Respiratory distress syndrome (RDS) results from insufficient pulmonary surfactant production by type II pneumocytes, which typically mature by 34-36 weeks gestation. Surfactant reduces alveolar surface tension, preventing alveolar collapse during expiration. Without adequate surfactant, alveoli collapse with each breath (atelectasis), requiring tremendous work of breathing to re-expand. This creates a cycle of progressive atelectasis, ventilation-perfusion mismatch, hypoxemia, and respiratory acidosis. Damaged alveolar epithelium allows plasma protein leakage, forming hyaline membranes that further impair gas exchange. Exogenous surfactant therapy dramatically improves outcomes when administered early.