Synergistic Effect of Hyperoxia and Biotrauma On Ventilator-Induced Lung Injury

Abstract

Patients undergoing mechanical ventilation in intensive care units (ICUs) may develop ventilator-induced lung injury (VILI). Beside the high tidal volume (Vt) and plateau pressure (Pplat), hyperoxia is supposed to precipitate lung injury. Oxygen toxicity is presumed to occur at levels of fraction of inspired oxygen (FiO2) exceeding 0.40. The exposure time to hyperoxia is certainly very important and patients who spend extended time on mechanical ventilation (MV) are probably more exposed to severe hyperoxic acute lung injury (HALI). Together, hyperoxia and biotrauma (release of cytokines) have a synergistic effect and can induce VILI. In the clinical practice, the reduction of FiO2 to safe levels through the appropriate use of the positive end expiratory pressure (PEEP) and the alignment of mean airway pressure is an appropriate goal. The strategy for lung protective ventilation must include setting up FiO2 to a safe level that is accomplished by using PaO2/FiO2 ratio with a lower limit of FiO2 to achieve acceptable levels of PaO2, which will be safe for the patient without local (lungs) or systemic inflammatory response. The protocol from the ARDS-net study is used for ventilator setup and adjustment. Cytokines (IL-1, IL-6, TNFα and MIP-2) that are involved in the inflammatory response are determined in order to help the therapeutic approach in counteracting HALI. Computed tomography findings reflect the pathological phases of the diffuse alveolar damage. At least preferably the lowest level of FiO2 should be used in order to provide full lung protection against the damage induced by MV.