Hypoxemic and hypercapnic respiratory failure !
- Mechanism
- Exam priority: medium
The lungs can fail in two ways: they can't get oxygen into the blood (type 1), or they can't clear CO₂ because breathing is too weak (type 2).
Updated 2026-11-01
Also called: Type 1 and type 2 respiratory failure
See it in 3D: Diaphragm · Medulla oblongata
What it is
Respiratory failure is the inability of the respiratory system to maintain gas exchange. In hypoxemic (type 1) failure PaO₂ falls with normal or low PaCO₂, from ventilation–perfusion mismatch, shunt or diffusion defects. In hypercapnic (type 2) failure alveolar ventilation is inadequate and PaCO₂ rises, from lack of drive, weak muscles or an excessive respiratory load.
How it works, step by step
- Type 1: areas with perfusion but no ventilation (filled or collapsed alveoli) add unoxygenated blood.
- Hypoxemia drives ventilation; CO₂, more diffusible, leaves easily and PaCO₂ stays normal or low.
- Type 2: alveolar ventilation falls from lack of drive (opioids, brainstem injury), weakness (Guillain-Barré) or fatigue against a high load (COPD).
- Because PaCO₂ is inversely proportional to alveolar ventilation, CO₂ accumulates as ventilation falls.
- Retained CO₂ displaces O₂ in the alveolus (alveolar gas equation), so PaO₂ falls too.
- Acute respiratory acidosis depresses consciousness and contractility; if it becomes chronic, the kidney compensates with bicarbonate.
Oxygen–hemoglobin dissociation curve
P50 26.8 mmHgArterial blood 97 %Mixed venous blood 75 %O₂ given up to the tissues 23 %
Normal curve. Tap a point (arterial, venous or P50) or move a control.
- Current curve
- Normal curve (pH 7.40 · 37 °C)
- Arterial blood (PO₂ 100)
- Mixed venous blood (PO₂ 40)
- O₂ given up to the tissues
The two types compared
| Feature | Type 1 (hypoxemic) | Type 2 (hypercapnic) |
|---|---|---|
| PaO₂ | Low | Low |
| PaCO₂ | Normal or low | High |
| A–a gradient | Raised | Normal if pure hypoventilation |
| Mechanism | V/Q, shunt, diffusion | Alveolar hypoventilation |
| Examples | ARDS, pneumonia, embolism, pulmonary edema | COPD exacerbation, opioids, Guillain-Barré |
Clinical notes
- COPD patient growing drowsy: suspect acute-on-chronic hypercapnia; the blood gas shows low pH with high bicarbonate.
- ARDS: refractory hypoxemia with bilateral infiltrates; the PaO₂/FiO₂ ratio grades severity.
- Opioid overdose: slow breathing, pinpoint pupils, hypercapnia; naloxone reverses the effect at the receptor.
- Nursing and NCLEX: drowsiness and morning headache can be the first signs of CO₂ retention.
Test yourself
Think of the answer, then tap the question to see it.
Why does opioid hypoventilation have a normal A–a gradient?
The lung is healthy: PaO₂ falls only because accumulated CO₂ takes up space in the alveolus, and blood equilibrates with that alveolar gas.
Why does hypoxemic failure usually come with a low PaCO₂?
Hypoxemia stimulates chemoreceptors and raises ventilation; CO₂ is cleared easily even from areas with V/Q mismatch.
What separates acute from chronic hypercapnia on a blood gas?
In acute hypercapnia pH clearly falls; in chronic hypercapnia the kidney has retained bicarbonate for days and pH is near normal.
Why does shunt hypoxemia improve little with oxygen while COPD hypoxemia does improve?
In shunt, blood passes unventilated alveoli that never see the O₂; in V/Q mismatch poorly ventilated alveoli still get some, and extra O₂ raises their PO₂.
See it in 3D
The structures of Durgical's 3D anatomy where it happens.
Related topics
- The causes of hypoxemia
- The alveolar gas equation and the A–a gradient
- Ventilation–perfusion matching and West zones
- Respiratory acidosis and alkalosis
- The work of breathing
- Control of breathing, chemoreceptors and lung reflexes
- Reading an arterial blood gas step by step
Related conditions
- Acute respiratory distress syndrome (ARDS)
- Chronic obstructive pulmonary disease (COPD)
- Respiratory acidosis
- Community-acquired pneumonia
- Guillain-Barré syndrome
- Pulmonary embolism
In Pharmacology
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: 22.4 Gas Exchange (OpenStax (Rice University), 2022); Acute Respiratory Distress Syndrome (StatPearls (NCBI Bookshelf), 2026); Chronic Obstructive Pulmonary Disease (COPD) (StatPearls (NCBI Bookshelf), 2026); Respiratory acidosis: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 43). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).
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Representative model, for educational purposes only.