Mechanical ventilation and its safety limits in anestesia and in critical care

ARDS does not homogeneously affect the lung parenchyma and the infiltrates visible at the chest X-ray may derive from atelectasis, interstitial or intra-acinar edema or consolidation.. The lung injury severity is widely distributed in ARDS population (5 to 70% of the total lung weight) and it is strictly associated with the severity of injury: greater is the amount of gasless tissue at 5 cmH2O PEEP, greater is the amount of gasless tissue regaining aeration at 45 cmH2O airway pressure. We hypothesized that the regions that experience the major amount of stress and strain during mechanical ventilation are the region near to the always closed ones. Recently we attempted to quantify the relationship between stress-strain and VILI in healthy animals. We found that edema formation was induced by mechanical ventilation when the global strain reaches a critical threshold which extended from 1.5 to 2. This threshold roughly corresponded to the point where the stress-strain curve lost its linearity, suggesting that some lung regions reach their own total capacity and cannot expand any further. Nevertheless, VILI may develop at stress and strain far lower than the threshold observed in experimental animals. A possible explanation is that the damaged lung is more “fragile” and injury develops at lower stress and strain thresholds. Either, that in a disomogenous lung the applied force, used to be evenly distributed, is locally concentrated leading to localized increase of stress. Mead et al described a mathematical model in which they simulated the effect, as an example, of letting decrease if lung volume down to one in a region of lung where that volume of gas was equal to 10. Referring to the ratio A1/A0 instead of V1/V0 by taking the V1/V0 to the power of 2/3 the stress, for an applied pressure of 30 cmH2O (transpulmonary) will result 30 * (V1/V0)2/3 i.e. 30*4.64 = 139.25 cmH2O. Thus there is a theoretical potential that location of disomogeneity throught the lung may act as a “pressure multiplier”. Accordingly, a pleural pressure below the threshold observed in “healthy lung”, if multiplied sufficiently, may locally reach a level recognized as surely injurious.