Acute Hypercapnic Respiratory Failure

Acute hypercapnic respiratory failure is a PaCO2 over 6.0 kPa (45 mmHg) with arterial pH under 7.35, caused by alveolar hypoventilation. It often coexists with hypoxaemia.

Epidemiology. COPD exacerbation is the commonest cause. Acidosis severity determines outcome, and in hospital mortality for acidotic COPD is about 10 to 15%.

Causes and associations.

• Airway disease: COPD, severe asthma, cystic fibrosis and bronchiectasis.
• Chest wall and pleural disease: obesity hypoventilation, kyphoscoliosis, flail chest and large effusion.
• Neuromuscular disease: Guillain-Barre syndrome, myasthenic crisis, motor neurone disease, muscular dystrophy and spinal cord injury.
• Central depression: opioids, sedatives, stroke and brainstem lesions.

Pathophysiology. Ventilatory demand exceeds capacity, because of increased load (airway resistance, hyperinflation), reduced drive or weakened muscles. Rising PaCO2 causes respiratory acidosis, which compensates over 3 to 5 days by renal bicarbonate retention. Oxygen therapy in COPD worsens hypercapnia through ventilation perfusion mismatch and a Haldane effect.

Presentation is breathlessness, drowsiness, headache, confusion, flapping tremor, bounding pulse, warm peripheries, papilloedema in severe cases and coma. Rapid shallow breathing, paradoxical abdominal movement and use of accessory muscles show muscle fatigue.

Red flags.

• GCS under 10 or falling, pH under 7.25 or rising PaCO2 despite treatment.
• Neuromuscular weakness (forced vital capacity under 15 mL/kg, weak cough, bulbar signs).
• Exhaustion, silent chest or inability to clear secretions.

Arterial blood gas on the current oxygen, chest radiograph, ECG, full blood count, urea and electrolytes, glucose, bicarbonate, culture of sputum and blood, and toxicology when drug use is possible. In neuromuscular disease measure forced vital capacity and maximum inspiratory pressure every 4 to 6 hours.

Differential diagnosis. Metabolic alkalosis with compensatory hypoventilation, sedative overdose and central causes, heart failure and pneumonia contributing to acute-on-chronic failure.

Controlled oxygen. Target saturation 88 to 92% until blood gases are known (94 to 98% when not at risk of hypercapnia). Use a venturi mask at 24 to 28% oxygen. Recheck gas within 30 to 60 minutes.

Bronchodilators. Salbutamol 2.5 to 5 mg and ipratropium 500 microgram nebulised, driven by air, with oxygen by nasal cannulae to keep the target saturation.

Corticosteroid and antibiotics in COPD exacerbation. Prednisolone 30 to 40 mg orally daily for 5 days. Doxycycline 200 mg on day 1 then 100 mg daily, or amoxicillin-clavulanate 625 mg orally every 8 hours, for 5 to 7 days when sputum is purulent.

Non-invasive ventilation (first line when pH is under 7.35 despite 1 hour of treatment).

• Start with inspiratory pressure 10 cmH2O and expiratory pressure 4 to 5 cmH2O. Increase inspiratory pressure by 2 to 5 cmH2O every 10 to 20 minutes to 20 to 30 cmH2O as tolerated.
• Check gas at 1 to 2 hours. Improvement in pH and respiratory rate means continue for at least 6 to 12 hours a day initially, with weaning over days.
• Contraindications: unprotected airway, vomiting, facial trauma, undrained pneumothorax and haemodynamic instability.

Invasive ventilation. Indications are failure of NIV (no improvement or pH under 7.25 after 1 to 2 hours), coma, respiratory arrest, copious secretions, haemodynamic instability and refusal of NIV when unrestricted treatment is intended. Use low tidal volume (6 to 8 mL/kg), long expiratory time, and a permissive approach in COPD.

Respiratory stimulant. Doxapram 1.5 to 4 mg/min IV (maximum duration 2 hours at first) only when NIV is not available, as a temporary measure. Avoid in seizure disorder, hypertension or arrhythmia.

Opioid or benzodiazepine overdose. Naloxone 0.4 mg IV titrated every 2 to 3 minutes to a maximum of 10 mg, followed by infusion of two thirds of the effective dose each hour. Flumazenil 0.2 mg IV titrated is used cautiously and is avoided in chronic benzodiazepine users and in mixed overdose with seizure risk.

Neuromuscular failure. Intubate for forced vital capacity under 15 mL/kg, maximum inspiratory pressure weaker than minus 30 cmH2O, bulbar failure or inability to clear secretions. Treat the cause (immunoglobulin 0.4 g/kg IV daily for 5 days, or plasma exchange, in Guillain-Barre syndrome and myasthenic crisis).

Monitoring. Arterial gas at 1 hour, 4 to 6 hours and with each change, respiratory rate, GCS, mask fit and air leak.

Referral and escalation. Intensive care for failure of NIV, pH under 7.25, GCS under 10, neuromuscular disease or need for invasive ventilation. Before discharge, assess for home ventilation in obesity hypoventilation and chronic hypercapnia.

Special groups. In obesity hypoventilation, use higher expiratory pressure (8 to 12 cmH2O). In pregnancy, target PaCO2 of 4.0 to 4.5 kPa, since hypercapnia harms the foetus. In children, specialist paediatric ventilation is required.