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. 2020 Mar 19;11:227. doi: 10.3389/fphys.2020.00227

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Copyright © 2020 Nieman, Al-Khalisy, Kollisch-Singule, Satalin, Blair, Trikha, Andrews, Madden, Gatto and Habashi.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Panels (A–F) depict leak progression caused by an applied stretch force. A single node fails (nf) at each time point with nf indicating the number of nodes that have failed in each panel. Computational model of an epithelial monolayer to simulate leak progression due to overdistension. Leak progression in a 45-cell (hexagon) network caused by applied stretch (i.e., Vt). After the force required to initiate the leak was reached, the leak area increased at a constant rate as the force increased further (Hamlington et al., 2016). Atelectrauma caused the initial tears, after which volutrauma expanded those tears. The tears progressed in a rich-get-richer mechanism in which the likelihood of a tear getting larger increased with the size of the initial tear. This mechanism explains why atelectrauma appears to be essential to the initiation of VILI in a normal lung, and why atelectrauma and volutrauma act synergistically once VILI is underway (Hamlington et al., 2018). Permissions obtained from Springer Nature. License 4699410825602.