Arterial Blood Gas Interpretation: A Five-Step Method

Introduction

An arterial blood gas measures the adequacy of oxygenation, ventilation and acid-base balance in a single sample. Interpreted systematically it is one of the highest-yield bedside investigations in medicine; interpreted by pattern recognition alone it produces confident wrong answers, which is why a fixed sequence is worth learning and using every time.

When to take one

• Any acutely breathless or hypoxic patient, including all suspected respiratory failure
• Any patient at risk of hypercapnic respiratory failure receiving oxygen
• Critical illness - sepsis, shock, major trauma, cardiac arrest
• Suspected metabolic disturbance - diabetic ketoacidosis, renal failure, poisoning, severe vomiting or diarrhoea
• Reduced conscious level of unclear cause
• Monitoring - after a change in oxygen, after starting NIV, and to track response to treatment

Arterial or venous?

In practice, a venous gas with pulse oximetry answers most questions, and an arterial sample is reserved for when oxygenation must be quantified or hypercapnia confirmed. Arterial puncture is painful and carries small risks of haematoma, arterial spasm, infection and, very rarely, distal ischaemia.

The five-step method

Step 1: assess oxygenation

• Is the patient hypoxaemic? A PaO2 below 8 kPa defines respiratory failure.
• Relate the PaO2 to the FiO2. A useful bedside approximation is that the PaO2 in kPa should be roughly the FiO2 percentage minus 10 - so about 11 kPa on air, 30 kPa on 40%, and 50 kPa on 60%. A PaO2 of 12 kPa on 60% oxygen represents severe gas exchange failure even though the number looks normal.
• Calculate the A-a gradient if the distinction matters. Breathing air at sea level, alveolar oxygen is approximately 20 minus PaCO2 divided by 0.8 in kPa, and the gradient is that value minus the measured PaO2. A normal gradient is under about 2 kPa in a young adult, rising with age.
• A raised A-a gradient means the lung is the problem - V/Q mismatch, shunt or diffusion impairment. A normal gradient with hypoxaemia means hypoventilation or a low inspired oxygen, and points to the respiratory pump rather than the lung.

Step 2: look at the pH

• pH below 7.35 - acidaemia
• pH above 7.45 - alkalaemia
• pH normal - either genuinely normal, fully compensated, or a mixed disorder with opposing effects. Do not stop here.
• The pH tells you which direction the primary disorder is pushing, and everything else in the interpretation follows from that

Step 3: look at the PaCO2 - the respiratory component

• CO2 is an acid. A high PaCO2 pushes the pH down, and a low PaCO2 pushes it up.
• High PaCO2 with a low pH - respiratory acidosis
• Low PaCO2 with a high pH - respiratory alkalosis
• Low PaCO2 with a low pH - the CO2 is not the cause; it is respiratory compensation for a metabolic acidosis
• High PaCO2 with a high pH - respiratory compensation for a metabolic alkalosis

Step 4: look at the bicarbonate and base excess - the metabolic component

• Bicarbonate is a base. A low bicarbonate pushes the pH down, and a high bicarbonate pushes it up.
• Low bicarbonate with a low pH - metabolic acidosis
• High bicarbonate with a high pH - metabolic alkalosis
• Base excess says the same thing in one number: more negative than minus 2 indicates a metabolic acidosis, more positive than plus 2 a metabolic alkalosis. It is often the quickest way to spot a metabolic component.

Step 5: assess compensation

• Uncompensated - the pH is abnormal and the other system has not moved
• Partially compensated - the other system has moved in the correcting direction but the pH is still abnormal
• Fully compensated - the pH is back within the normal range, but both the CO2 and the bicarbonate remain abnormal
• Compensation never overcorrects. If the pH has crossed to the opposite side of 7.40 from where the primary disorder would put it, there is a second primary disorder.
• Respiratory compensation is fast - minutes to hours, by changing minute ventilation. Metabolic (renal) compensation is slow - 2 to 3 days, by altering bicarbonate handling. This difference is what allows an acute problem to be distinguished from a chronic one.

The four primary disorders and their causes

Respiratory acidosis - high CO2

Always a failure of alveolar ventilation. Work down the respiratory pump from the brain outwards:

• Reduced drive - opioids, benzodiazepines, alcohol, anaesthetics, brainstem stroke, raised intracranial pressure
• Neuromuscular - Guillain-Barre syndrome, myasthenia gravis, motor neurone disease, high cervical cord injury, muscular dystrophy
• Chest wall - kyphoscoliosis, flail chest, obesity hypoventilation, circumferential burns
• Airway and lung - COPD, severe asthma in the exhausted phase, upper airway obstruction, advanced bronchiectasis and cystic fibrosis

Respiratory alkalosis - low CO2

Always hyperventilation, and the important task is to identify why - it is far more often a sign of serious illness than of anxiety.

• Hypoxia driving ventilation - pulmonary embolism, pneumonia, pulmonary oedema, asthma, high altitude
• Sepsis - one of the earliest gas abnormalities in sepsis
• Pain and anxiety - a diagnosis of exclusion, never a first assumption in an unwell patient
• Salicylate poisoning - early respiratory alkalosis from direct respiratory centre stimulation, later joined by a metabolic acidosis
• CNS causes - stroke, meningitis, encephalitis, head injury
• Liver failure, pregnancy (progesterone-driven), and mechanical over-ventilation

Metabolic acidosis - low bicarbonate

Divide by the anion gap, which distinguishes acid being added to the system from bicarbonate being lost from it.

Anion gap = (sodium + potassium) - (chloride + bicarbonate), normally 10 to 18 mmol/L. Some laboratories omit potassium, giving a normal range of 8 to 16. In hypoalbuminaemia the gap is falsely low: add roughly 2.5 mmol/L for every 10 g/L the albumin falls below 40.

The mnemonics are MUDPILES for the raised gap (methanol, uraemia, DKA, propylene glycol, isoniazid, lactate, ethylene glycol, salicylates) and, for the normal gap, HARDUPS (hyperalimentation, acetazolamide, renal tubular acidosis, diarrhoea, ureteroenterostomy, pancreatic fistula, saline).

Metabolic alkalosis - high bicarbonate

• Vomiting or nasogastric aspiration - loss of gastric acid, with hypokalaemia and hypochloraemia. Classic in pyloric stenosis, where the gas shows a hypochloraemic, hypokalaemic metabolic alkalosis.
• Diuretics - loop and thiazide
• Hypokalaemia from any cause
• Mineralocorticoid excess - Conn syndrome, Cushing syndrome, ectopic ACTH, liquorice excess
• Bartter and Gitelman syndromes
• Excess alkali - antacids, milk-alkali syndrome, large citrate loads in massive transfusion
• Chronic respiratory acidosis being over-corrected - a raised bicarbonate persisting after the CO2 has been brought down by ventilation

Worked examples

Common pitfalls

Beyond the numbers

Three additional values on the printout are worth reading deliberately rather than glancing at.

• Lactate - a marker of tissue hypoperfusion or impaired clearance. Above 2 mmol/L is abnormal, and above 4 mmol/L in suspected sepsis indicates high risk and triggers the sepsis pathway. Not all raised lactate is hypoperfusion: it also rises with salbutamol, metformin, seizures, liver failure and thiamine deficiency.
• Potassium - available within a minute, and in suspected hyperkalaemia this speed matters. Treat on the gas result while awaiting the laboratory sample if there are ECG changes.
• Carboxyhaemoglobin and methaemoglobin - reported by co-oximetry. Request them where there has been smoke exposure, a faulty boiler, or unexplained cyanosis with a normal PaO2.