The transition from intrauterine to extrauterine life requires dramatic physiological adaptations across multiple organ systems within minutes of birth. In utero, the fetus relies on the placenta for gas exchange, with fetal circulation shunting blood away from the lungs through the foramen ovale and ductus arteriosus. At birth, the infant's first breath creates negative intrathoracic pressure that expands the lungs, increases pulmonary blood flow, and initiates functional closure of fetal shunts. Surfactant, produced by type II alveolar cells beginning at approximately 24-28 weeks gestation, reduces alveolar surface tension and prevents atelectasis — its deficiency in preterm infants leads to respiratory distress syndrome (RDS).