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 |
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Summary: | 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. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 ObjectType-Undefined-3 |
ISSN: | 1387-1307 1573-2614 1573-2614 |
DOI: | 10.1007/s10877-016-9954-1 |