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Emphysema and influenza directly affect alveolar sacs and cause problems in lung performance during the breathing cycle. In this study, the effects of Emphysema and Influenza on alveolar sac’s air flow characteristics are investigated through Computational Fluid Dynamics (CFD) simulation. Both normal and Emphysemic alveolar sac models with varying collapsed volumes resulting from influenza virus replication were developed. Maximum, area average pressure, and wall shear stress (WSS) in collapsed and open alveolar sacs models were compared. It was found that a collapse at half of the volume at the bottom of the alveolar sacs’ models would cause a decrease in average and maximum pressure values and yield higher WSS values for fluid flow during the breathing cycle. On the other hand, a quarter volume collapse at the bottom and side of the model resulted in higher values for average and maximum pressure and WSS. Additionally, results also showed that a combination of alveolar sacs closure and Emphysema would generally lead to an increase in fluid pressure and average WSS during breathing. Maximum WSS was observed during exhalation and maximum WSS decrease occurred during inhalation. Findings are in good agreement with previous studies and suggest that emphysema and influenza virus affect fluid flow and may contribute to alveolar sac closure. However, more realistic simulations should include the fluid-solid interaction studies.

During mechanical ventilation, a sectional collapse of lung may occur when the lung air sacs become deflated and this condition is called Atelectasis. Some diseases including asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis are associated with atelectasis. Emphysema is one of the main types of COPD that causes a gradual loss of air sacs wall surface area within the lung. This surface area loss would affect the absorption of oxygen. As the destruction of air sacs’ structure progresses, there would be increasing difficulty in expelling the air during exhalation. Emphysema is considered to be the fourth leading cause of death in the United States based on statistics from the American Lung Association. Simulation of fluid flow under the effect of Emphysema would provide critical information for the respiratory specialists to prevent undesired injuries during mechanical ventilation (MV).

Computational fluid dynamics has been widely used over recent years to study different aspects of fluid flow related to the acinar region. Some studies employed CFD modeling and focused on flow patterns and effective parameters for assessing the influence of flow patterns on particle depositions and heat and mass transfer characteristics in alveolar cavities. Karl et al. [

As discussed in the preceding paragraphs, geometric changes significantly affect fluid flow in alveolar sacs. Accordingly, some studies focused on lung diseases which are associated with alveolar collapse and atelectasis to explore their effects on fluid flow in the alveolar region. Otis et al. [

Apart from Emphysema, some other diseases have also been reported to affect alveolar sac’s performance. For example, airways can be blocked by a foreign object or tumors that prevent the alveolar sacs from filling with air and collapse of lung tissue can occur in the affected area. Influenza viruses are among those foreign objects that cause alveolar sac closure and they are among the most common factors that lead to human respiratory infections and cause high morbidity and mortality rate [

Several studies focused on the effect of Emphysema and alveolar collapse on fluid flow through alveolar sacs separately but none of these studies focused on the effect of alveolar closure on Emphysemic alveolar sacs. In this study, a simplified bronchiole alveolar sac model was designed in Solid Works based on dimensions from real alveolar sacs models [

3D alveolar Sac Models were imported from Solid Works to ANSYS Workbench Fluent solver for generating the appropriate mesh and conducting the CFD simulation. Navier-stokes equations for laminar flow and second order implicit transient solver were used for the simulation. Inlet velocity boundary conditions for MV are loaded as user-defined functions (UDF) which are defined based on hospital data. Previous studies on flow in the lower airways showed that wall motion would not considerably affect fluid flow. Therefore, no-slip boundary conditions are applied at the entire model wall for simplicity [

Different geometric models have been considered for the alveolar studies, Fung et al. [

In this study, airflow in the acinar airways is assumed to be laminar and incompressible. Therefore the 3D incompressible laminar Navier-Stokes and continuity equations in a 3D mesh with a control volume approximation [

where u is the velocity field, p is the pressure, and μ is the dynamic viscosity. The continuity equation represents the conservation of mass, Equation (1), and the Navier-Stokes equations represent the conservation of momentum, Equation (2), that would be solved numerically on a moving grid using a commercial finite-volume based

program with fully implicit time marching techniques under isothermal conditions in ANSYS fluent solver [

Boundary conditions define the inputs of the CFD simulation model. Some conditions, like velocity and volumetric flow rate, define how a fluid enters or leaves the model. When solving the Navier-Stokes equation and continuity equation, appropriate initial conditions and boundary conditions need to be applied. In this study, the no-slip boundary condition is applied at the solid wall and inlet velocity boundary condition is defined as C++ subroutine User Defined-Function (UDF) that is written based on hospital data. These conditions would be applied at the inlet area geometry for the whole model and the generation number would specify fluid velocity through the model. For this purpose, inlet velocity profiles are subsequently defined in the form of constants and exponentially decreasing flow rate profiles for inhalation and exhalation during mechanical ventilation are presented in _{in}) and exhalation time (t_{ex}).

The flow rate (Q), is defined as the proportion of tidal volume to inhalation time that is the lung volume that represents the normal volume of air displaced between inhalation and exhalation when extra effort is not applied. A tidal volume of 420 mL is considered in this study.

Influenza virus replication causes bronchioles air flow closure. Once the sacs are internalized by respiratory epithelial cells, they replicate and lead to cell death and alveolar sac closure [

Airflow characteristics obtained from CFD simulation for two alveolar sacs models are discussed next? Wall shear stress (WSS) contours and velocity vectors were extracted and pressure and WSS curves versus time were analyzed to evaluate the influence of Emphysema on fluid flow through an alveolar sac model. Additionally, the

t_{in} ≤ 0.4 (s) | |
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t_{ex} > 0.4 (s) | |

Inlet velocity profile |

effect of alveolar volume closure on fluid flow during mechanical ventilation was investigated. For this purpose, fluid flow through collapsed cases was studied and compared with fluid flow in non-collapsed models for both normal and Emphysemic alveolar sac models to determine the effect of geometric changes and obstruction on fluid flow through alveolar sacs.

Velocity vectors for collapsed and open alveolar sac models are presented in

The fluid velocities have a parabolic profile for the laminar flow regime. This flow pattern is related to existing friction between the fluid and the alveolar wall and fluid itself, which is relevant to the fluid viscosity. A tangential force would be generated through fluid flow by discussed friction and is known as the “wall shear stress”. Wall shear stress’s magnitude depends on how fast the fluid velocity rises when flowing from the alveolar wall toward the center of the alveolar sac. Wall shear stress for Newtonian fluids is defined according to Newton’s law by the equation:

where μ, u, x and du/dx are the kinetic viscosity, fluid velocity, distance from the surface and the velocity gradient, respectively. As presented in

Different planes are defined through models and pressure and WSS curves versus time under mechanical ventilation were plotted and are shown in

of air with different pressure values during the respiratory cycle. When the flow is occluded, pressure at different locations is equalized. This equalized pressure multiplied by the total air volume represents total initial pressure-volume. In the case where alveoli have larger volume in comparison to other volumes, the equalized pressure would generally be equal to the existing pressure in the alveoli at the moment of interruption. Pressure equalization during each interruption indicates that the rate of flow suddenly drops or rises to zero, where it remains during the period of interruption. At the same time, the mouth pressure suddenly goes up and down and oscillates around a slowly rising or falling line [

Moreover, WSS-time curves are presented for both models in

Different models of collapsed cases were considered to investigate the influence of Influenza viruses on fluid flow. Case (І) considered half of the total volume and Case (ІI) considered a quarter of the total volume of alveolar sacs balloon geometries to be collapsed at the bottom. Case (ІII) considered a quarter of the total volume of alveolar sacs balloon geometries to be collapsed at the side. CFD simulations were conducted on all six collapsed models for both normal and Emphysemic alveolar sacs models, and results were post processed. The average pressure area at different locations through the models and WSS through whole model walls were extracted and comparisons were made between area average pressure and WSS results. As illustrated in

This study investigated the effects of Emphysema and Influenza on alveolar sacs air flow characteristics through a Computational Fluid Dynamics (CFD) simulation. For this purpose, several simulations were conducted on open and collapsed cases for both normal and Emphysemic alveolar sacs models. Results showed Emphysema caused an increase in fluid velocity and applied pressure on alveolar sacs wall and WSS during inhalation. It also led to lower WSS values in alveolar sacs during the exhalation cycle. As hypothesized, alvelolar sac collapse at half of the volume at the bottom of the alveolar sacs models yielded a decrease in average and maximum pressure values and an increase in WSS values for fluid flow during the breathing cycle. Additionally, it was found that a quarter volume collapse led to higher values for average and maximum pressure and WSS values. The influence of Emphysema and influenza virus replication on fluid flow through alveolar sacs models was simultaneously explored and it was shown that these two diseases would generally lead to an increase in fluid pressure. Although alveolar sacs’ collapse would cause WSS to rise, a reduction in WSS during inhalation was observed under the influence of Emphysema. The combination of Emphysema and alveolar closure caused a slight increase in average WSS during the breathing cycle with maximum WSS observed during exhalation and

a decrease in maximum WSS during inhalation. However, more realistic simulations should include the fluid- solid interaction studies. The results obtained provide useful information for respiratory specialists treating patients with diseases such as emphysema and influenza and assist them in developing patient specific guidelines for effective use of mechanical ventilation.

The authors thank the NSF for support this research through a grant CMMI-1430379.

Parya Aghasafari,Israr B. M. Ibrahim,Ramana M. Pidaparti, (2016) Investigation of the Effects of Emphysema and Influenza on Alveolar Sacs Closure through CFD Simulation. Journal of Biomedical Science and Engineering,09,287-297. doi: 10.4236/jbise.2016.96022