Ergotrauma – Composite Concept for Ventilation-induced Lung Injury

The pathological damage due to mechanical ventilation is characterised by inflammatory cell infiltrates, hyaline membranes and pulmonary oedema as a result of increased vascular permeability. Mechanical ventilation causing these constellations of features has been defined as ventilation-induced lung injury (VILI). The evolution of the aetiological causes has progressed from focusing on pressure, then on volume, then onto atelectasis and subsequently on dynamic factors such as flow and rate, and now, a unifying theory that incorporates all these concepts as a single entity called ergotrauma. While delivering mechanical ventilation with the intent to prevent VILI, we need to focus on tidal volume, respiratory rate, positive end-expiratory pressure, driving pressure, resistances and flow.[1] Tonetti etal.[2] described these components as a part of an irregular solid, with each component having a different area, thus contributing differently to the development of VILI. Each component by itself is important, but it is the combined or the composite effect that contributes to the development of VILI. This composite factor may be the mechanical power, and the resulting lung injury is referred to as ergotrauma. The physical and biological bases of ergotrauma can be understood by the following mechanism. If the power generated during ventilation is excessive, then chemical bonds of the polymers, which make up the extracellular matrix, disrupt. The physical distortion of the extracellular matrix, the microfractures and stress fractures also lead to inflammatory reactions, distorted epithelial cells release cytokine, which leads to a cascade of reactions leading to increased vascular permeability, activation of coagulation and recruitment of inflammatory cells. The main advantage of the theory of ergotrauma is that it accounts for all the key variables (both static and dynamic) involved in VILI. This hypothesis also suggests a possibility that the driving pressure is more contributory than plateau pressures towards the development of VILI. There are a few limitations to this theory. The lung heterogeneity is not quantified. Second, is the inclusion of flow, which acts in the airway, and how it dissipates to alveoli is still unclear. Nevertheless, we can hope that in the future, the ventilator software will incorporate composite power measurement to tailor ventilator support to adjust power to prevent VILI. Financial support and sponsorship Nil. Conflicts of interest There are no conflicts of interest.