To the Editor,

We read Drs Barak and Yussim’s comments with great interest.1 They raise the hypothesis that the end-tidal CO2 (ETCO2) variation observed following passive leg raising (PLR) is caused by a variation in alveolar dead space instead of an increase in cardiac output. Even if this hypothesis and argument are based on sound physiological principles, we cannot agree with their conclusions.

When alveolar ventilation is kept constant (assuming stable carbon dioxide production), simultaneous ETCO2 and cardiac output variations have been well described in the literature in multiple clinical situations.2,3 Also, in our study, cardiac output and ETCO2 measurements were performed simultaneously. Fluid responders had a significant change in their cardiac output and ETCO2 following the PLR maneuver, which is a well-recognized method to assess fluid responsiveness.4,5 Therefore, in our study, we think that the ETCO2 variation represents real cardiac output variation.