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Arterial Blood Gases - Indications and Interpretation

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Arterial blood gases (ABGs) are an important routine investigation to monitor the acid-base balance of patients.[1] They may help make a diagnosis, indicate the severity of a condition and help to assess treatment. ABGs provide the following information:

  • Oxygenation
  • Adequacy of ventilation
  • Acid-base levels

Also see the full separate article on Acid-base Disorders.

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Blood pH has to be maintained within a tight normal range to avoid cellular death. This can be achieved by buffer mechanisms which can be either renal or respiratory in nature.[2] 

Metabolic problems will require respiratory compensation and this occurs rapidly - eg, by increasing ventilation to blow off CO2. On the other hand respiratory problems leading to acid-base abnormalities require renal compensation. This is slow and may need secretion of H+ ions or reabsorption/new production of HCO3- ions.[3]

  • Respiratory failure - in acute and chronic states.
  • Any severe illness which may lead to a metabolic acidosis - for example:
    • Cardiac failure.
    • Liver failure.
    • Renal failure.
    • Hyperglycaemic states associated with diabetes mellitus.
    • Multiorgan failure.
    • Sepsis.
    • Burns.
    • Poisons/toxins.
  • Ventilated patients.
  • Sleep studies.
  • Severely unwell patients from any cause - affects prognosis.
  • Arterial blood can be obtained by direct arterial puncture most usually at the wrist (radial artery). Alternatives to the radial artery include the femoral and brachial artery - both of which are usually used in emergency settings. The dorsalis pedis artery and ulnar artery may also be used. It is important to ensure good collateral circulation (see below), as there is a theoretical risk of thrombus occlusion.
  • If multiple samples are required then an indwelling arterial cannula can be placed.
  • Allow the patient to titrate with the oxygen for 5-10 minutes (30 minutes if they have chronic obstructive pulmonary disease (COPD)) before taking a sample.
  • If the radial artery is to be used, perform Allen's test to confirm collateral blood flow to the hand.

    Allen's test

    • Elevate the hand and make a fist for approximately 30 seconds.
    • Apply pressure over the ulnar and the radial arteries occluding both (keep the hand elevated).
    • Open the hand which will be blanched.
    • Release pressure on the ulnar artery and look for perfusion of the hand (this takes under eight seconds).
    • If there is any delay then it may not be safe to perform radial artery puncture.
  • Explain the procedure to the patient - it is painful.
  • If there is time then local anaesthesia can be used.
  • ABG syringes usually come prepacked and are heparinised. Some contain a vacuum and thus the plunger does not always need to be pulled. (Check with your department as to which they use).
  • The wrist is extended - a pillow under the hand may improve comfort.
  • Palpate the artery and hold fingers firmly over the pulsation.
  • Then introduce the needle at a 45° angle slowly with the bevel facing upwards, aiming for the point of maximum pulsation.
  • Once you hit the artery, try to obtain at least a 1 ml sample.
  • Once you have taken your sample and withdrawn the needle, apply firm pressure for a minimum of two minutes (longer if the patient is on any antiplatelet medication or anticoagulants).

The following indices should be looked at in the following order (see local laboratory for reference ranges):

  • Blood pH - high indicates alkalosis, low indicates acidosis and normal indicates either normal, mixed defect or a compensated defect.
  • PaCO2 level - is it a respiratory problem? If not, look at the bicarbonate level. High PaCO2 with an acidosis indicates a respiratory problem. If the PaCO2 is normal or low it indicates compensation.
  • Bicarbonate - if the bicarbonate fits with the pH it suggests a primary metabolic problem. If not, it indicates compensatory changes.
  • Look for any compensation - eg, low PaCO2 in severe metabolic acidosis.
  • Anion gap in metabolic acidosis - see below under 'Other useful information from arterial blood gases'.
  • O2 level - is hypoxaemia present?
  • Alveolar-arterial oxygen gradient - (A-a)pO2; difference in oxygen partial pressures between the alveolar and arterial side.[4] It provides a measure of oxygen diffusion across the alveoli into the blood. Thus, will be impaired in lung disease such as COPD.[5] Raised (A-a)pO2 may also represent the presence of an intrapulmonary shunt, ie a lung that is perfused but not ventilated - for example, pneumonia. The following table provides a list of some of the causes in which (A-a)pO2 change:
    (A-a) pO2
    Normal (A-a)pO2 in type 2 respiratory failure
    Raised (A-a)pO2
    • Central nervous system (CNS) depression.
    • Neuromuscular disorders.
    • Intrinsic lung disease - eg, COPD.
  • Anion gap - this is useful in any cause of metabolic acidosis. In plasma, the sum of the cations (sodium plus potassium) is normally greater than that of the anions (chloride plus bicarbonate) by approximately 14 mmol/L (normal range 10-18 mmol/L). This is known as the anion gap. In some disorders, either the positive or negative ions may increase, leading to a change in the anion gap. The following table lists the causes of an abnormal anion gap:
    Causes of changes in anion gap
    Raised anion gap metabolic acidosis
    Normal anion gap (hyperchloraemia) metabolic acidosis
    Accumulation of acids, for example:
    • Ketoacids in diabetic ketoacidosis (DKA).
    • Lactic acid - eg, shock, infection.
    • Drugs/toxins - eg, salicylates, ethylene glycol, methanol.
    Loss of bicarbonate or ingestion of acid, for example:
    • Gastrointestinal tract causes - eg, diarrhoea, pancreatic fistula.
    • Renal tubular acidosis.
    • Addison's disease.
    • Drugs - eg, carbonic anhydrase inhibitors.
    Causes of a raised anion gap metabolic acidosis can be recalled using the 'MUDPILES' mnemonic (methanol, uraemia, DKA, paraldehyde, infection/ischaemia/isoniazid, lactic acidosis, ethylene glycol/ethanol, salicylates/starvation).
  • Respiratory acidosis: low pH, high PaCO2, normal or high normal bicarbonate.
    Causes: neuromuscular weakness, intrinsic lung disease - eg, COPD.
  • Respiratory alkalosis: high pH, low PaCO2, normal or high normal bicarbonate.
    Causes: any cause of hyperventilation - eg, anxiety, pain.
  • Metabolic acidosis: low pH, normal or low normal PaCO2, low bicarbonate.
    Causes: see anion gap table, above.
  • Metabolic alkalosis: high pH, normal PaCO2, high bicarbonate.
    Causes: vomiting, burns, ingestion of base.

Mixed acid-base disorders occur when there is a combination of primary acid-base disturbances (but not combined respiratory acidosis and alkalosis). Usually the ABG result does not fit into one of the above four clinical pictures easily. The therapy is directed towards correction of each primary acid-base disturbance.[6]

Further reading & references

  • Kurtz I, Kraut J, Ornekian V, et al; Acid-base analysis: a critique of the Stewart and bicarbonate-centered approaches. Am J Physiol Renal Physiol. 2008 May;294(5):F1009-31. doi: 10.1152/ajprenal.00475.2007. Epub 2008 Jan 9.
  1. Singh V, Khatana S, Gupta P; Blood gas analysis for bedside diagnosis. Natl J Maxillofac Surg. 2013 Jul;4(2):136-141.
  2. Koeppen BM; The kidney and acid-base regulation. Adv Physiol Educ. 2009 Dec;33(4):275-81. doi: 10.1152/advan.00054.2009.
  3. Ghosh AK; Diagnosing acid-base disorders. J Assoc Physicians India. 2006 Sep;54:720-4.
  4. Kellum JA; Disorders of acid-base balance. Crit Care Med. 2007 Nov;35(11):2630-6.
  5. Bruno CM, Valenti M; Acid-base disorders in patients with chronic obstructive pulmonary disease: a pathophysiological review. J Biomed Biotechnol. 2012;2012:915150. doi: 10.1155/2012/915150. Epub 2012 Feb 1.
  6. Adrogue HJ; Mixed acid-base disturbances. J Nephrol. 2006 Mar-Apr;19 Suppl 9:S97-103.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Gurvinder Rull
Current Version:
Peer Reviewer:
Dr Adrian Bonsall
Document ID:
8718 (v4)
Last Checked:
Next Review:
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