Pulmonary surfactant is a complex mixture of phospholipids (90%, primarily dipalmitoylphosphatidylcholine/DPPC) and surfactant proteins (SP-A, SP-B, SP-C, SP-D) produced by type II pneumocytes. Surfactant reduces alveolar surface tension according to the LaPlace equation (P = 2T/r), preventing alveolar collapse at end-expiration and reducing the work of breathing. In neonatal respiratory distress syndrome (RDS), premature infants (<34 weeks gestation) have insufficient surfactant production, leading to diffuse alveolar collapse, atelectasis, hyaline membrane formation, and progressive respiratory failure. In ARDS, surfactant dysfunction occurs through a different mechanism: direct or indirect lung injury causes diffuse alveolar damage with neutrophilic infiltration, protein-rich edema fluid inactivating surfactant, destruction of type II pneumocytes, and formation of hyaline membranes. The pathological cascade in ARDS follows three phases: exudative (0-7 days: bilateral infiltrates, refractory hypoxemia, reduced compliance), proliferative (7-21 days: type II pneumocyte proliferation, fibroblast activity), and fibrotic (>21 days: collagen deposition, architectural distortion). The Berlin definition classifies ARDS severity by PaO2/FiO2 ratio on PEEP ≥5 cmH2O: mild (200-300), moderate (100-200), severe (<100). Lung-protective ventilation (low tidal volume 6 mL/kg IBW, plateau pressure <30 cmH2O) reduces mortality by preventing...