Purpose of review
To discuss the relative role of dynamic and static tissue deformation (strain) generated by inflation of tidal volume and application of positive end-expiratory pressure in the pathogenesis of ventilator-induced lung injury.
Cellular, animal and human studies strongly suggest that dynamic strain is more injurious than static strain, at least when total lung capacity is not exceeded. One possible explanation for these findings is pulmonary viscoelasticity. Large and rapid dynamic deformations generate high and unevenly distributed tensions, internal frictions and energy dissipation in the form of heat, posing microstructure at risk for rupture. The most important strategy to protect the lung may thus be limiting the tidal volume. Increasing static strain may add benefit by diminishing inhomogeneities (stress raisers), especially in the already severely injured lung. On the other side, however, it may adversely affect the haemodynamics.
Large lung dynamic strain is more harmful than equivalent static strain.