Abstract:
Pulmonary function tests assess the function of a lung through a single integrated measurement. A computational model of forced expiration has been created in order to investigate the mechanisms behind lung disease and assess the effectiveness of this single measure to encompass the severity and variability of lung disease. The model incorporates· subject-specific anatomical geometry and physiologically realistic distributions of ventilation and static recoil pressures. These distributions are used as boundary conditions and localized values of tissue pressure for the solution were obtained through the computational solution of lung tissue deformation under gravity. An in-depth investigation into the most appropriate boundary conditions to obtain physiologically realistic distributions was carried out with the results that simplification of the geometry of the airway tree or applying uniform boundary conditions to the solution resulted in the introduction of errors and an unrealistic ventilation distribution. Verification of the forced expiration model was carried out by comparison to the clinical measurement of the subjects peak flow. The model was found to predict this maximum flow to within 0.3 % of the clinical measurement. The solution was tested at lower lung volumes through the effect of lower density Heliox gas on the maximum flows predicted. The peak flow was found to increase by 28% and a volume-iosflow point was predicted at a volume of 84 % vital capacity. These values indicate results within the bounds of clinical measurements for healthy lungs. The application of disease to the forced expiratory model was carried out to simulate the effects of emphysema and chronic bronchiolitis, both contributors to Chronic Obstructive Pulmonary Disease (COPD). The estimated severity of the disease indicated that the most severe cases involve varying degrees of the disease, isolated symptoms required significant levels of diseased parameters to reach these levels. The regional distribution of emphysematous tissue was investigated with application of the disease in predominantly apical and predominantly basal regions. The severity of the disease in the basal region was found to be greater for similar volumes of diseased tissue. The level of degradation was specified to be equivalent to that measured in severe COPD patients. These results are consistent with experiments carried out to assess the effect of regional distribution of COPD. Further degradation in the tissue resulted in these results swapping with the apical disease showing increased levels of severity over the basal region. These results indicate a variability in the effects of the disease based on the regional distribution which current screening does not account for.