Abstract
IntroductionSince normal or high central venous oxygen saturation (ScvO2) values cannot discriminate if tissue perfusion is adequate, integrating other markers of tissue hypoxia, such as central venous-to-arterial carbon dioxide difference (PcvaCO2 gap) has been proposed. In the present study, we aimed to evaluate the ability of the PcvaCO2 gap and the PcvaCO2/arterial-venous oxygen content difference ratio (PcvaCO2/CavO2) to predict lactate evolution in septic shock.MethodsObservational study. Septic shock patients within the first 24 hours of ICU admission. After restoration of mean arterial pressure, and central venous oxygen saturation, the PcvaCO2 gap and the PcvaCO2/CavO2 ratio were calculated. Consecutive arterial and central venous blood samples were obtained for each patient within 24 hours. Lactate improvement was defined as the decrease ≥ 10% of the previous lactate value.ResultsThirty-five septic shock patients were studied. At inclusion, the PcvaCO2 gap was 5.6 ± 2.1 mmHg, and the PcvaCO2/CavO2 ratio was 1.6 ± 0.7 mmHg · dL/mL O2. Those patients whose lactate values did not decrease had higher PcvaCO2/CavO2 ratio values at inclusion (1.8 ± 0.8vs. 1.4 ± 0.5, p 0.02). During the follow-up, 97 paired blood samples were obtained. No-improvement in lactate values was associated to higher PcvaCO2/CavO2 ratio values in the previous control. The ROC analysis showed an AUC 0.82 (p < 0.001), and a PcvaCO2/CavO2 ratio cut-off value of 1.4 mmHg · dL/mL O2 showed sensitivity 0.80 and specificity 0.75 for lactate improvement prediction. The odds ratio of an adequate lactate clearance was 0.10 (p < 0.001) in those patients with an elevated PcvaCO2/CavO2 ratio (≥1.4).ConclusionIn a population of septic shock patients with normalized MAP and ScvO2, the presence of elevated PcvaCO2/CavO2 ratio significantly reduced the odds of adequate lactate clearance during the following hours.
Highlights
Since normal or high central venous oxygen saturation (ScvO2) values cannot discriminate if tissue perfusion is adequate, integrating other markers of tissue hypoxia, such as central venous-to-arterial carbon dioxide difference (PcvaCO2 gap) has been proposed
Mesquida et al Critical Care (2015) 19:126 during the initial resuscitation does not rule out persistent tissue hypoxia, and some authors consider that ScvO2 should be used in combination with other tissue perfusion endpoints [7]
The PcvaCO2 gap at inclusion was inversely correlated to ScvO2 (r = –0.7, P
Summary
Since normal or high central venous oxygen saturation (ScvO2) values cannot discriminate if tissue perfusion is adequate, integrating other markers of tissue hypoxia, such as central venous-to-arterial carbon dioxide difference (PcvaCO2 gap) has been proposed. Some authors have advocated that the mixed and/or central venous-to-arterial carbon dioxide difference (PcvaCO2 gap) might be complementary tools to identify patients with persistent global hypoperfusion [10]. Both partial pressure of carbon dioxide gaps have demonstrated their prognostic value in different conditions [11,12,13,14], and a cutoff value of 6 mmHg seems to reflect whether global flow is adequate (gap >6 mmHg) or insufficient (gap ≥6 mmHg). Some authors have suggested that correcting the PcvaCO2 gap by an approximation of the oxygen consumption, the PcvaCO2/arterial-to-venous oxygen content difference (CavO2) ratio, might be superior to the PcvaCO2 gap to detect anaerobic metabolism [15], and should be a more reliable parameter to guide the resuscitation process
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