Arterial Blood Gases - Indications and Interpretation

Arterial blood gases (ABGs) are often required in sick patients. 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 full article on Acid-base Disorders.

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. Metabolic problems will require respiratory compensation and this occurs rapidly e.g. by increasing ventilation to blow of 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.¹

• Respiratory failure - in acute and chronic states
• Any severe illness which may lead to a metabolic acidosis e.g.
  • 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 patient to titrate with the oxygen for 5-10 minutes (30 minutes if COPD) before taking sample.
• If radial artery is to be used perform Allen's test to confirm collateral blood flow to the hand (see below).
  

  Allen's test Elevate hand and make a fist for approx 30 seconds. Apply pressure over the ulnar and the radial arteries occluding both (keep hand elevated). Open hand which will be blanched. Release pressure on ulnar artery and look for perfusion of hand (takes under 8 seconds). If 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 pre packed 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).
• Wrist is extended - a pillow under the hand may improve comfort.
• Palpate artery and hold fingers firmly over the pulsation.
• Then introduce needle at 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 2 minutes (longer if patient on any antiplatelet medication or anticoagulants).

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

1. Blood pH - high indicates alkalosis, low indicates acidosis and normal indicates either normal, mixed defect or a compensated defect.
2. CO₂ level - is it a respiratory problem if not look at bicarbonate level. High PaCO₂ with an acidosis indicates a respiratory problem. If the PaCO₂ is normal or low it indicates compensation.
3. Bicarbonate - if the bicarbonate fits with the pH it suggests a primary metabolic problem. If not it indicates compensatory changes.
4. Look for any compensation - e.g. low PaCO₂ in severe metabolic acidosis.
5. Anion gap in metabolic acidosis - see below.
6. O₂ level - is hypoxaemia present?

• Alveolar-arterial oxygen gradient - (A-a)pO₂; difference in oxygen partial pressures between alveolar and arterial side.² It provides a measure of oxygen diffusion across the alveoli into the blood. Thus will be impaired in lung disease such as COPD. Raised (A-a)pO₂ may also represent the presence of an intrapulmonary shunt i.e. lung that is perfused but not ventilated e.g. 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
  CNS depression Neuromuscular disorders	Intrinsic lung disease e.g. COPD

• Anion gap - this is useful in any cause of metabolic acidosis. Both negative (Cl^- and HCO₃^-) and positive ions (Na⁺ and K⁺) are present in the body.³ They are usually balanced, but when they are added together there is a gap representing the unmeasured anions e.g. plasma proteins. 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 e.g. Ketoacids in DKA Lactic acid e.g. shock, infection Drugs/toxins e.g. salicylates, ethylene glycol, methanol	Loss of bicarbonate or ingestion of acid e.g. GIT causes e.g. diarrhoea, pancreatic fistula Renal tubular acidosis Addison's disease Drugs e.g. 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 e.g. COPD.
• Respiratory alkalosis - high pH, low PaCO₂, normal or high normal bicarbonate. Causes - any cause of hyperventilation e.g. 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.⁴