Association Between End-Tidal Carbon Dioxide Pressure and Cardiac Output During Fluid Expansion in Operative Patients Depend on the Change of Oxygen Extraction

In a model of hemorrhagic shock, end-tidal carbon dioxide tension (EtCO(2)) has been shown to reflect the dependence of oxygen delivery (DO(2)) and oxygen consumption (VO(2)) at the onset of shock. The objectives of the present study were to determine whether variations in EtCO(2) during volume expansion (VE) are correlated with changes in oxygen extraction (O(2)ER) and whether EtCO(2) has predictive value in this respect. All patients undergoing cardiac surgery admitted to intensive care unit in whom the physician decided to perform VE were included. EtCO(2), cardiac output (CO), blood gas levels, and mean arterial pressure (MAP) were measured before and after VE with 500 mL of lactated Ringer solution. DO(2), VO(2), and O(2)ER were calculated from the central arterial and venous blood gas parameters. EtCO(2) responders were defined as patients with more than a 4% increase in EtCO(2) after VE. A receiver-operating characteristic curve was established for EtCO(2), with a view to predicting a variation of more than 10% in O(2)ER. Twenty-two (43%) of the 51 included patients were EtCO(2) responders. In EtCO(2) nonresponders, VE increased MAP and CO. In EtCO(2) responders, VE increased MAP, CO, EtCO(2), and decreased O(2)ER. Changes in EtCO(2) were correlated with changes in CO and O(2)ER during VE (P < 0.05). The variation of EtCO(2) during VE predicted a decrease of over 10% in O(2)ER (area under the curve [95% confidence interval]: 0.88 [0.77–0.96]; P < 0.0001). During VE, an increase in EtCO(2) did not systematically reflect an increase in CO. Only patients with a high O(2)ER (i.e., low ScvO(2) values) display an increase in EtCO(2). EtCO(2) changes during fluid challenge predict changes in O(2)ER.