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This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Type 1 (hypoxaemic): PaO2 <8 kPa with normal or low PaCO2 — V/Q mismatch (pneumonia, PE, pulmonary oedema, ARDS)
- Type 2 (hypercapnic): PaO2 <8 kPa with PaCO2 >6 kPa — alveolar hypoventilation (COPD, neuromuscular disease, chest wall disease, sedation)
- BTS oxygen guidelines: target SpO2 94–98% for most patients; 88–92% for patients at risk of hypercapnic failure (COPD, obesity hypoventilation)
- Type 2 failure in COPD: controlled oxygen (24–28% Venturi) + non-invasive ventilation (NIV, BiPAP) if pH <7.35 and PaCO2 >6 kPa despite initial treatment
- ABG is the essential investigation — always interpret PaO2, PaCO2, pH, HCO3, and base excess together
Overview
Respiratory failure is defined as failure of the respiratory system to maintain adequate oxygenation and/or carbon dioxide elimination. Type 1 (hypoxaemic) respiratory failure is characterised by PaO2 <8 kPa (60 mmHg) with normal or low PaCO2, caused by ventilation-perfusion (V/Q) mismatch, diffusion impairment, or shunt. Type 2 (hypercapnic) respiratory failure involves PaO2 <8 kPa with raised PaCO2 >6 kPa (45 mmHg), caused by inadequate alveolar ventilation. The distinction is critical because it determines oxygen therapy targets and the role of ventilatory support.
Epidemiology
Respiratory failure is a common reason for emergency admission and ICU care. Acute exacerbation of COPD is the most common cause of type 2 respiratory failure. Pneumonia, heart failure, and PE are the most common causes of type 1 failure. Chronic type 2 failure occurs in severe COPD, neuromuscular disease (MND, Duchenne), chest wall deformity (kyphoscoliosis), and obesity hypoventilation syndrome. Mortality is significant: approximately 25–30% in-hospital mortality for acute hypercapnic respiratory failure requiring NIV.
Clinical Features
Symptoms
Breathlessness (acute or progressive)
Confusion and drowsiness (particularly in type 2 — CO2 narcosis)
Morning headaches (chronic type 2 — nocturnal CO2 retention)
Signs
Cyanosis (central — lips and tongue)
Tachypnoea and increased work of breathing (accessory muscle use, nasal flaring)
Asterixis/flapping tremor (CO2 retention)
Bounding pulse, warm peripheries (vasodilation from hypercapnia)
Reduced level of consciousness (severe hypercapnia)
Tachycardia and hypertension (sympathetic response to hypoxia)
Investigations
First-line
Arterial blood gas (ABG)THE essential investigation. Type 1: PaO2 <8, PaCO2 normal/low. Type 2: PaO2 <8, PaCO2 >6. Assess pH, HCO3, base excess for acute vs chronic compensation
Pulse oximetryContinuous monitoring — but does NOT detect hypercapnia. Always pair with ABG
Chest X-rayIdentify underlying cause (consolidation, effusion, pulmonary oedema, pneumothorax)
Second-line
FBC, CRP, U&Es, BNPIdentify infection, renal impairment, heart failure
ECGArrhythmias, right heart strain (PE), ischaemia
CTPAIf PE suspected as cause of type 1 failure
Specialist
Spirometry and lung functionOnce stable — assess underlying lung disease severity
Sleep studyIf obesity hypoventilation syndrome or nocturnal hypoventilation suspected
1
Oxygen therapy
- Target SpO2 94–98% for MOST patients
- Target SpO2 88–92% for patients at risk of hypercapnic failure (COPD with previous type 2 RF, obesity hypoventilation, neuromuscular disease, chest wall deformity)
- Use controlled oxygen: 24–28% Venturi mask for at-risk patients; titrate up cautiously
- Repeat ABG 30–60 minutes after starting or changing oxygen therapy
2
Non-invasive ventilation (NIV/BiPAP) for type 2 failure
- Indications: pH <7.35 and PaCO2 >6 kPa DESPITE optimal medical therapy and controlled oxygen
- Bilevel positive airway pressure (BiPAP) — set IPAP (12–20 cmH2O) and EPAP (4–5 cmH2O)
- Start within 1 hour of ABG showing acidotic hypercapnia
- Repeat ABG at 1 hour — if no improvement, escalate (increase pressures, consider intubation)
- Do NOT delay NIV while awaiting other treatments
3
Treat the underlying cause
- COPD exacerbation: bronchodilators, steroids, antibiotics
- Pneumonia: antibiotics
- PE: anticoagulation
- Pulmonary oedema: diuretics, nitrates
- Opioid overdose: naloxone
4
Escalation
- If NIV fails or patient deteriorates: consider intubation and invasive mechanical ventilation
- Discuss ceiling of care with patient and family — important in advanced COPD or neuromuscular disease
Complications
- CO2 narcosis: Excessive oxygen in type 2 RF can worsen hypercapnia by reducing hypoxic drive — causes drowsiness, confusion, coma
- Multi-organ failure: Prolonged hypoxia damages brain, heart, kidneys, liver
- Cardiac arrhythmias: Hypoxia and acidosis are pro-arrhythmic
- Cor pulmonale: Right heart failure from chronic hypoxia-induced pulmonary vasoconstriction
UKMLA Exam Tips
- 1Type 1 = low PaO2 + normal/low PaCO2 (V/Q mismatch). Type 2 = low PaO2 + HIGH PaCO2 (hypoventilation)
- 2COPD patient: target SpO2 88–92% — too much oxygen can worsen hypercapnia (reduced hypoxic drive)
- 3NIV (BiPAP) for COPD exacerbation: when pH <7.35 and PaCO2 >6 kPa despite controlled O2
- 4ABG showing raised HCO3 and normal pH = CHRONIC compensated type 2 failure (kidneys have had time to retain bicarbonate)
- 5Flapping tremor (asterixis) = CO2 retention — also seen in hepatic encephalopathy and uraemia
- 6Always do an ABG — pulse oximetry does NOT detect hypercapnia
- 7Venturi mask gives precise FiO2 delivery — essential in type 2 RF management
practicetest your knowledge on respiratory failureApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — respiratory and beyond.
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