Abstract

The current main objective of mechanical ventilation during acute respiratory distress syndrome (ARDS) is to improve oxygenation while preventing ventilator-induced lung injury (VILI) in order to save a patient’s life. The major determinants of VILI are both hyperinflation of normally aerated lung and repetitive opening and closing of lung units. There are two methods of preventing VILI and, hence, making mechanical ventilation lung protective. The first is to reduce tidal volume to 6 ml/kg predicted body weight and to keep the end-inspiratory airway pressure below 30 cm H2O. This strategy reduced the mortality of patients with ARDS. In a large, multicenter, randomized, controlled trial, patients receiving lower tidal volume (6 ml/kg ideal body weight) had a better chance of survival than those patients receiving a higher tidal volume of 12 ml/kg. Keeping plateau pressure below 30 cm H2O was an associated strategy in this trial. However, it is likely that this value is not a safety threshold in every patient, since overdistension may be present even when plateau pressure is below 30 cm H2O. The second mechanism to prevent VILI is recruiting the nonaerated or poorly aerated lung areas and keeping them recruited. This strategy requires alveolar pressures much larger than 30 cm H2O transiently to overcome the critical opening pressures of the lung. One drawback is hemodynamic impairment. To date, this strategy has not been found to be associated with an improvement of patient outcome.

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