Effective management of asthma is dependent on achieving adequate delivery of the drugs into the lung. Inhalers come in the form of dry powder inhalers (DPIs) and metered dose inhalers (pMDIs) with the former requiring a deep fast breath for activation while there are no restrictions on inhalation rates for the latter. This study investigates two aerosol medication delivery methods (i) an idealised case for drug particle delivery under a normal breathing cycle (inhalation-exhalation) and (ii) for an increased effort during the inhalation with a breath hold. A computational model of a human tracheobronchial airway was reconstructed from computerised tomography (CT) scans. The model's geometry and lobar flow distribution were compared with experimental and empirical models to verify the current model. Velocity contours and secondary flow vectors showed vortex formation downstream of the bifurcations which enhanced particle deposition. The velocity contour profiles served as a predictive tool for the final deposition patterns. Different spherical aerosol particle sizes (3-10μm, 1.55g/cm(3)) were introduced into the airway for comparison over a range of Stokes number. It was found that a deep inhalation with a breath hold of 2s did not necessarily increase later deposition up to the sixth branch generation, but rather there was an increase in the deposition in the first few airway generations was found. In addition the breath hold allows deposition by sedimentation which assists in locally targeted deposition. Visualisation of particle deposition showed local "hot-spots" where particle deposition was concentrated in the lung airway.

Background: This study characterizes the distribution and components of plaque structure by presenting a three-dimensional blood-vessel modelling with the aim of determining mechanical properties due to the effect of lipid core and calcification within a plaque. Numerical simulation has been used to answer how cap thickness and calcium distribution in lipids influence the biomechanical stress on the plaque. Method: Modelling atherosclerotic plaque based on structural analysis confirms the rationale for plaque mechanical examination and the feasibility of our simulation model. Meaningful validation of predictions from modelled atherosclerotic plaque model typically requires examination of bona fide atherosclerotic lesions. To analyze a more accurate plaque rupture, fluid-structure interaction is applied to three-dimensional blood-vessel carotid bifurcation modelling. A patient-specific pressure variation is applied onto the plaque to influence its vulnerability. Results: Modelling of the human atherosclerotic artery with varying degrees of lipid core elasticity, fibrous cap thickness and calcification gap, which is defined as the distance between the fibrous cap and calcification agglomerate, form the basis of our rupture analysis. Finite element analysis shows that the calcification gap should be conservatively smaller than its threshold to maintain plaque stability. The results add new mechanistic insights and methodologically sound data to investigate plaque rupture mechanics. Conclusion: Structural analysis using a three-dimensional calcified model represents a more realistic simulation of late-stage atherosclerotic plaque. We also demonstrate that increases of calcium content that is coupled with a decrease in lipid core volume can stabilize plaque structurally.