INTRODUCTION —
An arterial blood gas (ABG) is one traditional method of estimating oxygenation, ventilation, and acid-base disturbances. However, ABGs can be painful and difficult to obtain. In the intensive care unit, emergency department, and respiratory floors, many clinicians use venous blood gases (VBGs) instead of ABGs to estimate indices of ventilation and acid-base disturbance (ie, systemic carbon dioxide [CO2] and pH). In select scenarios, for the assessment of systemic CO2 levels, some clinicians use end-tidal CO2 (PetCO2; eg, cardiac arrest) and transcutaneous CO2 (PtcCO2; eg, sleep laboratory).
VBG sampling, measurements, and interpretation as well as PetCO2 and PtcCO2 are discussed in this topic. ABGs, capnography, and acid-base disorders are reviewed separately. (See "Arterial blood gases" and "Carbon dioxide monitoring (capnography)" and "Simple and mixed acid-base disorders".)
VENOUS BLOOD GASES
Clinical uses — VBGs can assess the venous CO2 tension (PvCO2) and pH, but they cannot accurately assess oxygenation. Consequently, VBG use is often combined with peripheral oxygen saturation assessment by pulse oximetry [1]. (See "Pulse oximetry".)
Patients in whom VBG analysis may be useful include the following:
●Patients who need frequent arterial blood gas (ABG) testing but no arterial line is in place (eg, moderate acute exacerbation of chronic obstructive pulmonary disease, severe coagulopathy)
●Patients in whom daily assessment of ventilation informs ventilator changes (eg, patients weaning from invasive or noninvasive ventilation)
●Patients with acute kidney injury
●Patients who decline an ABG
●Patients in whom an ABG cannot be obtained (eg, diminished pulses, patient movement, arterial graft, Raynaud phenomenon)
A VBG is not useful in the following:
●Patients in whom an accurate assessment of oxygenation is needed (eg, calculation of the partial arterial oxygen tension:fraction of inspired oxygen ratio or Alveolar-arterial gradient, suspected carbon monoxide poisoning, suspected pulse oximetry error (table 1), evaluation for shunt)
●Patients with hemodynamic instability or shock
●Patients with extreme acid-base disturbance (eg, pH <7.2, >7.6)
●Patients in whom hyperoxemia is suspected
●Patients in whom doubt exists over a VBG test result
●Patients undergoing cardiopulmonary exercise testing
Several studies have described poor correlation between venous and arterial samples during states of shock [2-7]. For example, in a study of 168 matched sample pairs of VBG and ABGs, among patients with shock, the difference between mixed venous and arterial CO2 tension (PCO2) increased by a factor of three compared with patients without shock [2]. Similar observations were made during extremes of acid-base disturbance [8]. Nonetheless, VBG can still provide useful data if rapid screening is needed for acidosis and hypercarbia and arterial sampling has failed.
While VBGs have been used during in-laboratory sleep apnea testing, they are only helpful when the PvCO2 is <45.8 mmHg or ≥53.7 mmHg to exclude or diagnose hypercapnia, respectively [9]. (See "Clinical presentation and diagnosis of obstructive sleep apnea in adults", section on 'Polysomnography' and "Overview of polysomnography in adults", section on 'Measured variables'.)
Sampling sites — A VBG can be performed using the following:
●Central venous sampling (obtained from a central venous catheter) – We use central venous sampling because it best correlates with ABGs. (See 'Interpretation: Venous to arterial conversion estimates' below.)
●Peripheral venous sample (obtained by venipuncture) – Peripheral venous sampling is an alternative for patients without central venous access [10-12]. The tourniquet should be released about one minute before the sample is drawn to avoid changes induced by local ischemia [13].
●Mixed venous sampling (obtained from the distal port of a pulmonary artery catheter [PAC]) – Mixed venous sampling is a reasonable alternative when a PAC is in place. However, PAC placement is less common than in the past and should not be inserted for the sole purpose of obtaining a VBG. (See "Pulmonary artery catheterization: Indications, contraindications, and complications in adults".)
Measurements — A VBG measures the venous oxygen tension (PvO2), venous CO2 tension (PvCO2), acidity (pH), venous oxyhemoglobin saturation (SvO2; ScvO2 if taken from a central catheter [c representing central vein source]), base excess (BE), lactate, and bicarbonate (HCO3) concentration.
●PvCO2, venous pH, BE, and HCO3 concentration are used to assess ventilation and/or acid-base status. (See "Simple and mixed acid-base disorders".)
●ScvO2 has been used to guide resuscitation during septic shock, but is not an accurate indicator of oxygenation and has been replaced by lactate. (See "Evaluation and management of suspected sepsis and septic shock in adults".)
●PvO2 has no practical value because it cannot accurately assess oxygenation. By the time the blood reaches the venous circulation, oxygen has already been extracted by the tissues.
Interpretation: Venous to arterial conversion estimates — In general, venous measurements of PCO2, pH, and HCO3 are similar to arterial values with some minor adjustments as outlined in the table (table 2) [14-27]. We use the adjusted values for clinical decision-making. However, the values vary with the site of venous sampling and are inaccurate during states of shock or extreme acid-base disturbances. Thus, periodic correlation between ABG and VBG values is always reasonable when serial monitoring is needed.
●Central venous pH (ie, drawn from a central venous catheter) is usually 0.03 to 0.05 pH units lower than the arterial pH. The central venous PCO2 is usually 4 to 5 mmHg higher, with little or no increase in HCO3 values [14,15,25,28].
●Mixed venous blood (ie, drawn from the distal port of a pulmonary artery catheter) gives results similar to central venous blood [16-18].
●Peripheral venous pH is approximately 0.02 to 0.04 pH units lower than the arterial pH. The peripheral PvCO2 is approximately 3 to 8 mmHg higher, and the venous serum HCO3 concentration is approximately 2 to 3 mEq/L higher [1,9-11,19-24,29-35].
There are no venous to arterial conversions for SvO2, ScvO2, or PvO2.
Venous BE is approximately 0.15 higher than the arterial BE, and the venous lactate is approximately 0.12 higher than the arterial lactate [36].
ALTERNATIVE MEASUREMENTS OF CARBON DIOXIDE
End-tidal carbon dioxide (capnography) — End-tidal CO2 (PetCO2; also known as capnography) measures CO2 in exhaled breath, and the result is displayed as a numerical value or a graph (figure 1).
The PetCO2 is usually within 1 mmHg of the arterial CO2 tension (PaCO2) in healthy adults, but it is inaccurate in critically ill adults (likely due to an increase in dead space). Consequently, it is not commonly used in the intensive care unit (ICU) for CO2 tension (PCO2) monitoring. However, it is used frequently in newborn ICUs, operating rooms, and emergency departments for several indications. These indications are discussed separately. (See "Carbon dioxide monitoring (capnography)" and "Approach to mechanical ventilation in very preterm neonates", section on 'Monitoring'.)
Transcutaneous carbon dioxide — Transcutaneous CO2 (PtcCO2) measurement is uncommonly used. Although accuracy is improving, we do not use PtcCO2 in critically ill adults but do use it in critically ill neonates and in adult sleep laboratories when obstructive sleep apnea or sleep hypoventilation is suspected.
In general, PtcCO2 should not be used routinely outside of specific clinical circumstances defined by the device manufacturer, sampling site, sensor temperature, clinical diagnosis, and severity of illness [37]. PtcCO2 systems generally have a heating element that raises the skin temperature to 45ºC to increase local perfusion, an electrode to measure PtcCO2, and a light emitter and sensor to measure arterial oxyhemoglobin saturation [38]. Devices may be difficult to keep calibrated or mount in a way that prevents air trapping and may take up to an hour to sufficiently warm the skin [39]. In addition, the devices must be attached to an ear, which may be difficult in agitated patients.
Older studies suggested that PtcCO2 was inaccurate in critically ill adults especially those with poor skin perfusion (eg, due to vasopressors) or PaCO2 >56 mmHg [39-43]. Newer devices may be more accurate in critically ill patients, including those with a PaCO2 as high as 89 mmHg [44] and those on vasopressors and vasodilators [40].
PtcCO2 use for monitoring CO2 levels during sleep laboratory testing, for assessing the response to chronic noninvasive ventilation, and for critically ill neonates are discussed separately. (See "Noninvasive positive airway pressure therapy for the obesity hypoventilation syndrome", section on 'Assess indicators of alveolar hypoventilation' and "Noninvasive ventilation in adults with chronic respiratory failure from neuromuscular and chest wall diseases: Adaptation and follow-up after initiation", section on 'Measurement parameters' and "Approach to mechanical ventilation in very preterm neonates", section on 'Monitoring'.)
SOCIETY GUIDELINE LINKS —
Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Assessment of oxygenation and gas exchange".)
SUMMARY AND RECOMMENDATIONS
●Venous blood gases – Venous blood gas (VBG) analysis is an alternative method of estimating arterial carbon dioxide (CO2) tension and pH that does not require arterial blood sampling. Unlike arterial blood gas (ABG) analysis, VBG analysis cannot accurately assess oxygenation. Consequently, VBG use is often combined with peripheral oxygen saturation measurement by pulse oximetry. (See 'Venous blood gases' above.)
•Clinical uses – Our approach is the following (see 'Clinical uses' above):
VBGs may be useful in the following circumstances:
-Serial ABG monitoring without an arterial line
-Daily assessment to inform ventilator changes
-Acute kidney injury
-ABG refusal
-ABG cannot be obtained
VBG is not useful in the following:
-Accurate oxygenation assessment (eg, calculation of the partial arterial oxygen tension:fraction of inspired oxygen ratio or Alveolar-arterial gradient, carbon monoxide poisoning, pulse oximetry error (table 1), shunt)
-Hemodynamic instability or shock
-Extreme acid-base disturbance (eg, pH <7.2, >7.6)
-Suspected hyperoxemia
-Doubt exists over a VBG test result
-Cardiopulmonary exercise testing
•Sampling – We use central venous sampling (from a central venous catheter) because it best correlates with ABG samples. Peripheral venous sampling (by venipuncture) is an alternative for patients without central venous access. A mixed venous sample (from the distal port of a pulmonary artery catheter [PAC]) is also a reasonable alternative if a PAC is in place. (See 'Sampling sites' above.)
•Interpretation – In general, measurements of venous CO2 tension (PvCO2), pH, and bicarbonate are similar to arterial values with some minor adjustments as outlined in the table (table 2). However, the values vary with the site of venous sampling and are inaccurate during states of shock or extreme acid-base disturbances. Thus, periodic correlation between ABG and VBG values is reasonable when serial monitoring is needed. (See 'Interpretation: Venous to arterial conversion estimates' above.)
●Alternative ways to measure CO2 – End-tidal CO2 (PetCO2; also known as capnography) and transcutaneous CO2 (PtcCO2) are not routinely used in critically ill adults since they are inaccurate in this population. However, PetCO2 is used in newborn intensive care units, operating rooms, and emergency departments for several reasons. PtcCO2 is also commonly used in critically ill neonates and sleep laboratories when obstructive sleep apnea or sleep hypoventilation is suspected. These indications are discussed separately. (See "Carbon dioxide monitoring (capnography)" and "Approach to mechanical ventilation in very preterm neonates", section on 'Monitoring' and "Noninvasive positive airway pressure therapy for the obesity hypoventilation syndrome", section on 'Assess indicators of alveolar hypoventilation'.)