Blood Gases: ABG vs. VBG

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Determining if there are clinically important distinctions between the two results.

Arterial and venous blood gases provide crucial information about the acid-base status of critically ill ED patients. Arterial blood gases (ABGs) are considered the gold-standard, but they come at a cost. ABGs can be more difficult to obtain, are more painful and require arterial puncture that risks complications.


A peripheral venous blood gas (VBG) can be obtained as the nurse obtains IV access upon patient arrival, requiring no additional sticks or risk of arterial injury. This review will break down blood gas results into individual components to compare venous versus arterial results and evaluate whether these are clinically important differences.


The pH between a VBG and ABG correlates closely and accurately measures the severity of an acidosis. The average VBG pH is 0.03-0.04 less than the ABG pH values. (Kelly 2001, Razi 2012, Brandenburg 1998, McCanny 2012, Byrne 2014). This relationship appears to hold true even in shock states and in a severe metabolic acidosis such as diabetic ketoacidosis. (Zeserson 2018, Bradenburg 1998).



The difference in the pCO2 measurements between the VBG and ABG is the most contested in the literature. There is a correlation between the arterial and venous pCO2, but the confidence intervals are large with an average difference ranging from 5.7- 8.6mmHg. (Malinoski 2005, Kelly 2001, McCanny 2012, Malatesha 2007, Rang 2006, McKeever 2016). Kelly et al showed that the venous pCO2 can be used to screen for hypercarbia.

A venous pCO2 < 45 mmHg has a 100% negative predictive value for hypercarbia (Kelly 2005). In our opinion the use of a VBG to assess pCO2 depends on the clinical context. In a post-cardiac arrest or neuro trauma patient, it is critically important to closely and confidently follow and manage the pCO2. In this context an ABG is the test of choice. Conversely, in a COPD patient being treated with non-invasive positive pressure ventilation, it is unlikely that the wide confidence intervals of the venous pCO2 will be clinically significant. In hypercarbic patients, the venous or arterial pH is useful to differentiate an acute respiratory acidosis from a compensated chronic respiratory acidosis. Despite an elevated PCO2, a normal pH suggests your patient is at a compensated baseline (Kaynar 2017).



The blood gas can yield important information about oxygenation. The PaO2 level does not correlate between the venous and arterial blood gases (Malatesha 2007, Byrne 2014). The oxygenation saturation obtained by a pulse oximeter is a helpful surrogate in most patients, but not in all. In those with poor peripheral perfusion, severe acidosis, or in those with severe hypoxemia and acute respiratory distress syndrome (ARDS), an arterial blood gas is necessary for an accurate assessment of oxygenation. Intensivists most frequently use the ABG PaO2 to calculate a PaO2:FiO2 ratio in ARDS as it influences prognosis and treatment (JAMA 2012).


The bicarbonate (HCO3) correlates well between arterial and venous samples, and similar to the pH will closely approximate the arterial values, with a difference of 0.52-1.5 mmol/L (McCanny 2011, Kelly 2001, Malatesha 2007, Middleton 2006, Rang 2002).  Remember that the bicarbonate on a blood gas is a calculated value rather than a measured value, and if you are concerned about the patient’s bicarbonate level you should check the serum chemistry for an accurate measurement (Kaynar 2017).


The lactate level correlates well between arterial and venous blood gases, with a mean difference of 0.02-0.08 (Middleton 2006, Murdoch 1994). The venous lactic acid can be used to trend lactate while resuscitating your patient.

Base Deficit

Base deficit (BD) is a calculation, which can further quantify a patient’s acid-base status. The nomenclature requires some explanation-base deficit is the inverse of the standard base excess (SBE.) For example, a SBE of -6 and a BD of 6 are interpreted as a severe acidosis. The SBE is the amount of strong acid added to 1 liter of fully oxygenated whole blood to return the sample to a pH of 7.4 and pCO2 of 40 mmHg at a temperature of 37°F. (Berend 2018)

BD can help determine whether the patient has an acute or chronic, metabolic or respiratory, partially or fully compensated acidosis or alkalosis (Berend 2016.) BD is largely used in trauma and critical care as a marker of prognosis, metabolic derangement, and resuscitation (Ibraham, Dunham) and reflects the multiple factors including lactic acid, ventilation and fluid administration. A BD of greater than 6 is considered a severe acidosis, associated with worse outcomes (Ibraham) and usually requires more resuscitation. Arterial and venous base deficit values correlate and do not lead to clinically significant differences (Berend, Middleton 2006, Arnold 2011).

Who Still Needs an ABG?

Hypoxemic patients, those with ARDS, and patients with poor circulation that prohibits plethysmography by pulse oximeter should have an ABG, because a VBG cannot be used to determine oxygenation. In such patients, this means you can start with an ABG and then correlate your end tidal CO2 and oxygenation with pulse oximetry (if oximetry then improves). If you are concerned about the patient’s metabolic acid-base status, a VBG will give you a pH, HCO3, lactate and BD that closely approximates the ABG. A venous pCO2 <45 mmHg will reliably screen for hypercarbia on a VBG, but the actual value may vary from that of an ABG with an average difference ranging from 5.7- 8.6mmHg.

Take home

  1. Hypoxemic patients and those with shock get an arterial blood gas
  2. Venous blood gas can be used for pH, screening for hypercapnia and lactate trending
  3. HCO3 correlates between ABG and VBG, but if you’re really concerned about the value check a serum chemistry
  4. Base Deficit >6 is considered a severe acidosis and is associated with worse outcomes


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A-M Kelly et al. Venous pH can safely replace arterial pH in the initial evaluation of patients in the emergency department. Emerg Med J 2001;18:340-342.

Kelly, AM, Kerr, D, Middleton, P. Validation of venous pCO2 to screen for arterial hypercarbia in patients with chronic obstructive airways disease. J Emerg Med. 2005;28(4):377-379

Razi et al. Correlation of Arterial Blood Gas Measurements with Venous Blood Gas Values in Mechanically Ventilated Patients. Tanaffos 2012; 11(4):30-35

Brandenburg M, Dire D. Comparison of Arterial and Venous Blood Gas Values in the Initial Emergency Department Evaluation of Patients with Diabetic Ketoacidosis. Ann Emerg Med April 1998; 31:459-465

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Middleton P, Kelly AM, Brown J, et al. Agreement between arterial and venous values for pH, bicarbonate, base excess, and lactate. Emerg Med J. 2006;23:622-624.

McKeever, TM, Hearson, G, Housley, G, et al. Using venous blood gas analysis in the assessment of COPD exacerbations: a prospective cohort study. Thorax. 2016;71:210-215.

Murdoch IA, Turner C, Dalton RN. Arterial or mixed venous lactate measurement in critically ill children. Is there a difference? Acta Paediatr. 1994;83:412-413.

Adrogue HJ, Rashad MN, Gorin AB, et al. Assessing acid-base status in circulatory failure. Differences between arterial and central venous blood. N Engl J Med. 1989;320:1312-16.

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Byrne, AL et al. Peripheral venous and arterial blood gas analysis in adults: are they comparable? A systematic review and meta-analysis. Respirology (2014) 19, 168–175

The ARDS Definition Task Force. Acute Respiratory Distress Syndrome: The Berlin Definition. JAMA. 2012;307(23):2526-2533. doi:10.1001/jama.2012.5669

Zeserson, E, et al. Correlation of venous blood gas and pulse oximetry with arterial blood gas in the undifferentiated critically ill patient. J Intensive Care Med. 2018;33(3):176-181.

Kaynar, AM. (2017) Arterial blood gas interpretation. JL Vincent, E Abraham, FA Moore, PM Kochanek, MP Fink. 7th edition, Textbook of Critical Care (167-174).

Ibrahim I, et al. Is arterial base deficit still a useful prognostic marker in trauma? A systematic review. Am J Emerg Med. 2016 Mar;34(3):626-35



Skyler Lentz, MD is the Assistant Professor of Surgery and Medicine in the Divisions of Emergency Medicine and Pulmonary Critical Care at the University of Vermont Medical Center.

Matthew Roginski, MD, MPH, is an Assistant Professor of Medicine in the Sections of Emergency and Critical Care Medicine and the DHART Assistant Medical Director at Dartmouth-Hitchcock Medical Center.

Patricia Ruth Atchinson, DO, is a Critical Care Fellow at Dartmouth-Hitchcock Medical Center and an Emergency Medicine physician.

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