Central venous-to-arterial carbon dioxide difference and the effect of venous hyperoxia: A limiting factor, or an additional marker of severity in shock?
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Central venous-to-arterial carbon dioxide difference (PcvaCO2) has demonstrated its prognostic value in critically ill patients suffering from shock, and current expert recommendations advocate for further resuscitation interventions when PcvaCO2 is elevated. PcvaCO2 combination with arterial–venous oxygen content difference (PcvaCO2/CavO2) seems to enhance its performance when assessing anaerobic metabolism. However, the fact that PCO2 values might be altered by changes in blood O2 content (the Haldane effect), has been presented as a limitation of PCO2-derived variables. The present study aimed at exploring the impact of hyperoxia on PcvaCO2 and PcvaCO2/CavO2 during the early phase of shock. Prospective interventional study. Ventilated patients suffering from shock within the first 24 h of ICU admission. Patients requiring FiO2 ≥ 0.5 were excluded. At inclusion, simultaneous arterial and central venous blood samples were collected. Patients underwent a hyperoxygenation test (5 min of FiO2 100%), and arterial and central venous blood samples were repeated. Oxygenation and CO2 variables were calculated at both time points. Twenty patients were studied. The main cause of shock was septic shock (70%). The hyperoxygenation trial increased oxygenation parameters in arterial and venous blood, whereas PCO2 only changed at the venous site. Resulting PcvaCO2 and PcvaCO2/CavO2 significantly increased [6.8 (4.9, 8.1) vs. 7.6 (6.7, 8.5) mmHg, p 0.001; and 1.9 (1.4, 2.2) vs. 2.3 (1.8, 3), p < 0.001, respectively]. Baseline PcvaCO2, PcvaCO2/CavO2 and ScvO2 correlated with the magnitude of PO2 augmentation at the venous site within the trial (ρ −0.46, p 0.04; ρ 0.6, p < 0.01; and ρ 0.7, p < 0.001, respectively). Increased PcvaCO2/CavO2 values were associated with higher mortality in our sample [1.46 (1.21, 1.89) survivors vs. 2.23 (1.86, 2.8) non-survivors, p < 0.01]. PcvaCO2 and PcvaCO2/CavO2 are influenced by oxygenation changes not related to flow. Elevated PcvaCO2 and PcvaCO2/CavO2 values might not only derive from cardiac output inadequacy, but also from venous hyperoxia. Elevated PcvaCO2/CavO2 values were associated with higher PO2 transmission to the venous compartment, suggesting higher shunting phenomena.
KeywordsVenous-to-arterial carbon dioxide difference Circulatory shock Hemodynamic monitoring Tissue hypoxia
Arterial oxygen content
Arterial-to-venous oxygen content difference
Central venous oxygen content
Central venous-to-arterial carbon dioxide content difference
Global oxygen delivery
Mean arterial pressure
Arterial oxygen tension
Arterial carbon dioxide tension
Central venous oxygen tension
Central venous carbon dioxide tension
Central venous-to-arterial carbon dioxide difference
Central venous-to-arterial carbon dioxide difference/arterial–venous oxygen content difference ratio
Arterial oxygen saturation
Central venous oxygen saturation
Oxygen extraction ratio
Global carbon dioxide production
Global oxygen consumption
The authors want to thank David Suarez, PhD for his statistical support.
All the authors contributed to the elaboration of this manuscript. JM and PS conceived, designed, and coordinated the study. JM, PS, LP, GG, LE, APM, and CE performed data extraction. JM, PS and GG analyzed the data, and drafted the manuscript. All authors read and approved the final version of the manuscript.
Compliance with ethical standards
Conflict of interest
The authors declare that they have no conflict of interests.
Ethics approval and consent to participate
The local Ethics Committee (Comitè Ètic d’Investigació Clínica, Fundació Parc Taulí) approved the study (protocol reference CEIC-2014/636). Signed informed consent was obtained from each patient’s next of kin.
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