The presence of severe hypoxemia in critically ill patients with Adult Respiratory Distress Syndrome (ARDS) requires mechanical ventilation with large tidal volumes to produce adequate arterial oxygen tension (PaO2). However, this hyperventilation decreases arterial carbon dioxide tension (PaCO2), causing a profound depression of oxygen transport (decreased cardiac output and arterial oxygen content), delivery (left deviation of oxyhemoglobin dissociation curve) and adequacy of tissue oxygenation (O2 utilization coefficient and blood lactate concentration) together with an increase in oxygen consumption (VO2). As suggested by a previous study in our department (1), normalization of PaCO2 with addition of CO2 to inspired gases can acutely reverse the decrease in arterial oxygen content and cardiac output. Nevertheless, the long-term effects of PaCO2 normalization O2 transport and tissue O2 utilization in critically ill patients with ARDS remain unknown. This study proposed an evaluation of the long-term effects of PaCO2 normalization (48 hours) on O2 transport and delivery mechanisms, such as changes in cardiac output, PaO2, arterial oxygen content, oxygen consumption, blood lactate concentration, oxyhemoglobin dissociation curve and forces controlling the position of this curve (P50), such as 2,3 DPG concentration and pH. Since there are forces acting to move the oxyhemoglobin dissociation curve in opposite directions, net shift will be documented. We will evaluate the effects of PaCO2 normalization upon tissue oxygenation through examination of changes in oxygen consumption, O2 utilization coefficient and plasma lactate concentration. Acquisition of these data is essential to the understanding of oxygen delivery to and consumption by the tissues, when opposing forces are superimposed. Hopefully, PaCO2 normalization in these critically ill patients will result in improved tissue oxygenation with unchanged or decreased oxygen consumption and increased survival.