Stress amplification effect of lung.

Under a blast or impact load, rapid movement of the thoracic wall generates stress in lung, a foam-like structure of high compressibility, which is different from general solids. Due to this unique characteristic, it is hypothesized that when lung is subjected to a blast or impact load, there will be an initial low stress progressively developed into a high stress in a short duration in a thin layer of parenchyma at the lung surface. Compared to the incident stress, the actual stress value experienced by lung is amplified, which may cause alveolar-capillary walls to burst, subsequently results in injuries such as edema or hemorrhage. This hypothesis can explain one significant phenomenon observed in animal tests that the gross thoracic compression do not cause major lung injury and there is a close relationship between thoracic wall velocity and the lung injury degree. According to the hypothesis, under a blast or impact load, there should be a significant injury degree discrepancy between a thin layer of parenchyma at the lung surface and the rest of the lung. Serious injuries should be mainly found in this thin layer, which can be employed to test whether this amplified effect exists or not. The hypothesis may shed some light on the mechanism of blast lung injury.