Modeling lung tissue dynamics and injury under pressure and impact loading.

Abstract

A nonlinear viscoelastic model for the lung is implemented and evaluated for high-rate loading. Principal features of the model include a closed-cell approximation of the bulk compressibility accounting for air inside the lung and a damage-injury component by which local trauma is induced by cumulative normalized internal energy and amplified by gradients of energy density. The latter feature is adapted for use in standard numerical (i.e., explicit finite element) simulations in terms of the local rate of strain energy density and the longitudinal wave speed. Injury predictions for direct loading of a block of extracted lung material, rather than the entire thorax, via pressure pulses are in reasonably close agreement with experimental observations for an extracted rabbit lung: a threshold applied pressure exists above which edema is observed experimentally, correlating with low but non-negligible damage in the numerical results. Responses to impact by cylindrical and spherical projectiles are also interrogated. Penetration depths are comparable to those observed experimentally, as is drastically increasing damage with increasing impact velocity. Damage initiates and propagates from the impact surface, with local severity of injury decreasing with distance from the impact zone, in agreement with some empirical evidence. The model predicts more severe local injury, relative to the aforementioned surface pressure loading, than what is observed experimentally. Possible reasons for the discrepancy are analyzed, and adjustments to the model, with caveats, are suggested accordingly.