Next Article in Journal
Comparison of Total Antioxidant Capacity in COPD, Asthma, and Asthma–COPD Overlap Patients
Previous Article in Journal
Ultrasonographic Assessment of Meniscus Damage in the Context of Clinical Manifestations
 
 
Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
Journals
Medicina
Volume 61
Issue 8
10.3390/medicina61081337
medicina-logo
Submit to this Journal Review for this Journal Propose a Special Issue
► Article Menu

Article Menu

share Share announcement Help format_quote Cite question_answer Discuss in SciProfiles
first_page
settings
Order Article Reprints
Font Type:
Arial Georgia Verdana
Font Size:
Aa Aa Aa
Line Spacing:
Column Width:
Background:
Review

The Role of Venous Blood Gas Analysis in Critical Care: A Narrative Review

by
Dario Giani
1,
Michele Cosimo Santoro
2,*,
Maurizio Gabrielli
1,
Roberta Di Luca
2,
Martina Malaspina
2,
Maria Lumare
2,
Licia Antonella Scatà
2,
Martina Pala
2,
Alberto Manno
2,
Marcello Candelli
2,
Marcello Covino
2,
Antonio Gasbarrini
1 and
Francesco Franceschi
2
1
Department of Medical and Surgical Sciences, Fondazione Policlinico Universitario A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, 00168 Rome, Italy
2
Department of Emergency, Anesthesiological and Reanimation Sciences, Fondazione Policlinico Universitario A. Gemelli IRCCS, Università Cattolica del Sacro Cuore, 00168 Rome, Italy
*
Author to whom correspondence should be addressed.
Medicina 2025, 61(8), 1337; https://doi.org/10.3390/medicina61081337
Submission received: 27 May 2025 / Revised: 6 July 2025 / Accepted: 21 July 2025 / Published: 24 July 2025
(This article belongs to the Section Intensive Care/ Anesthesiology)
Review Reports Versions Notes

Abstract

ABG analysis is the gold standard for assessing acid–base balance, oxygenation, and ventilation in critically ill patients, but it is invasive and associated with patient discomfort and potential complications. Venous blood gas (VBG) analysis offers a less invasive alternative, although its clinical utility remains debated. This review evaluates the current evidence on VBG analysis, exploring its correlation with ABG, clinical applications, and limitations. Studies show a strong correlation between ABG and VBG for pH and a good correlation for bicarbonate and base excess in most cases, while the correlation for pCO2 remains controversial. Predictably, pO2 values differ significantly due to oxygen consumption gradients between the arterial and venous blood. VBG analysis is especially valuable for initial assessments, monitoring therapeutic responses, and guiding resuscitation in intensive care settings. It is not merely an alternative to ABG but a complementary tool that can provide unique insights, such as mixed venous oxygen saturation (SvO2) or indices that require combined ABG and VBG data, like the pCO2 gap. This review highlights the diagnostic equivalence of VBG in appropriate contexts and advocates for its use when arterial sampling is unnecessary or impractical. Furthermore, VBG analysis could enhance patient care by enabling the timely, less invasive assessment of hemodynamic and metabolic conditions. Future research should focus on refining interpretation algorithms and expanding the clinical applications of VBG to fully realize its potential in critical care practice.

1. Introduction

ABG analysis is currently considered the gold standard for measuring blood gases O2, and CO2. It is the test of choice for assessing oxygenation, ventilation, and acid–base status in acute or critically ill patients. Consequently, point-of-care blood gas analyzers have become a standard tool in critical care settings, particularly in the Emergency Department [1,2]. However, obtaining an arterial blood sample requires a procedure that is often painful for the patient and carries potential complications, such as thrombosis, ischemia, rupture, pseudoaneurysm, as well as the risk of needlestick injury to the operator. VBG analysis offers a less invasive alternative, though its clinical utility remains debated.
The aim of this review is to evaluate the current evidence on the utility of VBG, assessing its correlation with ABG, clinical applications, and limitations. An in-depth discussion of the pathophysiological basis of the presented data is also provided in order to support the use of VBG as a practical tool, not only as an alternative to arterial blood, but also as a complement to it in specific clinical settings.

2. The Literature Research

We conducted a review of the medical literature from the past 10 years to identify studies and reports on the clinical use of mixed, central, and peripheral venous blood in critically ill patients. The following electronic databases were searched: PubMed®, MEDLINE®, Scopus®, and the Cochrane Library®, using the following search terms:
  • ‘Venous blood gas analysis’ AND ‘Emergency Department’;
  • ‘Venous blood gas analysis’ AND ‘Critical Care’;
  • ‘Venous blood gas analysis’ AND ‘ICU (Intensive Care Unit)’.
This search yielded English-language articles, and it was primarily focused on reviews, systematic reviews, meta-analyses, abstracts, and clinical trials. Article selection was conducted independently by two reviewers (MCS and DG). Additionally, a manual search of the reference lists of the selected articles was performed to identify other potentially relevant studies. The results of this literature review are summarized in Table 1.
We did not assess the quality of the studies using validated tools due to the narrative nature of this review, which explores various aspects of the potential clinical utility of venous blood. In addition to systematic reviews and meta-analyses, we prioritized clinical studies with robust methodological designs, large sample sizes, and, when possible, more recent publication dates.

3. Differences in the Main Gas Analysis Parameters of Arterial and Venous Blood

Clinicians utilizing venous blood must be aware of the differences between arterial and venous blood gas values. Firstly, unlike arterial blood sampling, the site of venous sampling (e.g., peripheral or central venous catheter) significantly influences blood gas parameters—particularly oxygen and carbon dioxide values—which are affected by the local metabolic activity. Secondly, venous blood gas analysis does not simply serve as a substitute for arterial analysis but can also provide complementary information.
Under physiological conditions, electrolyte and hemoglobin levels are generally consistent between arterial and venous samples. Although pH and HCO3− values differ slightly, they remain largely comparable: venous blood typically has a pH approximately 0.04 units lower and a bicarbonate level about 1 mEq/L higher than arterial blood [3]. In contrast, carbon dioxide and especially oxygen values differ substantially between arterial and venous blood (see Table 2).
PH tends to show a more consistent agreement between arterial and venous blood, whereas bicarbonate demonstrates slightly less concordance. Combined with the heterogeneity of patient populations and sampling types (i.e., mixed, central, and peripheral venous blood), this may help explain why many studies report a lack of agreement between arterial and venous pCO2 values. Intuitively, based on the Henderson–Hasselbalch equation, when pH and bicarbonate show enough concordance, one would expect a corresponding agreement in pCO2. However, as previously noted, this is not consistently observed in the literature. Table 3 summarizes the differences in blood gas values between arterial and mixed, central, and peripheral venous samples in normal conditions [3,4,5].
So, in conclusion, these values are similar but not identical. In the following chapters, it is explained how to interpret them and how to use them in clinical practice.

4. Mixed, Central, and Peripheral Venous Blood

4.1. Central Mixed Venous Blood

As previously mentioned, the site of venous blood sampling significantly influences blood gas values, particularly pO2 and pCO2, due to their susceptibility to local metabolic activity. Among the different types of venous samples, mixed venous blood is considered the most representative of the entire body, as it results from the combination of blood returning from both the superior and inferior vena cava. It is collected via a catheter positioned in the pulmonary artery (Swan-Ganz catheter), where blood flows from the right ventricle. The normal reference values for blood gas analysis performed on mixed venous blood are shown in Table 3.
Given these characteristics, mixed venous blood is commonly used for venous oximetry, i.e., the measurement of SvO2, where “v” denotes venous. SvO2 is considered a surrogate marker of CO. Under normal physiological conditions, arterial oxygen saturation is approximately 100%, while mixed venous saturation is around 75% [6,7]. The remaining 25% reflects the amount of oxygen extracted by the tissues. In pathological states with hemodynamic instability, tissue oxygen extraction increases, resulting in lower SvO2, typically falling below 70–75%, so it can be used as a marker of cardiac output, as described in Section 5.1.
In intensive care settings where a pulmonary artery catheter is available, SvO2 is a widely used parameter to assess hemodynamic instability in conditions such as sepsis, heart failure, and the perioperative and postoperative periods of major surgery, particularly cardiac surgery. However, due to the declining use of pulmonary artery catheters in clinical practice, ScvO2 is now more commonly measured using central venous blood.
The mean differences between arterial and venous values for all studies included in the Byrne’s meta-analysis [8], along with their 95% confidence intervals, are summarized in Table 2. The mean arterial pH across studies ranged from 7.15 to 7.46, while mean venous pH values ranged from 7.10 to 7.43. The estimated mean difference between venous and arterial pH was 0.033, with venous values being lower and the difference statistically significant [9].
Regarding pCO2 and pO2, the results revealed a wide range of values. Mean arterial pCO2 values ranged from 29.6 to 75.9 mmHg, while the mean venous pCO2 values ranged from 34.9 to 82.5 mmHg. The estimated bias was −4.15 mmHg. Heterogeneity was substantial, indicating that most of the variability was due to differences between studies. A venous pCO2 value of 55 mmHg could correspond to an arterial pCO2 between 44.3 mmHg (within the normal range) and 57.4 mmHg (consistent with type 2 respiratory failure).
A random-effects meta-analysis further demonstrated wide variability in pO2 values. Mean arterial pO2 ranged from 55.4 to 146.5 mmHg, while mean venous pO2 values ranged from 33.1 to 107.1 mmHg. The differences between arterial and venous pO2 were substantial across all studies [5,10].

4.2. Central Venous Blood

Central venous blood is obtained via a CVC, which is inserted into a large-caliber vein leading to the right atrium—commonly the internal jugular, subclavian, or femoral vein. Compared to the Swan-Ganz catheter used to measure SmvO2, the placement of a CVC is a less invasive method for assessing venous oxygenation. The oxygen saturation measured from central venous blood is referred to as ScvO2 and it is a marker of cardiac output, as reported below, in Section 5.1.
In clinical practice, ScvO2 is often used as a surrogate for SvO2. Although blood gas values from central venous blood do not perfectly match those from mixed venous blood, several studies have demonstrated a reasonable agreement, with ScvO2 typically differing from SvO2 by approximately 5–10% (Table 3).
As noted by Janotka et al., under physiological conditions, SvO2 tends to be slightly higher (typically 75–70%) than ScvO2 (~70%). However, this relationship may reverse in critically ill patients with hemodynamic instability due to the preferential redistribution of blood flow to vital organs, such as the brain and heart, at the expense of peripheral tissues, a phenomenon known as “circulatory centralization” [6]. In such cases, differences of up to 18% between ScvO2 and SvO2 have been reported [6].
It is not recommended to assess ScvO2 using a CVC inserted via the femoral vein, as this accesses the inferior vena cava. The resulting measurement (SfvO2) has been shown to differ significantly from values obtained from subclavian or jugular venous blood. In 2015, Martí et al. demonstrated that, unlike lactate, SfvO2 does not correlate well with ScvO2 or SvO2 [7], and these findings have since been corroborated by other studies [11,12]. For example, after intubation, venous oxygen saturation measured from the internal jugular or subclavian veins typically rises significantly, whereas SfvO2 remains unchanged. This discrepancy is largely attributed to circulatory centralization during cardiovascular compromise, wherein vasoconstriction reduces blood flow to splanchnic and peripheral regions. As perfusion to organs like the brain and heart is prioritized, their oxygen extraction requirements diminish, thereby increasing ScvO2. In contrast, reduced oxygen delivery to peripheral and splanchnic regions necessitates greater tissue-level oxygen extraction, resulting in lower SfvO2 values. Thus, ScvO2 and SfvO2 cannot be considered interchangeable.

4.3. Peripheral Venous Blood

Until a few decades ago, research focused exclusively on the use of central and mixed venous blood. However, with the widespread adoption of pulse oximeters in clinical practice, an increasing number of studies have begun to investigate peripheral venous blood as well [13].
Despite this interest, peripheral venous blood differs from mixed or central venous blood, particularly due to its proximity to the microcirculation, which makes it significantly influenced by local metabolic activity. Recent studies have concluded that peripheral venous blood gas (VBG) analysis cannot replace arterial blood gas (ABG) analysis in patients with respiratory disorders. Nevertheless, Bloom et al. demonstrated that a venous pCO2 < 45 mm Hg effectively rules out arterial hypercapnia, with a negative predictive value of approximately 99%.
Therefore, peripheral venous blood can be used as a substitute for arterial blood to assess hemoglobin and electrolytes and for pH and bicarbonate levels—but only in the absence of respiratory disorders [8,14,15,16,17,18]. With regards to lactate, under physiological conditions, peripheral venous lactate levels tend to correlate well with arterial values. However, in pathological states, this concordance is not consistently observed. As the arterial blood composition is independent of the sampling site, it is generally recommended in clinical practice for lactate measurement. Nevertheless, recent studies have demonstrated good agreement between arterial and both central and peripheral venous lactate concentrations [19,20,21,22].
In clinical settings, several parameters are routinely employed to manage patients with cardiovascular compromise, such as those with cardiogenic or septic shock and associated organ dysfunction. However, the literature still lacks consensus on the optimal sample type for evaluating these parameters [16,17]. Currently, arterial and central venous blood are most used, though peripheral venous blood may hold promise as a reliable marker of tissue metabolism due to its proximity to the capillary bed.

5. Other Hemodynamic Blood Gas Analytical Indices

5.1. Venous Oxygen Saturation

Venous oxygen saturation measured in mixed (SvO2) or central (ScvO2) venous blood, but not in peripheral venous blood, is considered a surrogate marker of cardiac output [23,24,25,26]. The primary function of the cardiovascular system is to deliver an adequate supply of oxygen to tissues in order to meet the body’s metabolic demands. In cases of cardiovascular impairment, signs of tissue hypoxia may appear and, if prolonged, can progress to MODS and eventually to MOF. Evaluating the adequacy of tissue oxygenation in critically ill patients is therefore essential from both diagnostic and therapeutic standpoints.
The pathophysiological rationale for the clinical use of SvO2 is well described by Bloos et al. [27]. Under physiological conditions, arterial oxygen saturation (SaO2) is approximately 100%, while SvO2 in mixed or central venous blood is around 75%. The remaining 25% represents the oxygen extracted by tissues—termed oxygen extraction ratio (O2ER), calculated as SaO2 − SvO2.
If
  • CaO2 = 1.34 × Hb × SaO2;
  • CvO2 = 1.34 × Hb × SvO2;
  • VO2 = CO × (CaO2 − CvO2).
Then CO can be expressed as: CO = VO2/[1.34 × Hb × (SaO2 − SvO2)].
This equation demonstrates that oxygen consumption (VO2) is directly proportional to O2ER and therefore inversely proportional to SvO2. This is the reason SvO2 is used in clinical practice as a surrogate marker of cardiac output. Furthermore, the formula highlights that when cardiac output decreases, O2ER increases in an attempt to maintain oxygen consumption (VO2). However, O2ER can only increase up to a point, beyond which oxygen delivery (DO2) falls below the critical threshold, referred to as “critical DO2”, leading to anaerobic metabolism and lactate production. The value of critical DO2 varies among individuals and is reached more rapidly in frail patients or those with comorbidities [9].
SvO2 monitoring is commonly employed to evaluate the effects of various therapies, including mechanical ventilation, inotropic support, blood transfusions, and sedation. Achieving a normal SvO2 value (~75%) is often considered a therapeutic target. In the setting of hemodynamic compromise, SvO2 values below 75% are associated with a poor prognosis [27].
Unfortunately, while SvO2 is highly sensitive, it is not particularly specific. It can be influenced by a range of conditions, including both reduced oxygen delivery (e.g., low cardiac output, hypoxemia, and anemia) and increased oxygen consumption (e.g., fever, pain), even when DO2 is preserved. Conversely, SvO2 may appear deceptively normal in cases of low cardiac output if microcirculatory dysfunction prevents effective tissue oxygen extraction. This condition, commonly referred to as “cytopathic hypoxia” or “dysoxia,” is thought to be related to endothelial injury, glycocalyx degradation, or microvascular shunting. In such cases, SvO2 must be interpreted alongside other markers, particularly lactate levels, for accurate assessment [28].

5.2. Relationship Between Lactate and Venous Oxygen Saturation

Tissue hypoperfusion occurs when oxygen demand exceeds the body’s delivery capacity (DO2), as seen in sepsis and other critical conditions. Consequently, elevated blood lactate levels are commonly used for the prognostic stratification of critically ill patients, as they suggest a shift toward anaerobic metabolism secondary to inadequate oxygen delivery and result in lactic acid production.
However, lactate elevation is not a specific marker of hypoperfusion. Increased lactate levels may also be observed in the absence of tissue hypoxia, such as in diabetic ketoacidosis (due to an altered glucose metabolism) or during intense physical exertion in untrained individuals. Furthermore, lactate accumulation can occur in liver disease due to impaired hepatic clearance, and in states of elevated adrenergic activity. Catecholamines released during stress stimulate glycolysis, leading to excessive pyruvate production, which is then converted into lactate.
Thus, elevated lactate in septic patients may reflect either an increased adrenergic tone or hypoperfusion associated with organ dysfunction. Interestingly, recent studies have questioned the exclusively negative prognostic value of lactate elevation in sepsis, suggesting that it may also represent an adaptive response. In this view, elevated lactate levels could indicate adrenergic activation in response to a noxious insult, potentially associated with a more favorable prognosis in some cases [29,30].
Like SvO2, lactate is a highly sensitive but non-specific parameter. Therefore, their combined interpretation can be particularly valuable in the assessment and stratification of critically ill patients, especially in the context of sepsis. A decrease in SvO2, reflecting a reduced cardiac output, does not necessarily correspond to an immediate rise in lactate levels, as lactic acid is only produced when anaerobic metabolism is triggered, i.e., when DO2 drops below the so-called critical DO2 threshold. Conversely, SvO2 values may appear falsely reassuring in the presence of impaired tissue oxygen utilization, such as in the late stages of septic shock, where reduced cardiac output coexists with elevated lactate levels due to a cellular inability to extract or utilize oxygen effectively.

5.3. The pCO2 Gap: Pathophysiological Basis

In clinical practice, lactate is the most commonly used parameter to assess tissue hypoperfusion, while SvO2 is widely employed in intensive care units as a surrogate marker for reduced cardiac output. However, both lactate and SvO2 have limitations, as they may yield false positives or negatives. Therefore, the pCO2 gap has been introduced and is increasingly utilized to evaluate the hemodynamic status of critically ill patients.
The pCO2 gap, also referred to as the venous-arterial (or arterial-venous) pCO2 gap or Pv—aCO2, reflects the adequacy of the cardiovascular system in clearing CO2 produced by tissues. A reduced cardiac output leads to CO2 accumulation in the venous blood, resulting in an increased pCO2 gap. Several studies have demonstrated that a pCO2 gap > 6 mmHg is associated with a worse prognosis and should therefore be considered pathological [31,32]. The pCO2 gap is usually calculated using central venous blood, which is more accessible than mixed venous blood. A few studies suggest that peripheral venous blood might also be used [25,26], but current recommendations favor central venous sampling.
CO2 is a highly soluble gas generated by energy metabolism under both aerobic and anaerobic conditions. Glycolysis breaks down glucose into two molecules of pyruvate. In the presence of oxygen, pyruvate is converted into acetyl-CoA and enters the Krebs cycle, producing CO2. In the absence of oxygen, two types of fermentation occur:
  • Lactic fermentation: Pyruvate is converted into lactate with ATP hydrolysis and CO2 production. Lactate may accumulate or be reconverted to pyruvate once aerobic conditions are restored.
  • Alcoholic fermentation: Pyruvate is transformed into ethanol and CO2.
Regardless of the metabolic pathway, CO2 (or total CO2 content, CCO2) circulates in the blood in three forms:
  • Bicarbonate ion (HCO3−): Accounts for 90% of total CO2 in arterial blood, formed via the reaction CO2 + H2O → H2CO3 → H+ + HCO3−, catalyzed by carbonic anhydrase.
  • Dissolved in plasma: Represented by the partial pressure of CO2 (PaCO2), approximately 5% of the total CO2 in arterial blood.
  • Carbamino compounds: CO2 bound to hemoglobin (carbaminohemoglobin), constituting around 1–5% of the total CO2 in arterial blood.
Under physiological conditions, the total CO2 in arterial blood is approximately 490 mL/L (PaCO2 ~40 mmHg), while in venous blood it is about 535 mL/L (PvCO2 ~42–45 mmHg). Thus, the normal arterial-venous CO2 gap ranges from 2 to 5 mmHg.
Applying Fick’s principle to CO2 production (VCO2), the arteriovenous pCO2 gap can be expressed as a function of cardiac output (CO). Given that
  • VCO2 = CO × (CaCO2 − CvCO2);
  • PaCO2 − PvCO2 = K × (CaCO2 − CvCO2);
  • Then:
  • VCO2 = CO × K × (PaCO2 − PvCO2);
  • Therefore: (PaCO2 − PvCO2) = VCO2/(CO × K).
From this equation, an inverse relationship between CO and the pCO2 gap can be deduced. However, the constant K is influenced by several factors, so the relationship is not strictly proportional. Despite these limitations, numerous studies have confirmed that a pCO2 gap > 6 mmHg is a reliable hemodynamic marker, particularly in the context of reduced CO [9,32] and a poor prognosis [33].
The relationship between CO and the arteriovenous CO2 gap indicates that a marked increase in the pCO2 gap occurs only with a significant decrease in CO—typically below 2–3 L/min, and more notably under 1–2 L/min [33,34,35].
Several physiological factors can influence the constant K and affect the pCO2 gap.
Haldane Effect: As PaO2 increases (e.g., due to oxygen therapy), PaCO2 decreases, since oxygenated hemoglobin binds less CO2. Conversely, hypoxemia increases the CO2 binding to hemoglobin, reducing PaCO2 levels.
pH: Changes in bicarbonate (HCO3−) levels alter the CO2 content. In metabolic acidosis, PaCO2 tends to be lower, while in alkalosis, it increases.
Hematocrit: Higher hematocrit reduces the plasma volume available for bicarbonate buffering, decreasing PaCO2 relative to total CO2.
Temperature: Lower temperatures increase CO2 solubility, resulting in a higher PaCO2 relative to CCO2.
These factors shift the CO2–CCO2 curve to the right under conditions such as hyperoxia, metabolic acidosis, hemoconcentration, and hypothermia, increasing the proportion of dissolved CO2 relative to total CO2 [9,36].

5.3.1. The pCO2 Gap in Clinical Practice

Several studies support the clinical utility of the pCO2 gap for the following reasons:
  • It is inversely related to CO in animal models of hemorrhage, hypovolemia, and obstructive shock, like an intermediate-high risk pulmonary embolism [37,38];
  • Persistent elevation after fluid resuscitation in septic shock correlates with a poor prognosis [39];
  • It serves as an early and sensitive marker of impaired venous return [33];
  • It predicts a 28-day mortality in patients with sepsis and organ dysfunction [40];
  • Serial measurements can help monitor therapy effectiveness and guide fluid management when lactate levels remain high but the pCO2 gap is normal [38,41].
Thus, combining ScvO2, lactate (LAC), and the pCO2 gap can enhance diagnostic and therapeutic strategies in hemodynamically unstable patients [42]. For example, elevated lactate (>2 mmol/L) with normal ScvO2 (70–75%) and a normal pCO2 gap (<6 mmHg) indicates dysoxia—impaired oxygen utilization at the tissue level—rather than circulatory failure, as seen in conditions like anemia.
In sepsis, the pCO2 gap may be an earlier indicator of severe hemodynamic compromise than lactate, which only increases when compensatory mechanisms (e.g., O2 extraction) are exhausted. A Pv–aCO2 gap > 6 mmHg, even with normal lactate, is significantly associated with mortality [43]. Moreover, a persistently elevated Pv–aCO2 gap after lactate normalization suggests ongoing hemodynamic dysfunction and predicts poor outcomes. Retrospective studies have also linked elevated postoperative Pv-aCO2 gaps to major complications and mortality after cardiac surgery, though diagnostic performance remains limited [44,45].

5.3.2. Limitations of the pCO2 Gap

As previously discussed, pCO2 is a valuable parameter in hemodynamic monitoring. However, it presents several important limitations. For example: (a) Its interpretation can be misleading in cases of impaired microcirculatory flow or altered CO2 production, such as in distributive shock (e.g., anaphylactic shock), where reduced capillary density results in heterogeneous perfusion despite normal cardiac output (CO) and an elevated pCO2 gap; (b) as demonstrated by Bakker et al. [46], the pCO2 gap in patients with septic shock is primarily influenced by cardiac output and also by the degree of pulmonary dysfunction. Although the pCO2 gap is typically larger in non-survivors, its prognostic value remains modest.
Most studies have relied on mixed or central venous blood, and data regarding the clinical utility of peripheral venous samples for pCO2 gap measurement are limited. Nonetheless, recent research suggests a good level of agreement between peripheral and mixed venous values [47]. However, to date, no studies have validated the use of the pCO2 gap derived from peripheral venous blood for monitoring the hemodynamic status of critically ill patients. Further research is therefore needed before this approach can be routinely implemented in clinical practice.

5.4. Ratio of the pCO2 Gap to the Arteriovenous O2 Content Difference (pCO2 Gap/Ca-vO2 Gap)

Lactate is a widely used marker of hypoperfusion, reflecting anaerobic metabolism due to reduced oxygen delivery (DO2). However, lactate elevation can also result from adrenergic stimulation. This dual origin complicates interpretation in septic patients. Thus, additional tools are needed, such as the ratio between the pCO2 gap and the arteriovenous O2 content difference (pCO2 gap/Ca-vO2 gap), which may better reflect anaerobic metabolism [48].
This ratio is derived from the respiratory quotient (RQ = VCO2/VO2), which is approximately one under normal conditions, as O2 consumption matches CO2 production. In anaerobic states, VO2 decreases disproportionately to VCO2, leading to an RQ > 1. A ratio > 1.4 has been associated with anaerobic metabolism in various studies. In practice, elevated lactate combined with a pCO2 gap/Ca-vO2 gap > 1.4 indicates a true anaerobic metabolism (i.e., DO2 deficit), whereas a ratio close to one suggests a lactate increase due to adrenergic stimulation.
These insights may guide therapy, although further studies are needed to determine the ratio’s utility in interpreting lactate dynamics in sepsis and tailoring interventions [49,50].

6. Conclusions

Venous blood gas analysis provides not only an alternative but also complementary information to the arterial blood gas analysis. In conclusion, we propose the following recommendations for clinical use:
  • Central venous blood can be used to evaluate ScvO2 as a surrogate for SvO2 measured from mixed venous blood, with a reasonable agreement of approximately 85–90%, and to assess the pCO2 gap in conjunction with the arterial blood gas analysis.
  • Peripheral venous blood is suitable for assessing hemoglobin and electrolytes and for evaluating pH and bicarbonate levels, but only in the absence of respiratory disorders.
  • Arterial blood gas analysis remains the gold standard in critically ill patients for evaluating hemoglobin, electrolytes, lactate, and the acid–base balance, particularly in the presence of respiratory dysfunction.
Table 4 summarizes the practical applications of different blood sample types in critically ill patients.
Peripheral venous lactate shows a good agreement with arterial levels under normal conditions, but this correlation is less consistent in acute illness. Nonetheless, recent evidence suggests central and peripheral venous lactate may be comparable to arterial lactate [19] and a recent review highlights peripheral venous as a reliable marker of metabolic derangements due to its proximity to the capillary exchange [51].
The arteriovenous CO2 gap, measured from mixed or central venous blood, is a non-invasive tool for hemodynamic monitoring. It is inversely correlated with CO and can identify early cardiovascular compromise, particularly before DO2 becomes critically low and lactate rises. Data on the peripheral venous pCO2 gap remain limited [52,53], but it could become a useful and easily accessible tool for assessing hemodynamics in critically ill patients without central venous access.
Given that neither the pCO2 gap nor lactate alone reliably reflects anaerobic metabolism or hypoperfusion in all scenarios, the pCO2 gap/Ca-vO2 gap ratio has emerged as a promising marker of anaerobic conditions in critically ill patients. More research is needed to assess its clinical usefulness in guiding therapy and interpreting lactate trends in sepsis.

Author Contributions

Conceptualization, D.G., M.C.S., M.M. and M.C. (Marcello Candelli); methodology, M.P., A.M. and M.C. (Marcello Candelli); resources, R.D.L., M.M., M.L. and A.M.; writing—original draft preparation, D.G., M.C.S., M.G. and R.D.L.; writing—review and editing, M.C. (Marcello Covino), A.G. and F.F.; visualization, M.L., L.A.S. and M.P.; supervision, M.G., M.C. (Marcello Covino), A.G. and F.F. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Conflicts of Interest

The authors declare no conflicts of interest.

Abbreviations

The following abbreviations are used in this manuscript:
ABGarterial blood gas
CaO2arterial content of oxygen
CvO2venous content of oxygen
CaO2 − CvO2 (or Ca–vO2 gap)arterial-venous O2 content difference
CCO2total content of CO2
COcardiac output
CO2carbon dioxide
CVCcentral venous catheter
DO2delivery of oxygen
MODSmultiple organ dysfunction
MOFmultiple organ failure
O2oxygen
O2ERoxygen extraction rate
pCO2partial CO2 pressure (not specified whether arterial or venous)
PaCO2arterial partial CO2 pressure
PvCO2venous partial CO2 pressure
pO2partial O2 pressure (not specified whether arterial or venous)
PaO2arterial partial O2 pressure
pCO2 gap or Pv–aCO2venous-arterial CO2 pressure difference
RQrespiratory quotient
SO2oxygen saturation (not specified whether arterial or venous)
SaO2arterial O2 saturation
SvO2venous O2 saturation (generic term)
ScvO2central venous O2 saturation
SfvO2femoral venous O2 saturation
SmvO2mixed venous O2 saturation
SpvO2peripheral venous O2 saturation
VBGvenous blood gas
VO2O2 consumption

References

  1. Korpi-Steiner, N.; Horowitz, G.; Tesfazghi, M.; Suh-Lailam, B.B. Current Issues in Blood Gas Analysis. J. Appl. Lab. Med. 2023, 8, 372–381. [Google Scholar] [CrossRef] [PubMed]
  2. Giuliano, K.K.; Grant, M.E. Blood analysis at the point of care: Issues in application for use in critically ill patients. AACN Clin. Issues 2002, 13, 204–220. [Google Scholar] [CrossRef] [PubMed]
  3. Bijapur, M.B.; Kudligi, N.A.; Asma, S. Central Venous Blood Gas Analysis: An Alternative to Arterial Blood Gas Analysis for pH, PCO2, Bicarbonate, Sodium, Potassium and Chloride in the Intensive Care Unit Patients. Indian J. Crit. Care Med. 2019, 23, 258–262. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  4. Tahvanainen, J.; Meretoja, O.; Nikki, P. Can central venous blood replace mixed venous blood samples? Crit. Care Med. 1982, 10, 758–761. [Google Scholar] [CrossRef] [PubMed]
  5. Rang, L.C.; Murray, H.E.; Wells, G.A.; Macgougan, C.K. Can peripheral venous blood gases replace arterial blood gases in emergency department patients? CJEM 2002, 4, 7–15. [Google Scholar] [CrossRef] [PubMed]
  6. Janotka, M.; Ostadal, P. Biochemical markers for clinical monitoring of tissue perfusion. Mol. Cell Biochem. 2021, 476, 1313–1326. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  7. Marti, Y.N.; de Freitas, F.G.; de Azevedo, R.P.; Leão, M.; Bafi, A.T.; Machado, F.R. Is venous blood drawn from femoral access adequate to estimate the central venous oxygen saturation and arterial lactate levels in critically ill patients? Rev. Bras. Ter. Intensive 2015, 27, 340–346. [Google Scholar] [CrossRef] [PubMed]
  8. Byrne, A.L.; Bennett, M.; Chatterji, R.; Symons, R.; Pace, N.L.; Thomas, P.S. Peripheral venous and arterial blood gas analysis in adults: Are they comparable? A systematic review and meta-analysis. Respirology 2014, 19, 168–175. [Google Scholar] [CrossRef] [PubMed]
  9. Brandenburg, M.A.; Dire, D.J. Comparison of arterial and venous blood gas values in the emergency department and evaluation of patients with diabetic ketoacidosis. Ann. Emerg. Med. 1998, 31, 459–465. [Google Scholar] [CrossRef] [PubMed]
  10. Razi, E.; Moosavi, G. Comparison of arterial and venous blood gas analysis in patients with exacerbation of chronic obstructive pulmonary disease. Saudi Med. J. 2007, 28, 862–865. [Google Scholar] [PubMed]
  11. van Beest, P.A.; van der Schors, A.; Liefers, H.; Coenen, L.G.; Braam, R.L.; Habib, N.; Braber, A.; Scheeren, T.W.; Kuiper, M.A.; Spronk, P.E. Femoral venous oxygen saturation is no surrogate for central venous oxygen saturation. Crit. Care Med. 2012, 40, 3196–3201. [Google Scholar] [CrossRef] [PubMed]
  12. Davison, D.L.; Chawla, L.S.; Selassie, L.; Jones, E.M.; McHone, K.C.; Vota, A.R.; Junker, C.; Sateri, S.; Seneff, M.G. Femoral-based central venous oxygen saturation is not a reliable substitute for subclavian/internal jugular-based central venous oxygen saturation in patients who are critically ill. Chest 2010, 138, 76–83. [Google Scholar] [CrossRef] [PubMed]
  13. Zeserson, E.; Goodgame, B.; Hess, J.D.; Schultz, K.; Hoon, C.; Lamb, K.; Maheshwari, V.; Johnson, S.; Papas, M.; Reed, J.; et al. Correlation of venous blood gas and pulsi oximetry with arterial blood gas in undifferentiated critical ill patient. J. Intensive Care Med. 2018, 33, 176–181. [Google Scholar] [CrossRef] [PubMed]
  14. Ak, A.; Ogun, C.; Bayir, A.; Kayis, S.; Koylu, R. Prediction of arterial blood gas values in patients with acute exacerbation of chronic obstructive pulmonary disease. Tohoku J. Exp. Med. 2006, 210, 285–290. [Google Scholar] [CrossRef] [PubMed]
  15. Razi, E.; Nasiri, O.; Akbari, H.; Razi, A. Correlation of arterial blood gas measurements with venous blood gas values in mechanically ventilated patients. Tanaffos 2012, 11, 30–35. [Google Scholar] [PubMed] [PubMed Central]
  16. Gennis, P.R.; Skoron, M.L.; Gallagher, E.J. The usefulness of peripheral venous blood in estimating acid-base status in acutely ill patients. Ann. Emerg. Med. 1985, 14, 845–849. [Google Scholar] [CrossRef] [PubMed]
  17. Toftegaard, M.; Rees, S.; 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. [Google Scholar] [CrossRef] [PubMed]
  18. Bloom, B.M.; Grundlingh, J.; Bestwick, J.P.; Harris, T. The role of venous blood gas in the Emergency Department: A systematic review and meta-analysis. Eur. J. Emerg. Med. 2014, 21, 81–88. [Google Scholar] [CrossRef] [PubMed]
  19. Theerawit, P.; Na Petvicharn, C.; Tangsujaritvijit, V.; Sutherasan, Y. The Correlation Between Arterial Lactate and Venous Lactate in Patients With Sepsis and Septic Shock. J. Intensive Care Med. 2018, 33, 116–120. [Google Scholar] [CrossRef] [PubMed]
  20. Oi, Y.; Mori, K.; Yamagata, H.; Nogaki, A.; Takeda, T.; Watanabe, C.; Sakaguchi, Y.; Ogawa, F.; Abe, T.; Imaki, S.; et al. Peripheral venous lactate levels substitute arterial lactate levels in the emergency department. Int. J. Emerg. Med. 2022, 15, 7. [Google Scholar] [CrossRef]
  21. Browning, R.; Datta, D.; Gray, A.J.; Graham, C. Peripheral venous and arterial lactate agreement in septic patients in the emergency department: A pilot study. Eur. J. Emerg. Med. 2014, 21, 139–141. [Google Scholar] [CrossRef] [PubMed]
  22. Datta, D.; Grahamslaw, J.; Gray, A.J.; Graham, C.; Walker, C.A. Lactate—Arterial and Venous Agreement in Sepsis: A prospective observational study. Eur. J. Emerg. Med. 2018, 25, 85–91. [Google Scholar] [CrossRef] [PubMed]
  23. Lemoël, F.; Govciyan, S.; El Omri, M.; Marquette, C.H.; Levraut, J. Improving the validity of peripheral venous blood gas analysis as an estimate of arterial blood gas by correcting the venous values with SvO2. J. Emerg. Med. 2013, 44, 709–716. [Google Scholar] [CrossRef] [PubMed]
  24. Reinhart, K.; Rudolph, T.; Bredle, D.L.; Hannemann, L.; Cain, S.M. Comparison of central-venous to mixed-venous oxygen saturation during changes in oxygen supply/demand. Chest 1989, 95, 1216–1221. [Google Scholar] [CrossRef] [PubMed]
  25. Ramakrishna, M.N.; Hegde, D.P.; Kumaraswamy, G.N.; Gupta, R.; Girish, T.N. Correlation of mixed venous and central venous oxygen saturation and its relation to cardiac index. Indian J. Crit. Care Med. 2006, 10, 230–234. [Google Scholar] [CrossRef]
  26. Dueck, M.H.; Klimek, M.; Appenrodt, S.; Weigand, C.; Boerner, U. Trends but not individual values of central venous oxygen saturation agree with mixed venous oxygen saturation during varying hemodynamic conditions. Anesthesiology 2005, 103, 249–257. [Google Scholar] [CrossRef] [PubMed]
  27. Bloos, F.; Reinhart, K. Venous oximetry. Intensive Care Med. 2005, 31, 911–913. [Google Scholar] [CrossRef] [PubMed]
  28. Fink, M.P. Cytopathic hypoxia. Is oxygen use impaired in sepsis as a result of an acquired intrinsic derangement in cellular respiration? Crit. Care Clin. 2002, 18, 165–175. [Google Scholar] [CrossRef] [PubMed]
  29. Garcia-Alvarez, M.; Marik, P.; Bellomo, R. Sepsis-associated hyperlactatemia. Crit. Care 2014, 18, 503. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  30. Garcia-Alvarez, M.; Marik, P.; Bellomo, R. Stress hyperlactatemia: Present understanding and controversy. Lancet Diabetes Endocrinol. 2014, 2, 339–347. [Google Scholar] [CrossRef] [PubMed]
  31. Dres, M.; Monnet, X.; Teboul, J.L. Hemodynamic management of cardiovascular failure by using PCO(2) venous-arterial difference. J. Clin. Monitor Comput. 2012, 26, 367–374. [Google Scholar] [CrossRef] [PubMed]
  32. Guo, Z.; Yin, M.; Kong, J.; Wang, B.; Dai, K.; Zuo, T.; Yu, G.; Bao, Y. Relationship Analysis of Central Venous-to-arterial Carbon Dioxide Difference and Cardiac Index for Septic Shock. Sci. Rep. 2019, 9, 8822. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  33. Ospina-Tascón, G.A.; Umaña, M.; Bermúdez, W.F.; Bautista-Rincón, D.F.; Valencia, J.D.; Madriñán, H.J.; Hernandez, G.; Bruhn, A.; Arango-Dávila, C.; De Backer, D. Can venous-to-arterial carbon dioxide differences reflect microcirculatory alterations in patients with septic shock? Intensive Care Med. 2016, 42, 211–221. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  34. Mallat, J.; Lemyze, M.; Tronchon, L.; Vallet, B.; Thevenin, D. Use of venous-to-arterial carbon dioxide tension difference to guide resuscitation therapy in septic shock. World J. Crit. Care Med. 2016, 5, 47–56. [Google Scholar] [CrossRef] [PubMed]
  35. van Beest, P.A.; Lont, M.C.; Holman, N.D.; Loef, B.; Kuiper, M.A.; Boerma, E.C. Central venous-arterial pCO(2) difference as a tool in resuscitation of septic patients. Intensive Care Med. 2013, 39, 1034–1039. [Google Scholar] [CrossRef] [PubMed]
  36. Pinsky, M.R.; Cecconi, M.; Chew, M.S.; De Backer, D.; Douglas, I.; Edwards, M.; Hamzaoui, O.; Hernandez, G.; Martin, G.; Monnet, X.; et al. Effective hemodynamic monitoring. Crit. Care 2022, 26, 294. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  37. Yuriditsky, E.; Zhang, R.S.; Bakker, J.; Horowitz, J.M.; Zhang, P.; Bernard, S.; Greco, A.A.; Postelnicu, R.; Mukherjee, V.; Hena, K.; et al. Relationship between the mixed venous-to-arterial carbon dioxide gradient and the cardiac index in acute pulmonary embolism. Eur. Heart J. Acute Cardiovasc. Care 2024, 13, 493–500. [Google Scholar] [CrossRef] [PubMed]
  38. Zhang, H.; Vincent, J.L. Arteriovenous differences in PCO2 and pH are good indicators of critical hypoperfusion. Am. Rev. Respir. Dis. 1993, 148 Pt 1, 867–871. [Google Scholar] [CrossRef] [PubMed]
  39. Ospina-Tascón, G.A.; Bautista-Rincón, D.F.; Umaña, M.; Tafur, J.D.; Gutiérrez, A.; García, A.F.; Bermúdez, W.; Granados, M.; Arango-Dávila, C.; Hernández, G. Persistently high venous-to-arterial carbon dioxide differences during early resuscitation are associated with poor outcomes in septic shock. Crit. Care 2013, 17, R294. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  40. Jiang, L.; Wang, Z.; Wang, L.; Liu, Y.; Chen, D.; Zhang, D.; Shi, X.; Xiao, D. Predictive value of the serum anion gap for 28-day in-hospital all-cause mortality in sepsis patients with acute kidney injury: A retrospective analysis of the MIMIC-IV database. Ann. Transl. Med. 2022, 10, 1373. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  41. Nassar, B.; Badr, M.; Van Grunderbeeck, N.; Temime, J.; Pepy, F.; Gasan, G.; Tronchon, L.; Thevenin, D.; Mallat, J. Central venous-to-arterial PCO2 difference as a marker to identify fluid responsiveness in septic shock. Sci. Rep. 2021, 11, 17256. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  42. Du, W.; Liu, D.W.; Wang, X.T.; Long, Y.; Chai, W.Z.; Zhou, X.; Rui, X. Combining central venous-to-arterial partial pressure of carbon dioxide difference and central venous oxygen saturation to guide resuscitation in septic shock. J. Crit. Care 2013, 28, e1–e5. [Google Scholar] [CrossRef] [PubMed]
  43. Ltaief, Z.; Schneider, A.G.; Liaudet, L. Pathophysiology and clinical implications of the veno-arterial PCO2gap. Crit Care 2021, 25, 318. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  44. Mukai, A.; Suehiro, K.; Kimura, A.; Funai, Y.; Matsuura, T.; Tanaka, K.; Yamada, T.; Mori, T.; Nishikawa, K. Comparison of the venous-arterial CO2 to arterial-venous O2 content difference ratio with the venous-arterial CO2 gradient for the predictability of adverse outcomes after cardiac surgery. J. Clin. Monit. Comput. 2020, 34, 41–53. [Google Scholar] [CrossRef] [PubMed]
  45. Huette, P.; Beyls, C.; Mallat, J.; Martineau, L.; Besserve, P.; Haye, G.; Guilbart, M.; Dupont, H.; Guinot, P.-G.; Diouf, M.; et al. Central venous-to-arterial CO2 difference is a poor tool to predict adverse outcomes after cardiac surgery: A retrospective study. Can. J. Anaesth. 2021, 68, 467–476. [Google Scholar] [CrossRef] [PubMed]
  46. Bakker, J.; Vincent, J.-L.; Gris, P.; Leon, M.; Coffernils, M.; Kahn, R.J. Veno-arterial carbon dioxide gradient in human septic shock. Chest 1992, 101, 509–515. [Google Scholar] [CrossRef] [PubMed]
  47. Orso, D.; Molinari, C.; Bacchetti, G.; Zanini, V.; Montanar, V.; Copetti, R.; Guglielmo, N.; Bove, T. Correlation and Agreement Between the CO2 Gap Obtained From Peripheral Venous Blood and From Mixed Venous Blood in Mechanically Ventilated Septic Patients. Semin. Cardiothorac. Vasc. Anesth. 2024, 28, 18–27. [Google Scholar] [CrossRef] [PubMed]
  48. Ospina-Tascón, G.A.; Hernández, G.; Cecconi, M. Understanding the venous-arterial CO2 to arterial-venous O2 content difference ratio. Intensive Care Med. 2016, 42, 1801–1804. [Google Scholar] [CrossRef] [PubMed]
  49. Mallat, J.; Lemyze, M.; Meddour, M.; Pepy, F.; Gasan, G.; Barrailler, S.; Durville, E.; Temime, J.; Vangrunderbeeck, N.; Tronchon, L.; et al. Ratios of central venous-to-arterial carbon dioxide content or tension to arteriovenous oxygen content are better markers of global anaerobic metabolism than lactate in septic shock patients. Ann. Intensive Care 2016, 6, 10. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  50. He, H.; Long, Y.; Liu, D.; Wang, X.; Tang, B. The Prognostic Value of Central Venous-to-Arterial CO2 Difference/Arterial-Central Venous O2 Difference Ratio in Septic Shock Patients with Central Venous O2 Saturation ≥80. Shock 2017, 48, 551–557. [Google Scholar] [CrossRef] [PubMed]
  51. Saberian, L.; Sharif, M.; Aarabi, M.; Broumand, B.; Shafiee, M.A. Arterial Versus Venous Blood Gas Analysis Comparisons, Appropriateness, and Alternatives in Different Acid/Base Clinical Settings: A Systematic Review. Cureus 2023, 15, e41707. [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  52. Gao, W.; Zhang, Y.; Ni, H.; Zhang, J.; Zhou, D.; Yin, L.; Zhang, F.; Chen, H.; Zhang, B.; Li, W. Prognostic value of difference between peripheral venous and arterial partial pressure of carbon dioxide in patients with septic shock: A pilot study. Nan Fang Yi Ke Da Xue Xue Bao 2018, 38, 1312–1317. (In Chinese) [Google Scholar] [CrossRef] [PubMed] [PubMed Central]
  53. Gao, W.; Zhu, Q.; Ni, H.; Zhang, J.; Zhou, D.; Yin, L.; Zhang, F.; Chen, H.; Zhang, B.; Li, W. Prognostic value of differences between peripheral arterial and venous blood gas analysis in patients with septic shock. Zhonghua Wei Zhong Bing Ji Jiu Yi Xue 2018, 30, 722–726. (In Chinese) [Google Scholar] [CrossRef] [PubMed]
Table 1. Results of the literature research; VBG = venous blood gas analysis; ED = Emergency Department; ICU = intensive care unit.
Table 1. Results of the literature research; VBG = venous blood gas analysis; ED = Emergency Department; ICU = intensive care unit.
VBG and ED VBG and CRITICAL CARE VBG and ICU
Abstract180308112
Review7285
Systematic review020
Systematic review and meta-analysis220
Clinical trial11239
Table 2. Difference between arterial and venous blood of pH, pCO2, HCO3−, and pO2, respectively, indicated as Δ(a-v) pH, Δ(a-v) pCO2, Δ(a-v) HCO3−, and Δ(a-v) pO2.
Table 2. Difference between arterial and venous blood of pH, pCO2, HCO3−, and pO2, respectively, indicated as Δ(a-v) pH, Δ(a-v) pCO2, Δ(a-v) HCO3−, and Δ(a-v) pO2.
Δ(a-v) pH~0.04 units
Δ(a-v) pCO2~6 mm Hg
Δ(a-v) HCO3−~1 mEq/L
Δ(a-v) pO2~55 mmHg
Table 3. Difference between arterial and mixed, central, and peripheral blood gas analysis in normal conditions.
Table 3. Difference between arterial and mixed, central, and peripheral blood gas analysis in normal conditions.
ParameterArterialMixed VenousCentral VenousPeripheral Venous
pH7.40 (7.35–7.45)7.36 (7.35–7.45)7.35–7.377.36 (7.29–7.45)
pO280–100 mmHg35–40 mmHg35–40 mmHg35–40 mmHg
SO295–100%~75%70–75% (lower due to cardiac and cerebral oxygen consumption)65–75% (variable)
pCO235–45 mmHg41–51 mmHg44–45 mmHg (range: 35–48)43–48 mmHg
HCO3−22–26 mmol/L23–29 mmol/L25 mmol/L (range: 22–27)25–26 mmol/L
Electrolytes, HemoglobinIdentical valuesIdentical valuesIdentical valuesIdentical values
Lactate0.5–1.8 mmol/LComparable under normal conditions; agreement is controversial in pathological statesSimilar to mixed venousSimilar to mixed venous
Table 4. Practical use of different blood samples in critically ill patients. Details are extensively discussed in the text. ✔: reliable; ✖: not reliable.
Table 4. Practical use of different blood samples in critically ill patients. Details are extensively discussed in the text. ✔: reliable; ✖: not reliable.
Arterial Blood Mixed Venous Blood Central Venous Blood Peripheral Venous Blood
pH✔✔✔✔
pO2✔✖✖✖
SO2✔✔ (useful for venous oxygen saturation)✔ (useful for venous oxygen saturation)✖
pCO2✔✖ (but useful for pCO2 gap)✖ (but useful for pCO2 gap)✖
HCO3−✔✔✔✔
Electrolytes, Hemoglobin✔✔✔✔
Lactate✔✔  (only in normal conditions) ✔  (only in normal conditions) ✔  (only in normal conditions)
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content.

Share and Cite

MDPI and ACS Style

Giani, D.; Santoro, M.C.; Gabrielli, M.; Di Luca, R.; Malaspina, M.; Lumare, M.; Scatà, L.A.; Pala, M.; Manno, A.; Candelli, M.; et al. The Role of Venous Blood Gas Analysis in Critical Care: A Narrative Review. Medicina 2025, 61, 1337. https://doi.org/10.3390/medicina61081337

AMA Style

Giani D, Santoro MC, Gabrielli M, Di Luca R, Malaspina M, Lumare M, Scatà LA, Pala M, Manno A, Candelli M, et al. The Role of Venous Blood Gas Analysis in Critical Care: A Narrative Review. Medicina. 2025; 61(8):1337. https://doi.org/10.3390/medicina61081337

Chicago/Turabian Style

Giani, Dario, Michele Cosimo Santoro, Maurizio Gabrielli, Roberta Di Luca, Martina Malaspina, Maria Lumare, Licia Antonella Scatà, Martina Pala, Alberto Manno, Marcello Candelli, and et al. 2025. "The Role of Venous Blood Gas Analysis in Critical Care: A Narrative Review" Medicina 61, no. 8: 1337. https://doi.org/10.3390/medicina61081337

APA Style

Giani, D., Santoro, M. C., Gabrielli, M., Di Luca, R., Malaspina, M., Lumare, M., Scatà, L. A., Pala, M., Manno, A., Candelli, M., Covino, M., Gasbarrini, A., & Franceschi, F. (2025). The Role of Venous Blood Gas Analysis in Critical Care: A Narrative Review. Medicina, 61(8), 1337. https://doi.org/10.3390/medicina61081337

Article Metrics

Back to TopTop