Respiratory Failure
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Direct answer
Respiratory failure is the inability of the respiratory system to maintain arterial blood gases: type 1 (hypoxaemic) failure is a PaO2 below 60 mmHg with a normal or low PaCO2, produced by ventilation-perfusion mismatch, shunt, diffusion impairment or low inspired oxygen; type 2 (hypercapnic, ventilatory) failure adds a PaCO2 above 50 mmHg, produced by ventilatory pump failure from obstructive disease, sedation, obesity-hypoventilation or neuromuscular weakness. Management titrates oxygen to a target range while treating the cause, escalating from oxygen through non-invasive to invasive ventilation.
What you must remember
- Numerical definitions: type 1 — PaO2 below 60 mmHg with PaCO2 normal or low; type 2 — PaO2 below 60 mmHg with PaCO2 above 50 mmHg, both at rest on room air; a "type 3" label sometimes covers perioperative hypoventilation and atelectasis.
- Mechanisms of hypoxaemia: hypoventilation (normal alveolar-arterial gradient — narcotics, obesity-hypoventilation); ventilation-perfusion mismatch, the commonest clinically (pneumonia, embolism, COPD — responds to oxygen); right-to-left shunt (consolidation, arteriovenous malformation — refractory to oxygen); diffusion impairment (fibrosis, worse on exercise); and low inspired oxygen at altitude.
- The 100 per cent oxygen test separates shunt from mismatch: shunt physiology barely corrects because blood bypasses ventilated alveoli, whereas mismatch corrects well.
- Causes of type 2 failure: COPD exacerbations (the prototype), acute severe asthma late, chest wall and neuromuscular disease (Guillain-Barre syndrome, myasthenia, kyphoscoliosis), depressed drive from opioids and sedatives, obesity-hypoventilation and upper airway obstruction.
- Clinical recognition: cyanosis, tachypnoea, accessory muscle use and agitation of hypoxaemia; the hypercapnic patient shows flapping tremor (asterixis), warm peripheries, papilloedema, morning headache, confusion and drowsiness progressing to carbon dioxide narcosis with small pupils and coma.
- Assessment: arterial blood gas with the alveolar-arterial gradient, continuous pulse oximetry with serial gases, and a chest radiograph to identify the cause.
- Management sequence: titrate oxygen — 94 to 98 per cent generally, 88 to 92 per cent in chronic hypercapnia risk; treat the cause; apply non-invasive ventilation for type 2 failure with acidosis (pH below about 7.35) in COPD; intubate for airway compromise, exhaustion, refractory hypoxaemia or failure of non-invasive support. Oxygen-induced hypercapnia in COPD works through lost hypoxic vasoconstriction, the Haldane effect and blunted drive — a reason for controlled targets, never for withholding oxygen.
Typing a failure from the gas machine
An arterial sample on room air gives you the whole classification. PaO2 of 48 with PaCO2 of 31 in a febrile patient with unilateral crackles: type 1, mechanism most likely ventilation-perfusion mismatch — the commonest clinical mechanism — expected to correct well with oxygen. PaO2 of 52 with PaCO2 of 68 and pH 7.28 in a drowsy smoker with asterixis: A PaO2 that stays low despite 100 per cent oxygen points to shunt, whereas mismatch corrects readily. A normal alveolar-arterial gradient with hypoxaemia and hypercapnia together means pure hypoventilation, localising to the drive rather than the lung. Management follows the same ladder in every case: titrated oxygen — 94 to 98 generally, 88 to 92 where chronic hypercapnia threatens — treatment of the cause, non-invasive ventilation for type 2 failure with acidosis in COPD, and intubation for airway compromise, exhaustion or refractory hypoxaemia.
Where students slip
Cyanosis and a normal saturation mislead: early hypoxaemia is often compensated, and the diagnosis rests on gases. The type split is misapplied when early asthma and pulmonary embolism — both type 1 — are memorised as ventilatory failure. The oxygen question is the highest-stakes slip: withholding oxygen from a cyanosed COPD patient is a fatal over-remembering; the correct act is a controlled 88 to 92 target with blood-gas reassessment. Guillain-Barre syndrome appearing as pure ventilatory failure with clear lungs is the favourite crossover stem.
Frequently asked questions
What are the definitions of type 1 and type 2 respiratory failure?
Type 1 is PaO2 below 60 mmHg with normal or low PaCO2; type 2 adds PaCO2 above 50 mmHg, both on room air at rest.
Which mechanism causes hypoxaemia refractory to oxygen?
Right-to-left shunt, since shunted blood never contacts the alveolar gas enriched with 100 per cent oxygen.
What is the commonest mechanism of hypoxaemia?
Ventilation-perfusion mismatch, typical of pneumonia, pulmonary embolism and obstructive disease, and largely correctable with supplemental oxygen.
Which clinical features signal carbon dioxide retention?
Asterixis, warm hands, bounding pulse, papilloedema, morning headache, confusion and drowsiness proceeding to coma.
Why does oxygen worsen hypercapnia in COPD?
By releasing hypoxic pulmonary vasoconstriction, via the Haldane effect on carbon dioxide transport, and by blunting ventilatory drive — hence the 88 to 92 per cent target.
When is invasive ventilation preferred over non-invasive?
For coma or inability to protect the airway, respiratory exhaustion, refractory hypoxaemia, failure or contraindication of non-invasive support.