Constant Tidal Volume Ventilation and Surfactant Dysfunction: An Overlooked Cause of Ventilator-Induced Lung Injury.

Ventilator-induced lung injury (VILI) is currently ascribed to volutrauma and/or atelectrauma but the effect of constant tidal volume ventilation (CVTV) has received little attention. This Perspective summarizes the literature documenting that CVTV causes VILI and reviews the mechanisms by which it occurs. Surfactant is continuously inactivated, depleted, displaced or desorbed as a function of the duration of ventilation, the tidal volume, the level of PEEP and possibly the respiratory rate. Accordingly, surfactant must be continuously replenished and secretion primarily depends on intermittent delivery of large ventilatory excursions. The surfactant abnormalities resulting from CVTV result in atelectasis and VILI. While surfactant secretion is reduced by the absence of intermittent deep breaths continuous administration of large tidal volumes depletes surfactant and impairs subsequent secretion. Low or normal lung volumes result in desorption of surfactant. PEEP can be protective by reducing surface film collapse and subsequent film rupture on re-expansion, and/or by reducing surfactant displacement into the airways, but PEEP can also down-regulate surfactant release. Conclusions: The effect of CVTV on surfactant is complex. If attention is not paid to facilitating surfactant secretion and limiting its inactivation, depletion, desorption or displacement surface tension will increase and atelectasis and VILI will occur.