Analysis for stress environment in the alveolar sac model

Abstract

Better understanding of alveolar mechanics is very important in order to avoid lung injuries for patients undergoing mechanical ventilation for treatment of respiratory problems. The objective of this study was to investigate the alveolar mechanics for two different alveolar sac models, one based on actual geometry and the other an idealized spherical geometry using coupled fluid-solid computational analysis. Both the models were analyzed through coupled fluid-solid analysis to estimate the parameters such as pressures/velocities and displacements/stresses under mechanical ventilation conditions. The results obtained from the fluid analysis indicate that both the alveolar geometries give similar results for pressures and velocities. However, the results obtained from coupled fluid-solid analysis indicate that the actual alveolar geometry results in smaller displacements in comparison to a spherical alveolar model. This trend is also true for stress/strain between the two models. The results presented indicate that alveolar geometry greatly affects the pressure/velocities as well as displacements and stresses/strains.

Mathematical modeling of ventilator-induced lung inflammation

“…Mathematical models have studied a host of causes of lung inflammation including bacterial and viral infections and allergic reactions (Brown et al, 2011;Day et al, 2009;Manchanda et al, 2014;Smith et al, 2011). Models have also been studied to examine the effects of biomechanical strain on the lungs (Pidaparti et al, 2013). Our model combines the varied effects of macrophage activation with a more detailed epithelial subsystem.…”

“…Many models have examine the immune response to bacterial and viral infections, such as pneumonia (Schirm et al, 2016;Mochan et al, 2014;Smith et al, 2011), tuberculosis (Day et al, 2009;Raman et al, 2010;Segovia-Juarez et al, 2004), and influenza (Manchanda et al, 2014;Anderson et al, 2016;Hancioglu et al, 2007). Additionally, models related to smoking and asthma (Brown et al, 2011;Chernyavsky et al, 2014;Golov et al, 2017;Pothen et al, 2015), mechanical ventilation (Hickling, 1998;Marini et al, 1989;Pidaparti et al, 2013), and general inflammatory stress (Reynolds et al, 2010) have been developed, but these models generally deal with the mechanics of the airways, including airflow, pressure, and gas exchange, and how these mechanics respond to inflammation and particle inhalation without accounting for the various cells types involved in the immune response. Models have also been developed to understand and analyze the molecular mechanisms that govern the phenotype switch that macrophages undergo from pro-inflammatory to anti-inflammatory, as well as other important subcellular pathways (Anderson et al, 2016;Braun et al, 2013;Maiti et al, 2014).…”

“…Common modeling approaches used in these papers include agent based modeling (Brown et al, 2011;Pothen et al, 2015;Segovia-Juarez et al, 2004), partial differential equations (Pidaparti et al, 2013;Reynolds et al, 2010), ordinary differential equations (Chernyavsky et al, 2014;Day et al, 2009;Hancioglu et al, 2007;Mochan et al, 2014;Schirm et al, 2016;Smith et al, 2011), and Boolean models (Anderson et al, 2016). Each technique has its advantages and disadvantages, but we choose to model the inflammatory response to VILI, specifically the resulting damage to epithelial cells, using a set of coupled ordinary differential equations (ODEs), which we describe further in the following section.…”

“…Many models have examine the immune response to bacterial and viral infections, such as pneumonia [22–24], tuberculosis [25–27], and influenza [28–30]. Additionally, models related to smoking and asthma [31–34], mechanical ventilation [35–42], and general inflammatory stress [4, 43] have been developed, but these models generally deal with the mechanics of the airways, including airflow, pressure, and gas exchange, and how these mechanics respond to inflammation and particle inhalation without accounting for the various cells types involved in the immune response. Models have also been developed to understand and analyze the molecular mechanisms that govern the phenotype switch that macrophages undergo from pro-inflammatory to antiinflammatory, as well as other important subcellular pathways [29, 44, 45].…”

An Analytical Model for Estimating Alveolar Wall Elastic Moduli From Lung Tissue Uniaxial Stress-Strain Curves

“…These models, however, all fail to capture the foam-like structure of lung parenchyma comprised of alveoli and alveolar ducts. Models based on 3-dimensional alveolar geometry have been proposed (Denny and Schroter, 2006;Parameswaran et al, 2011;Pidaparti et al, 2013), but these all assume constitutive properties for the alveolar wall and predict tissue behavior on this basis. Here we seek to do the reverse, namely to infer alveolar wall properties from the macroscopic mechanical behavior of lung parenchyma.…”