Mechanical ventilation is inarguably a necessary life-sustaining medical treatment for acute respiratory distress syndrome. However, mechanical stresses and strains exerted on the delicate tissues of the airways and alveoli may result in ventilation-induced lung injury (VILI). This presentation describes the coupling between fluid flows, mechanical stresses, and surfactant biophysical interactions that occurs during the recruitment of obstructed airways and alveoli that can result in atelectrauma.
Our investigations couple computational simulation with in vitro experimental investigations. We idealize the system as an airway that is lined with epithelial cells, with reopening occurring through the migration of a finger of air that displaces the obstruction. Mechanical stress fields and surfactant transport processes are assessed by computational fluid dynamic simulation, flow visualization is completed with microparticle image velocimetry, and cell damage is evaluated using biomimetic airway constructs of respiratory bronchioles.
These studies demonstrate the strong coupling between interfacial flows and atelectrauma. Finally, we asked whether it is possible to enhance the surface activity of endogenous surfactant, using unsteady flows to reduce atelectrauma. Our investigations demonstrate that the use of pulsatile flow to enhance surfactant function provides an opportunity for “endogenous surfactant delivery” that diminishes epithelial damage and thus may reduce VILI.
Footnotes
Supported by NIH R01-HL81266 and NSF CBET-1033619.
The views expressed in this article do not communicate an official position of Tulane University, the National Institutes of Health, or the National Science Foundation.
Author disclosures are available with the text of this abstract at www.atsjournals.org.
