Barotrauma

Abstract

Clinical barotrauma to the lung induced by mechanical ventilation, including pneumothorax, has been recognized as a problem for many years, but it is only in the past 10 years that the more subtle effects of mechanical ventilation on the lung have been recognized (1). The first comprehensive study that showed mechanical ventilation with high pressures and high tidal volumes in normal lungs caused pulmonary edema was carried out by Webb and Tierney in 1974 (2). In 1988, Dreyfus and colleagues, by using thoracoabdominal strapping to limit lung stretch during mechanical ventilation with high airway pressures, showed no ensuing pulmonary edema occurred with high pressures when the lung was not allowed to stretch (3). A negative pressure extrathoracic ventilator was then used, showing that pulmonary edema occurred at large tidal volumes, even though airway pressures were low. This demonstrated that lung stretch occurring with artificial ventilation, and not airway pressure, was the mechanism causing lung injury. Positive end-expiratory pressure may modify the response to lung stretch as occurs at disproportionately high tidal volumes. Although some data in rats support this concept (1), applying positive end-expiratory pressure to humans with lung injury and lowering the tidal volume simultaneously did not protect the lung (4). Along with lung edema, mechanical ventilation with high tidal volume ventilation has been shown to cause a release of inflammatory cytokines and chemokines with a subsequent influx of neutrophils into the lung (5). This combination of pulmonary edema and lung inflammation caused by barotrauma, or, perhaps more correctly, volutrauma, secondary to mechanical ventilation, has been termed ventilator-induced lung injury (VILI).