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J Clin Monit Comput. 2017 Dec;31(6):1203-1211. doi: 10.1007/s10877-016-9954-1. Epub 2016 Nov 10.

Central venous-to-arterial carbon dioxide difference and the effect of venous hyperoxia: A limiting factor, or an additional marker of severity in shock?

Author information

1
Critical Care Department, Hospital de Sabadell, Corporació Sanitària Universitària Parc Taulí, Universitat Autònoma de Barcelona, Parc Tauli, 1, 08208, Sabadell, Spain.
2
Serviço de Medicina Interna, Hospital Prof. Dr. Fernando Fonseca, Amadora, Portugal.
3
Critical Care Department, Hospital de Sabadell, Corporació Sanitària Universitària Parc Taulí, Universitat Autònoma de Barcelona, Parc Tauli, 1, 08208, Sabadell, Spain. jmesquida@tauli.cat.

Abstract

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.

KEYWORDS:

Circulatory shock; Hemodynamic monitoring; Tissue hypoxia; Venous-to-arterial carbon dioxide difference

PMID:
27832407
DOI:
10.1007/s10877-016-9954-1
[Indexed for MEDLINE]

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