ARDS is characterized by diffuse alveolar damage from pulmonary or extrapulmonary insults. The exudative phase (days 1-7) involves damage to the alveolar-capillary membrane: type I pneumocyte injury allows protein-rich edema fluid to flood alveoli, forming hyaline membranes. Neutrophil-mediated inflammation releases proteases and reactive oxygen species, amplifying damage. Surfactant dysfunction increases surface tension, promoting alveolar collapse. The result is bilateral pulmonary infiltrates, severe hypoxemia refractory to supplemental oxygen, and reduced lung compliance. Berlin criteria classify severity by PaO2/FiO2 ratio on PEEP >= 5: mild (200-300), moderate (100-200), severe (< 100). Lung-protective ventilation targeting low tidal volumes (6 mL/kg IBW) reduces ventilator-induced lung injury (VILI) from overdistention (volutrauma), cyclic opening/closing of atelectatic alveoli (atelectrauma), and biotrauma (cytokine release). The ARDS Network trial demonstrated a 22% mortality reduction with low Vt strategy.