Clinical overview
The arterial blood gas (ABG) is the single most decision-changing bedside test you will order in a deteriorating obstetric or post-operative patient. It tells you four things at once that no other test does so quickly: whether the patient is oxygenating, whether she is ventilating, what her acid–base status is, and — increasingly with modern analysers — her lactate, glucose, electrolytes and haemoglobin. For the O&G registrar this matters most in three recurring scenarios: the collapsed or septic mother, the woman with pre-eclampsia with severe features or pulmonary oedema, and the post-operative patient (post-caesarean, post-laparotomy) who is tachypnoeic, hypotensive or oliguric. In each, an ABG converts a vague clinical impression into a quantified physiological problem you can act on.
Interpreting a gas is not the work of an intensivist. It means taking a printed result, working through it in a disciplined, reproducible order, naming the disturbance correctly, calculating the expected compensation, and translating the numbers into a safe management decision and an escalation call. The skill lies in the interpretation and reasoning, not in reciting normal values. The commonest mistake is reading the pH and pO₂ and stopping there. Pregnancy adds a crucial twist — the normal maternal ABG is not the normal non-pregnant one, and treating a "low" maternal bicarbonate or pCO₂ as pathology is a classic error. The systematic approach below interprets any gas, in any patient, reliably.
Core knowledge
Figure F3.1 — Pregnancy resets the ABG: progesterone-driven hyperventilation lowers PaCO₂, the kidney excretes bicarbonate, and the result is a chronic compensated respiratory alkalosis — so a "normal" maternal PaCO₂ of 5 kPa signals CO₂ retention.
The normal arterial blood gas — and how pregnancy shifts it
Standard adult arterial reference ranges (textbook physiology, breathing room air at sea level):
| Parameter | Non-pregnant adult | Term pregnancy (approximate) |
|---|---|---|
| pH | 7.35–7.45 | 7.40–7.47 (mild alkalaemia) |
| paCO₂ | 4.7–6.0 kPa (35–45 mmHg) | 3.7–4.3 kPa (28–32 mmHg) |
| paO₂ | 11–13 kPa (80–100 mmHg) | 13–14 kPa (often higher) |
| HCO₃⁻ | 22–26 mmol/L | 18–22 mmol/L |
| Base excess | −2 to +2 mmol/L | slightly negative |
Progesterone is a direct respiratory stimulant. From early pregnancy it drives an increase in tidal volume (and hence minute ventilation by ~30–50%), producing a chronic compensated respiratory alkalosis. The pCO₂ falls to roughly 3.7–4.3 kPa, the kidney excretes bicarbonate to compensate (HCO₃⁻ falls to ~18–22 mmol/L), and the pH settles slightly alkalaemic. The practical consequences are large and examinable:
- A maternal pCO₂ of 5.0 kPa — perfectly normal in a non-pregnant adult — represents relative CO₂ retention in a term mother and may signal impending respiratory failure or exhaustion (for example in severe asthma or magnesium toxicity). A "normalising" pCO₂ in a tiring asthmatic is an ominous sign.
- The lowered buffering reserve (lower baseline bicarbonate) means a pregnant woman tolerates a metabolic acidosis less well — she has less bicarbonate to spare. Diabetic ketoacidosis, including euglycaemic DKA, develops faster and at lower glucose levels in pregnancy.
- Maternal alkalosis shifts the oxyhaemoglobin dissociation curve and, with the placenta, helps offload oxygen to the fetus (the maternal–fetal "double Bohr / double Haldane" effect — standard teaching).
Acid–base first principles
pH is governed by the Henderson–Hasselbalch relationship, which simplifies clinically to: pH depends on the ratio of bicarbonate (the metabolic, renal-controlled component) to carbon dioxide (the respiratory, lung-controlled component).
- Acidosis = a process lowering pH. Acidaemia = an actually low blood pH (<7.35). Alkalosis/alkalaemia mirror these. Use the words precisely; a patient can have a normal pH yet harbour two opposing primary disorders.
- A respiratory disturbance is a primary change in pCO₂: a high pCO₂ acidifies (respiratory acidosis), a low pCO₂ alkalinises (respiratory alkalosis).
- A metabolic disturbance is a primary change in bicarbonate/base: a low HCO₃⁻/negative base excess acidifies (metabolic acidosis), a high HCO₃⁻/positive base excess alkalinises (metabolic alkalosis).
- Compensation is the body's attempt to push the pH back toward normal by adjusting the other system. The lungs compensate fast (minutes–hours) by changing ventilation; the kidneys compensate slowly (hours–days) by retaining or excreting bicarbonate. Compensation never fully corrects the pH — if the pH is normal but both pCO₂ and HCO₃⁻ are deranged, suspect either full compensation of a chronic single disorder or a mixed disorder.