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A Microfluidic Model of Biomimetically Breathing Pulmonary Acinar Airways
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Micrometer aerosol deposition in normal and emphysematous subacinar models
Jinxiang Xi1, Mohamed Talaat1, Xiuhua April Si2
1Department of Biomedical Engineering, University of Massachusetts, Lowell, MA, USA.
Respiratory Physiology & Neurobiology
|October 3, 2020
Summary
Emphysema alters airflow and particle deposition in the lungs. As septal destruction progresses, particle doses increase, especially in outer regions, escalating risks to acinar health.
Area of Science:
- Pulmonary biomechanics
- Respiratory physiology
- Computational fluid dynamics
Background:
- Emphysema involves alveolar septa destruction and enlarged air sacs.
- Particle deposition patterns in emphysematous lungs are not fully understood.
Purpose of the Study:
- To numerically assess how septal destruction in emphysema affects particle deposition within pulmonary acini.
- To quantify spatial and temporal particle deposition changes in emphysematous models.
Main Methods:
- A pyramid-shaped subacinar model with 496 alveoli was used.
- Four emphysematous models were created by progressively removing septa.
- A discrete-phase Lagrangian model simulated airflow and particle deposition.
Main Results:
- Emphysema alters airflow, causing unsymmetrical and recirculating flows.
- Particle deposition increases significantly in outer walls and bases with disease progression.
- Smaller particles (1-1.5 μm) deposition is more sensitive to septal destruction than larger particles (2.5-3 μm).
- Unexpectedly higher deposition occurs on outer walls and bases compared to inner septal walls.
Conclusions:
- Progressive septal destruction in emphysema leads to increased subacinar-averaged particle doses.
- Altered deposition patterns pose an escalating risk to acinar health in later stages of emphysema.
