ABSTRACT
Critically ill patients requiring mechanical ventilation frequently develop
the acute respiratory distress syndrome (ARDS) (1,2). Over the past 15 years,
improvements in ventilatory management and other supportive care mea-
sures have led to a decreased mortality related to ARDS. However, the mortality rate in patients with ARDS remains high at 30% to 40% (3). This
devastating syndrome results in decreased lung compliance, requiring ven-
tilation with a higher airway pressure to maintain tidal volume (4). Patients
with ARDS are at risk for developing further lung injury secondary to the
potentially harmful effects of mechanical ventilation. Ventilator-induced
lung injury (VILI) can develop secondary to increased pressure and/or vol-
ume in the alveoli (5,6). Barotrauma secondary to increased pressure
within the alveoli can lead to alveolar rupture, while volutrauma secondary to increased volume within the alveoli can lead to alveolar overdistention.
Animal studies of mechanical ventilation have demonstrated that increased
pressure and overdistention of the alveoli lead to increases in membrane
permeability, edema, and inflammation (7-9). These processes may then
lead to a worsening of the lung injury and deterioration of the lung function in patients with ARDS. Concerns over these harmful effects of mechanical
ventilation have led to the development of lung-protective ventilation stra-
tegies, which attempt to minimize VILI by lowering the tidal volume and
limiting airway pressure.
