Ventilator-Dependent Factors

It is now known, in general terms, that the mechanisms of VILI are alveolar overdistension (volutrauma), alveolar instability leading to alveolar collapse and reopening with each breath (atelectrauma), and the secondary inflammation caused by these mechanical injuries which is known as biotrauma [9].

Times ago, Lachmann [33] proposed that the optimal lung-protective strategy would be to “open the lung and keep it open.” He hypothesized that heterogeneous lung inflation, which is a hallmark of ARDS pathology, plays a major role in driving mechanical ventilation-induced progressive acute lung injury. The corollary to this hypothesis is that keeping the lung open would result in a homogeneously ventilated lung, minimizing VILI and reducing ARDS mortality. If the approach of opening the ARDS lung and keeping it open can significantly reduce injury, then protective mechanical ventilation should be applied early in patients at a high risk of developing ARDS, in an attempt to “never let the lung collapse” and significantly reduce ARDS incidence [34]. As we will see in the next paragraphs, barotrauma, volu- trauma, atelectrauma, and biotrauma are considered as undisputable truth and represent the background for the development and universal acceptance of the so-called lung-protective strategy.