The venous–arterial difference in CO2 should be interpreted with caution in case of respiratory alkalosis in healthy volunteers

Morel, J.; Gergelé, Laurent; Dominé, Alexandre; Molliex, Serge; Perrot, Jean‐Luc; Labeille, B.; Costes, Frédéric

doi:10.1007/s10877-016-9897-6

Cited by 10 publications

(9 citation statements)

References 32 publications

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“…As a consequence, the reducing trend of the CO 2 partial pressure of venous blood is less marked than that of arterial blood. This has been demonstrated by other scholars as well [18]. The increase in alveolar ventilation increases CO 2 excretion and should increase the alveolar PaO 2 provided other factors stay the same.…”

Section: Discussionsupporting

confidence: 60%

Effects of respiratory rate on venous-to-arterial CO2 tension difference in septic shock patients undergoing volume mechanical ventilation

Guo

Wang

Xie³

et al. 2020

Eur J Med Res

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Background: To explore the effects of the respiratory rate (RR) on the venous-to-arterial CO 2 tension difference (gapCO 2 ) in septic shock patients undergoing volume mechanical ventilation. Methods:Adult patients with septic shock underwent volume mechanical ventilation between October 2015 and October 2016. RR was started at 10 breaths/min, and 2 breaths/min were added every 60 min until 16 breaths/min was reached. At every point, central venous and arterial blood gas measurements were obtained simultaneously.Results: In this study, gapCO 2 induced by hyperventilation significantly increased, while the central venous carbon dioxide pressure (PvCO 2 ) and the partial pressure of CO 2 (PaCO 2 ) in arteries decreased. The decreasing trend of the PaCO 2 was more obvious than that of the PvCO 2 . HCO 3 − and ctCO 2 were markedly decreased, when the RR was increased (P < 0.05). Central venous oxygen saturation (S cv O 2 ) had a decreasing trend between 14 (77.1 ± 8.3%) and 16 (75.2 ± 8.7%) breaths/min; however, the difference was not significant. Conclusions:In septic patients undergoing ventilation, respiratory alkalosis induced by hyperventilation caused an increase in the gapCO 2 . Clinicians should cautiously interpret the gapCO 2 in hemodynamically stable ventilated septic shock patients and its relationship with low cardiac output and inadequate perfusion.

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Section: Discussionsupporting

confidence: 60%

Effects of respiratory rate on venous-to-arterial CO2 tension difference in septic shock patients undergoing volume mechanical ventilation

Guo

Wang

Xie³

et al. 2020

Eur J Med Res

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“…The authors concluded that the decrease in mean blood flow, which was the result of increased vascular tone induced by hyperventilation, was responsible for the rise in peripheral venous-to-arterial CO 2 difference that they observed after acute hyperventilation. Similarly, Morel et al [ 20 ] found a significant drop in the skin microcirculatory blood flow of healthy volunteers, evaluated with in vivo reflectance confocal microscopy, secondary to acute hypocapnia. In our study, we observed a significant increase in systemic vascular resistance in parallel with the elevation of alveolar ventilation (Table 2 ).…”

Section: Discussionmentioning

confidence: 87%

“…In anesthetized paralyzed patients, contradictory findings were observed with some authors reporting a significant increase in whole-body VO 2 [ 27 ], whereas others failed to demonstrate any significant variation [ 14 ]. Recently, Morel et al [ 20 ], reported a twofold increase in VO 2 in healthy volunteers with hypocapnic condition compared to hypercapnic condition for the same minute volume, suggesting a possible contribution of this mechanism to the observed increase in peripheral venous-to-arterial CO 2 difference after induced acute respiratory alkalosis. The mechanism by which an acute respiratory alkalosis stimulates oxygen consumption is unclear and may involve many intracellular processes.…”

Section: Discussionmentioning

confidence: 99%

“…However, acute changes in PaCO 2 or arterial pH might have direct effects on microvascular tone and/or might induce variations in systemic oxygen consumption [ 15 – 18 ], and could then affect ∆PCO 2 . Recently, in healthy volunteers, acute hyperventilation was shown to be associated with an increase in the peripheral venous-to-arterial CO 2 difference due to a reduction in peripheral blood flow induced by acute hypocapnia [ 19 , 20 ]. Furthermore, Morel et al [ 21 ] found, in a small study that included mechanically ventilated postoperative patients, that acute decreases in PaCO 2 resulted in significant increases in ∆PCO 2 without any change in cardiac output.…”

Section: Introductionmentioning

confidence: 99%

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Acute hyperventilation increases the central venous-to-arterial PCO2 difference in stable septic shock patients

Mallat

Mohammad

Lemyze

et al. 2017

Ann. Intensive Care

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BackgroundTo evaluate the effects of acute hyperventilation on the central venous-to-arterial carbon dioxide tension difference (∆PCO2) in hemodynamically stable septic shock patients.MethodsEighteen mechanically ventilated septic shock patients were prospectively included in the study. We measured cardiac index (CI), ∆PCO2, oxygen consumption (VO2), central venous oxygen saturation (ScvO2), and blood gas parameters, before and 30 min after an increase in alveolar ventilation (increased respiratory rate by 10 breaths/min).ResultsArterial pH increased significantly (from 7.35 ± 0.07 to 7.42 ± 0.09, p < 0.001) and arterial carbon dioxide tension decreased significantly (from 44.5 [41–48] to 34 [30–38] mmHg, p < 0.001) when respiratory rate was increased. A statistically significant increase in VO2 (from 93 [76–105] to 112 [95–134] mL/min/m2, p = 0.002) was observed in parallel with the increase in alveolar ventilation. While CI remained unchanged, acute hyperventilation led to a significant increase in ∆PCO2 (from 4.7 ± 1.0 to 7.0 ± 2.6 mmHg, p < 0.001) and a significant decrease in ScvO2 (from 73 ± 6 to 67 ± 8%, p < 0.001). A good correlation was found between changes in arterial pH and changes in VO2 (r = 0.67, p = 0.002). Interestingly, we found a strong association between the increase in VO2 and the increase in ∆PCO2 (r = 0.70, p = 0.001).ConclusionsAcute hyperventilation provoked a significant increase in ∆PCO2, which was the result of a significant increase in VO2 induced by hyperventilation. The clinician should be aware of the effects of acute elevation of alveolar ventilation on ∆PCO2.Electronic supplementary materialThe online version of this article (doi:10.1186/s13613-017-0258-5) contains supplementary material, which is available to authorized users.

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“…This relationship is shifted to the right, with a pH decrease resulting in an increased pCO 2 gap for the same value of CvCO 2 . Consequently, an increase in CO will be associated with lower pCO 2 gap if the tissue acid production is decreased by the improvement in oxygen supply (10). Finally, the mechanisms implicated in the elevation of the pCO 2 gap during shock states are not completely understood, and interpretation of the pCO 2 gap could sometimes be difficult.…”

Section: Physiological Backgroundmentioning

confidence: 99%

Venous-to-arterial pCO2 difference in high-risk surgical patients

et al. 2019

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Alteration of tissue perfusion is a main contributor to organ dysfunction in high-risk surgical patients. The difference between venous carbon dioxide and arterial carbon dioxide pressure (pCO 2 gap) has been described as a parameter reflecting tissue hypoperfusion in critically ill patients who are insufficiently resuscitated. The pCO 2 gap/CavO 2 ratio has also been described as an indicator of the respiratory quotient, thus the relationship between DO 2 and VO 2 . Most of the knowledge about the pCO 2 gap and the pCO 2 gap/ CavO 2 ratio has come from studies in the literature on animal models or intensive care unit (ICU) patients. To date, publications pertaining to the operative setting are sparse. In the present review, we will first discuss the physiological background of the pCO 2 gap and CO 2 -O 2 derived parameters used in the operating room. Few studies have focused on the clinical relevance of the pCO 2 gap in high-risk non-cardiac surgical patients. Prospective observational studies with a small sample size and retrospective studies have shown that the pCO 2 gap may be a useful complementary tool to identify patients who remain insufficiently optimized hemodynamically. In a few studies, a high pCO 2 gap was associated with postoperative complications following non-cardiac high-risk surgery. Results of observational studies conducted in patients undergoing cardiac surgery are contradictory. We focused on the divergence between non-cardiac surgery, cardiac surgery, and septic critically ill patients. When analyzing the literature, we can find some explanations for the discrepancies in the published results between cardiac and non-cardiac surgery. Finally, we will discuss the clinical utility of the pCO 2 gap in high-risk surgical patients.

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The venous–arterial difference in CO2 should be interpreted with caution in case of respiratory alkalosis in healthy volunteers

Cited by 10 publications

References 32 publications

Effects of respiratory rate on venous-to-arterial CO2 tension difference in septic shock patients undergoing volume mechanical ventilation

Effects of respiratory rate on venous-to-arterial CO2 tension difference in septic shock patients undergoing volume mechanical ventilation

Acute hyperventilation increases the central venous-to-arterial PCO2 difference in stable septic shock patients

Venous-to-arterial pCO2 difference in high-risk surgical patients

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