Towards ultraprotective mechanical ventilation

ARDS does not homogeneously affect the lung parenchyma and the nature of infiltrates visible at the chest X-ray may derive from atelectasis, interstitial or intra-acinar edema or consolidation. The potentially recruitable lung varies widely in the ARDS population, ranging from 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. In fact we recently found in an animal model that the damage occurs when the strain and stress are in the region of total lung capacity. Nevertheless, in mechanically ventilated patients, 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. Moreover in a dishomogenous lung the applied force, which should be evenly distributed in a normal lung, is locally concentrated leading to localized increase of stress. Mead et al, in the seventies, simulated the effects of a lung volume decrease from 10 to 1 in a single lung region. The pressure applied, in this case, was computed as the product of the applied pressure (as an example 30 cmH2O transpulmonary pressure) to the ratio Area1/Area0 (mathematically equivalent to (Volume1/Volume0)2/3): i.e. 30*4.64 = 139.25 cmH2O. Accordingly the location of dishomogeneity throughout the lung may act as a “pressure multiplier” and a pressure below the threshold observed in “healthy lung”, if multiplied sufficiently, may locally reach a level recognized as surely injurious.