VILI from Ventilation with Low End Expiratory Volume and Pressure

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 [8].

2. Lowvolume/lowpressure VILI may occurfrom excessive stress in theparenchy-mal attachments between atelectatic and aerated lung units [21].

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.

Was this article helpful?

0 0

Post a comment