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.

Mechatronic Design and Active Disturbance Rejection Control of a Bag Valve-Based Mechanical Ventilator

“…Mechanical and electrical components may fail, jeopardizing the ventilator's ability to maintain the settings required by the clinician and, therefore, making it unable to provide a proper ventilation. Improper ventilation may induce lung injuries such as lung overdistension (volutrauma) [16], overpressure within distal airways and alveoli (barotrauma) [17], and repeated alveolar collapse and expansion (atelectrauma) [18][19][20][21]. The respiratory settings in an invasive mechanical ventilation are a key factor to avoid additional lung injury.…”

“…While measurable pressure and volume can reflect the stresses and strains on the lung tissue induced by the mechanical ventilation, further analysis of the exhaled gas, blood gas analysis, and lung imaging are recommended to better inform clinicians of the appropriateness of the ventilation [40]. An adequate monitoring of the lung mechanical function during the mechanical ventilation provides a feedback signal to adequately set ventilation parameters and minimize VILI [20,21].…”

Loss of SOX18/CLAUDIN5 disrupts the pulmonary endothelial barrier in ventilator-induced lung injury

“…A major feature of VILI is disruption of the endothelial barrier resulting in increased pulmonary vascular permeability and edema ( Parker et al, 1984 ; Dreyfuss et al, 1985 ; Dreyfuss and Saumon, 1993 ). The disruption to the lung barrier function in VILI occurs by two main mechanisms, increased lung microvascular pressure from surfactant loss and, more importantly, increased pulmonary alveolar and vascular permeability ( Webb and Tierney, 1974 ; Parker et al, 1984 ; Parker et al, 1990 ; De Prost et al, 2011 ; Mori et al, 2020 ). Increased vascular permeability leads to edema, which is one of the hallmarks of inflammation.…”