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Over the past 30 to 40 years, mechanical ventilation (MV) has become an indispensable therapeutic modality for the management of respiratory failure. However, soon after its inception, it became apparent that MV per se could lead to a number of deleterious complications, including initiation or exacerbation of underlying lung injury.1 Research over the past two decades has focused primarily on the mechanical factors (i.e., pressure and volume) that affect ventilator-induced lung injury (VILI).2-4 Despite considerable amount of experimental work and a number of innovations in ventilator therapy aimed at minimizing such injury, the morbidity and mortality of acute respiratory failure remain high, and VILI remains a significant problem in the care of critically ill patients. The concept of VILI came into light after animal experimental studies clearly demonstrated that MV with high airway pressure and tidal volume led to a rapidly developing permeability-type pulmonary edema with diffuse alveolar damage accompanied by severe lung inflammation when protracted. High lung volume rather than pressure was identified as responsible for these abnormalities, hence the term volutrauma.5 Earlier, generous tidal volumes (VT) (15–20 mL/kg) were delivered to patients to provide adequate CO2 elimination and counterbalance the formation of atelectasis. In the following years, practices progressively moved toward a reduction of tidal volume to values lower than 10 mL/kg and interestingly it was associated with a more rapid attenuation of the inflammatory response.6,7 Definite proof of a causal relation between mortality and ventilator strategy was given by the results of a multicenter randomized controlled trial that showed a decreased mortality rate of 22% in patients ventilated with a 6 mL/kg rather than a 12 mL/kg VT. 8

Systemic Cytokine Response predicts the Outcome of Patients from Mechanical Ventilation