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Featured Articles: Narrative Review Article

Comparing Central Venous Blood Gas to Arterial Blood Gas and Determining Its Utility in Critically Ill Patients: Narrative Review

Chong, Woon H. MD*; Saha, Biplab K. MD; Medarov, Boris I. MD*

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doi: 10.1213/ANE.0000000000005501
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Arterial blood gas (ABG) analysis is an important step in assessing the adequacy of oxygenation and ventilation while diagnosing and monitoring acid-base disturbances. However, an arterial puncture is needed to obtain the sample and can be associated with complications such as pain, infection, nerve injury, bleeding/hematoma, arterial aneurysm/pseudoaneurysm, dissection, thrombosis, and limb ischemia.1 Arterial access can cause more pain than venous access and may also be difficult due to patient movement or diminished pulses, which may delay care, especially when serial results are needed.2 Central venous blood gas (VBG) analysis may allow an estimate of ABG values and can be obtained from an indwelling central venous catheter.

Critically ill patients often have indwelling central venous catheters for administration of intravenous medications, monitoring of central venous pressure, and venous blood sampling. Although venous blood Po2 cannot estimate arterial Po2, pulse oximetry is more commonly used for monitoring oxygenation.3 Moreover, multiple studies have examined the utility of peripheral VBG in assessing ventilation and acid-base status. Existing meta-analyses suggest that pH and Pco2 in peripheral venous blood closely approximate arterial levels.4,5 In addition, peripheral venous sampling has since been widely used in emergency settings and initial assessments of patients with chronic obstructive pulmonary disease (COPD) and diabetic ketoacidosis (DKA).4–8 However, the value of using central VBG to guide clinical decisions in critical care and perioperative settings remains less certain. The purpose of this review is to explore the relationship between pH and Pco2 values obtained by arterial and central venous blood samples in critically ill patients.


We reviewed the current English language literature available between 1989 and 2019 via a MEDLINE and Pubmed search using the combination of the following search terms: “ABG,” “VBG,” “venous blood gas,” “arterial blood gas,” and “central venous blood gas.” We selected only articles that compared central VBG with ABG obtained simultaneously in human subjects and excluded studies that involved peripheral VBG. All cited references from included studies were also reviewed to identify relevant literature. We assessed and summarized the differences in pH and Pco2 between the arterial and central venous samples in the studies included.

Studies Comparing Central VBG and ABG in Critically Ill Patients

We identified 7 studies comparing central VBG and ABG values that met our criteria (Table 1). Four studies were focused on intensive care unit (ICU) patients.10–13 A 2010 study by Walkey et al12 reviewed 187 critically ill patients enrolled from medical (39%) and surgical (5%) ICUs, and the remainder from cardiac catheterization laboratory (56%). The reason for ICU admission in this study was primarily cardiac-related, and most were hemodynamically stable. The authors observed only a small difference between central venous and arterial pH (0.035 units) and Pco2 (4.5 mm Hg).12 A 2015 study by Mallat et al13 assessed 192 medical and surgical critically ill patients, most of whom were admitted for pneumonia (37%) and peritonitis (24%). About 88% required mechanical ventilation, and 32% had septic shock. Again, a close relationship between central venous and arterial pH (0.03 units) and Pco2 (6.5 mm Hg) was observed.13

Table 1. - Summary of Studies Comparing Central Venous and Arterial pH and Pco2
Author, year Study design and population N Mean difference pH, units (95% CI) Mean difference Pco 2, mm Hg (95% CI)
Adrogué et al, 19899 Single-center prospective study/different types of circulatory compromise 105 +0.03 (±0.01) normal CO −5.70 (±1.1) normal CO
+0.10 (±0.08) shock −24.0 (±17.7) shock
+0.35 (±0.04) cardiac arrest, ventilated −48.9 (±8.3) cardiac arrest, ventilated
+0.04 (±0.07) cardiac arrest, nonventilated −8.9 (±4.9) cardiac arrest, nonventilated
Malinoski et al, 200510 Single-center prospective study/SICU 25 +0.03 (±0.03) −4.36 (±3.4)
Treger et al, 201011 Single-center prospective study/MICU 40 +0.027 (±0.03) −3.80 (±4.3)
Walkey et al, 201012 Single-center prospective study/all ICU and cardiac catheterization 187 +0.035 (±0.02) −4.5 (±3.5)
Mallat et al, 201513 Single-center prospective study/all ICU 192 +0.03 (±0.02) −6.5 (−7.4 to −4.6)
Singh et al, 201514 Single-center prospective study/cardiac surgery 30 +0.008 (−0.04 to +0.06) −3.5 (−9.6 to +2.7)
Esmaeilivand et al, 201715 Single-center prospective study/cardiac surgery 100 +0.046 (0.03-0.07) −6.59 (−8.3 to −4.6)
Abbreviations: −, lower arterial value; +, higher arterial value; CI, confidence interval; CO, cardiac output; ICU, intensive care unit; MICU, medical intensive care unit; N, number of patients, SICU, surgical intensive care unit.

Relationships between the central VBG and ABG variables in patients after adult and pediatric cardiac surgery are similar. In a 2017 study of 100 patients after coronary artery bypass surgery, Esmaeilivand et al15 found a strong correlation between pH and Pco2 values obtained via arterial and central venous samples with a mean difference of 0.046 units and 6.59 mm Hg, respectively. A smaller 2015 study involving 30 pediatric cardiac ICU patients by Singh et al14 also found a slight difference in the mean pH of 0.008 units and mean Pco2 of 3.5 mm Hg (Table 1; Figure 1). Patients with hemodynamic instability and multiorgan failure or who were mechanically ventilated were excluded from both studies.

Figure 1.
Figure 1.:
pH (A) and Pco 2 (B) mean difference and 95% CI based on the studies in Table 1. CI indicates confidence interval.
Figure 2.
Figure 2.:
pH (A) and Pco 2 (B) difference between central venous and arterial blood during different circulatory states according to study by Adrogué et al.9 CI indicates confidence interval.

Although VBGs were reasonable approximations to arterial values in hemodynamically stable patients, the relationship deteriorates in unstable patients. A 1989 study assessed 105 patients with normal cardiac output (25%) and those with circulatory failure (75%), a mean difference in the pH and Pco2 of 0.03 units and 5.7 mm Hg was observed with normal cardiac output, but the gap widened as circulatory failure progressed.9 The discrepancy was 2–4 times greater in the individuals whose mean arterial pressure was <60 mm Hg or cardiac index <1 L/min/m2 or were mechanically ventilated during cardiac arrest. Interestingly, during cardiac arrest in nonmechanically ventilated patients, differences between the arterial and venous pH and Pco2 were small (0.04 units and 8.9 mm Hg, respectively). Another important finding in the study was that the gap between central venous and arterial pH as well as Pco2 in those receiving mechanical ventilation (pH 0.35 units and Pco2 48.9 mm Hg) was larger than in those not receiving mechanical ventilation (Table 1; Figure 2).9

Correlation Between Central VBG and ABG Summary

We found a clinically relevant correlation between central venous and arterial pH and Pco2 in hemodynamically stable patients across multiple studies, with a mean difference of 0.03 units and 4.5–6.5 mm Hg, respectively (Table 1; Figure 1). These correlations are similarly noted in meta-analyses comparing peripheral venous and arterial pH and Pco2 with a mean difference of 0.03 units and 4.4–5.7 mm Hg.4,5 However, in hemodynamically unstable patients, this correlation is unreliable. The difference between central venous and arterial pH/Pco2 can be 2–4 times greater in shock states than when hemodynamic stability is preserved (Table 1; Figure 2). The decoupling of the central venous and arterial values is especially striking during cardiac arrest in patients requiring mechanical ventilation where pH and CO2 difference may exceed 0.3 units and 50 mm Hg, respectively. During cardiogenic shock, a low cardiac output state will result in CO2 retention in the central venous system from a decrease in delivery and elimination of CO2 by the lungs.9,16,17 Furthermore, the increase in transit time of the blood in the tissue capillaries leads to greater CO2 extraction and higher CO2 serum levels (Figure 3).9,13,16,17 Severe respiratory failure during a circulatory failure will attenuate the observed difference between central venous and arterial Pco2 because of the poor CO2 clearance. Conversely, mechanical ventilation in the setting of cardiac arrest will lead to a marked discrepancy between those values.9 The likely explanation is that when respiratory failure ensues in the absence of mechanical ventilation in the setting of circulatory failure during cardiac arrest, arterial Pco2 will keep pace with the central venous Pco2 due to the lack of adequate ventilation to expel CO2 from the circulatory system. Therefore, a huge difference in pH will not be appreciated in these patients. However, patients receiving mechanical ventilation will have a wide disparity in mean Pco2 and mean pH due to effective alveolar ventilation, causing more CO2 elimination from the central venous system, leading to lower Pco2 in the arterial system.

Figure 3.
Figure 3.:
The mechanism of increased central venous Pco 2 in a low cardiac output state.

Central venous Pco2 may also be considered as a screening tool for arterial hypercapnia with a high degree of certainty.14,15 Several studies suggest that central venous Pco2 <50 mm Hg is extremely sensitive for ruling out arterial hypercapnia (defined as arterial Pco2 >45 mm Hg) with close to a 100% sensitivity.12,14,15 These findings have been replicated in multiple prospective studies comparing peripheral venous and arterial Pco2.4,8,18–21 Central VBG measurement may thus be a reasonable alternative to ABG monitoring in several clinical circumstances.

Several meta-analyses have discussed the close relationship between pH and Pco2 obtained from peripheral venous blood and arterial blood among COPD and DKA patients, especially in emergency care settings.4,5 With the close correlation described between central venous and arterial pH and Pco2 in hemodynamically stable patients, central venous sampling can supplant arterial puncture in many clinical situations in critical care and perioperative settings (Table 1). Central VBG parameters of pH and Pco2 should be considered during clinical scenarios in which circulatory failure has resolved or not present, such as the following: (1) determination of readiness for extubation during the ventilator weaning phase of critical illness or postcardiac surgery, (2) acid-base or respiratory disorders in critically ill patients not in the clinical state of shock, and (3) even unstable, nonventilated patient who suffered a cardiac arrest without arterial access. Nevertheless, due to the observed discrepancy with central VBG, ABG parameters remain essential during hemodynamic instability in critically ill patients suffering from the clinical state of shock or cardiac arrest while receiving mechanical ventilation.

Regression Equations for Central VBG and ABG

Table 2. - Table for Regression Equations Based on Multiple Studies Comparing Central VBG and ABG
Author Regression equations’ pH Regression equations’ Pco 2
Treger et al11 Arterial pH = −0.307 + (1.05 × central venous pH) Arterial Pco 2 = 0.805 + (0.936 × central venous Pco 2)
Esmaeilivand et al15 Arterial pH = 1.33 + (0.83 × central venous pH) Arterial Pco 2 = 4.63 + (0.73 × central venous Pco 2)
Singh et al14 Arterial pH = −0.3778 + (1.0518 × central venous pH) Arterial Pco 2 = 5.2923 + (0.7574 × central venous Pco 2)
Walkey et al12 Arterial pH = 0.26 + (0.97 × central venous pH) Arterial Pco 2 = 0.29 + (0.89 × central venous Pco 2)
Abbreviations: ABG, arterial blood gas; VBG, venous blood gas.

Several regression equations have been proposed to estimate arterial gas variables from central VBG values (Table 2). In a 2010 review of 187 patients, Walkey et al12 described a simplified formula with venous-arterial correlation coefficients of 0.95 and 0.84 for arterial pH and Pco2, respectively: (1) arterial pH = venous pH + 0.05 units and (2) arterial Pco2 = venous Pco2 − 5 mm Hg.12


In this review of 7 studies comparing arterial and central VBG analyses in perioperative and critically ill patients, we found a reasonable correlation between arterial and central VBG values. Our findings suggest that measuring blood gas values from centrally obtained venous blood is a good substitute for estimating arterial pH and Pco2 values in critically ill patients who are hemodynamically stable. Across all studies of hemodynamically stable patients, the mean difference between arterial and central venous pH and Pco2 is 0.03 units and 4–6.5 mm Hg with narrow 95% confidence intervals (CIs), respectively. These findings are similar in patients undergoing cardiac surgery. However, existing data suggest that such estimates are less accurate in patients with shock or after cardiac arrest. In multiple studies, a central venous Pco2 of 50 mm Hg or less makes arterial hypercapnia unlikely and can be used as a screening tool for hypoventilation in hospitalized patients with central venous access.


Name: Woon H. Chong, MD.

Contribution: This author helped write, edit, revise, and submit the manuscript.

Name: Biplab K. Saha, MD.

Contribution: This author helped write and edit the manuscript.

Name: Boris I. Medarov, MD.

Contribution: This author helped write, edit, revise, and supervise the manuscript.

This manuscript was handled by: Avery Tung, MD, FCCM.


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