Key Concepts
Introduction
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. On the exam, writers often pair stable-sounding options with unstable data—notice the mismatch before you commit. If the stem names a license or role, reread that line; scope errors are classic trap answers even when the clinical topic is familiar. Run a 60-second scan: breathing work and oxygenation, perfusion and end organs, neuro baseline, likely infection sources, and devices that can fail quietly. When two answers feel partly right, pick the one that reduces imminent harm and matches orders for the role you were given. Train yourself to state the primary risk in one short phrase...