Effect of oxygen on chronic obstructive pulmonary disease

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In some individuals, the effect of oxygen on chronic obstructive pulmonary disease is to cause increased carbon dioxide retention, which may cause drowsiness, headaches, and in severe cases lack of respiration, which may lead to death. People with lung ailments or with central respiratory depression, who receive supplemental oxygen, require careful monitoring.

Signs and symptoms[edit]

In individuals with chronic obstructive pulmonary disease and similar lung problems, the clinical features of oxygen toxicity are due to high carbon dioxide content in the blood (hypercapnia).[1] This leads to drowsiness (narcosis), deranged acid-base balance due to respiratory acidosis, and death.[2]


Many people with chronic obstructive pulmonary disease have a low partial pressure of oxygen in the blood. Treatment with supplemental oxygen may improve their well-being; alternatively, in some this can lead to the adverse effect of elevating the carbon dioxide content in the blood (hypercapnia) to levels that may become toxic.[3][4]


In individuals with chronic obstructive pulmonary disease who receive supplemental oxygen, carbon dioxide accumulation may occur through three main mechanisms:[5]

  • Ventilation/perfusion matching: under-ventilated lung usually has a low oxygen content which leads to localised vasoconstriction limiting blood flow to that lung tissue. Supplemental oxygen abolishes this constriction, leading to poor ventilation/perfusion matching. This redistribution of blood to areas of the lung with poor ventilation reduces the amount of carbon dioxide eliminated from the system.
  • The Haldane effect: most carbon dioxide is carried by the blood as bicarbonate, and deoxygenated hemoglobin promotes the production of bicarbonate. Increasing the amount of oxygen in the blood by administering supplemental oxygen reduces the amount of deoxygenated hemoglobin, and thus reduces the capacity of blood to carry carbon dioxide.
  • Respiratory homeostasis: in healthy individuals, a rise in carbon dioxide causes an increase in the drive to breathe. However, in some patients with chronic obstructive pulmonary disease, this response has been blunted, leaving low oxygen levels as the main stimulus of respiration (hypoxic drive). Hence, giving supplemental oxygen reduces their stimulus to breathe, causing respiration to slow (hypoventilation), and allowing carbon dioxide to accumulate in the body.


In people with chronic obstructive pulmonary disease, carbon dioxide toxicity can be prevented by careful control of the supplemental oxygen. Just enough oxygen is given to maintain an oxygen saturation of 88 - 92%.[6]


  1. ^ Tinits, P (1983). "Oxygen therapy and oxygen toxicity". Annals of Emergency Medicine. 12 (5): 321–8. doi:10.1016/S0196-0644(83)80520-4. PMID 6414343. 
  2. ^ Young, IH (2007). "Revisiting oxygen therapy in patients with exacerbation of chronic obstructive pulmonary disease". The Medical Journal of Australia. 186 (5): 239. PMID 17391085. 
  3. ^ Kim, V; Benditt, JO; Wise, RA; Sharafkhaneh, A (2008). "Oxygen therapy in chronic obstructive pulmonary disease". Proceedings of the American Thoracic Society. 5 (4): 513–8. doi:10.1513/pats.200708-124ET. PMC 2645328Freely accessible. PMID 18453364. 
  4. ^ Patel, Dharmeshkumar N; Goel, Ashish; Agarwal, SB; Garg, Praveenkumar; Lakhani, Krishna K (2003). "Oxygen toxicity" (PDF). Journal, Indian Academy of Clinical Medicine. 4 (3): 234–7. Retrieved 2008-09-28. 
  5. ^ Lumb, AB (2000). Nunn's Applied Respiratory Physiology (5th ed.). Butterworth Heinemann. p. 533. ISBN 0-7506-3107-4. 
  6. ^ Agustí, AG; Carrera, M,; Barbé, F; Muñoz, A; Togores, B (1999). "Oxygen therapy during exacerbations of chronic obstructive pulmonary disease" (full text). European Respiratory Journal. 14 (4): 934–9. doi:10.1034/j.1399-3003.1999.14d34.x. PMID 10573245.