Type 1 and type 2 respiratory failure

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

The type 1/type 2 classification describes gas exchange, not a diagnosis. Pneumonia can begin as type 1 failure and become type 2 when fatigue supervenes; COPD can produce either.

PaCO2 reflects alveolar ventilation. A low PaCO2 in severe type 1 failure can represent compensatory hyperventilation; a 'normalising' PaCO2 in a tiring asthmatic patient can be ominous.

ABG interpretation should state pH, PaCO2, bicarbonate/base excess, PaO2, inspired oxygen and the clinical process. Without FiO2/device and prior gases, chronicity and severity are easily misread.

Respiratory support is a bridge to cause control. Oxygen corrects hypoxaemia; NIV assists ventilation; invasive ventilation supports a failing airway or patient when non-invasive support is inappropriate or failing.

Key points

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.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Alveolar or vascular disease

Pneumonia, pulmonary oedema, acute respiratory distress syndrome and pulmonary embolism impair oxygen transfer, usually causing hypoxaemia without primary global hypoventilation.

Obstructive airway disease

Severe asthma or COPD creates ventilation-perfusion mismatch and increased work of breathing; fatigue can add hypercapnia to initial hypoxaemia.

Respiratory pump failure

Neuromuscular weakness, chest-wall restriction, obesity hypoventilation and central depressant medicines reduce effective alveolar ventilation and produce carbon dioxide retention.

Environmental or iatrogenic factors

Low inspired oxygen, excessive oxygen in susceptible hypercapnic patients, sedation and inappropriate ventilatory settings can cause or worsen failure.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Oxygen-transfer failure
Ventilation-perfusion mismatch, shunt or diffusion limitation lowers arterial oxygen even when total minute ventilation is maintained or increased.
2
Alveolar hypoventilation
When effective ventilation is inadequate for carbon dioxide production, arterial carbon dioxide rises and acute respiratory acidosis develops.
3
Compensatory response
Tachypnoea and sympathetic activation initially support gas exchange; with chronic hypercapnia, renal bicarbonate retention partially restores pH.
4
Systemic dysfunction
Hypoxaemia compromises cellular oxygen delivery while severe acidaemia impairs cardiovascular and neurological function, creating further respiratory instability.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Type 1 patternRed flag

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

Acute type 2 patternRed flag

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.

Chronic compensated hypercapnia

Raised PaCO2 with raised bicarbonate and near-normal pH suggests chronic ventilatory failure; compare previous gases and do not overcorrect oxygen.

Acute-on-chronic failureRed flag

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 arrestRed flag

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.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Arterial blood gas with recorded oxygen device/FiO2First step
Why
Classify oxygenation, ventilation and acid–base status.
Interpretation and limitations
Type 1: PaO2 low with PaCO2 normal/low. Type 2: PaCO2 raised; pH and bicarbonate distinguish acute, chronic and acute-on-chronic patterns.
02
Repeat blood gas after 30–60 minutes or sooner after intervention
Why
Detect rising CO2/falling pH and measure response to oxygen, bronchodilation or ventilation.
Interpretation and limitations
Improving pH and falling PaCO2 support response; worsening acidosis, persistent tachypnoea or confusion demands escalation.
03
Chest X-ray or immediate thoracic ultrasound when indicated
Why
Identify consolidation, oedema, pneumothorax, effusion or collapse.
Interpretation and limitations
Do not delay decompression for suspected tension pneumothorax to obtain imaging.
04
ECG, FBC, U&E, CRP, cultures and lactate
Why
Identify infection, arrhythmia, electrolyte disturbance, anaemia and hypoperfusion.
Interpretation and limitations
Interpret lactate with work of breathing, beta-agonists and shock; it does not define respiratory-failure type.
05
Peak flow/spirometry only when safe
Why
Assess obstruction in cooperative, non-exhausted patients.
Interpretation and limitations
Do not force manoeuvres in severe distress; bedside clinical trajectory and gases take priority.
06
Medication/toxicology review
Why
Find opioids, sedatives or other ventilatory depressants and treatment interactions.
Interpretation and limitations
Pinpoint pupils and bradypnoea support opioid toxicity, but mixed ingestion and other neurological causes remain possible.
07
Vital capacity and cough assessment in neuromuscular disease
Why
Detect pump failure before late gas deterioration.
Interpretation and limitations
A falling vital capacity, weak cough or bulbar dysfunction warrants early respiratory/critical-care support even before profound acidosis.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Oximetry artefact

Poor perfusion, motion, nail products and device bias can produce a misleading saturation; repeat measurement and arterial sampling resolve discordance with the patient.

Metabolic acidosis

Deep rapid breathing with low carbon dioxide may be compensation for metabolic acid accumulation rather than primary respiratory disease; pH and bicarbonate distinguish the process.

Dysfunctional breathing

Breathlessness and tachypnoea with preserved gas exchange may reflect a functional pattern, but this is considered only after acute cardiopulmonary disease is excluded.

Dyshemoglobinaemia

Carbon monoxide or methaemoglobin can impair oxygen carriage despite a misleading arterial oxygen tension or saturation; co-oximetry and exposure history discriminate.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01InitialStabilise and classifyFirst stepAny suspected acute respiratory failure.

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

02Type 1Hypoxaemic failureLow PaO2 with normal or low PaCO2.

1EscalationEscalate oxygen device to achieve the prescribed target while checking probe reliability and obtaining gas values.
2Treat the cause: antibiotics/sepsis care for infection, diuresis for congestion, reperfusion/anticoagulation for PE, drainage for pneumothorax, bronchodilation for obstructive disease.
3If oxygen requirement rises or work of breathing/organ dysfunction worsens, obtain early critical-care review for HFNO, CPAP in selected cardiogenic oedema or invasive ventilation rather than persistently increasing oxygen alone.

03Type 2Hypercapnic ventilatory failureRaised PaCO2, particularly with pH below 7.35.

1Target SpO2 88–92%, stop/reverse respiratory depressants where appropriate, optimise bronchodilators/steroids/antibiotics or airway clearance for the cause.
2EscalationRepeat ABG after initial treatment. In COPD with persistent pH below 7.35 and PaCO2 above 6.5 kPa, start NIV promptly with a documented escalation plan.
3If pH is very low, consciousness/airway is impaired, NIV is contraindicated or gases/clinical state worsen despite optimised NIV, involve critical care immediately for invasive ventilation or an agreed ceiling-of-care plan.

04Opioid causeVentilate and reverse safelyClinically important respiratory depression with suspected opioid toxicity.

1Open/support the airway and ventilate with oxygen; do not wait for naloxone to start basic respiratory support.
2Give titrated naloxone IV to restore adequate ventilation; larger initial doses are appropriate in coma/apnoea, while small increments reduce severe withdrawal in dependent patients.
3Observe for recurrent respiratory depression because naloxone may wear off first; repeat doses or an infusion may be required and mixed toxicity must still be managed.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Reverses opioid-mediated ventilatory depression while airway and ventilation are supported.

Naloxone for suspected opioid overdose

400–2000 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.

Treats reversible bronchospasm contributing to ventilatory failure.

Nebulised salbutamol

2.5–5 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.

Reduces inflammatory airflow obstruction in acute COPD exacerbation.

Prednisolone for COPD exacerbation

30 mg orally once daily for 5 days when a COPD exacerbation is the cause, unless contraindicated or an alternative steroid route is required.

Hyperglycaemia, infection, delirium and GI effects. Do not give merely because a blood gas shows type 2 failure; confirm an obstructive exacerbation context.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Cardiorespiratory arrest

Progressive hypoxaemia, acidosis and respiratory muscle exhaustion can culminate in arrhythmia, loss of consciousness and arrest.

Hypoxic organ injury

Sustained inadequate oxygen delivery damages the brain, myocardium, kidneys and other vulnerable tissues even if respiratory support later succeeds.

Carbon dioxide narcosis

Severe or rapidly rising hypercapnia can cause headache, confusion, drowsiness and coma, while other neurological causes still require assessment.

Pulmonary hypertension

Chronic hypoxaemia promotes pulmonary vasoconstriction and vascular remodelling, increasing right-ventricular workload and eventually causing cor pulmonale.

Ventilator-associated harm

Escalated support can introduce pressure injury, haemodynamic compromise, aspiration or infection, making close reassessment and cause-specific treatment essential.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Continuous SpO2 in severe disease, but use serial blood gases to monitor ventilation and pH; saturation alone cannot detect CO2 retention.
Trend respiratory rate, effort, ability to speak, consciousness, cough strength, haemodynamics and urine output; a falling rate can mean fatigue, not recovery.
Repeat ABG 30–60 minutes after changing oxygen in a hypercapnia-risk patient and approximately 1 hour after starting or materially changing NIV.
Monitor potassium, glucose and lactate during frequent beta-agonists; check ECG when tachyarrhythmia or electrolyte disturbance is possible.
Document escalation status early, including NIV suitability, intubation plan and patient wishes; review it when physiology changes.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

pH tells the time course

PaCO2 labels hypercapnia; pH and bicarbonate reveal whether kidneys have compensated and whether a dangerous acute component is present.

Oxygenation and ventilation are separate

Supplemental oxygen can normalise SpO2 while alveolar ventilation continues to fail and PaCO2 rises.

A normalising PaCO2 can be bad

In a patient who was hypocapnic from intense respiratory effort, a rise toward normal with worsening fatigue may signal impending ventilatory collapse.

Neuromuscular failure may look quiet

Minimal wheeze and modest distress do not exclude severe pump failure; vital capacity, cough, bulbar function and trajectory are crucial.

Support buys time for cause control

Neither oxygen nor NIV treats pneumonia, oedema, PE, secretions or intoxication; every support prescription needs a parallel cause-specific plan.

11Common pitfallsFrequent interpretation and management errors.

01
Calling all hypoxaemia type 1 without checking PaCO2 and pH.
02
Using SpO2 alone to declare type 2 respiratory failure resolved.
03
Withholding oxygen from a critically hypoxaemic COPD patient rather than giving controlled oxygen and checking gases.
04
Abruptly stopping oxygen when hypercapnia is detected and causing rebound hypoxaemia.
05
Starting NIV without treating bronchospasm, infection, fluid overload, secretions or drug depression.
06
Interpreting a falling respiratory rate as improvement in an increasingly drowsy patient.