Respiratory Acidosis

Respiratory acidosis is a primary rise in PaCO₂ producing a fall in pH, resulting from alveolar hypoventilation: the lungs failing to clear CO₂ at the rate it is produced.

Renal compensation retains bicarbonate, but this takes 3–5 days to become fully established, which is why the distinction between acute and chronic matters so much.

Acute respiratory acidosis shows a markedly low pH with only a small rise in bicarbonate (roughly 1 mmol/L per 10 mmHg rise in PaCO₂), because compensation has not had time to develop.

Chronic respiratory acidosis shows a near-normal pH with a substantially raised bicarbonate (roughly 3.5–4 mmol/L per 10 mmHg), reflecting established renal compensation.

Causes include central respiratory depression (opioids, sedatives, brainstem pathology), neuromuscular disease (Guillain-Barré, myasthenia, motor neurone disease), chest wall and pleural disease, and airways and parenchymal disease, principally COPD, severe asthma and obesity hypoventilation.

• Blood gas showing low pH with raised PaCO₂. An arterial sample is preferred where precise PaCO₂ matters, though venous CO₂ correlates well enough for screening
• Distinguish acute from chronic by the bicarbonate, using the compensation rules above. A patient with PaCO₂ of 70 mmHg and bicarbonate of 26 is acutely decompensated and in danger; the same PaCO₂ with a bicarbonate of 38 reflects chronic adaptation. Mistaking chronic compensated hypercapnia for acute failure leads to unnecessary intervention, and mistaking acute failure for chronic leads to dangerous delay
• Acute-on-chronic is common and is identified by a bicarbonate that is raised but insufficient for the degree of hypercapnia
• Identify the cause: chest examination and imaging, drug chart review for opioids and sedatives, neurological assessment for neuromuscular weakness, and assessment for airway obstruction
• Serial gases are more informative than a single measurement, since the trajectory determines management
• In neuromuscular disease, forced vital capacity predicts respiratory failure earlier and more reliably than blood gases, which can remain normal until decompensation is imminent

• Treat the underlying cause, which is the priority: bronchodilators, steroids and antibiotics for COPD exacerbation; naloxone for opioid-induced respiratory depression; treatment of the neuromuscular disorder
• Controlled oxygen therapy in patients at risk of CO₂ retention, targeting saturations of 88–92% rather than normal values. The concern is real but is often misunderstood: the mechanism is principally increased ventilation-perfusion mismatch and the Haldane effect rather than simple loss of hypoxic drive. Critically, hypoxia kills before hypercapnia does, so oxygen should never be withheld from a hypoxic patient for fear of retention; it should be titrated
• Non-invasive ventilation (BiPAP) is the key intervention in acute hypercapnic respiratory failure, particularly in COPD, where it has clear mortality benefit. Indications include a pH below 7.35 with PaCO₂ above roughly 45–50 mmHg persisting despite initial medical therapy
• Invasive ventilation where non-invasive ventilation fails or is contraindicated: reduced consciousness with an unprotected airway, haemodynamic instability, copious secretions, facial trauma, or vomiting
• Avoid over-correcting chronic hypercapnia: rapidly normalising PaCO₂ in a chronically compensated patient produces a post-hypercapnic metabolic alkalosis, since the raised bicarbonate persists after the CO₂ has fallen
• Stop or reverse contributing sedatives and opioids
• Discuss ceiling of care early in patients with advanced chronic lung disease, since decisions about escalation to invasive ventilation are best made before the patient deteriorates rather than during a crisis

Referral: respiratory medicine and critical care for acute hypercapnic failure; neurology for neuromuscular causes, with early critical care involvement given the speed of decompensation.