ARDS and ventilator-induced lung injury is still high. The concept of modulating the inflammatory response seems rational and promising, but the results to date are disappointing, since none of the therapies aimed at reducing or controlling the lung inflammatory response have showed any benefit in terms of outcome. Innovative approaches to inflammation modulation (such as the infusion of mesenchymal stromal cells) are still under evaluation and could deliver results in the next years.
2021
Cardiopulmonary Monitoring: Basic Physiology, Tools, and Bedside Management for the Critically III
729
739
Tonetti T.; Ranieri V.M.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11585/929419
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