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alveolar collapse, alveoli, atelectasis, hyaline membrane disease, neonatal, RDS, respiratory distress syndrome of the newborn, surface tension


To explore basic mechanisms of action of pulmonary surfactant in preventing alveolar collapse, a first-principles analysis is done analyzing forces on the shared walls separating adjacent alveolar gas bubbles. The analysis holds for concave alveolar models with either rounded, dome-like surfaces or flat, box-like surfaces. The analysis also holds for neighboring alveoli of varying size and shape. Surfactant action is characterized by two parameters describing reduction in surface tension vs. log concentration. The resulting equations describe the net pressure tending to shift the shared position of a wall, as a function of the perturbation from a balanced initial state. In the absence of surfactant, the bubbles exist in an unstable equilibrium. Any perturbation causes runaway positive feedback such that one bubble shrinks and the other enlarges. In the presence of surfactant having adequate concentration and potency the initial normal bubble volumes are maintained by stabilizing negative feedback. With borderline surfactant activity there is stable partial enlargement of one bubble and partial shrinkage of the other bubble. The present analysis shows quantitatively how pulmonary surfactant normally works to equalize the sizes of neighboring alveolar gas bubbles in small, local regions of lung. Once a threshold surfactant effect is exceeded this local stability is robust. However, inadequate surfactant can lead to microatelectasis, intrapulmonic shunting of venous blood past poorly alveoli, and arterial hypoxemia. The presence of giant alveoli surrounded by smaller collapsed alveoli, as well as the presence of hyaline membranes, characteristic of respiratory distress syndrome of the newborn, are also explained by the underlying biomechanics.