Lung Alveolar and Tissue Analysis Under Mechanical Ventilation

Mechanical ventilation has been a major therapy used by physicians in support of surgery as well as for treating patients with reduced lung function. Despite its many positive outcomes and ability to maintain life, in many cases, it has also led to increased injury of the lungs, further exacerbating the diseased state. Numerous studies have investigated the effects of long term ventilation with respect to lungs, however, the connection between the global deformation of the whole organ and the strains reaching the alveolar walls remains unclear. The walls of lung alveoli also called the alveolar septum are characterized as a multilayer heterogeneous biological tissue. In cases where damage to this parenchymal structure insist, alveolar overdistension occurs. Therefore, damage is most profound at the alveolar level and the deformation as a result of such mechanical forces must be investigated thoroughly. This study investigates a three-dimensional lung alveolar model from generations 22 (alveolar ducts) through 24 (alveoli sacs) in order to estimate the strain/stress levels under mechanical ventilation conditions. Additionally, a multilayer alveolar tissue model was generated to investigate localized damage at the alveolar wall. Using ANSYS, a commercial finite element software package, a fluid-structure interaction analysis (FSI) was performed on both models. Various cases were simulated that included a normal healthy lung, normal lung with structural changes to model disease and normal lung with mechanical property changes to model aging. In the alveolar tissue analysis, strains obtained from the aged lung alveolar analysis were applied as a boundary condition and used to obtain the mechanical forces exerted as a result. This work seeks to give both a qualitative and quantitative description of the stress/strain fields exerted at the alveolar region of the lungs. Regions of stress/strain concentration will be identified in order to gain perspective on where excess damage may occur. Such damage can lead to overdistension and possible collapse of a single alveolus. Furthermore, such regions of intensified stress/strain are translated to the cellular level and offset a signaling cascade. Hence, this work will provide distributions of mechanical forces across alveolar and tissue models as well as significant quantifications of damaging stresses and strains