Modeling airflow-related shear stress during heterogeneous constriction and mechanical ventilation.
Ventilator-induced lung injury has been proposed as being caused by overdistention and closure and reopening of small airways and alveoli. Here we investigate the possibility that heterogeneous constriction increases airflow-related shear stress to a dangerously high level that may be sufficient to cause injury to the epithelial cells during mechanical ventilation. We employed an anatomically consistent model of the respiratory system, based on Horsfield morphometric data, and solved for the time evolution of pressure and flow along the airway tree during mechanical ventilation. We simulated constant-flow ventilation with passive expiration in two different conditions: baseline and highly heterogeneous constriction. The constriction was applied with two strategies: establishing a simple diameter reduction or adding also a length shortening. The shear stress distribution on airway walls was analyzed for airways ranging from the trachea to the acini. Our results indicate that 1). heterogeneous constriction can amplify the maximal values of shear stress up to 50-fold, with peak values higher than 0.6 cmH2O; 2). the highest shear stress is found in pathways constricted by 60-80%; 3). simultaneous diameter reduction and shortening amplifies the shear stresses by three- to fourfold, with shear stresses reaching 2 cmH2O; and 4). there is a range of airways (diameters from 0.6 to 0.3 mm at baseline) that appear to be at risk of very high stresses. We conclude that elevated airflow-related shear stress on the epithelial cell layer can occur during heterogeneous constriction and conjecture that this may constitute a mechanism contributing to ventilator-induced lung injury.
Nucci
Gianluca
G
Department of Information Engineering, University of Padova, Padova 35131, Italy. nucci@dei.unipd.it
Suki
Bela
B
Lutchen
Kenneth
K
D000399:Air Pressure; D000465:Algorithms; D016084:Bronchoconstriction / Q000502:physiology*; D004847:Epithelial Cells / Q000502:physiology; D006801:Humans; D008170:Lung Compliance / Q000502:physiology; D008954:Models, Biological; D012121:Respiration, Artificial / Q000009:adverse effects*; D015656:Respiratory Mechanics / Q000502:physiology*; D014132:Trachea / Q000502:physiology; D014783:Viscosity