Medicine chapters
Respiratory failure
Respiratory failure is a PaO2 below 8 kPa, with (type 2) or without (type 1) a raised PaCO2; this chapter covers causes, ABG recognition, oxygen and ventilation, ARDS and complications.
- Respiratory failure means PaO2 <8 kPa (60 mmHg); type 1 has a normal or low PaCO2 (V/Q mismatch or shunt, e.g. pneumonia, PE, oedema, ARDS) and type 2 has PaCO2 raised from alveolar hypoventilation (COPD, neuromuscular weakness, opioids, chest wall disease).
- The A–a gradient separates lung disease (wide) from pure hypoventilation (normal); pulse oximetry misses a rising CO2 when the patient is on oxygen.
- Treat the cause, give oxygen to target (94–98%, or 88–92% if at risk of CO2 retention), use CPAP for type 1, NIV (BiPAP) for acidotic type 2, and intubate when these fail; watch for CO2 narcosis, barotrauma, VAP and oxygen toxicity.
On this page
Overview
Respiratory failure happens when the lungs (the gas exchanger) or the breathing pump (brainstem, nerves, muscles, chest wall) cannot keep arterial gases normal.
In practice it is diagnosed on an arterial blood gas (ABG):
- Type 1 (hypoxaemic): PaO2 <8 kPa (60 mmHg) with a normal or low PaCO2.
- Type 2 (hypercapnic, ventilatory): PaO2 <8 kPa with a raised PaCO2 (above about 6.5–7 kPa, 50–55 mmHg).
The TOS asks you to recognise its complications and manage them: hypoxic organ damage, acidosis and CO2 narcosis, and the complications of oxygen and ventilation.
Mechanisms of hypoxaemia
| Mechanism | Example | A–a gradient | Corrects with O2? |
|---|---|---|---|
| V/Q mismatch (commonest) | Pneumonia, asthma, COPD, PE, pulmonary oedema | Wide | Yes |
| Right-to-left shunt | ARDS, lobar collapse, cyanotic heart disease, AV malformation | Wide | Poorly |
| Alveolar hypoventilation | Opioid overdose, neuromuscular weakness, chest wall disease | Normal | Yes |
| Diffusion defect | Fibrosis (mainly on exercise) | Wide | Yes |
| Low inspired O2 | High altitude | Normal | Yes |
In a shunt, blood passes unventilated alveoli, so extra oxygen barely raises the PaO2. Hyperventilation of normal alveoli usually keeps PaCO2 normal or low.
The A–a gradient
Alveolar gas equation (sea level, breathing air): PAO2 ≈ 150 − (PaCO2 ÷ 0.8) in mmHg. A–a gradient = PAO2 − PaO2. Normal is roughly under 15–20 mmHg in young adults (rises with age).
Inspired PO2 = 0.21 × (760 − 47) ≈ 150 mmHg
Patient 1 (pneumonia): PaCO2 40, PaO2 60 → PAO2 = 150 − 40 ÷ 0.8 = 100; A–a = 100 − 60 = 40 → wide → lung disease (type 1)
Patient 2 (opioid overdose): PaCO2 72, PaO2 54 → PAO2 = 150 − 72 ÷ 0.8 = 60; A–a = 60 − 54 = 6 → normal → pure hypoventilation (type 2)
Causes
| Type 1 | Type 2 |
|---|---|
| Pneumonia | COPD (commonest) |
| Pulmonary oedema | Severe or life-threatening asthma (tiring patient) |
| Pulmonary embolism | Drugs: opioids, benzodiazepines, alcohol |
| ARDS | Neuromuscular: Guillain–Barré syndrome, myasthenia gravis, motor neurone disease, high cord injury, polio |
| Asthma (early attack) | Chest wall: kyphoscoliosis, flail chest, gross obesity (obesity hypoventilation) |
| Interstitial lung disease | Obstructive sleep apnoea; brainstem lesions |
| Pneumothorax | Exhaustion in any type 1 failure |
COPD is the commonest cause of type 2 respiratory failure. In a young person with type 2 failure and clear lungs, think of drugs (opioids) or neuromuscular weakness.
Recognition
Clinical features
- Respiratory distress: tachypnoea (the most sensitive early sign), accessory muscles, recession, inability to speak in sentences, sweating, tachycardia.
- Hypoxaemia: central cyanosis (needs enough deoxygenated haemoglobin, so it may be absent in anaemia), restlessness, confusion, arrhythmia, then bradycardia and arrest.
- Hypercapnia: headache (worse in the morning), warm peripheries, bounding pulse, flapping tremor, drowsiness, coma (CO2 narcosis), papilloedema.
- Tiring patient: paradoxical (see-saw) chest and abdominal movement, falling respiratory rate, rising PaCO2, exhaustion.
Investigations
- ABG: type of failure, acid–base state and whether it is acute or chronic.
- Pulse oximetry for continuous monitoring; unreliable with poor perfusion and carbon monoxide.
- Vital capacity in neuromuscular disease.
- Chest X-ray, ECG, FBC, cultures, drug screen; echo and CT pulmonary angiogram as indicated.
| ABG pattern | Meaning |
|---|---|
| Low PaO2, low or normal PaCO2 | Type 1 |
| High PaCO2, low pH, normal HCO3− | Acute type 2 |
| High PaCO2, near-normal pH, high HCO3− | Chronic (compensated) type 2, e.g. stable COPD |
| High PaCO2, low pH, high HCO3− | Acute-on-chronic type 2 (COPD exacerbation) |
A normal SpO2 on supplemental oxygen does not exclude hypoventilation. Only a blood gas shows the rising CO2.
In Guillain–Barré syndrome and myasthenia, SpO2 and even PaCO2 change late. Monitor forced vital capacity regularly; a falling VC (around 10 mL/kg or less) means ventilation is needed.
Management
General principles
- Airway and position (sit up unless hypotensive).
- Oxygen to a target saturation:
- Most acutely ill patients: 94–98%.
- Those at risk of hypercapnic failure (COPD, obesity hypoventilation, neuromuscular or chest wall disease): 88–92%, adjusted by ABG.
- Treat the cause: bronchodilators and steroids, antibiotics, diuretics, anticoagulation, naloxone for opioids, drain a pneumothorax.
- Clear secretions (physiotherapy, suction); correct hypophosphataemia and malnutrition that weaken muscles.
- Repeat ABG 30–60 minutes after any change in oxygen or ventilation.
Oxygen devices
| Device | Typical FiO2 | Use |
|---|---|---|
| Nasal cannula (1–4 L/min) | About 24–40% | Mild hypoxaemia, comfortable |
| Simple face mask (5–10 L/min) | About 35–55% (variable) | Moderate hypoxaemia |
| Non-rebreather mask with reservoir (15 L/min) | Up to about 85% | Critically ill, type 1 |
| Venturi (fixed-performance) mask | 24, 28, 31, 35, 40, 60% | Controlled O2 in type 2 risk (COPD) |
| High-flow nasal oxygen | Up to 100%, heated and humidified | Severe type 1 failure |
Ventilatory support
| Method | How it helps | Main use |
|---|---|---|
| CPAP | Constant pressure splints alveoli open, raises PaO2 | Type 1: acute cardiogenic pulmonary oedema, some pneumonia; obstructive sleep apnoea |
| NIV (BiPAP) | Higher pressure on inspiration (IPAP) boosts ventilation and removes CO2; lower expiratory pressure (EPAP) | Type 2 with acidosis: COPD exacerbation (pH <7.35, PaCO2 >6.5 kPa), obesity hypoventilation, neuromuscular and chest wall disease |
| Invasive ventilation (intubation) | Full control of ventilation and oxygenation | Failure of NIV; coma or unprotected airway; exhaustion; severe hypoxaemia despite high FiO2; respiratory arrest |
Contraindications to NIV include an unprotected airway or reduced consciousness, vomiting, facial trauma, undrained pneumothorax, copious secretions, and haemodynamic instability.
CPAP does not reduce CO2, so it is the wrong choice for hypercapnic COPD; use BiPAP.
Acute respiratory distress syndrome (ARDS)
A severe form of type 1 failure from leaky alveolar capillaries after a direct or indirect insult.
Causes: pneumonia, aspiration, sepsis, major trauma, burns, acute pancreatitis, massive transfusion (TRALI), near-drowning, drug overdose, fat embolism.
Berlin criteria:
- Onset within 1 week of the insult.
- Bilateral opacities on chest imaging not fully explained by effusion, collapse or nodules.
- Not fully explained by heart failure or fluid overload (echo if no risk factor).
- PaO2/FiO2 ratio measured with PEEP or CPAP ≥5 cmH2O:
| Severity | PaO2/FiO2 (mmHg) |
|---|---|
| Mild | 200–300 |
| Moderate | 100–200 |
| Severe | <100 |
PaO2 80 mmHg on FiO2 0.5 (50%) with PEEP 8
P/F = 80 ÷ 0.5 = 160 → between 100 and 200 → moderate ARDS
Management: treat the cause; lung-protective ventilation (tidal volume about 6 mL/kg predicted body weight, plateau pressure ≤30 cmH2O, adequate PEEP, accept a high CO2, "permissive hypercapnia"); prone positioning in severe cases; conservative fluids; ECMO in specialist centres.
Complications and how to manage them
Of respiratory failure itself
| Complication | Management |
|---|---|
| Hypoxic brain injury, confusion, seizures | Correct oxygenation fast; airway protection |
| Arrhythmias, myocardial ischaemia, cardiac arrest | Oxygen, correct potassium and acidosis, ALS |
| Respiratory acidosis and CO2 narcosis | Controlled oxygen, NIV, then intubation |
| Pulmonary hypertension and cor pulmonale (chronic hypoxia) | Long-term oxygen, diuretics |
| Secondary polycythaemia | LTOT; venesection if haematocrit is very high |
| Acute kidney injury, stress ulcers | Fluids, monitor, ulcer prophylaxis in ventilated patients |
Of treatment
| Complication | Points |
|---|---|
| Oxygen-induced hypercapnia | In COPD, uncontrolled high-flow oxygen raises PaCO2 → drowsiness, acidosis. Step down to the 88–92% target and consider NIV; do not abruptly stop oxygen (rebound hypoxaemia) |
| Oxygen toxicity | Very high FiO2 for long periods damages lung tissue through reactive oxygen species and causes absorption collapse; use the lowest FiO2 that meets the target |
| Barotrauma / volutrauma | Pneumothorax, pneumomediastinum, surgical emphysema; a sudden drop in saturation and rise in airway pressure on the ventilator needs a check for tension pneumothorax |
| Ventilator-associated pneumonia | Gram-negative organisms (Pseudomonas, Klebsiella, Acinetobacter) and MRSA; prevent with head-up 30–45°, oral care, daily sedation holds |
| Tube problems | Oesophageal or right main bronchus intubation, blockage, displacement, laryngeal and tracheal injury or stenosis |
| Low cardiac output | Positive pressure reduces venous return → hypotension; give fluids |
| Sedation and immobility | Delirium, ICU weakness, DVT (thromboprophylaxis), pressure sores |
| NIV-related | Mask pressure ulcers, gastric distension, aspiration, eye irritation |
Sudden deterioration on a ventilator: DOPE = Displaced tube, Obstructed tube, Pneumothorax, Equipment failure.
Expect: ABG definitions of type 1 and type 2 failure (PaO2 <8 kPa; raised PaCO2), COPD as the commonest cause of type 2 failure, shunt not correcting with oxygen, normal A–a gradient in hypoventilation (opioids, neuromuscular disease), acute versus chronic compensation (bicarbonate), vital capacity monitoring in Guillain–Barré syndrome, oxygen targets 94–98% and 88–92%, Venturi masks, CPAP for type 1 versus BiPAP for acidotic type 2, NIV contraindications, Berlin ARDS criteria and P/F ratio, lung-protective ventilation, and complications such as CO2 narcosis, barotrauma, VAP and oxygen toxicity.
Quick revision
- Type 1: PaO2 <8 kPa, PaCO2 normal or low (V/Q mismatch, shunt).
- Type 2: PaO2 <8 kPa plus high PaCO2 (hypoventilation); COPD commonest.
- Shunt: poor response to O2. Hypoventilation: normal A–a gradient.
- Chronic type 2: high HCO3−, near-normal pH; acute-on-chronic: high HCO3− but low pH.
- Targets 94–98%; 88–92% if CO2 retainer.
- CPAP for type 1; BiPAP (NIV) for acidotic type 2; intubate if failing.
- GBS and myasthenia: monitor vital capacity.
- ARDS: bilateral infiltrates, non-cardiac, P/F ≤300 on PEEP ≥5; ventilate at 6 mL/kg.
Written by The House Job from standard references (Kumar and Clark's Clinical Medicine).
FAQ
What is the difference between type 1 and type 2 respiratory failure?
Both have a PaO2 below 8 kPa; type 1 has a normal or low PaCO2 from V/Q mismatch or shunt, while type 2 has a raised PaCO2 because alveolar ventilation is inadequate.
Why does pulse oximetry miss CO2 retention?
Oximetry measures only haemoglobin saturation; a patient breathing extra oxygen can keep a normal SpO2 while PaCO2 climbs, so an ABG is needed.
Should oxygen be withheld from a hypoxic COPD patient?
No. Severe hypoxaemia is more dangerous than hypercapnia; give controlled oxygen to 88–92%, recheck the blood gas, and use NIV if acidosis develops.
What is permissive hypercapnia?
Accepting a raised PaCO2 (with a pH that is not dangerously low) during lung-protective ventilation, so that small tidal volumes can be used without injuring the lungs.