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

Abstract

Central venous-to-arterial carbon dioxide difference (PCO) has demonstrated its prognostic value in critically ill patients suffering from shock, and current expert recommendations advocate for further resuscitation interventions when PCO is elevated. PCO combination with arterial-venous oxygen content difference (PCO/CO) 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 PCO and PCO/CO 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 PCO and PCO/CO 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 PCO, PCO/CO and SO 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 PCO/CO 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]. PCO and PCO/CO are influenced by oxygenation changes not related to flow. Elevated PCO and PCO/CO values might not only derive from cardiac output inadequacy, but also from venous hyperoxia. Elevated PCO/CO values were associated with higher PO transmission to the venous compartment, suggesting higher shunting phenomena.

Changes in central venous-to-arterial carbon dioxide tension induced by fluid bolus in critically ill patients

“…Second, the absence of correlation between P va CO 2 changes and S cv O 2 suggests that the Haldane effect has only a minor impact on the changes of P va CO 2 during fluid bolus. Given that arterial saturation and PCO 2 did not change in our cohort increases in S cv O 2 secondary to a positive fluid response could cause an increase in venous partial pressure of CO 2 and consequently an increase in P va CO 2 [34].…”

Changes in central venous to arterial carbon dioxide gap (PCO2gap) in response to acute changes in ventilation

“…8 10 A high ∆PCO 2 /∆tO 2 ratio, with cut-offs of ≥1.8, ≥1.6 or ≥1.68 mm Hg/mL have been associated with a worse prognosis. [8][9][10] Although the routine use of this ratio in critical care is controversial, 22 the narrow difference in the cut-offs make it imperative to understand the various influences on blood gas parameters, to be applied during clinical interpretation.…”

Pathophysiology and clinical implications of the veno-arterial PCO2 gap

“…It has been observed that, in patients with circulatory shock, ventilation at 100% inspired oxygen fraction (FiO 2 ) for 5 min increased venous PCO 2 , and hence the Pv-aCO 2 gap, independent of changes in the hemodynamic status [44]. While this observation may be explained by a lower CO 2 affinity of hemoglobin due to elevated venous PO 2 (Haldane effect) [44], it may also reflect some impairment in microcirculatory blood flow, owing to the vasoconstrictive effects of hyperoxia [45]. The second confounder is acute hyperventilation with respiratory alkalosis.…”