alveoli

Alveoli are the functional units of gas exchange in the respiratory system. Each alveolus is lined by type I pneumocytes (95% of surface area, thin squamous cells optimized for diffusion) and type II pneumocytes (cuboidal cells that produce surfactant and can differentiate into type I cells after injury). Surfactant, composed of dipalmitoylphosphatidylcholine (DPPC), reduces surface tension via LaPlace's law (P=2T/r), preventing alveolar collapse (atelectasis) especially in smaller alveoli. Surfactant production begins around week 26 of gestation and matures by week 35; deficiency causes neonatal respiratory distress syndrome (NRDS), assessed clinically via lecithin-to-sphingomyelin (L/S) ratio in amniotic fluid (mature if >2). The alveolar-capillary interface (respiratory membrane) consists of alveolar epithelium, fused basement membranes, and capillary endothelium, allowing rapid diffusion of O2 and CO2 governed by Fick's law. Alveolar macrophages (dust cells) reside in alveoli to phagocytose inhaled particles and pathogens; hemosiderin-laden macrophages ('heart failure cells') indicate pulmonary edema/hemorrhage, classically seen in left heart failure. Pores of Kohn connect adjacent alveoli, allowing collateral ventilation but also facilitating spread of infection (e.g., pneumonia). Clinically relevant conditions include emphysema (destruction of alveolar walls, decreased surface area, increased compliance), pulmonary edema (fluid in alveolar space impairing gas exchange), and diffuse alveolar damage (seen in ARDS). Understanding alveolar physiology is essential for interpreting diffusion capacity (DLCO), V/Q mismatch, and oxygen-hemoglobin dynamics in pulmonary pathology.