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

Central venous-to-arterial carbon dioxide difference (P cva CO 2 ) has demonstrated its prognostic value in critically ill patients suffering from shock, and current expert recommendations advocate for further resuscitation interventions when P cva CO 2 is elevated. P cva CO 2 combination with arter...

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Published inJournal of clinical monitoring and computing Vol. 31; no. 6; pp. 1203 - 1211
Main Authors Saludes, P., Proença, L., Gruartmoner, G., Enseñat, L., Pérez-Madrigal, A., Espinal, C., Mesquida, J.
Format Journal Article
LanguageEnglish
Published Dordrecht Springer Netherlands 01.12.2017
Springer Nature B.V
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Online AccessGet full text
ISSN1387-1307
1573-2614
1573-2614
DOI10.1007/s10877-016-9954-1

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Abstract Central venous-to-arterial carbon dioxide difference (P cva CO 2 ) has demonstrated its prognostic value in critically ill patients suffering from shock, and current expert recommendations advocate for further resuscitation interventions when P cva CO 2 is elevated. P cva CO 2 combination with arterial–venous oxygen content difference (P cva CO 2 /C av O 2 ) seems to enhance its performance when assessing anaerobic metabolism. However, the fact that PCO 2 values might be altered by changes in blood O 2 content (the Haldane effect), has been presented as a limitation of PCO 2 -derived variables. The present study aimed at exploring the impact of hyperoxia on P cva CO 2 and P cva CO 2 /C av O 2 during the early phase of shock. Prospective interventional study. Ventilated patients suffering from shock within the first 24 h of ICU admission. Patients requiring FiO 2  ≥ 0.5 were excluded. At inclusion, simultaneous arterial and central venous blood samples were collected. Patients underwent a hyperoxygenation test (5 min of FiO 2 100%), and arterial and central venous blood samples were repeated. Oxygenation and CO 2 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 PCO 2 only changed at the venous site. Resulting P cva CO 2 and P cva CO 2 /C av O 2 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 P cva CO 2 , P cva CO 2 /C av O 2 and S cv O 2 correlated with the magnitude of PO 2 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 P cva CO 2 /C av O 2 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]. P cva CO 2 and P cva CO 2 /C av O 2 are influenced by oxygenation changes not related to flow. Elevated P cva CO 2 and P cva CO 2 /C av O 2 values might not only derive from cardiac output inadequacy, but also from venous hyperoxia. Elevated P cva CO 2 /C av O 2 values were associated with higher PO 2 transmission to the venous compartment, suggesting higher shunting phenomena.
AbstractList Central venous-to-arterial carbon dioxide difference (P cva CO 2 ) has demonstrated its prognostic value in critically ill patients suffering from shock, and current expert recommendations advocate for further resuscitation interventions when P cva CO 2 is elevated. P cva CO 2 combination with arterial–venous oxygen content difference (P cva CO 2 /C av O 2 ) seems to enhance its performance when assessing anaerobic metabolism. However, the fact that PCO 2 values might be altered by changes in blood O 2 content (the Haldane effect), has been presented as a limitation of PCO 2 -derived variables. The present study aimed at exploring the impact of hyperoxia on P cva CO 2 and P cva CO 2 /C av O 2 during the early phase of shock. Prospective interventional study. Ventilated patients suffering from shock within the first 24 h of ICU admission. Patients requiring FiO 2  ≥ 0.5 were excluded. At inclusion, simultaneous arterial and central venous blood samples were collected. Patients underwent a hyperoxygenation test (5 min of FiO 2 100%), and arterial and central venous blood samples were repeated. Oxygenation and CO 2 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 PCO 2 only changed at the venous site. Resulting P cva CO 2 and P cva CO 2 /C av O 2 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 P cva CO 2 , P cva CO 2 /C av O 2 and S cv O 2 correlated with the magnitude of PO 2 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 P cva CO 2 /C av O 2 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]. P cva CO 2 and P cva CO 2 /C av O 2 are influenced by oxygenation changes not related to flow. Elevated P cva CO 2 and P cva CO 2 /C av O 2 values might not only derive from cardiac output inadequacy, but also from venous hyperoxia. Elevated P cva CO 2 /C av O 2 values were associated with higher PO 2 transmission to the venous compartment, suggesting higher shunting phenomena.
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.
Central venous-to-arterial carbon dioxide difference (P CO ) has demonstrated its prognostic value in critically ill patients suffering from shock, and current expert recommendations advocate for further resuscitation interventions when P CO is elevated. P CO combination with arterial-venous oxygen content difference (P CO /C O ) seems to enhance its performance when assessing anaerobic metabolism. However, the fact that PCO values might be altered by changes in blood O content (the Haldane effect), has been presented as a limitation of PCO -derived variables. The present study aimed at exploring the impact of hyperoxia on P CO and P CO /C O during the early phase of shock. Prospective interventional study. Ventilated patients suffering from shock within the first 24 h of ICU admission. Patients requiring FiO  ≥ 0.5 were excluded. At inclusion, simultaneous arterial and central venous blood samples were collected. Patients underwent a hyperoxygenation test (5 min of FiO 100%), and arterial and central venous blood samples were repeated. Oxygenation and CO 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 PCO only changed at the venous site. Resulting P CO and P CO /C O 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 P CO , P CO /C O and S O correlated with the magnitude of PO 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 P CO /C O 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]. P CO and P CO /C O are influenced by oxygenation changes not related to flow. Elevated P CO and P CO /C O values might not only derive from cardiac output inadequacy, but also from venous hyperoxia. Elevated P CO /C O values were associated with higher PO transmission to the venous compartment, suggesting higher shunting phenomena.
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.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.
Author Pérez-Madrigal, A.
Proença, L.
Espinal, C.
Mesquida, J.
Gruartmoner, G.
Enseñat, L.
Saludes, P.
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/27832407$$D View this record in MEDLINE/PubMed
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Tue Jul 01 00:29:54 EDT 2025
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Issue 6
Keywords Tissue hypoxia
Circulatory shock
Venous-to-arterial carbon dioxide difference
Hemodynamic monitoring
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– reference: 16682934 - Minerva Anestesiol. 2006 Jun;72(6):597-604
– reference: 11904655 - Intensive Care Med. 2002 Mar;28(3):272-7
– reference: 17666946 - Shock. 2008 Jan;29(1):3-6
– reference: 26842697 - Ann Intensive Care. 2016 Dec;6(1):10
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Snippet Central venous-to-arterial carbon dioxide difference (P cva CO 2 ) has demonstrated its prognostic value in critically ill patients suffering from shock, and...
Central venous-to-arterial carbon dioxide difference (P CO ) has demonstrated its prognostic value in critically ill patients suffering from shock, and current...
Central venous-to-arterial carbon dioxide difference (PcvaCO2) has demonstrated its prognostic value in critically ill patients suffering from shock, and...
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StartPage 1203
SubjectTerms Aged
Anesthesiology
Augmentation
Blood
Blood Gas Analysis
Carbon dioxide
Carbon Dioxide - chemistry
Cardiac output
Critical Care Medicine
Female
Health Sciences
Humans
Hyperoxia
Hypoxia - pathology
Intensive
Male
Mathematical analysis
Medicine
Medicine & Public Health
Metabolism
Middle Aged
Monitoring, Physiologic - methods
Original Research
Oxygen - chemistry
Oxygen content
Oxygenation
Patients
Prognosis
Prospective Studies
Reproducibility of Results
Resuscitation
Shock - blood
Shock - diagnosis
Statistics for Life Sciences
Treatment Outcome
Veins - pathology
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Title Central venous-to-arterial carbon dioxide difference and the effect of venous hyperoxia: A limiting factor, or an additional marker of severity in shock?
URI https://link.springer.com/article/10.1007/s10877-016-9954-1
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Volume 31
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