Patterns of air flow and particle deposition in the diseased human lung
No Thumbnail Available
Files
Date
2001-07-05
Authors
Journal Title
Series/Report No.
Journal ISSN
Volume Title
Publisher
Abstract
In this work, we investigate particle deposition and air flow in thehuman lung. In particular we are interested in how the motion ofparticulate matter and air is affected by the presence of lungdisease. Patients with compromised lung function are more sensitiveto air pollution; understanding the extent of that sensitivity canlead to more effective air quality standards. Also, understanding ofair flow andparticle trajectories could lead to the development of better aerosoldrugs to treat the lung diseases.We focus our efforts on twodiseases: chronic obstructive pulmonary disease (COPD) and bronchialtumors. Because COPD affects the majority of airways in a patientwith the disease, we are able to take a more global approach toanalyzing the effects of the disease. Using a FORTRAN codewhich computes total deposition in the lung over the course of onebreath, we modified the pre-existing code to account forthe difference between healthy subjects and patients with COPD. Usingthe model, itwas possible to isolate the different disease components of COPD andsimulate their effects separately. It was determined thatthe chronic bronchitis component of COPD was responsible for the increaseddeposition seen in COPD patients.While COPD affects the whole lung, tumors tend to belocalized to one or several airways. This led us to investigate theeffects of bronchial tumors in detail within these individualairways. Using a computational fluid dynamics package, FIDAP, wedefined a Weibel type branching network of airways.In particular, we modeled theairways of a four-year-old child.In the work with the tumors, we ran numerous simulations with variousinitial velocities and tumor locations. It was determined that tumorslocated on the carinal ridge had the dominant effect on the flow. Athigher initial velocities, areas of circulation developed downstream from the tumors. Extensive simulations were run with a 2-D model. Theresults from the 2-D model were then compared with some initial 3-Dsimulations.In the development of the FIDAP model, we avoided thecomplications of flow past the larynx, by limiting the model togenerations 2-5 of the Weibel lung. We developed a realistic inletvelocity profile to be used as the input into the model. The skewednature ofthis inlet profile led to thequestion of boundary layer development and the determination of theentrance length needed to achieve fully developed parabolicflow. Simple scale analysis of the Navier-Stokes equations did notcapture the results we were seeing with the CFD simulations.We turned to a more quantitative, energy correctionanalysis to determine the theoretical entrance length.In conclusion, the presence of disease in the lunghas a large effect both on global deposition patterns and on localizedairflow patterns. This indicates the need for different protocolsregarding susceptibility of people to airborne pollutants that take intoaccount lung disease. It also suggests that treatment should accountfor changes in airflow in the diseased lung.
Description
Keywords
Citation
Degree
PhD
Discipline
Applied Mathematics
