Acute Respiratory Distress Syndrome (ARDS) results from diffuse alveolar damage (DAD) to the alveolar-capillary membrane, leading to non-cardiogenic pulmonary edema and refractory hypoxemia. The pathological process occurs in three phases: (1) Exudative phase (days 1-7): An inciting event triggers a massive inflammatory cascade with neutrophil activation, releasing proteases, reactive oxygen species, and pro-inflammatory cytokines (IL-1, IL-6, IL-8, TNF-alpha). Damage to type I alveolar epithelial cells and pulmonary capillary endothelium increases permeability, allowing protein-rich fluid to flood the alveoli. Surfactant-producing type II pneumocytes are damaged, causing surfactant deficiency, increased surface tension, and alveolar collapse (atelectasis). Hyaline membranes form along the alveolar walls. (2) Proliferative phase (days 7-21): Type II pneumocytes proliferate to restore the alveolar epithelium, fibroblasts begin collagen deposition. (3) Fibrotic phase (after day 21): Some patients develop pulmonary fibrosis with irreversible changes. The Berlin criteria classify severity by PaO2/FiO2 ratio on PEEP >=5 cmH2O: mild (200-300), moderate (100-200), severe (<100).