Effect of oxygen on chronic obstructive pulmonary disease

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

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]

Causes

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]

Mechanism

In individuals with chronic obstructive pulmonary disease who receive supplemental oxygen, carbon dioxide accumulation may occur through two 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.

Prevention

In people with chronic obstructive pulmonary disease, carbon dioxide toxicity can be prevented by careful control of the supplemental oxygen. In those with an acute exacerbation of COPD, hypoxic pulmonary vasoconstriction can improve gas exchange, and so just enough oxygen is given to maintain an oxygen saturation of 88%–92%.[6]

References
  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 2645328. 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. Abdo, Wilson F; Heunks, Leo MA (October 2012). "Oxygen-induced hypercapnia in COPD: myths and facts". Critical Care (London, England). 16 (5): 323. doi:10.1186/cc11475. PMC 3682248. PMID 23106947.
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