Fig. 2
The impact of dynamic versus static lung strain on lung injury in normal pigs ventilated for 54 h. Four groups of animals were studied and in all four groups the lungs were ventilated with a very high static strain (2.5) at total lung capacity (TLC). High dynamic strain was caused by the tidal volume (VT) being 100% of the lung volume with no positive end-expiratory pressure (VPEEP). Thus there was a large change in lung volume (i.e. high dynamic strain) with each breath. In the lowest dynamic strain group VT accounted for 25% of the lung volume and VPEEP for 75% of the lung volume. Thus there would be a very small change in lung volume (i.e. low dynamic strain) with each breath. In the high dynamic-strain group all animals developed pulmonary edema and died before the end of the study. Conversely, none of the low dynamic-strain group developed edema and all lived until the end of the experiment [22]. This study suggest that high static strain does not damage normal lung tissue as previously hypothesize [34] but rather must be combined with a high dynamic strain to cause VILI. These data were supported in a heterogeneous porcine lung injury model (Fig. 4) in which high static strain caused no lung damage, whereas high dynamic strain injured the normal tissue and exacerbated damage in the acutely injured tissue [23]