The role of pulmonary surfactant on lung fluid balance

Karl von Neegaard's classic publication, in 1929, first identified the physiological function of pulmonary surfactant on alveolar mechanics. Dr. John Allen Clements brought this work to the clinic in the 1960s, culminating in the development of surfactant replacement therapy for infant respiratory distress syndrome (RDS). In this mini-review, we discuss pulmonary surfactants' role in maintaining lung fluid balance, which is essential in preventing pulmonary edema. Alveolar surface tension (γ) is transmitted into the perialveolar space surrounding pulmonary capillaries and corner vessels. Increasing surface tension at end expiration would increase alveolar recoil pressure and decrease alveolar radius, thus causing more subatmospheric pressure in the perialveolar space, generating an increased gradient for microvascular filtration. Studies have demonstrated a positive correlation between increased pulmonary extravascular water volume (PEWV) and high γ (γ = 8.3 ± 1.7 dyn/cm; PEWV = 3.4 ± 0.2 mL/g vs. γ = 23.2 ± 0.4 dyn/cm; PEWV = 6.1 ± 1.0 mL/g dry lung). A subsequent study demonstrated that the high γ did not increase capillary permeability, supporting the mechanism of high γ-induced pulmonary edema as a decrease in interstitial hydrostatic pressure. Computational modeling, as presented in our previous publications based on the Starling equation of fluid flux, identifies the impact of elevated alveolar surface tension on lung fluid balance. Loss of surfactant function favors fluid moving from the capillary across the endothelium into the perialveolar space and across the epithelium into the alveoli. We conclude that elevated alveolar surface tension plays a pivotal role in lung fluid balance and, if sufficiently elevated, can cause pulmonary edema even with normal capillary permeability.