학술논문
Central venous-to-arterial carbon dioxide difference and the effect of venous hyperoxia: A limiting factor, or an additional marker of severity in shock?
Document Type
Original Paper
Author
Source
Journal of Clinical Monitoring and Computing: Including a Specialty Section on Surgical Neuromonitoring. :1-9
Subject
Language
English
ISSN
1387-1307
1573-2614
1573-2614
Abstract
Central venous-to-arterial carbon dioxide difference (Pcva CO2 ) has demonstrated its prognostic value in critically ill patients suffering from shock, and current expert recommendations advocate for further resuscitation interventions when Pcva CO2 is elevated. Pcva CO2 combination with arterial–venous oxygen content difference (Pcva CO2 /Cav O2 ) 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 Pcva CO2 and Pcva CO2 /Cav O2 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 Pcva CO2 and Pcva CO2 /Cav O2 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 Pcva CO2 , Pcva CO2 /Cav O2 and Scv O2 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 Pcva CO2 /Cav O2 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]. Pcva CO2 and Pcva CO2 /Cav O2 are influenced by oxygenation changes not related to flow. Elevated Pcva CO2 and Pcva CO2 /Cav O2 values might not only derive from cardiac output inadequacy, but also from venous hyperoxia. Elevated Pcva CO2 /Cav O2 values were associated with higher PO2 transmission to the venous compartment, suggesting higher shunting phenomena.