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. 2004 Aug 18;9(1):60–65. doi: 10.1186/cc2934

Figure 1.

Figure 1

Schematic representation of mechanisms of injury during tidal ventilation. Dependent areas are poorly aerated at end-expiration because of compressing hydrostatic pressures. At end-inspiration, patent alveoli may become over-stretched (A), excessive stresses may be generated at the boundary between aerated and nonaerated lung tissue (B), and dependent alveoli may be repetitively opened and closed producing tissue damage (C).