Supplementary Figure 1

Schematic illustration of trigger mechanisms leading to acute respiratory distress syndrome (ARDS). Four key pathophysiological and clinical findings are encountered in ARDS: firstly, noxious agents may attack the alveolar compartment directly or hit the lung via the intravascular compartment (indirect, classical ARDS). Secondly, during the early exudative phase, a self-perpetuating inflammatory process involves the entire gas exchange unit leading to type II cell injury, loss of epithelial (and endothelial) integrity, alveolar edema formation, and severe impairment of surfactant function. Thirdly, as a result a ventilation-perfusion mismatch with extensive shunt flow is observed. Fourthly, aggravating complications including new inflammatory events, such as recurrent or persistent sepsis, or acquisition of secondary (nosocomial) pneumonia may repetitively worsen the state of lung function and then progressively favour proliferative processes characterized by mesenchymal cell activation and ongoing lung fibrosis. infl., inflammatory, interst., interstitial.