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Review Article
Surgery Clinical applications of blood gas analysis: a comparative review of arterial and venous blood gas monitoring in critical care
Acute and Critical Care 2025;40(2):153-159.
DOI: https://doi.org/10.4266/acc.000900
Published online: May 30, 2025

Division of Trauma and Surgical Critical Care, Department of Surgery, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul, Korea

Corresponding author: Gyeo Ra Lee Division of Trauma and Surgical Critical Care, Department of Surgery, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, 222 Banpo-daero, Seocho-gu, Seoul 06591, Korea Tel: +82-2-2258-2159 Fax: +82-2-595-2822 Email: leegyoura@naver.com
• Received: March 14, 2025   • Revised: May 19, 2025   • Accepted: May 22, 2025

© 2025 The Korean Society of Critical Care Medicine

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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  • Blood gas analysis is an essential diagnostic tool used for assessing acid-base balance, ventilation, and oxygenation in critically ill patients. Arterial blood gas analysis (ABGA) remains the gold standard, primarily due to its accuracy in measuring oxygenation. Venous blood gas analysis (VBGA), in contrast, serves as a less invasive alternative and is particularly useful for evaluating acid-base status and metabolic function. Important parameters such as central venous oxygen saturation (ScvO2) and venous-to-arterial carbon dioxide pressure difference (∆pv-aCO2) provide critical insights into hemodynamic status, cardiac output, and tissue perfusion. Although VBGA cannot replace ABGA for the precise assessment of oxygenation, it remains a valuable tool in clinical scenarios involving hemodynamic monitoring, shock management, and critical care decision-making.
  • Key Words: blood; blood gas analysis; carbon dioxide; catheterization; central venous; hemodynamics; Veins
Blood gas analysis (BGA) is a frequently performed point-of-care test intended to assess acid-base balance, ventilation status, and O2 delivery in patients with critical or acute illnesses. This analysis enables rapid evaluation of respiratory function, oxygenation, electrolyte levels, and metabolic conditions, making it indispensable in emergency rooms, intensive care units (ICUs), and operating rooms, as well as for managing patients with respiratory and metabolic disorders. In particular, BGA is vital for assessing critically ill patients and determining appropriate treatment strategies, emphasizing the necessity of rapid and accurate analysis. The most preferable sample for BGA is arterial blood, collected anaerobically through arterial puncture or via an indwelling arterial catheter, making arterial sampling the gold standard method. This distinguishes BGA from general blood tests, which typically utilize venous blood obtained via peripheral venipuncture. Occasionally, capillary blood is used, primarily for neonates and infants. Although venous blood is helpful for assessing acid-base balance, it cannot be used to accurately evaluate oxygenation status, thereby limiting its usefulness in BGA.
Arterial blood gas analysis (ABGA) involves drawing blood from an artery, most commonly the radial artery, due to its easy accessibility and lower risk of complications. Prior to using the radial artery, verifying adequate collateral circulation through the Allen test is essential. Alternative sites include the brachial and femoral arteries, although the brachial artery poses a risk of nerve injury, and the femoral artery carries greater risks of bleeding and infection, usually restricting its use to emergency scenarios. Possible complications of ABGA include pain, bleeding, hematoma formation, arterial spasm, thrombosis, infection, and damage to adjacent tissues or nerves. Such complications can be minimized by employing proper techniques and careful handling [1,2]. Given the critical need for expertise to ensure patient safety and comfort, only trained medical professionals are authorized to perform arterial blood collection.
Venous blood gas analysis (VBGA) is less invasive and simpler than ABGA, enhancing patient comfort and reducing complications such as bleeding, hematoma, and arterial spasm. It also enables repeated sampling, a significant advantage for continuous patient monitoring. Critically ill ICU patients frequently have arterial catheters placed primarily for continuous blood pressure monitoring, facilitating easier and more comfortable arterial blood sampling for BGA, although arterial catheter insertion remains an invasive procedure requiring technical expertise [3]. However, many critically ill patients needing frequent blood gas analyses have central venous catheters (CVCs), enabling safe venous blood collection and reducing the need for repeated venipuncture. Using venous blood for BGA enhances convenience for healthcare providers and offers a safer, more comfortable option for patients. Table 1 presents a comparison of the key differences between ABGA and VBGA. VBGA provides notable advantages, including ease of sampling, reduced invasiveness, and suitability for repeated testing. Venous samples can be collected via peripheral venipuncture or a CVC, decreasing pain and complications such as bleeding, hematoma, or ischemia compared to arterial puncture. Additionally, VBGA facilitates rapid patient assessment and treatment monitoring in emergency rooms and ICUs, increasing patient comfort and clinical workflow efficiency.
VBGA is valuable for assessing acid-base status to a certain degree, but it cannot deliver accurate oxygenation data provided by ABGA. Consequently, ABGA is indispensable for evaluating respiratory status and O2 delivery, while VBGA serves effectively as a supplementary tool. Most clinical BGA research has historically focused on arterial blood, and established reference ranges are extensively validated using arterial samples. Although these arterial values are well-established among clinicians, there is increasing interest in exploring the potential of venous blood as an alternative in specific circumstances, driven mainly by practical challenges related to arterial sampling.
Since the partial pressures of gases are measured directly, the three primary parameters evaluated in BGA are pH, partial pressure of carbon dioxide (pCO2), and partial pressure of oxygen (pO2). The bicarbonate (HCO3–) concentration, on the other hand, is calculated indirectly from these measurements. Together, pH, pCO2, and HCO3– are essential for assessing the patient's acid-base status. The differences between arterial and venous blood result from the physiological exchange of O2 and CO2 occurring within the capillary beds of tissues and alveoli. This two-step gas exchange process is vital for blood's fundamental role: delivering O2 from the lungs to peripheral cells and transporting CO2 from cells back to the lungs for removal. Proper functioning of this exchange process is critical for maintaining adequate metabolic activity and respiration.
Venous blood returns to the heart after delivering O2 and nutrients to tissues. As blood traverses tissues, it accumulates CO2 and metabolic wastes. Consequently, venous blood contains lower O2 levels, reduced O2 saturation, and higher CO2 concentrations compared to arterial blood, resulting in a slightly lower pH. Recognizing these differences is crucial when selecting an appropriate blood sample for diagnostic evaluation. In contrast, arterial blood becomes oxygenated as it passes through the lungs, absorbing O2 and releasing CO2, before traveling to the left side of the heart via pulmonary veins. Previous studies [4-13] exploring the feasibility of venous blood for BGA follow a consistent and straightforward methodology. Accurate comparisons between arterial and venous BGA require anaerobic sampling and timely analysis using identical equipment. Research has consistently demonstrated that central venous pH is slightly lower than arterial pH, with an average arterial-venous (A-V) difference of approximately 0.03 pH units; this difference is clinically acceptable when accounted for in interpretation. Similarly, central venous pCO2 is higher than arterial pCO2, with a systematic negative bias of roughly –0.6 kPa (–5.0 mm Hg), making it a viable substitute in most clinical scenarios. Because HCO3– is derived from pH and pCO2, central venous HCO3– typically shows slightly higher values than arterial HCO3–, and thus can also serve as an appropriate alternative. In contrast, arterial and venous pO2 values demonstrate no reliable correlation due to variations in tissue O2 consumption and blood flow dynamics, exhibiting an average A-V difference of approximately 8.33 kPa (63 mm Hg)±7.88 kPa (59 mm Hg). As a consequence, venous pO2 cannot accurately predict arterial pO2 levels, necessitating direct ABGA for precise oxygenation assessments. However, pulse oximetry offers a noninvasive method for continuously monitoring arterial O2 saturation. Except in situations where assessing oxygenation is essential due to respiratory issues, VBGA is preferable for evaluating acid-base status, avoiding the complications associated with arterial sampling. Furthermore, patients requiring frequent BGA also routinely undergo venous blood draws for other diagnostic tests. Utilizing a single venous sample for multiple diagnostic evaluations would enhance efficiency, improve patient safety, and reduce healthcare costs.
Numerous previous studies evaluating the reliability of venous blood have utilized samples obtained through peripheral venipuncture [4,8,14,15]. Peripheral blood collected via venipuncture differs in gas variables from central venous and mixed venous blood. Unlike arterial blood, which maintains stable gas values until it reaches the tissue capillary bed, venous blood gas measurements may vary depending on the collection site. Central venous blood specifically refers to blood samples obtained through a CVC. Besides facilitating blood sampling for diagnostics, CVCs allow continuous central venous pressure monitoring, which is vital for managing hemodynamically unstable patients. Additionally, these catheters provide vascular access for the administration of medications, fluids, and blood transfusions. Typically, a CVC is inserted via the jugular or subclavian vein, and its tip is positioned near the junction of the superior vena cava and the right atrium, thereby collecting venous blood predominantly from the upper body. However, as this blood excludes input from the inferior vena cava, central venous blood does not represent true mixed venous blood. Complete mixing of venous blood occurs only after it circulates to the pulmonary artery. Consequently, only pulmonary artery catheterization enables the collection of fully mixed venous blood. This distinction is crucial for accurately evaluating systemic oxygenation and hemodynamic status. However, pulmonary artery catheters are seldom employed in our ICU. Thus, central venous blood often serves as a substitute for mixed venous blood in clinical practice. While central venous blood cannot fully replace mixed venous blood, it can function as a partial alternative in specific clinical scenarios. Mixed venous blood, obtained directly from the pulmonary artery, reflects a comprehensive mixture of venous return from the entire body, thereby accurately representing overall tissue O2 consumption and metabolic state. In contrast, central venous blood is drawn from the superior vena cava or other central veins and primarily includes venous return from the upper body, offering only partial metabolic and oxygenation information (Figure 1). Typically, the central venous oxygen saturation (ScvO2) is approximately 2%–3% lower than that of mixed venous oxygen saturation (SvO2), and thus it can be used as a supplementary indicator, particularly in patients with conditions such as sepsis or shock [16].
Hemodynamic monitoring supports clinical decision-making, thus playing a crucial role in critical care [17]. A key objective is to provide timely alerts to facilitate decision-making before adverse events occur. Most variables in hemodynamic monitoring reflect macro-circulation parameters, as optimizing macro-hemodynamic conditions is generally assumed to enhance micro-circulation; however, this is often not the case [18]. Over time, BGA has remained superior to lactate, base deficit, and ScvO2, as it provides essential information on cardiac output, microcirculatory perfusion, and anaerobic metabolic activity. Specifically, the venous-to-arterial CO2 pressure difference (∆pv-aCO2) serves as a critical indicator of these physiological processes. Given that these parameters represent fundamental targets for hemodynamic monitoring, BGA holds significant clinical value in assessing a patient's circulatory and metabolic status [19]. The data obtained from BGA more accurately reflect the true microcirculatory flow and metabolic state, indicating impaired O2 utilization and hemodynamic instability [20,21].
In healthy individuals, ScvO2 is typically around 3% lower than SvO2, which is attributable to the lower O2 extraction ratio (O2ER) in the lower body compared to the upper body [16]. However, in shock conditions, this ScvO2/SvO2 relationship reverses due to increased O2 extraction in the lower body. Specifically, in patients with septic shock, ScvO2 may exceed SvO2 by up to 8% because of enhanced O2ER in the lower extremities [16]. Some studies indicate that ScvO2 can reliably substitute SvO2 values in clinical assessments [22]. ScvO2 is directly influenced by the O2 consumption-to-delivery ratio (VO2/DO2), decreasing when O2 transport is insufficient and increasing when O2 utilization is reduced [23]. When DO2 declines, the body compensates by elevating O2ER. Without timely intervention, however, this compensation eventually fails, causing VO2 to become dependent on DO2 [24]. Up to this critical threshold, known as cellular dysoxia, ScvO2 decreases proportionally to reductions in DO2. Beyond this point, delayed or insufficient interventions result in severe tissue hypoxia, causing disproportionate shifts toward anaerobic metabolism. Thus, ScvO2 is a valuable marker of cellular oxygenation. If ScvO2 is low, enhancing DO2 initially leads to increased VO2, yet ScvO2 remains low despite appropriate intervention. ScvO2 begins to rise only when VO2 becomes independent of DO2, marking entry into the independent zone [25]. However, low ScvO2 does not always warrant increased DO2, as this intervention can produce adverse effects. Instead, interventions that lower VO2—such as sedation, pain management, fever control, and managing agitation or tremors—should be prioritized [26]. Thus, personalized therapeutic strategies are essential. A high ScvO2 may indicate clinical improvement but can also reflect inappropriately low VO2, suggesting that elevated ScvO2 alone does not necessarily exclude the need for therapeutic interventions. Regardless of ScvO2 values—low, normal, or high—it is most effective when assessed alongside ∆pv-aCO2 [27]. Although lactate is a commonly used indicator, it does not always accurately represent tissue hypoxia or anaerobic metabolism, as nonhypoxic processes can also elevate lactate levels. Hence, lactate should be considered in conjunction with other parameters [28].
CO2 measurements offer deeper insights into macro- and micro-hemodynamics than O2 parameters and respond more rapidly than lactate [29]. As a metabolic byproduct of the Krebs cycle, increased tissue CO2 during aerobic metabolism suggests heightened oxidative activity or elevated carbohydrate intake [30]. Conversely, elevated CO2 can also indicate increased anaerobic metabolism [28,31]. ∆pv-aCO2, which is calculated from central venous and arterial blood gas analyses, represents the difference between venous and arterial partial pressures of CO2. Its normal range is 2–6 mm Hg [32]. Variations in ∆pv-aCO2 are primarily influenced by changes in blood flow rather than tissue hypoxia. Elevated ∆pv-aCO2 typically reflects decreased tissue perfusion, assuming adequate O2 delivery is maintained [33]. According to Fick's equation applied to CO2 metabolism, CO2 elimination depends on the difference between venous CO2 content (CvCO2) and arterial CO2 content (CaCO2), multiplied by cardiac output (CO): (CvCO2 – CaCO2) × CO [34]. Consequently, the primary determinant of ∆pv-aCO2 variations is CO, with an inverse proportional relationship [34]. Even with low CO, hyperventilation may maintain a normal or reduced ∆pv-aCO2. Consequently, ∆pv-aCO2 serves as a practical bedside marker of CO and microcirculatory blood flow. Research indicates that in hypoxic hypoxia, ∆pv-aCO2 remains below 6 mm Hg [29]. Conversely, ischemic hypoxia, characterized by reduced blood flow without altered arterial O2 pressure, elevates ∆pv-aCO2 above 6 mm Hg [29]. Hemodynamic monitoring using BGA has long provided bedside diagnostic capabilities, enabling timely and effective interventions, and will continue to be valuable. No single hemodynamic monitoring method—static or dynamic—is perfect, as measurement interpretation and clinical decision-making remain operator-dependent, each approach presenting distinct advantages and limitations. Unlike sophisticated monitoring devices, blood gas analyzers are broadly available in hospitals, making them highly practical tools for evaluating circulatory status. Thus, utilizing BGA for hemodynamic monitoring effectively informs diagnosis and therapy.
VBGA is an increasingly valuable alternative to ABGA, offering a less invasive, safer, and more practical method for evaluating acid-base balance and ventilation in critically ill patients. While ABGA remains indispensable for precise oxygenation assessment, VBGA reliably measures pH, pCO2, and HCO3–, making it particularly beneficial in emergency and intensive care settings. VBGA’s ease of sampling, reduced complication risk, and suitability for repeated measurements enhance workflow efficiency and patient comfort. As clinical practice continues to evolve, integrating VBGA alongside ABGA will optimize patient management by balancing diagnostic accuracy with clinical practicality, ultimately enhancing patient outcomes.
▪ Arterial blood gas (ABG) and venous blood gas (VBG) analyses are critical diagnostic tools in intensive care, each possessing distinct advantages and limitations that should be carefully considered.
▪ ABG is crucial for the accurate assessment of oxygenation and ventilation, yet it is invasive and carries procedural risks.
▪ In contrast, VBG is less invasive, allowing more frequent monitoring, but is limited in evaluating specific clinical parameters, notably oxygenation status.
▪ Integrating ABG and VBG according to individual patient needs in the intensive care unit can minimize invasive procedures while ensuring effective and timely clinical decision-making.

CONFLICT OF INTEREST

No potential conflict of interest relevant to this article was reported.

FUNDING

None.

ACKNOWLEDGMENTS

None.

AUTHOR CONTRIBUTIONS

All the work was done by GRL.

Figure 1.
Chest radiograph showing the position of a central venous catheter in the superior vena cava, which is used for measuring central venous oxygen saturation (ScvO2) as part of hemodynamic monitoring.
acc-000900f1.jpg
Table 1.
Comparison between ABGA and VBGA
Category ABGA VBGA
Sampling site Artery (radial, femoral, etc.) Peripheral or central vein
Invasiveness More invasive, more painful Less invasive, less painful
Oxygenation information Accurate (PaO2, SaO2) Limited, unreliable
pCO2 Accurate; reflects ventilation Differs from that in arterial blood by approximately 2 to 6 mm Hg
pH & HCO3– Standard values Slightly lower or comparable; can be estimated
Indication Essential for respiratory failure, acid-base imbalance Used in emergencies or if central access available
Emergency use Gold standard Possible alternative with limitations

ABGA: arterial blood gas analysis; VBGA: venous blood gas analysis; PaO2: partial pressure of oxygen; SaO2: saturation of oxygen; pCO2: partial pressure of carbon dioxide; HCO3–: bicarbonate.

  • 1. Okeson GC, Wulbrecht PH. The safety of brachial artery puncture for arterial blood sampling. Chest 1998;114:748-51.ArticlePubMed
  • 2. Giner J, Casan P, Belda J, González M, Miralda RM, Sanchis J. Pain during arterial puncture. Chest 1996;110:1443-5.ArticlePubMed
  • 3. Eisen LA, Minami T, Berger JS, Sekiguchi H, Mayo PH, Narasimhan M. Gender disparity in failure rate for arterial catheter attempts. J Intensive Care Med 2007;22:166-72.ArticlePubMedPDF
  • 4. Rang LC, Murray HE, Wells GA, Macgougan CK. Can peripheral venous blood gases replace arterial blood gases in emergency department patients? CJEM 2002;4:7-15.ArticlePubMed
  • 5. Chu YC, Chen CZ, Lee CH, Chen CW, Chang HY, Hsiue TR. Prediction of arterial blood gas values from venous blood gas values in patients with acute respiratory failure receiving mechanical ventilation. J Formos Med Assoc 2003;102:539-43.PubMed
  • 6. Ak A, Ogun CO, Bayir A, Kayis SA, Koylu R. Prediction of arterial blood gas values from venous blood gas values in patients with acute exacerbation of chronic obstructive pulmonary disease. Tohoku J Exp Med 2006;210:285-90.ArticlePubMed
  • 7. Kelly AM. The case for venous rather than arterial blood gases in diabetic ketoacidosis. Emerg Med Australas 2006;18:64-7.ArticlePubMed
  • 8. Bilan N, Behbahan AG, Khosroshahi AJ. Validity of venous blood gas analysis for diagnosis of acid-base imbalance in children admitted to pediatric intensive care unit. World J Pediatr 2008;4:114-7.ArticlePubMedPDF
  • 9. O'Connor TM, Barry PJ, Jahangir A, Finn C, Buckley BM, El-Gammal A. Comparison of arterial and venous blood gases and the effects of analysis delay and air contamination on arterial samples in patients with chronic obstructive pulmonary disease and healthy controls. Respiration 2011;81:18-25.ArticlePubMedPDF
  • 10. Malinoski DJ, Todd SR, Slone S, Mullins RJ, Schreiber MA. Correlation of central venous and arterial blood gas measurements in mechanically ventilated trauma patients. Arch Surg 2005;140:1122-5.ArticlePubMed
  • 11. Toftegaard M, Rees SE, Andreassen S. Correlation between acid-base parameters measured in arterial blood and venous blood sampled peripherally, from vena cavae superior, and from the pulmonary artery. Eur J Emerg Med 2008;15:86-91.ArticlePubMed
  • 12. Treger R, Pirouz S, Kamangar N, Corry D. Agreement between central venous and arterial blood gas measurements in the intensive care unit. Clin J Am Soc Nephrol 2010;5:390-4.ArticlePubMedPMC
  • 13. Walkey AJ, Farber HW, O'Donnell C, Cabral H, Eagan JS, Philippides GJ. The accuracy of the central venous blood gas for acid-base monitoring. J Intensive Care Med 2010;25:104-10.ArticlePubMedPDF
  • 14. Brandenburg MA, Dire DJ. Comparison of arterial and venous blood gas values in the initial emergency department evaluation of patients with diabetic ketoacidosis. Ann Emerg Med 1998;31:459-65.ArticlePubMed
  • 15. Yildizdaş D, Yapicioğlu H, Yilmaz HL, Sertdemir Y. Correlation of simultaneously obtained capillary, venous, and arterial blood gases of patients in a paediatric intensive care unit. Arch Dis Child 2004;89:176-80.ArticlePubMedPMC
  • 16. Bloos F, Reinhart K. Venous oximetry. Intensive Care Med 2005;31:911-3.ArticlePubMedPDF
  • 17. Saugel B, Malbrain ML, Perel A. Hemodynamic monitoring in the era of evidence-based medicine. Crit Care 2016;20:401.ArticlePubMedPMCPDF
  • 18. Ince C. Hemodynamic coherence and the rationale for monitoring the microcirculation. Crit Care 2015;Suppl 3(Suppl 3):S8.ArticlePubMedPMCPDF
  • 19. Ospina-Tascón GA, Umaña M, Bermúdez WF, Bautista-Rincón DF, Valencia JD, Madriñán HJ, et al. Can venous-to-arterial carbon dioxide differences reflect microcirculatory alterations in patients with septic shock? Intensive Care Med 2016;42:211-21.ArticlePubMedPMCPDF
  • 20. Wang J, Weng L, Xu J, Du B. Blood gas analysis as a surrogate for microhemodynamic monitoring in sepsis. World J Emerg Med 2023;14:421-7.ArticlePubMedPMC
  • 21. Molnar Z, Nemeth M. Monitoring of tissue oxygenation: an everyday clinical challenge. Front Med (Lausanne) 2018;4:247.ArticlePubMedPMC
  • 22. Edwards JD, Mayall RM. Importance of the sampling site for measurement of mixed venous oxygen saturation in shock. Crit Care Med 1998;26:1356-60.ArticlePubMed
  • 23. Walley KR. Use of central venous oxygen saturation to guide therapy. Am J Respir Crit Care Med 2011;184:514-20.ArticlePubMed
  • 24. Lorente JA, Renes E, Gómez-Aguinaga MA, Landín L, de la Morena J, Liste D. Oxygen delivery-dependent oxygen consumption in acute respiratory failure. Crit Care Med 1991;19:770-5.ArticlePubMed
  • 25. Tánczos K, Molnár Z. The oxygen supply-demand balance: a monitoring challenge. Best Pract Res Clin Anaesthesiol 2013;27:201-7.ArticlePubMed
  • 26. van Beest P, Wietasch G, Scheeren T, Spronk P, Kuiper M. Clinical review: use of venous oxygen saturations as a goal - a yet unfinished puzzle. Crit Care 2011;15:232.ArticlePubMedPMC
  • 27. Mesquida J, Saludes P, Gruartmoner G, Espinal C, Torrents E, Baigorri F, et al. Central venous-to-arterial carbon dioxide difference combined with arterial-to-venous oxygen content difference is associated with lactate evolution in the hemodynamic resuscitation process in early septic shock. Crit Care 2015;19:126.ArticlePubMedPMCPDF
  • 28. Ospina-Tascón GA, Umaña M, Bermúdez W, Bautista-Rincón DF, Hernandez G, Bruhn A, et al. Combination of arterial lactate levels and venous-arterial CO2 to arterial-venous O2 content difference ratio as markers of resuscitation in patients with septic shock. Intensive Care Med 2015;41:796-805.ArticlePubMedPMCPDF
  • 29. Waldauf P, Jiroutkova K, Duska F. Using pCO2 gap in the differential diagnosis of hyperlactatemia outside the context of sepsis: a physiological review and case series. Crit Care Res Pract 2019;2019:5364503.ArticlePubMedPMCPDF
  • 30. Doyle J, Cooper JS. Physiology, carbon dioxide transport [Internet]. StatPearls Publishing; 2025 [cited 2025 May 15]. Available from: https://pubmed.ncbi.nlm.nih.gov/30422582
  • 31. Saludes P, Proença L, Gruartmoner G, Enseñat L, Pérez-Madrigal A, Espinal C, et al. Central venous-to-arterial carbon dioxide difference and the effect of venous hyperoxia: a limiting factor, or an additional marker of severity in shock? J Clin Monit Comput 2017;31:1203-11.ArticlePubMedPDF
  • 32. Dres M, Monnet X, Teboul JL. Hemodynamic management of cardiovascular failure by using PCO2 venous-arterial difference. J Clin Monit Comput 2012;26:367-74.ArticlePubMedPDF
  • 33. Mallat J, Vallet B. Difference in venous-arterial carbon dioxide in septic shock. Minerva Anestesiol 2015;81:419-25.PubMed
  • 34. Lamia B, Monnet X, Teboul JL. Meaning of arterio-venous PCO2 difference in circulatory shock. Minerva Anestesiol 2006;72:597-604.PubMed

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      Clinical applications of blood gas analysis: a comparative review of arterial and venous blood gas monitoring in critical care
      Acute Crit Care. 2025;40(2):153-159.   Published online May 30, 2025
      DOI: https://doi.org/10.4266/acc.000900
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    Clinical applications of blood gas analysis: a comparative review of arterial and venous blood gas monitoring in critical care
    Image
    Figure 1. Chest radiograph showing the position of a central venous catheter in the superior vena cava, which is used for measuring central venous oxygen saturation (ScvO2) as part of hemodynamic monitoring.

    Figure 1.

    Clinical applications of blood gas analysis: a comparative review of arterial and venous blood gas monitoring in critical care
    Category ABGA VBGA
    Sampling site Artery (radial, femoral, etc.) Peripheral or central vein
    Invasiveness More invasive, more painful Less invasive, less painful
    Oxygenation information Accurate (PaO2, SaO2) Limited, unreliable
    pCO2 Accurate; reflects ventilation Differs from that in arterial blood by approximately 2 to 6 mm Hg
    pH & HCO3– Standard values Slightly lower or comparable; can be estimated
    Indication Essential for respiratory failure, acid-base imbalance Used in emergencies or if central access available
    Emergency use Gold standard Possible alternative with limitations
    Table 1. Comparison between ABGA and VBGA

    ABGA: arterial blood gas analysis; VBGA: venous blood gas analysis; PaO2: partial pressure of oxygen; SaO2: saturation of oxygen; pCO2: partial pressure of carbon dioxide; HCO3–: bicarbonate.

    Table 1.

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