Arterial blood gas analysis - principles, interpretation and relevance to nephrology
Arterial blood gases (ABGs) are essential for assessing ventilatory status, oxygenation and acid-base balance in acutely unwell patients.
In nephrology they guide management of severe metabolic acidosis (uraemic acidosis, diabetic ketoacidosis), indications for urgent dialysis, therapy for life‑threatening electrolyte disturbance (notably hyperkalaemia), and ventilation management in patients with fluid overload or chronic lung disease.
This section summarises the physiological basis, a practical interpretation method, common mixed disorders seen in acute nephrology, and key safety and sampling points for UK practice.
Key physiology (concise)
- pH and hydrogen ions: pH = -log10[H+]. Normal arterial pH 7.35-7.45. Small changes in [H+] produce clinically important pH shifts.
- Buffers: bicarbonate (HCO3-)/carbonic acid is the major extracellular buffer; haemoglobin, plasma proteins and phosphate also buffer H+.
- Henderson-Hasselbalch: clinically used as the bicarbonate-CO2 framework - pH reflects the relationship between HCO3- (metabolic) and PaCO2 (respiratory).
- Renal (metabolic) control: kidneys reabsorb HCO3- and generate new bicarbonate while excreting H+. Renal compensation is slow (hours-days).
- Respiratory control: alveolar ventilation determines PaCO2 and thus quickly influences pH.
- Oxygen carriage: Hb carries most O2; shifts in the oxyhaemoglobin dissociation curve (right/left) affect tissue O2 delivery and are influenced by pH, PaCO2, temperature and CO exposure.
What an ABG reports (core elements) and normal ranges
Conversion: 1 kPa ≈ 7.5 mmHg.