ards is produced in a pulmonary edema picture due to increased vascular patency. in this way, the initial alteration consists in an alveolar occupation due to protein rich edema. this occupation reduces the alveolar surface available for gas exchange, increasing the pulmonary areas with poor or null v/q ratio. as ards progresses, vascular phenomena occur that affect the gas exchange differently, giving rise to heterogeneity in the v/q ratio. this situation worsens due to the appearance of areas with null ventilation in relationship with the appearance of atelectasis in lung dependent zones. all these factors form the hypoxemia picture refractory to the increase of the inspired oxygen fraction characteristic of this clinical entity. in this article, we make a review of these physiological mechanisms and the effect on the oxygenation of different ventilatory and drug maneuvers.