Abstract
Lung cells react to forces applied during mechanical ventilation by activating a large variety of biological responses, from proliferation to inflammation or cell death. In heterogeneous lungs, regional volumes and pressures are unevenly distributed, enhancing these mechanosensitive cell responses and causing tissue damage. Inflammation, apoptosis, and matrix remodeling are hallmarks of this condition, termed Ventilator-Induced Lung Injury (VILI). Limitation of VILI is a major goal in the current critical care, but there is no gold standard for its monitoring. As no pharmacological treatment has shown a clinical benefit, optimization of mechanical ventilation remains the only available approach in critically ill patients. Protective ventilatory strategies limit tidal volumes to avoid overdistension and apply positive end-expiratory pressure to ensure a lung rest volume that guarantees gas exchange and minimizes cyclic changes in aeration. However, only reduction of tidal volume in patients with previous lung injury has shown a significant reduction in mortality. Improvements in monitoring and patient selection can help to personalize ventilatory therapy to avoid further lung damage caused by mechanical ventilation.
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Albaiceta, G.M., Amado-Rodríguez, L. (2022). Ventilator-Induced Lung Injury and Lung Protective Ventilation. In: Bellani, G. (eds) Mechanical Ventilation from Pathophysiology to Clinical Evidence. Springer, Cham. https://doi.org/10.1007/978-3-030-93401-9_15
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DOI: https://doi.org/10.1007/978-3-030-93401-9_15
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