Lung metabolism during ventilator-induced lung injury: Stretching the relevance of the normally aerated lung

摘要

Concerns about pulmonary complications of positive pressure ventilation (1) are at least as old as the description of the acute respiratory distress syndrome (ARDS) (2). Yet, it took about a decade until experimental findings (3) shifted the focus from air leaks and oxygen toxicity to the biological effects of large excursions of the lung parenchyma (4). The demonstration that mechanical ventilation with high peak inspiratory pressures and low positive end-expiratory pressure (PEEP) could produce edema, increased alveolocapillary permeability, leukocyte infiltration, and inflammation in normal lungs established the current understanding of ventilator-induced lung injury (VILI) (4, 5).