Key Facts

Respiratory failure is defined as failure of the respiratory system to maintain adequate gas exchange. It is classified into Type 1 (hypoxaemic) and Type 2 (hypercapnic, ventilatory failure). Both may be acute, chronic, or acute-on-chronic.

Epidemiology

Respiratory failure is one of the commonest reasons for hospital admission and ICU referral. COPD exacerbations account for approximately 115,000 emergency admissions annually in the UK, many with Type 2 respiratory failure. Community-acquired pneumonia affects 1-5 per 1,000 adults annually, frequently causing Type 1 failure.

Aetiology

Type 1 (hypoxaemic):

• V/Q mismatch: pneumonia, asthma, PE, atelectasis
• Shunt: ARDS, pulmonary AVM, hepatopulmonary syndrome
• Diffusion impairment: pulmonary fibrosis (usually exercise-limited)
• Low inspired O₂: altitude

Type 2 (hypercapnic):

• Reduced drive: opioid/sedative overdose, brainstem lesion, central sleep apnoea
• Neuromuscular: motor neurone disease, Guillain-Barré, myasthenia gravis, muscular dystrophy
• Chest wall: kyphoscoliosis, flail chest, obesity hypoventilation syndrome
• Airways: severe COPD, life-threatening asthma

Pathophysiology

Type 1: V/Q mismatch occurs when ventilation and perfusion are mismatched (e.g. perfused but poorly ventilated alveoli in pneumonia). True shunt (blood bypassing ventilated alveoli) is refractory to supplemental O₂. The A-a gradient is elevated.

Type 2: Alveolar hypoventilation leads to CO₂ accumulation. Using the alveolar gas equation: PAO₂ = PIO₂ − (PaCO₂/R), rising PaCO₂ directly reduces PAO₂. In chronic Type 2 failure, renal compensation retains bicarbonate to buffer the respiratory acidosis.

Type 1 Respiratory Failure

• Dyspnoea, tachypnoea (RR >20)
• Tachycardia, use of accessory muscles
• Cyanosis (central — tongue, lips)
• Features of underlying cause (e.g. crackles in pneumonia, wheeze in asthma)
• Confusion and agitation (hypoxia)

Type 2 Respiratory Failure

• Dyspnoea (may be less prominent if chronic)
• CO₂ retention signs: drowsiness, confusion, flapping tremor (asterixis), bounding pulse, warm peripheries, headache (especially morning)
• Papilloedema (chronic hypercapnia)
• Reduced respiratory rate if cause is reduced drive

Red Flags

• SpO₂ <85% or rapidly falling
• RR <8 or >35
• GCS falling or inability to speak in sentences
• Silent chest in asthma (near-fatal)
• pH <7.25 on ABG
• Signs of respiratory muscle fatigue (paradoxical abdominal movement)

Bedside

• ABG: essential — determines type (PaO₂, PaCO₂, pH, HCO₃⁻, A-a gradient, lactate)
• SpO₂ monitoring: continuous pulse oximetry
• PEFR: if asthma/COPD suspected
• ECG: arrhythmia, RV strain (PE), ischaemia

Bloods

• FBC: anaemia (reduced O₂ carrying capacity), raised WCC (infection)
• CRP/procalcitonin: infection markers
• U&Es: renal function, electrolyte derangement
• BNP/NT-proBNP: cardiac failure assessment
• D-dimer: PE screening (if low pre-test probability)
• Venous blood gas: can screen for hypercapnia if ABG delayed

Imaging

• CXR: consolidation, pulmonary oedema, pneumothorax, pleural effusion
• CTPA: if PE suspected
• CT thorax: if ILD, malignancy, or complex pathology
• Lung ultrasound: pleural effusion, consolidation, pneumothorax, B-lines

Special Tests

• Forced vital capacity (FVC): serial measurement in neuromuscular disease — FVC <1L or <15 ml/kg indicates need for ventilatory support
• Sleep study (polysomnography): if obesity hypoventilation or sleep-disordered breathing suspected
• Diaphragm ultrasound/sniff test: diaphragmatic paralysis

Non-pharmacological

• Controlled oxygen therapy: target SpO₂ 94-98% (most patients) or 88-92% (COPD, obesity hypoventilation, neuromuscular disease) per BTS oxygen guideline
• Venturi mask for precise FiO₂ delivery in Type 2 failure risk patients
• Positioning: sit upright to optimise diaphragmatic excursion
• NIV (BiPAP): first-line for acute hypercapnic respiratory failure with pH 7.25-7.35 in COPD — start IPAP 12-15 cmH₂O, EPAP 4-5 cmH₂O (NICE NG115)
• CPAP: for Type 1 failure (e.g. pulmonary oedema, obesity)

Pharmacological

• Treat underlying cause: antibiotics for pneumonia, bronchodilators for COPD/asthma, anticoagulation for PE
• Doxapram 1.5-4 mg/min IV: respiratory stimulant if NIV unavailable or not tolerated (rarely used now)
• Naloxone 400 mcg IV (repeat every 2-3 min, max 10 mg): opioid overdose causing Type 2 failure
• Aminophylline 5 mg/kg IV loading (if not on theophylline), then 0.5 mg/hr: adjunct in severe COPD

Surgical/Interventional

• Invasive mechanical ventilation: if NIV fails (pH <7.25 after 1-2 hours), GCS <8, or respiratory arrest
• Intercostal drain: tension/large pneumothorax
• Tracheostomy: prolonged ventilatory weaning, bulbar neuromuscular disease

Referral Criteria

• Refer to ICU/HDU if failing NIV, pH <7.25, or requiring FiO₂ >0.6
• Respiratory/neurology referral for new neuromuscular presentations
• Home NIV service referral for chronic Type 2 failure (obesity hypoventilation, neuromuscular, chest wall disease)

Prognosis depends on the underlying cause. In-hospital mortality for acute COPD exacerbations requiring NIV is approximately 12-15%. Mortality from ARDS-related respiratory failure is 35-46%. Neuromuscular causes (e.g. Guillain-Barré) may have full recovery with supportive care. Patients requiring invasive ventilation have ICU mortality of 20-40% depending on age and comorbidities. Survivors of prolonged ventilation may have persistent functional impairment; 25% of ICU survivors have impaired lung function at 1 year.

Classification Summary

ABG Interpretation Pattern