VILI occurred in experimental animal models of ALI when positive pressure ventilation was delivered with low end-expiratory volumes and airway pressures
[1, 8, 9]. At least three mechanisms for this form of VILI have been suggested:
1. Low volume/low pressure VILI may occur if there is some atelectasis at end-expiration, which is more likely when low end-expiratory airway pressures are applied. This may allow repeated opening and closing of small bronchioles and alveoli, which could involve injurious mechanical stresses .
2. Lowvolume/lowpressure VILI may occurfrom excessive stress in theparenchy-mal attachments between atelectatic and aerated lung units .
3. Low volume/low pressure VILI may occur if there is substantial atelectasis or alveolar filling, leading to maldistribution of the Vt to the aerated lung units, causing overdistention[22, 23]. Several studies in experimental models demonstrated decreased VILI when higher levels of positive end-expiratory pressure (PEEP) were applied, to raise end-expiratory lung volume by recruiting atelectasis or flooded alveoli [1, 8, 9]. Higher levels of PEEP were recommended by some investigators to prevent this form of VILI in ARDS patients [24, 25]. However, higher levels of PEEP may cause higher levels of end-inspiratory pressure and volume, which could cause VILI from overdistention. Moreover, higher levels of PEEP may cause circulatory depression [26, 27]. Therefore, it was not clear that modifying traditional mechanical ventilation approaches with higher PEEP would improve clinical outcomes.
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