Modeling Lung Derecruitment in VILI Due to Fluid-Occlusion: The Role of Emergent Behavior

Abstract

Ventilator-induced lung injury (VILI) is driven by the processes of volutrauma and atelectrauma, which can act synergistically to compromise the blood-gas barrier. We have postulated that this synergy arises through a rich-get-richer mechanism whereby atelectrauma causes holes to form in the blood-gas barrier while concomitant volutrauma causes susceptible holes to progressively enlarge as VILI worsens. We previously developed an analytical model based on this idea that accurately predicts the progressive increases in lung elastance seen immediately following a recruitment maneuver as VILI progresses over the course of hours. In the present study we extend this model to account for the rate of change of elastance, due to closure of lung units, in the minutes following a recruitment maneuver. We found that the distribution of unit closing velocities throughout the lung can be described by a power law with an exponent of −2 that matches previously published power laws associated with the dynamics of lung recruitment. Our model thus reveals lung collapse as an example of emergent complex behavior and links the dynamics of altered function in the injured lung to structural damage in a way that explains the mechanisms of injury progression arising from the ongoing stresses and strains applied by mechanical ventilation.