What are the normal ABG values?
An arterial blood gas (ABG) measures arterial pH, the partial pressures of oxygen (PaO2) and carbon dioxide (PaCO2), and reports bicarbonate (HCO3-) — usually calculated from pH and PaCO2 — plus base excess. PaO2 tells you about oxygenation, PaCO2 about ventilation, and the pH–PaCO2–HCO3- trio about acid–base status.
| Parameter | Normal range | Tells you about |
|---|---|---|
| pH | 7.35–7.45 | Acidaemia (below 7.35) or alkalaemia (above 7.45) |
| PaCO2 | 35–45 mm Hg | Ventilation — the respiratory component |
| HCO3- | 22–26 mEq/L | The metabolic component |
| PaO2 | 75–100 mm Hg | Oxygenation |
| Base excess | −4 to +2 | Metabolic component (negative = base deficit) |
| SaO2 | 95–100% | Haemoglobin saturation |
- The radial artery is preferred (superficial, easily felt); the femoral is next. Do a modified Allen test before radial puncture to confirm collateral flow through the ulnar artery.
- PaCO2 is a more sensitive marker of ventilatory failure than PaO2, especially on supplemental oxygen — a normal PaO2 on oxygen does not rule out respiratory failure.
- Venous bicarbonate is generally 2–4 mEq/L higher than arterial.
What is the stepwise approach to interpreting an ABG?
- Look at the pH. Below 7.35 = acidaemia; above 7.45 = alkalaemia. If the pH is within range, use 7.40 as the cut-off — 7.37 counts as the acidotic side, 7.42 as the alkalotic side.
- Find the primary disorder. Which value moves in the direction that explains the pH? High PaCO2 with low pH = respiratory acidosis; low HCO3- with low pH = metabolic acidosis; low PaCO2 with high pH = respiratory alkalosis; high HCO3- with high pH = metabolic alkalosis.
- Check compensation. The other value moves in the same direction to limit the pH change. Use the expected-compensation formulas below. If the measured value is outside the expected range, a second primary disorder is present.
- In metabolic acidosis, calculate the anion gap, correct it for albumin, and if it is high, calculate the delta ratio.
- Assess oxygenation — PaO2 and, where useful, the alveolar–arterial (A–a) gradient.
- Match to the clinical picture — the history usually tells you which disorder is plausible.
What are the compensation formulas for each acid–base disorder?
| Primary disorder | Compensation | Expected change |
|---|---|---|
| Metabolic acidosis | Hyperventilation (within 12–24 h) | Winter's formula: expected PaCO2 = (1.5 × HCO3-) + 8 ± 2 |
| Metabolic alkalosis | Hypoventilation | Expected PaCO2 = 0.7 × HCO3- + 20 ± 5 (some texts use a rise of 0.6 mm Hg per 1 mEq/L) |
| Acute respiratory acidosis | Cell buffering (minutes) | HCO3- rises 1 mEq/L per 10 mm Hg rise in PaCO2 |
| Chronic respiratory acidosis | Renal (days) | HCO3- rises 4 mEq/L per 10 mm Hg rise in PaCO2 |
| Acute respiratory alkalosis | Cell buffering | HCO3- falls 2 mEq/L per 10 mm Hg fall in PaCO2 (usually not below 18) |
| Chronic respiratory alkalosis | Renal (days) | HCO3- falls 4 mEq/L per 10 mm Hg fall in PaCO2 (usually not below 14) |
Why timing matters. The lungs change PaCO2 within minutes to hours, so respiratory compensation for a metabolic disorder is largely in place within 12–24 hours. The kidneys adjust bicarbonate — reabsorbing it and excreting fixed acid — over days. So in a respiratory disorder, a bicarbonate that has moved a lot tells you the problem has been present for days (chronic), while a small shift means it is acute. In the StatPearls worked example, a raised bicarbonate in a respiratory acidosis is read as metabolic compensation that 'takes days', pointing to a non-acute disorder.
Winter's formula: expected PaCO₂ = (1.5 × HCO₃⁻) + 8 ± 2
Measured PaCO₂ higher than expected → added respiratory acidosis; lower than expected → added respiratory alkalosis. Shortcut: the expected PaCO₂ roughly equals the last two digits of the pH.
How are the anion gap and delta ratio used in metabolic acidosis?
Anion gap = Na⁺ − (Cl⁻ + HCO₃⁻)
Normal range is about 4–12 mmol/L (8 ± 4); potassium is usually left out. Most of the normal gap is albumin.
Correct for albumin. Albumin is the main unmeasured anion, so a low albumin hides a raised gap: corrected AG = measured AG + 2.5 × (4.0 − albumin in g/dL). A measured gap of 10 with an albumin of 2.0 g/dL is really 15 — a true high anion gap acidosis. An anion gap above 18 almost always means an organic acid is present. For the full list of causes see the anion gap page.
Delta ratio = (corrected AG − 12) ÷ (24 − measured HCO₃⁻)
In a pure high anion gap acidosis the rise in the gap roughly equals the fall in bicarbonate.
| Delta ratio | Interpretation |
|---|---|
| Less than 1 | High anion gap acidosis plus a normal anion gap (hyperchloraemic) acidosis |
| 1 to 2 | Pure high anion gap metabolic acidosis |
| More than 2 | High anion gap acidosis plus metabolic alkalosis (or pre-existing high bicarbonate) |
- High anion gap causes — CAT MUDPILES: Cyanide and CO, Arsenic, Toluene, Methanol and Metformin, Uraemia, DKA, Paraldehyde, Iron and INH, Lactate, Ethylene glycol, Salicylates.
- Normal anion gap (hyperchloraemic) causes: mainly diarrhoea and renal tubular acidosis — chloride rises as bicarbonate falls. The urine anion gap (urine Na + K − Cl) helps separate gut from renal loss; see renal tubular acidosis types.
- Deep, rapid breathing of metabolic acidosis is Kussmaul breathing — the respiratory compensation you can see at the bedside.
What are the main causes of each primary acid–base disorder?
| Disorder | Common causes | Exam clue |
|---|---|---|
| Metabolic acidosis — high AG | DKA, lactic acidosis, renal failure, methanol, ethylene glycol, salicylates | Low HCO3-, high gap |
| Metabolic acidosis — normal AG | Diarrhoea, renal tubular acidosis | Hyperchloraemia |
| Metabolic alkalosis | Vomiting or gastric loss, diuretics, excess bicarbonate, milk–alkali syndrome | Chloride-responsive if urine Cl- below 10 mEq/L; chloride-resistant if above 20 mEq/L |
| Respiratory acidosis | Hypoventilation — COPD, opioid overdose, myasthenia gravis, Guillain–Barré syndrome | High PaCO2 |
| Respiratory alkalosis | Hyperventilation — anxiety, head injury or stroke, pulmonary embolism, early salicylate poisoning | Low PaCO2 |
Chloride-responsive metabolic alkalosis (vomiting, previous diuretic use) is corrected by replacing fluid, chloride and potassium.
How is oxygenation assessed, and what sampling errors distort an ABG?
The acid–base reading is only half of the ABG. PaO2 is the main reason for taking an arterial rather than a venous sample, because oxygen is where arterial and venous values differ most. Three common ways to judge oxygenation:
| Index | What it is | Use |
|---|---|---|
| A–a gradient | Difference between alveolar and arterial oxygen | Separates hypoventilation (normal gradient) from shunt, V/Q mismatch or diffusion defects; designed for room air and less accurate at high FiO2 |
| P/F ratio | PaO2 ÷ FiO2 | Simple bedside measure; used to grade ARDS severity |
| Oxygenation index | Mean airway pressure × FiO2 (%) ÷ PaO2 | Ventilated neonates and children — guides inhaled nitric oxide, surfactant and ECMO decisions |
- Collect the sample anaerobically in a 1–3 mL syringe with lyophilised heparin; liquid heparin or saline dilutes the sample with room-air gas values.
- Put the sample on ice and analyse it as soon as possible.
- Wrong or misstated FiO2, barometric pressure or body temperature produce erroneous values; temperature and acid–base changes can also make PaO2 and SaO2 disagree.
- Hypoxaemia itself can feed the acid–base picture: tissue hypoxia drives anaerobic metabolism and a lactic (metabolic) acidosis.
How do you work through ABG questions — worked examples?
Example 1 — a diabetic with vomiting and confusion. pH 7.25, PaCO2 30 mm Hg, HCO3- 12 mEq/L, Na+ 140, Cl- 100, albumin normal.
- pH 7.25 → acidaemia. Low HCO3- explains it → metabolic acidosis.
- Winter's: 1.5 × 12 + 8 = 26 ± 2 → expected PaCO2 24–28. Measured 30 is higher → an added respiratory acidosis.
- Anion gap = 140 − (100 + 12) = 28 → high anion gap.
- Delta ratio = (28 − 12) ÷ (24 − 12) = 16 ÷ 12 ≈ 1.3 → the metabolic part is a pure high anion gap acidosis.
- Final answer: high anion gap metabolic acidosis with a concurrent respiratory acidosis.
Example 2 — a long-standing COPD patient. pH 7.34, PaCO2 60 mm Hg, HCO3- 31 mEq/L.
- pH 7.34 → acidaemia; high PaCO2 explains it → respiratory acidosis.
- PaCO2 is 20 above 40. Acute rule: HCO3- should rise by 2 → about 26. Chronic rule: rise by 8 → about 32.
- Measured 31 fits the chronic rule → chronic (compensated) respiratory acidosis. A bicarbonate near 26 would suggest an acute rise in PaCO2 instead.