Mechanical ventilation markedly affects pulmonary circulation and is more pronounced in the setting of reduced lung compliance. Several studies have correlated a reduced ARDS survival to the development of ACP.6,7 PP, which is a reflection of transpulmonary pressure, has direct effects on pulmonary capillaries with alterations on RV afterload. In a study of 352 patients with ARDS who were mechanically ventilated, an ACP incidence of 13% was noted in PP < 27 cm H2O, 30% for PP range 27 to 35 cm H2O, and 60% for PP greater than > 35 cm H2O. Corresponding mortality rates for these three PP ranges were 30%, 40%, and 80% respectively. Similarly, the application of high extrinsic PEEP also has deleterious effects on RV function and results in overloading the right ventricle.7 Limiting tidal volumes is ideal in reducing PP, but it is also responsible for the development of hypercapnia. Hypercapnia likewise will induce pulmonary arterial vasoconstriction and worsen ACP. To control for the development of hypercapnia in the treatment of ACP, one should not increase the tidal volume, but should correct by increasing the respiratory rate and avoiding the development of intrinsic PEEP.