Arterial Blood Gas Interpretation

Arterial blood gas (ABG) measurement is a quick and handy way to identify chemical abnormalities such as problems with gas exchange, acid-base balance and electrolyte derangements in the blood that aid in analysing a clinical picture - remember that the background history and examination of a patient can provide useful clues for the interpretation of ABGs!

  1. Assess Oxygenation - should be >10kPa on room air. Always note the FiO2 (what % oxygen they’re on); as a rule of thumb, PaO2 ≈ FiO2 - 10. Clinical context is important here - a patient may only be sustaining a ‘normal’ PaO2 through supplemental oxygen or hyperventilation!If the patient is hypoxic, assess PaCO2 to determine the type of respiratory failure:
    1. ↓PaO2 without ↑PaCO2 = Type 1 Respiratory Failure (gas exchange problem: O2 unable to get in but more soluble CO2 can still diffuse out)
    2. ↓PaO2 with ↑PaCO2 = Type 2 Respiratory Failure (ventilation problem: alveolar air is not being replenished hence no O2 entering or CO2 leaving)
  2. Determine Acid-Base Status - Acidosis is pH <7.35 and Alkalosis is pH >7.45
  3. Is it a respiratory problem?
  • If pH <7.35 and the PaCO2 >6.0kPa – respiratory acidosis
  • If pH >7.45 and the PaCO2 <4.7kPa – respiratory alkalosis

OR           

Is it a metabolic problem?

  • If pH <7.35 and the HCO3- (bicarbonate) < 22mmol/L – metabolic acidosis
  • If pH >7.45 and the HCO3- (bicarbonate) > 26mmol/L – metabolic alkalosis
    • BE > 2 = metabolic alkalosis
    • BE <-2 = metabolic acidosis

Alternatively, base excess measures the concentration of acid/base that must be added to the sample to return it to pH 7.4 corrected for PaCO2, i.e. isolating the metabolic component

  1. Are there compensatory changes?
  • Respiratory compensation (hypo/hyperventilation) occurs in minutes-hours
    • i.e. ↑pCO2 in metabolic alkalosis and ↓pCO2 in metabolic acidosis
  • Metabolic compensation (by kidneys) occurs in hours-days 
    • i.e. ↑HCO3- in respiratory acidosis and ↓HCO3- in respiratory alkalosis
  1. If there is metabolic acidosis, where is the acid coming from?
  • A drop in HCO3- is sometimes a consequence, rather than the primary cause, of a metabolic acidosis.
  • Calculate the anion gap: [Na+] + [K+] - ([Cl] + [HCO3]) 
  • If raised (N.R. 10-16mmol/L), this suggests that an additional acid is present:
    • Intake of exogenous acid: e.g. salicylate (e.g. aspirin) poisoning
  • If the anion gap is normal, this suggests an electrolyte derangement is the primary cause e.g. renal tubular acidosis.

Increased production of endogenous acids or decreased acid excretion: e.g. ketoacidosis (DKA)

  1. What are the other values like?
    1. Electrolytes
    2. Lactate - quick way to identify a potential cause of a raise anion gap
    3. Glucose
    4. Haemoglobin (Hb) - notoriously inaccurate on ABGs!
    5. Methaemoglobin (MetHb) - oxidised form of Hb caused by errors of metabolism or by exposure to toxins such as nitrates.
    6. Carbon Monoxide (CO) - in city dwellers or smokers levels can be raised up to 10% but a level >10% indicates poisoning
  2. Determine the Cause:

ACIDOSIS (T2RF)


ALKALOSIS

RESPIRATORY

Acute: asthma, NM disease, ↓resp drive

Type 1 Resp Failure:

Pneumonia, pneumothorax, pulmonary oedema, pleural effusion, PE

Anxiety, Excessive Mechanical Ventilation, Compensation

Chronic: COPD, MND, pulmonary fibrosis

METABOLIC

Methanol
Uraemia
Diabetic Ketoacidosis
Paraldehyde
Iron/Isoniazid/IEM
Lactate
Ethanol
Salicylate

⇐ Raised Anion Gap

H+ depletion (e.g. persistent vomiting), 


K+ depletion (e.g. diuretics, Conn’s syndrome, burns, liquorice excess)


HCO3- ingestion/retention


Pancreatobilary
Acetazolamide
Normal Saline
Diarrhoea
Aldosterone antag
Renal Tubular Acidosis
Ureterogastic conduit
Small bowel fistula
Hyperalimentation

⇐ Normal Anion Gap