⚕️ Step	Type 1 (Hypoxaemic (PaO₂ < 8 kPa) )	Type 2 (Hypoxaemic (PaO₂ < 8 kPa) and Hypercapnic)
🫁 Oxygen	High-flow O₂ (non-rebreather) → SpO₂ 94–98%	Controlled O₂ (Venturi 24–28%) → SpO₂ 88–92%
🎯 Treat cause	Diuretics → pulmonary oedema Chest drain → pneumothorax Antibiotics → pneumonia Anticoagulation → PE	Bronchodilators/steroids → COPD/asthma Chest physio/suction → sputum plugs Stop/reverse sedatives → Naloxone, Flumazenil
💻 Support	Consider CPAP, NIV, or invasive ventilation ± ECMO	NIV (BiPAP): IPAP 10 / EPAP 5; escalate to intubation if failing
📞 Escalation	Urgent ITU referral if deteriorating (tachycardia, tachypnoea, hypotension, confusion, rising PaCO₂ or falling PaO₂)

It is quite possible for a patient with COPD to also have a PE. Patients may go from Type 1 to Type 2 when they tire, hypoventilate, or receive sedation. Intubation and ventilation can treat both types.

📖 About

🫁 Respiratory failure (PaO₂ < 8 kPa) is a common emergency.
Reflects failure of the lungs to perform gas exchange: oxygenation ± CO₂ clearance.
Classified as Type 1 (hypoxaemic) or Type 2 (hypercapnic).
📟 Pulse oximetry → O₂ saturation only, no CO₂ info.
💉 ABG → PaO₂, PaCO₂, pH, HCO₃⁻, acid–base status.

📊 Classification

Type	Oxygen (PaO₂)	Carbon Dioxide (PaCO₂)
Type 1 🩵	< 8 kPa	< 6 kPa
Type 2 ❤️	< 8 kPa	> 6 kPa

💨 How much Oxygen?

🌍 Most patients: aim SpO₂ 94–98%.
🌫️ COPD / Type 2 RF: aim 88–92%, PaO₂ > 7 kPa.
⬆️ If sats < 94% → ↑ O₂ (unless chronic hypercapnic COPD).
⬇️ If sats > 98% → ↓ O₂.
⚠️ Special cases (e.g. COVID O₂ conservation): follow local guidance.

🩺 Causes

Type 1 (Hypoxaemic, V/Q mismatch or shunt):
- 🌊 Pulmonary oedema
- 🩸 Pulmonary embolism
- 🔥 ARDS
- 🌪️ Asthma
- 🦠 Pneumonia
- 🏔️ High altitude
- 🚫 Upper airway obstruction
Type 2 (Hypercapnic, alveolar hypoventilation):
- 😮‍💨 Fatigue in COPD/pneumonia
- 🧠 CNS: stroke, tumour, sedation, head injury
- 🫁 COPD exacerbation
- 💪 Neuromuscular weakness (GBS, MND, SMA, polio, dystrophies, Pompe)
- 🦴 Chest wall deformity (flail chest, kyphoscoliosis)
- ⚖️ Obesity hypoventilation, alcohol, sedatives
- 🟤 Sputum retention, mucus plugging

🔍 Investigations

📟 Pulse oximetry → O₂ only.
💉 ABG → gold standard.
📈 ECG → arrhythmias, RV strain, S1Q3T3 (PE).
🩻 CXR → pneumonia, COPD, pneumothorax.
🧪 CTPA if Wells suggests PE in Type 1 RF.

⚕️ Management of Type 1 RF

ABC; give high-flow O₂ (unless risk of hypercapnia).
🎯 Treat cause:
- 💊 Diuretics → pulmonary oedema
- 🩹 Chest drain → pneumothorax
- 🦠 Antibiotics → infection
- 💨 Bronchodilators/steroids → asthma/COPD
- 🩸 Anticoagulation/thrombolysis → PE
May require CPAP, NIV, invasive ventilation ± ECMO.

⚕️ Management of Type 2 RF

ABC; controlled O₂ (24% Venturi, aim PaO₂ > 7 kPa).
🧪 Watch for CO₂ retention: warm peripheries, bounding pulse, drowsiness, flap.
🫁 Typical COPD signs: prolonged expiration, wheeze, hyperinflated chest.
❤️ Right heart failure signs: oedema, raised JVP, hepatomegaly, ascites.
🧹 Chest physio ± suction for sputum plugs.
NIV (BiPAP): start IPAP 10, EPAP 5 cm H₂O.
If failing → intubation & ventilation:
- FiO₂ 1.0
- Tidal vol 6–10 ml/kg
- RR 10–12
- PEEP 5 cm H₂O
Consider ECMO if refractory.
💊 Drug-induced: Naloxone (opiates), Flumazenil (benzos).

🚨 Important Scenarios

⚡ Impending arrest: HR >120, RR >30, hypotension, agitation, confusion, rising PaCO₂/falling PaO₂ → urgent ITU call.
😵 Mask intolerance: confused patients → nasal prongs 1–2 L/min safer.
🎭 High-flow O₂ with normal PaO₂ can mask deterioration → repeat ABG.
🌪️ Asthma + “normal PaCO₂” = fatigue/worsening → escalate urgently.
🧪 Low PaO₂ but normal sats may be venous sample error.

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Respiratory Failure

🚨 Emergency Management at the Bedside