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Educational draft · awaiting clinical reviewUse Rapid for revision, not patient-care decisions. Check current national and local guidance and the BNF or BNFC before acting.

Type 1 and type 2 respiratory failure

Respiratory · UK scope · Sources checked 27 Aug 2026 · Clinical review pending

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Escalate

Exhaustion, reduced consciousness, silent chest, severe acidaemia, refractory hypoxaemia, haemodynamic instability or a falling respiratory rate in a tiring patient requires immediate senior airway/critical-care support. Give life-saving oxygen and ventilation; do not wait for a perfect diagnostic label.

Synopsis

Interpret respiratory failure from the blood gas, identify the failing physiological process and match oxygen, ventilatory support and cause-specific treatment to the patient rather than to a label alone.

  • Type 1 respiratory failure is hypoxaemia (commonly PaO2 below 8 kPa) with normal or low PaCO2, caused mainly by V/Q mismatch, shunt or diffusion failure.
  • Type 2 respiratory failure is hypercapnia (PaCO2 above the laboratory upper reference, often over 6.0 kPa) from inadequate alveolar ventilation, often with hypoxaemia.
  • Acute hypercapnic respiratory failure requiring NIV assessment is conventionally pH below 7.35 with PaCO2 above 6.5 kPa after initial treatment.
  • A raised bicarbonate/base excess suggests renal compensation and chronicity; acidaemia indicates acute or acute-on-chronic ventilatory failure.
  • Start with ABCDE, prescribe an SpO2 target and obtain an ABG promptly when hypercapnia is possible, SpO2 is unexpectedly low, the patient is deteriorating or ventilatory support may be needed.
  • Target 94–98% for most acutely ill adults; target 88–92% for COPD or another risk of hypercapnic respiratory failure while awaiting blood gases.
  • Treat the cause in parallel: airway obstruction, pneumonia/sepsis, pulmonary oedema, PE, pneumothorax, CNS depression, neuromuscular weakness or chest-wall/obesity hypoventilation.
  • Persistent acidotic hypercapnia in COPD despite optimal medical therapy is an NIV indication; severe acidosis, inability to protect the airway or rapid deterioration may require intubation.
  • Normal SpO2 on supplemental oxygen does not prove adequate ventilation: a patient can have dangerous CO2 retention with a reassuring saturation.
  • Never abruptly stop oxygen in oxygen-induced hypercapnia; step down to maintain 88–92% and reassess gases because rebound hypoxaemia can be severe.
  • Key red flags

    Type 1 pattern

    Low PaO2 with normal/low PaCO2: consider pneumonia, pulmonary oedema, PE, pneumothorax, acute asthma, ARDS or interstitial lung disease.

    Acute type 2 pattern

    Raised PaCO2 with pH below 7.35 and limited metabolic compensation: consider COPD/bronchiectasis exacerbation, drug/CNS depression, severe obesity hypoventilation, neuromuscular weakness or fatigue.

    Acute-on-chronic failure

    Known or suspected chronic CO2 retention with new acidaemia, worsening hypercapnia and illness. This is not reassuring compensation; it often needs urgent NIV assessment.

    Impending ventilatory arrest

    Reduced consciousness, inability to speak, paradoxical breathing, weak cough, falling tidal volume, bradypnoea or exhaustion can precede arrest even if the SpO2 appears acceptable on oxygen.

    Investigation priorities

    01
    Arterial blood gas with recorded oxygen device/FiO2First step

    Classify oxygenation, ventilation and acid–base status.

    Management branches

    InitialStabilise and classify

    Any suspected acute respiratory failure.

    1. Perform ABCDE, sit upright if appropriate, call for senior help when severe and prescribe a target saturation.
    2. Give controlled oxygen: usually 94–98%, or 88–92% if hypercapnia risk. Obtain an ABG promptly and record device/flow.
    3. Identify immediate reversible causes at the bedside—bronchospasm, secretions, opioid effect, oedema, pneumothorax, PE, sepsis—and treat in parallel.
    4. Repeat clinical assessment and gas within 30–60 minutes, sooner if deteriorating; decide ward, respiratory-support unit or critical-care location.

    Key medicines

    Naloxone for suspected opioid overdose400–2000 micrograms IV initially in coma or significant respiratory depression, repeated every 2–3 minutes if needed up to 10 mg; in opioid-dependent or postoperative patients, titrate smaller 100–200 microgram IV increments to adequate ventilation.Shorter action than many opioids; recurrent depression needs observation/re-dosing or infusion. Abrupt reversal can cause severe withdrawal, pain, hypertension, arrhythmia or pulmonary oedema.
    Nebulised salbutamol2.5–5 mg nebulised, repeated according to severity and response; in hypercapnia risk, drive the nebuliser with compressed air and maintain target oxygen separately where possible.Tachycardia, tremor, hypokalaemia and lactate rise; it does not replace NIV or airway support when ventilation is failing.
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    Sources and review status4 sources · checked 27 Aug 2026 · clinical review pending+
    Sources

    Sources and review status

    National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.

    • BTS/ICS guideline for ventilatory management of acute hypercapnic respiratory failureDefinitions, NIV thresholds, monitoring and escalation.
    • BTS guideline for oxygen use in healthcare and emergency settingsTarget saturation and repeat-gas recommendations.
    • NICE NG115: COPD in over 16s—recommendationsExacerbation treatment and NIV for persistent hypercapnic failure.
    • Naloxone 400 micrograms/mL SmPCLicensed adult naloxone dosing and safety information.

    Editorial contact: Doctor’s Passport editorial team. Source-check date is separate from clinical approval. Report a content problem · Content changes

    Authoring stateRapid draftClinical stateAwaiting reviewJurisdictionUnited Kingdom