Preparatory Mindset
Respiratory failure is the final common pathway of nearly all pulmonary and many non-pulmonary diseases — and the exam hinges on blood-gas classification: Type I (hypoxaemic): PaO₂ <60 mmHg with normal/low PaCO₂ (gas-exchange failure: pneumonia, PE, ARDS) vs Type II (hypercapnic): PaCO₂ >50 mmHg ± hypoxaemia (ventilatory failure: COPD, asthma, neuromuscular, CNS depression) (17CM exam tested). Once classified, the treatment logic follows: oxygen for Type I, but controlled oxygen for Type II (too much O₂ suppresses the hypoxic drive and worsens CO₂ retention), with NIV first for hypercapnic acidosis, intubation if NIV fails. Underlying mechanisms (hypoventilation, diffusion impairment, V/Q mismatch, true shunt) are classic short-answer and MCQs — know the shunt physiology cold.
Core Concepts
Definition & diagnostic criteria
- Respiratory failure = failure of gas exchange such that arterial blood gases fall outside normal while breathing air at sea level: PaO₂ <60 mmHg OR PaCO₂ >50 mmHg.
- Under oxygen therapy: PaO₂/FiO₂ <300 mmHg indicates respiratory failure (with FiO₂ = 21% on room air at sea level).
- Diagnosis requires ABG analysis + clinical manifestations + history.
Classification by blood gas
| Type I — Hypoxaemic | Type II — Hypercapnic | |
|---|---|---|
| Definition | PaO₂ <60 mmHg, PaCO₂ normal or decreased | PaCO₂ >50 mmHg (with or without PaO₂ <60 mmHg) |
| Mechanism | Impaired gas exchange (oxygenation) | Impaired ventilation (alveolar hypoventilation) |
| Causes | Pneumonia, PE, ARDS, pulmonary fibrosis, pulmonary oedema | COPD and asthma (most common obstructive causes), neuromuscular disease, chest-wall deformity, CNS depression (drugs), hypoventilation syndrome |
*(Classification by site: central vs peripheral ventilatory failure; by causes: obstructive, restrictive, vascular.)*
Pathophysiology — the four mechanisms
- Low V/Q (V↓, Q normal) — shunt-like: e.g., pneumonia, atelectasis, asthma. - High V/Q (Q↓, V normal) — dead space: e.g., PE, emphysema.
- Hypoventilation (ventilatory failure): ↓ alveolar ventilation → PaO₂↓ + PaCO₂↑ (Type II) — corrected by ventilation, NOT just oxygen.
- Diffusion impairment: thickening of the alveolar-capillary membrane (fibrosis, oedema) → hypoxaemia on exertion; O₂-responsive.
- V/Q mismatch (most common cause of hypoxaemia):
- Intrapulmonary shunt (true shunt): venous blood completely bypasses oxygenation (pneumonia, ARDS, atelectasis, pulmonary AV malformation) — the hallmark: hypoxaemia does NOT correct with 100% O₂. Normally shunt <3% of cardiac output; functional shunt 3%–30–50%; larger shunts (30–60–70%) predict failure of oxygen therapy.
Clinical manifestations
- Hypoxaemia: cyanosis, tachypnoea, tachycardia, confusion, restlessness; chronic — clubbing, polycythaemia.
- Hypercapnia: headache (CO₂ vasodilatation), papilloedema, flapping tremor (asterixis), sweating, drowsiness → CO₂ narcosis (coma), bounding pulse.
- Organ effects: arrhythmias, hypotension (hypoxic myocardium), renal/hepatic dysfunction; acid-base disturbance (respiratory acidosis ± metabolic compensation).
Management
Treatment principles: (1) correct hypoxaemia, (2) correct hypercapnia/acidosis, (3) treat the underlying cause, (4) prevent and treat complications (acid-base, arrhythmias, multi-organ).
- Type I: give O₂ generously to maintain SaO₂ ≥90–94%. - Type II (COPD): CONTROLLED low-flow O₂ (start 1–2 L/min), target SpO₂ 88–92% — avoid suppressing hypoxic respiratory drive and causing CO₂ retention; monitor ABG 30–60 min. - High-flow nasal cannula (HFNC) for refractory hypoxaemia.
- NIV (BIPAP/CPAP): first-line for hypercapnic respiratory failure (COPD) with pH ≤7.35 + PaCO₂ >6.0 kPa; also cardiogenic pulmonary oedema (CPAP). - Invasive mechanical ventilation: NIV failure/intolerance, depressed consciousness, inability to protect airway, haemodynamic instability, massive aspiration, respiratory/cardiac arrest.
- Oxygen therapy:
- Ventilatory support:
- Treat the cause: antibiotics (pneumonia), bronchodilators + steroids (COPD/asthma), anticoagulation (PE), diuretics (pulmonary oedema), naloxone (opioid depression), treat neuromuscular disease.
- Complications management: correct acid-base, fluids/electrolytes, nutrition, prevent VAP/immobility.
HKHA Handbook (LMCHK) — Key Points
- Oxygen therapy (P 6–7): oxygen is a drug — prescribe by target saturation; for patients at risk of hypercapnic failure (COPD), start 1–2 L/min and target SpO₂ 88–92%, with ABG re-check 30–60 min; titrate to avoid CO₂ retention; high-concentration O₂ for hypoxaemic (Type I) failure.
- NIV (P 22–24): consider for acute hypercapnic respiratory acidosis (PaCO₂ >6.0 kPa, pH ≤7.35) — e.g., AECOPD — severe dyspnoea with respiratory-muscle fatigue, persistent hypoxaemia despite O₂; check ABG 30–60 min after initiation; do not delay intubation if NIV fails (falling pH, deteriorating consciousness, haemodynamic instability).
- Mechanical ventilation (P 20–21): indications — NIV failure/intolerance with life-threatening hypoxaemia, diminished consciousness/agitation, massive aspiration/persistent vomiting, inability to clear secretions, severe haemodynamic instability/arrhythmia, post-arrest; ICU setting.
- Massive haemoptysis (P 1): secure airway, reverse coagulopathy, bronchial artery embolisation / surgery for massive haemoptysis.
- Type I vs Type II classification is universal; in HK practice the PaO₂/FiO₂ <300 (under O₂) criterion for defining respiratory failure is used (as in ARDS).
High-Yield Points
- Type I: PaO₂ <60, PaCO₂ normal/low — gas-exchange failure; Type II: PaCO₂ >50 ± PaO₂ <60 — ventilatory failure.
- Under O₂: PaO₂/FiO₂ <300 = respiratory failure.
- Four mechanisms: hypoventilation, diffusion impairment, V/Q mismatch, true shunt.
- True shunt: hypoxaemia persists with 100% O₂; normal shunt <3%.
- COPD + asthma = most common causes of Type II.
- Type II: controlled O₂, target SpO₂ 88–92%; NIV for pH ≤7.35; intubate if NIV fails.
- Treat the cause — O₂ and ventilation are supportive, not curative.
Topic Summary
Respiratory failure is defined by ABG (PaO₂ <60 or PaCO₂ >50 mmHg breathing air; PaO₂/FiO₂ <300 on oxygen) and split into Type I hypoxaemic (gas-exchange failure — pneumonia, PE, ARDS) and Type II hypercapnic (ventilatory failure — COPD, asthma, neuromuscular, CNS depression). The four pathophysiologic mechanisms — hypoventilation, diffusion impairment, V/Q mismatch and true shunt (hypoxaemia unresponsive to 100% O₂) — explain the clinical patterns and guide oxygen strategy: generous O₂ for Type I, controlled O₂ (SpO₂ 88–92%) for Type II, NIV for hypercapnic acidosis, and intubation when NIV fails. Treating the underlying cause and preventing complications completes the picture — with the HKHA oxygen-therapy and NIV criteria as LMCHK priorities.