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Research Papers

Simulation of Forced Expiration in a Biophysical Model, With Homogeneous and Clustered Bronchoconstriction

[+] Author and Article Information
Kerry L. Hedges

Auckland Bioengineering Institute,
University of Auckland,
Private Bag 92019,
Auckland 1142,
New Zealand
e-mail: k.hedges@auckland.ac.nz

Merryn H. Tawhai

Auckland Bioengineering Institute,
University of Auckland,
Private Bag 92019,
Auckland 1142,
New Zealand
e-mail: m.tawhai@auckland.ac.nz

1Corresponding author.

Manuscript received August 12, 2015; final manuscript received April 6, 2016; published online May 9, 2016. Assoc. Editor: Tim David.

J Biomech Eng 138(6), 061008 (May 09, 2016) (10 pages) Paper No: BIO-15-1404; doi: 10.1115/1.4033475 History: Received August 12, 2015; Revised April 06, 2016

One limitation of forced spirometry is that it integrates the contribution of the complex and dynamic behavior of all of the airways and tissue of the lung into a single exhaling unit, hence, it is not clear how spirometric measures are affected by local changes to the airways or tissue such as the presence of “ventilation defects.” Here, we adapt a wave-speed limitation model to a spatially distributed and anatomically based airway tree that is embedded within a deformable parenchyma, to simulate forced expiration in 1 s (FEV1). This provides a model that can be used to assess the consequence of imposed constrictions on FEV1. We first show how the model can be parameterized to represent imaging and forced spirometry data from nonasthmatic healthy young adults. We then compare the effect of homogeneous and clustered bronchoconstriction on FEV1 in six subject-specific models (three male and three female). The model highlights potential sources of normal subject variability in response to agonist challenge, including the interaction between sites of airway constriction and sites of flow limitation at baseline. The results support earlier studies which proposed that the significant constriction of nondefect airways must be present in order to match to clinical measurements of lung function.

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Figures

Grahic Jump Location
Fig. 1

Illustration of sites of clustered bronchoconstriction in subject F1. Constricted airways are shown in green. (a) six small clusters per lung and (b) two large clusters per lung.

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Fig. 2

Simulated MEFV (maximum flow against expired volume) curves for normal young adult female (left-hand column) and male (right-hand column) subjects. Individual subject measurements of PEF and FVC are superimposed.

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Fig. 3

Simulated results for expired volume against time for normal young adult female (left-hand column) and male (right-hand column) subjects. Individual subject measurements of FEV1 and FEF25–75 are superimposed.

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Fig. 4

Airway resistance (Raw) normalized by its baseline value against FEV1 for homogeneous airway constriction in all the subjects. (a) shows the simulated FEV1 postconstriction normalized by the FEV1 simulated at baseline and (b) shows the simulated FEV1 postconstriction normalized by the subject's predicted value (based on their demographic data).

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Fig. 5

Calculated sites of flow limitation in all the subjects at PEF. Clusters of same colored airways indicate regions that are distal to a flow limited airway. The color scale indicates the trachea (whole lung) flow at which the limited airway reached its maximum flow.

Grahic Jump Location
Fig. 6

Illustration of effect of variation in pressure at the bifurcations. Solid line shows results using average pressure at each bifurcation in airway tree. Dashed lines show results for ten solutions carried out using pressure values randomly chosen between maximum and minimum pressure entering each bifurcation.

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