{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T05:18:37Z","timestamp":1790486317740,"version":"4.1.0"},"reference-count":30,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2021,8,26]],"date-time":"2021-08-26T00:00:00Z","timestamp":1629936000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2021,8,26]],"date-time":"2021-08-26T00:00:00Z","timestamp":1629936000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Sci Rep"],"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Defining the hemodynamic response to volume therapy is integral to managing critically ill patients with acute circulatory failure, especially in the absence of cardiac index (CI) measurement. This study aimed at investigating whether changes in central venous-to-arterial CO<jats:sub>2<\/jats:sub> difference (\u0394-\u0394PCO<jats:sub>2<\/jats:sub>) and central venous oxygen saturation (\u0394ScvO<jats:sub>2<\/jats:sub>) induced by volume expansion (VE) are reliable parameters to define fluid responsiveness in sedated and mechanically ventilated septic patients. We prospectively studied 49 critically ill septic patients in whom VE was indicated because of circulatory failure and clinical indices. CI, \u0394PCO<jats:sub>2<\/jats:sub>, ScvO<jats:sub>2<\/jats:sub>, and oxygen consumption (VO<jats:sub>2<\/jats:sub>) were measured before and after VE. Responders were defined as patients with a\u2009&gt;\u200910% increase in CI (transpulmonary thermodilution) after VE. We calculated areas under the receiver operating characteristic curves (AUCs) for \u0394-\u0394PCO<jats:sub>2<\/jats:sub>, \u0394ScvO<jats:sub>2<\/jats:sub>, and changes in CI (\u0394CI) after VE in the whole population and in the subgroup of patients with an increase in VO<jats:sub>2<\/jats:sub> (\u0394VO<jats:sub>2<\/jats:sub>)\u2009\u2264\u200910% after VE (oxygen-supply independency). Twenty-five patients were fluid responders. In the whole population, \u0394-\u0394PCO<jats:sub>2<\/jats:sub> and \u0394ScvO<jats:sub>2<\/jats:sub> were significantly correlated with \u0394CI after VE (r\u2009=\u2009\u2009\u2212\u20090.30, <jats:italic>p<\/jats:italic>\u2009=\u20090.03 and r\u2009=\u20090.42, <jats:italic>p<\/jats:italic>\u2009=\u20090.003, respectively). The AUCs for \u0394-\u0394PCO<jats:sub>2<\/jats:sub> and \u0394ScvO<jats:sub>2<\/jats:sub> to define fluid responsiveness (increase in CI\u2009&gt;\u200910% after VE) were 0.76 (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001) and 0.68 (<jats:italic>p<\/jats:italic>\u2009=\u20090.02), respectively. In patients with \u0394VO<jats:sub>2<\/jats:sub>\u2009\u2264\u200910% (n\u2009=\u200936) after VE, the correlation between \u0394ScvO<jats:sub>2<\/jats:sub> and \u0394CI was 0.62 (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001), and between \u0394-\u0394PCO<jats:sub>2<\/jats:sub> and \u0394CI was\u2009\u2212\u20090.47 (<jats:italic>p<\/jats:italic>\u2009=\u20090.004). The AUCs for \u0394-\u0394PCO<jats:sub>2<\/jats:sub> and \u0394ScvO<jats:sub>2<\/jats:sub> were 0.83 (<jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001) and 0.73 (<jats:italic>p<\/jats:italic>\u2009=\u20090.006), respectively. In these patients, \u0394-\u0394PCO<jats:sub>2<\/jats:sub>\u2009\u2264\u2009-37.5% after VE allowed the categorization between responders and non-responders with a positive predictive value of 100% and a negative predictive value of 60%. In sedated and mechanically ventilated septic patients with no signs of tissue hypoxia (oxygen-supply independency), \u0394-\u0394PCO<jats:sub>2<\/jats:sub> is a reliable parameter to define fluid responsiveness.<\/jats:p>","DOI":"10.1038\/s41598-021-96806-6","type":"journal-article","created":{"date-parts":[[2021,8,26]],"date-time":"2021-08-26T10:05:29Z","timestamp":1629972329000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":17,"title":["Central venous-to-arterial PCO2 difference as a marker to identify fluid responsiveness in septic shock"],"prefix":"10.1038","volume":"11","author":[{"given":"Boulos","family":"Nassar","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohamed","family":"Badr","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicolas","family":"Van Grunderbeeck","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Johanna","family":"Temime","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Florent","family":"Pepy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gaelle","family":"Gasan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Laurent","family":"Tronchon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Didier","family":"Thevenin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jihad","family":"Mallat","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,8,26]]},"reference":[{"key":"96806_CR1","doi-asserted-by":"publisher","first-page":"2000","DOI":"10.1378\/chest.121.6.2000","volume":"121","author":"F Michard","year":"2002","unstructured":"Michard, F. & Teboul, J. 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