Arterial blood gas analysers are designed to measure multiple components in the arterial blood. The readout from the machine quotes normal values based on the assumption that the sample analysed is arterial (an ABG). There is currently a plague of ‘venous’ blood gases (VBG) in clinical practice. A VBG is obtained by placing a venous sample in the arterial blood gas analyser. VBGs are popular as it is far less painful for the patient to obtain a venous sample compared to an arterial sample. In addition, obtaining ABGs carries well known risks. VBGs are useful if you know how to interpret them and have a knowledge of their limitations.
An ABG has a number of uses, the VBG can be substituted for some of these uses but not for others.
The pO2 on a VBG bears no relationship to the paO2. The VBG is of no value in assessing oxygenation status.
In patients with COPD we need to detect the presence of CO2 retention. This has an important impact on treatment.
If the pCO2 on the VBG is above the normal arterial range (ie >45 mmHg, >6 kPa) the patient has CO2 retention. (100% sensitivity reported, so, at least in studies, it does not appear to miss any cases)
However, the absolute value of pCO2 on the VBG above this range correlates poorly with the paCO2 and cannot be used to monitor the response to treatment in a CO2 retainer.
This is probably where the VBG is of most use but there are still limitations.
The venous pH correlates well with the arterial pH. The venous pH tends to be more acidic than the arterial pH. Add 0.035 to the venous pH to estimate the arterial pH. In conditions such as DKA, it is probably reasonable to follow the pH response to treatment with VBGs. In addition, if there is no concern over a patient’s oxygenation status, it is reasonable to screen for pH disturbances with a VBG. Sometimes this can be very helpful. For example, in an elderly person with abdominal pain, identification of an unsuspected acidosis could drastically alter the differential.
The venous bicarbonate correlates reasonably well with the arterial bicarbonate. However, there are outliers. If in doubt do an ABG.
There are limitations to the VBG in assessment of pH status.
All correlations break down in the presence of shock. The VBG has no role in the assessment of critically ill patients.
The ‘bedside rules’ (see our video tutorial) have not been validated for VBGs, therefore, at the present time, VBGs have no role in the assessment of mixed acid-base disturbances.
Elevated venous lactate levels show no relationship with the arterial lactate. A venous lactate level elevated above the normal arterial range quoted on the arterial blood gas analyser has no meaning clinically.
The arterial blood gas analyser will measure electrolyte levels in the plasma. People often use a VBG to obtain a rapid assessment of electrolyte levels in a patient, as we can analyse the sample in the Emergency Department avoiding the time needed to send the sample to the lab. Be careful! Remember the concentration of key electrolytes is influenced by the presence of hemolysis. The most important example is K+. In vitro hemolysis of red cells in a blood sample will give rise to release of K+ from red cells and may produce an artefactual hyperkalemia on the readout. Venous samples sent to the laboratory are screened for hemolysis, VBG samples analysed in the Department are not. Be cautious when analysing K+ levels on a VBG or indeed on an ABG for that matter.
There is an excellent correlation between the levels of carboxyhemoglobin and methemoglobin on a VBG and an ABG.
Some people say that the VBG will replace the ABG in clinical practice. This is a little premature and may reflect the fact that many of us don’t know how to read an ABG properly to maximise the information available (see our detailed video tutorials).