Acute respiratory failure (hypoxaemic and hypercapnic) !

Acute respiratory failure is when the lungs suddenly cannot take in enough oxygen or remove enough carbon dioxide. It is a medical emergency.

Updated 2026-11-01

Structures involved

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In the clinical exam

Why it happens

What it is

A syndrome in which gas exchange fails over minutes to days, so arterial oxygen falls (hypoxaemic, type 1) and/or carbon dioxide rises (hypercapnic, type 2). It is defined by arterial blood gases, not by a single disease.

Who gets it

One of the most common reasons for admission to intensive care units worldwide and in Latin America. Pneumonia, sepsis, exacerbations of COPD and heart failure are the usual causes in adults; in Colombia, tuberculosis and high-altitude cities (where normal oxygen levels are lower) add to the context for interpreting gases.

Causes

Hypoxaemic (type 1): pneumonia, ARDS, pulmonary oedema, pulmonary embolism, atelectasis, pneumothorax
Hypercapnic (type 2) from the lungs or airways: COPD or severe asthma exacerbation, end-stage cystic fibrosis
Hypercapnic from the respiratory centre: opioid or sedative overdose, stroke or injury of the brainstem
Hypercapnic from nerves, muscles or chest wall: Guillain-Barré syndrome, myasthenic crisis, high spinal cord injury, flail chest, severe obesity
Low inspired oxygen (high altitude) as a contributing factor

Risk factors

Chronic lung disease (COPD, interstitial disease, cystic fibrosis)
Neuromuscular disease or high spinal cord injury
Use of opioids, benzodiazepines or other sedatives
Older age, frailty and immunosuppression
Major surgery, trauma or sepsis

Pathophysiology

Hypoxaemia comes mainly from ventilation-perfusion mismatch and shunt (alveoli filled with fluid or pus, or collapsed), with diffusion limitation and hypoventilation as other mechanisms; shunt responds poorly to extra oxygen. Hypercapnia comes from alveolar hypoventilation, because the drive, the pump (nerves, diaphragm, chest wall) or the load on the airways fails. Rising CO2 lowers blood pH (acute respiratory acidosis); in chronic CO2 retention the kidney retains bicarbonate to compensate.

Classification

Type 1, hypoxaemic: PaO2 below about 60 mmHg with normal or low PaCO2
Type 2, hypercapnic: PaCO2 above about 45–50 mmHg with acidaemia (pH below 7.35)
Acute, chronic, or acute-on-chronic (e.g. COPD exacerbation)
Perioperative (type 3) and shock-related (type 4) forms are sometimes added

Symptoms and signs

Shortness of breath, fast breathing and use of accessory neck muscles
Restlessness, anxiety or confusion from hypoxaemia
Cyanosis of the lips and nail beds
Tachycardia and sweating
Headache, drowsiness, flushed warm skin and a flapping tremor (asterixis) when CO2 is high
Paradoxical abdominal movement when the diaphragm tires

Diagnosis

Clinical: Rate, work of breathing, mental status and pulse oximetry at the bedside, then a search for the cause (history, chest examination, signs of heart failure, sepsis or overdose). Nursing priorities: airway, positioning upright, continuous oximetry and frequent reassessment.
Tests: Arterial blood gas is the key test: PaO2, PaCO2, pH and bicarbonate classify the type and whether it is acute or chronic; the alveolar-arterial gradient separates hypoventilation (normal gradient) from lung disease (raised gradient). Blood count, lactate, electrolytes, cultures, BNP or troponin and toxicology according to the suspected cause.
Imaging: Chest X-ray first; bedside lung ultrasound for pneumothorax, effusion, consolidation or B-lines of oedema; CT pulmonary angiography if pulmonary embolism is suspected; echocardiography for heart function.

Differential diagnosis

Anxiety with hyperventilation (low CO2, normal oxygen)
Metabolic acidosis with compensatory fast breathing (e.g. diabetic ketoacidosis)
Severe anaemia or carbon monoxide poisoning (oximetry can be misleading)
Upper airway obstruction (foreign body, angio-oedema)
Cardiogenic shock with pulmonary oedema

Goal of treatment

Restore adequate oxygenation and ventilation quickly, protect the airway, and treat the underlying cause while avoiding complications of oxygen and mechanical ventilation.

Treatment

Acute: Controlled supplemental oxygen titrated to a target saturation, with a lower target in people at risk of CO2 retention (e.g. COPD); high-flow nasal oxygen in hypoxaemic failure.
Procedure: Non-invasive positive-pressure ventilation is first choice in hypercapnic COPD exacerbations and cardiogenic pulmonary oedema; intubation and invasive mechanical ventilation when it fails, consciousness falls or the airway is not protected.
Medical: Treatment of the cause: antibiotics for pneumonia or sepsis, bronchodilators and systemic corticosteroids for asthma or COPD, diuretics and vasodilators for pulmonary oedema, anticoagulation for pulmonary embolism, opioid antagonist for opioid overdose.
Follow-up: Continuous oximetry, repeated blood gases, capnography when ventilated, vital signs and level of consciousness; nursing care includes head-of-bed elevation, suctioning and ventilator-safety checks.

Drugs for this condition

Oxygen

Complications

Cardiac arrest and hypoxic brain injury
Arrhythmias and myocardial ischaemia
Ventilator-associated pneumonia and ventilator-induced lung injury
Barotrauma and pneumothorax
ICU-acquired weakness, delirium and pressure injuries

Prognosis

Depends on the cause and on how fast it is reversed: drug overdose or pulmonary oedema often recover quickly, while ARDS, sepsis or advanced chronic lung disease carry substantial mortality. Survivors of long ICU stays may have lasting weakness and reduced quality of life.

Prevention

Vaccination against influenza, pneumococcus and COVID-19 in people at risk
Optimal control of COPD and asthma and stopping smoking
Careful use and monitoring of opioids and sedatives
Early mobilisation and breathing exercises after surgery

Test yourself

Think of the answer, then tap the question to see it.

How are type 1 and type 2 respiratory failure defined on blood gases?

Type 1 is hypoxaemia (PaO2 below about 60 mmHg) with normal or low PaCO2; type 2 is hypercapnia (PaCO2 above about 45–50 mmHg) with respiratory acidosis.

Which mechanism of hypoxaemia responds poorly to supplemental oxygen?

Shunt, where blood passes alveoli that are not ventilated (filled with fluid or collapsed), as in ARDS or lobar consolidation.

What does a normal alveolar-arterial gradient with hypoxaemia suggest?

Pure hypoventilation (e.g. opioid overdose or neuromuscular weakness) or low inspired oxygen, rather than lung disease.

In which situation is non-invasive ventilation the first-line support?

Hypercapnic respiratory acidosis in a COPD exacerbation, and also cardiogenic pulmonary oedema.

Which bedside signs suggest the patient is tiring and may need intubation?

Falling consciousness, a slowing respiratory rate or paradoxical abdominal breathing despite distress, and worsening acidosis on repeat gases.

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Respiratory Failure (National Heart, Lung, and Blood Institute (NHLBI, NIH), 2022).

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Representative model, for educational purposes only.

Right lower lobe highlighted on the Durgical 3D model