Purpose of review: Mechanical ventilation is essential for the support of critically ill patients, but may aggravate lung damage, leading to ventilator-associated lung injury (VALI). VALI results from a succession of events beginning with mechanical alteration of lung parenchyma, because of disproportionate stress and strain. The resulting structural tension initiates a biological inflammatory cascade; however, tension can reach the limits of stress, triggering the destruction of structures. This article reviews and discusses the ongoing research into the mechanisms of VALI and their implications for the management of ventilated patients.
Recent findings: Several experimental and clinical studies have been performed to evaluate the contribution of pathogenic mechanical forces to organ and cellular deformation and the implications for guiding ventilator management in patients at risk for VALI. VALI may be attenuated by reducing tidal volume, but the key variable in determining pulmonary overdistension is transpulmonary pressure. Other parameters associated with the induction of VALI include positive end-expiratory pressure, inspiratory airflow and time, and respiratory frequency.
Summary: How ventilation strategy, specific mechanisms of mechanotransduction, and their individual threshold values impact on VALI remains to be elucidated. In addition, clinical studies are required to evaluate the usefulness of individualized ventilator strategies based on lung mechanics.