Oxygen and Carbon Dioxide Retention in COPD

Revised and reviewed 6 March 2014


  • Excessive oxygen administration can lead to hypercapnic respiratory failure in some COPD patients
  • COPD patients with more severe hypoxemia are at higher risk of CO2 retention from uncontrolled O2 administration
  • The same phenomenon has also been described in severe asthma, community-acquired pneumonia and obesity hypoventilation syndrome and any patient with chronic respiratory failure may be at risk


The traditional explanation is wrong

  • the traditional theory is that oxygen administration to CO2 retainers causes loss of hypoxic drive, resulting in hypoventilation and type 2 respiratory failure. This is a myth.
  • Patients suffering from COPD exacerbation, regardless of whether they have CO2 retention, generally have supra-normal respiratory drive (unless there is impending hypercapnic coma)

The real explanation involves:

  • increased V/Q mismatch (most important)
  • the Haldane effect

V/Q mismatch

  • In COPD, patients optimise their gas exchange by hypoxic vasoconstriction leading to altered alveolar ventilation-perfusion (Va/Q) ratios
  • Excessive oxygen administration overcomes this, leading to increased blood flow to poorly ventilated alveoli, and thus increased Va/Q mismatch and increased physiological deadspace
  • this increase in Va/Q mismatch occurs in both CO2 retainers and non-retainers, the difference is presumably one of degree

The Haldane effect

  • deoxygenated hemoglobin (Hb) binds CO2 with greater affinity than oxygenated hemoglobin (HbO2)
  • hence oxygen induces a rightward shift of the CO2 dissociation curve, which is called the Haldane effect
  • in patients with severe COPD who cannot increase minute ventilation, the Haldane effect accounts for about 25% of the total PaCO2 increase due to O2 administration


  • Target SaO2 88-92% in these patients
  • the targeted approach is associated with decreased mortality in COPD patients and less respiratory acidosis
  • The oxygen flow rate administered is not important, the (alveolar) PAO2 (and, indirectly, the SaO2) achieved is
  • Never withhold oxygen from a seriously ill hypoxic patient due to fear of cause hypercapnic respiratory failure

Journal articles

  • Abdo WF, Heunks LM. Oxygen-induced hypercapnia in COPD: myths and facts. Crit Care. 2012 Oct 29;16(5):323. PMC3682248

FOAM and web resources

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC


  1. Hi Chis,

    Just a question in regards to V/Q mismatch. The article states that excessive oxygen administration results in increased physiological dead space but now that poorly ventilated areas of lung are receiving increased perfusion wouldn’t this be an example of increased shunt?


  2. hi, quick question for clarity, it says the Haldane effect causes right shift of the ODC, however when I google imagine of the ODC, right shift is labeled Bohr effect and LEFT shift is labeled Haldane effect. Am I getting confused, or is there a mistake in the article?
    Any clarification is much appreciated
    QLD Intern

Leave a Reply

This site uses Akismet to reduce spam. Learn how your comment data is processed.