Step by step

How to read an arterial blood gas (ABG) in six steps

To read an arterial blood gas, it helps to take it in the same order every time: the patient and sample, pH, primary disorder, compensation, anion gap, then oxygenation. Done that way, a wall of numbers becomes a short, repeatable piece of reasoning.

· Last updated: 2 November 2026 · 8 min read

Before you start: normal blood gas values

Parameter Typical adult range In kPa What it tells you
pH 7.35–7.45 — Acidaemia or alkalaemia
PaCO₂ 35–45 mmHg 4.7–6.0 kPa Respiratory component
HCO₃⁻ 22–26 mmol/L — Metabolic component
Base excess −2 to +2 mmol/L — Metabolic component, independent of CO₂
PaO₂ (room air) 80–100 mmHg 10.7–13.3 kPa Oxygenation
Lactate < 2 mmol/L — Tissue perfusion and metabolism

To convert, mmHg = kPa × 7.50062 (about 7.5). Reference ranges vary slightly between laboratories and analysers; it is advisable to use the ones printed on the report. PaO₂ also falls with age and depends entirely on the inspired oxygen.

Step 1: Start with the patient and the sample

Before the numbers, it helps to note three things: how the patient looks, how much oxygen they were receiving when the sample was taken (FiO₂, flow rate or ventilator settings), and whether the sample is truly arterial. An air bubble, a long delay before analysis or an accidental venous sample can all distort the result. A gas that does not fit the patient deserves a second look before a long interpretation.

Step 2: Look at the pH

  • pH below 7.35: acidaemia.
  • pH above 7.45: alkalaemia.
  • pH 7.35–7.45: normal, which does not rule out a disorder. Either nothing is wrong, or two opposing processes cancel each other out.

The pH tells you which way the balance has tipped. The next step tells you why.

Step 3: Identify the primary disorder

The next step is to look at PaCO₂ and HCO₃⁻ and ask which one explains the pH.

pH PaCO₂ HCO₃⁻ Primary disorder
Low High Normal or high Respiratory acidosis
Low Normal or low Low Metabolic acidosis
High Low Normal or low Respiratory alkalosis
High Normal or high High Metabolic alkalosis

A rise in CO₂ lowers pH; a rise in bicarbonate raises it. If PaCO₂ and HCO₃⁻ both point towards the same pH change (for example high CO₂ and low bicarbonate in an acidaemic patient), there are two primary processes: a mixed disorder.

The base excess supports the reading: clearly negative in metabolic acidosis, clearly positive in metabolic alkalosis.

Step 4: Check the compensation

The body responds to a primary disorder by shifting the other component in the same direction. Lungs act within minutes to hours; kidneys take days. The rules below predict the expected response; a measured value outside the range suggests a second disorder.

Primary disorder Expected compensation (mmHg, mmol/L)
Metabolic acidosis Expected PaCO₂ = 1.5 × HCO₃⁻ + 8 ± 2 (Winter’s formula)
Metabolic alkalosis Expected PaCO₂ ≈ 0.7 × HCO₃⁻ + 21 ± 2
Acute respiratory acidosis HCO₃⁻ rises about 1 mmol/L per 10 mmHg rise in PaCO₂
Chronic respiratory acidosis HCO₃⁻ rises about 3.5 mmol/L per 10 mmHg rise
Acute respiratory alkalosis HCO₃⁻ falls about 2 mmol/L per 10 mmHg fall in PaCO₂
Chronic respiratory alkalosis HCO₃⁻ falls about 4–5 mmol/L per 10 mmHg fall

If your analyser reports kPa, it is advisable to convert PaCO₂ to mmHg first, or to remember that 10 mmHg is about 1.3 kPa. In metabolic acidosis, a PaCO₂ above the Winter range means the lungs are not keeping up (a coexisting respiratory acidosis); a PaCO₂ below it means extra hyperventilation (a coexisting respiratory alkalosis).

Step 5: In metabolic acidosis, calculate the anion gap

The anion gap separates acidoses caused by added acids from those caused by loss of bicarbonate:

Anion gap = Na⁺ − (Cl⁻ + HCO₃⁻)

Without potassium, about 8–12 mmol/L is often quoted, but the local range applies. A raised gap points to unmeasured acids such as lactate, ketones, uraemic acids or certain toxins; a normal gap points to bicarbonate loss (for example diarrhoea) or chloride gain (for example large volumes of saline).

Albumin is the main unmeasured anion, so low albumin hides a raised gap. The adjustment used by the anion gap calculator is:

Adjusted gap = gap + 0.25 × (40 − albumin in g/L)

Two optional refinements:

  • Delta ratio = (gap − 12) ÷ (24 − HCO₃⁻). Roughly, below 1 suggests an added normal-gap acidosis; 1–2 fits a pure raised-gap acidosis; above 2 suggests an added metabolic alkalosis. It is an approximation, not a rule.
  • If toxic alcohol ingestion is a concern, the serum osmolality calculator gives the osmolal gap.

Step 6: Assess oxygenation

PaO₂ only makes sense alongside the oxygen being given. A PaO₂ of 90 mmHg is unremarkable on room air but worrying on 60% oxygen. The P/F ratio puts the two together:

P/F = PaO₂ (mmHg) ÷ FiO₂ (as a fraction)

On room air, healthy lungs give a P/F of roughly 400–500 mmHg. Values of 300 mmHg or less are one of the Berlin criteria for ARDS, but only when the other criteria (timing, imaging, cause, PEEP) are met. The P/F ratio calculator accepts PaO₂ in mmHg or kPa and FiO₂ as a percentage or fraction.

Also note whether the patient is hypoxaemic (low PaO₂) and whether PaCO₂ is raised, which separates mainly oxygenation failure from ventilatory failure.

Worked examples

These examples are for practising the method, not for interpreting a real patient’s result.

Example 1. Raised anion gap metabolic acidosis with appropriate compensation

pH 7.21, PaCO₂ 25 mmHg (3.33 kPa), HCO₃⁻ 10 mmol/L, Na⁺ 138, Cl⁻ 102 mmol/L, albumin 40 g/L, glucose markedly raised.

  1. pH 7.21: acidaemia.
  2. HCO₃⁻ low, PaCO₂ low: primary metabolic acidosis.
  3. Winter: 1.5 × 10 + 8 = 23, range 21–25 mmHg. Measured 25: compensation appropriate.
  4. Anion gap = 138 − (102 + 10) = 26 mmol/L: raised. Albumin normal, no adjustment needed.
  5. Delta ratio = (26 − 12) ÷ (24 − 10) = 14 ÷ 14 = 1.0: consistent with a pure raised-gap acidosis.

With high glucose this pattern is typical of diabetic ketoacidosis, though ketones and the clinical picture confirm it.

Example 2. Acute-on-chronic respiratory acidosis

pH 7.24, PaCO₂ 70 mmHg (9.33 kPa), HCO₃⁻ 30 mmol/L, PaO₂ 55 mmHg (7.33 kPa) on FiO₂ 0.28.

  1. pH 7.24: acidaemia.
  2. PaCO₂ high: primary respiratory acidosis.
  3. PaCO₂ is 30 mmHg above 40. Acute rule: 24 + 3 × 1 = 27 mmol/L. Chronic rule: 24 + 3 × 3.5 = 34.5 mmol/L. Measured 30 lies between the two: more bicarbonate than a purely acute rise would explain, less than a fully chronic state. This is the typical picture of acute-on-chronic hypercapnia, as in an exacerbation of COPD.
  4. P/F = 55 ÷ 0.28 = 196 mmHg. The calculator places this in the Moderate (100–200) Berlin band but also reminds you that the Berlin bands describe ARDS only when the other criteria are met.

Example 3. A hidden raised gap and a mixed acidosis

pH 7.28, PaCO₂ 32 mmHg (4.27 kPa), HCO₃⁻ 15 mmol/L, Na⁺ 136, Cl⁻ 110 mmol/L, albumin 24 g/L, lactate 4.5 mmol/L, PaO₂ 72 mmHg (9.60 kPa) on FiO₂ 0.40.

  1. pH 7.28: acidaemia; low HCO₃⁻: primary metabolic acidosis.
  2. Winter: 1.5 × 15 + 8 = 30.5, range 28.5–32.5 mmHg. Measured 32: appropriate.
  3. Anion gap = 136 − (110 + 15) = 11 mmol/L, apparently normal. Adjusted for albumin: 11 + 0.25 × (40 − 24) = 15 mmol/L, raised, in keeping with the lactate.
  4. Delta ratio = (15 − 12) ÷ (24 − 15) = 3 ÷ 9 = 0.33: the fall in bicarbonate is larger than the rise in the gap, suggesting a coexisting normal-gap (hyperchloraemic) acidosis, for example after large volumes of saline.
  5. P/F = 72 ÷ 0.40 = 180 mmHg (24.0 kPa).

Without the albumin adjustment, the lactic component would have been easy to miss.

Arterial or venous blood gas?

Venous blood gases are easier and less painful to obtain, and are widely used in emergency departments and for monitoring trends. Two reviews compared them: Byrne and colleagues (pH, PCO₂, PO₂) and an earlier one by Kelly that also covered bicarbonate. They found:

  • pH: venous values on average only about 0.03 lower than arterial; usually close enough for screening.
  • Bicarbonate: venous on average about 1.4 mmol/L higher, with individual differences up to about ±5 mmol/L (Kelly).
  • PCO₂: venous on average a few mmHg higher, but with wide individual variation. Kelly suggests a normal venous PCO₂ can help screen out arterial hypercapnia; a raised one does not quantify it reliably.
  • PO₂: no useful agreement. Oxygenation needs an arterial sample, or at least pulse oximetry with its own limits. The guide to normal vital signs by age covers SpO₂ ranges and how to get a reliable reading.

Lactate, electrolytes and glucose from a venous gas are generally usable, provided the sample is handled correctly. Whether a venous sample is acceptable for a given question is set by local practice.

Common pitfalls

  • Ignoring FiO₂. A PaO₂ without the oxygen being delivered cannot be interpreted.
  • Calling a normal pH normal. Abnormal PaCO₂ and HCO₃⁻ with a normal pH usually mean a mixed disorder.
  • Mixing units. Applying Winter’s formula to a PaCO₂ in kPa gives nonsense; it is best to convert first.
  • Expecting full compensation. Compensation does not overshoot; a pH pushed past normal in the opposite direction suggests a second process.
  • Forgetting albumin. In critically ill patients, low albumin often hides a raised anion gap.
  • Using a different gap formula. Including potassium raises the gap by about 4 mmol/L; it is best compared with the matching reference range.
  • Delay and bubbles. A sample left at room temperature or with air in the syringe can change PO₂, PCO₂ and lactate.

Frequently asked questions

What are the normal arterial blood gas values?

Typical adult reference values are pH 7.35–7.45, PaCO₂ 35–45 mmHg (4.7–6.0 kPa), bicarbonate 22–26 mmol/L, base excess −2 to +2 mmol/L and, on room air, PaO₂ 80–100 mmHg (10.7–13.3 kPa). Lactate is usually below 2 mmol/L. Each laboratory sets its own ranges.

What is the difference between acidaemia and acidosis?

Acidaemia describes the blood: a pH below 7.35. Acidosis describes a process that adds acid or removes base. A patient can have an acidosis with a normal pH if another process, or compensation, pulls the pH back. That is why a normal pH never rules out a disorder on its own.

What is Winter’s formula?

It predicts the PaCO₂ expected when the lungs compensate for a metabolic acidosis: expected PaCO₂ (mmHg) = 1.5 × HCO₃⁻ + 8, ± 2. A measured PaCO₂ above the range suggests an added respiratory acidosis; below it, an added respiratory alkalosis. With HCO₃⁻ 10 mmol/L, for example, the expected range is 21–25 mmHg.

How do I convert kPa to mmHg?

Multiply kPa by 7.50062 (about 7.5) to get mmHg, and divide mmHg by the same factor to get kPa. A PaCO₂ of 5.3 kPa is about 40 mmHg, and 10 mmHg is about 1.3 kPa. Convert before applying Winter’s formula or the other compensation rules, which are written in mmHg.

Does compensation ever bring the pH fully back to normal?

Rarely. Compensation usually moves the pH towards normal without reaching the middle of the range. A completely normal pH with clearly abnormal PaCO₂ and bicarbonate should prompt a search for a mixed disorder; chronic respiratory alkalosis is the main exception. Compensation does not overshoot: a pH pushed past normal in the opposite direction points to a second process.

Can a venous blood gas replace an arterial one?

For pH, bicarbonate, electrolytes and lactate, a venous sample is often close enough for screening and trends. Venous PCO₂ agrees less well, and venous PO₂ says nothing reliable about oxygenation, so an arterial sample is still needed when those questions matter.

What is the P/F ratio?

It is PaO₂ divided by FiO₂ expressed as a fraction, also called the Horowitz index. It shows how well the lungs oxygenate for the oxygen given. Healthy lungs on room air give roughly 400–500 mmHg; 300 mmHg or less is one element of the Berlin definition of ARDS, alongside timing, imaging, cause and PEEP.

Sources

  1. Berend K, de Vries APJ, Gans ROB. Physiological approach to assessment of acid–base disturbances. N Engl J Med 2014;371:1434–1445
  2. Albert MS, Dell RB, Winters RW. Quantitative displacement of acid-base equilibrium in metabolic acidosis. Ann Intern Med 1967;66:312–322
  3. Kraut JA, Madias NE. Serum anion gap: its uses and limitations in clinical medicine. Clin J Am Soc Nephrol 2007;2:162–174
  4. Byrne AL et al. Peripheral venous and arterial blood gas analysis in adults: are they comparable? A systematic review and meta-analysis. Respirology 2014;19:168–175
  5. ARDS Definition Task Force. Acute respiratory distress syndrome: the Berlin Definition. JAMA 2012;307:2526–2533
  6. Kelly AM. Review article: Can venous blood gas analysis replace arterial in emergency medical care. Emerg Med Australas 2010;22(6):493–498