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 in | Journal of clinical monitoring and computing Vol. 31; no. 6; pp. 1203 - 1211 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
Dordrecht
Springer Netherlands
01.12.2017
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
ISSN | 1387-1307 1573-2614 1573-2614 |
DOI | 10.1007/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. |
Author_xml | – sequence: 1 givenname: P. surname: Saludes fullname: Saludes, P. organization: Critical Care Department, Hospital de Sabadell, Corporació Sanitària Universitària Parc Taulí, Universitat Autònoma de Barcelona – sequence: 2 givenname: L. surname: Proença fullname: Proença, L. organization: Critical Care Department, Hospital de Sabadell, Corporació Sanitària Universitària Parc Taulí, Universitat Autònoma de Barcelona, Serviço de Medicina Interna, Hospital Prof. Dr. Fernando Fonseca – sequence: 3 givenname: G. surname: Gruartmoner fullname: Gruartmoner, G. organization: Critical Care Department, Hospital de Sabadell, Corporació Sanitària Universitària Parc Taulí, Universitat Autònoma de Barcelona – sequence: 4 givenname: L. surname: Enseñat fullname: Enseñat, L. organization: Critical Care Department, Hospital de Sabadell, Corporació Sanitària Universitària Parc Taulí, Universitat Autònoma de Barcelona – sequence: 5 givenname: A. surname: Pérez-Madrigal fullname: Pérez-Madrigal, A. organization: Critical Care Department, Hospital de Sabadell, Corporació Sanitària Universitària Parc Taulí, Universitat Autònoma de Barcelona – sequence: 6 givenname: C. surname: Espinal fullname: Espinal, C. organization: Critical Care Department, Hospital de Sabadell, Corporació Sanitària Universitària Parc Taulí, Universitat Autònoma de Barcelona – sequence: 7 givenname: J. orcidid: 0000-0003-3670-5021 surname: Mesquida fullname: Mesquida, J. email: jmesquida@tauli.cat organization: Critical Care Department, Hospital de Sabadell, Corporació Sanitària Universitària Parc Taulí, Universitat Autònoma de Barcelona |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27832407$$D View this record in MEDLINE/PubMed |
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Copyright | Springer Science+Business Media Dordrecht 2016 Journal of Clinical Monitoring and Computing is a copyright of Springer, 2017. |
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DOI | 10.1007/s10877-016-9954-1 |
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Keywords | Tissue hypoxia Circulatory shock Venous-to-arterial carbon dioxide difference Hemodynamic monitoring |
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PublicationSubtitle | Including a Specialty Section on Surgical Neuromonitoring |
PublicationTitle | Journal of clinical monitoring and computing |
PublicationTitleAbbrev | J Clin Monit Comput |
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Snippet | Central venous-to-arterial carbon dioxide difference (P
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CO
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) 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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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? |
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