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,
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]
Causes
[edit]Many people with chronic obstructive pulmonary disease have a low partial pressure of oxygen in the blood and high partial pressure of carbon dioxide. 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] With normal lung function, a stimulation to take another breath occurs when a patient has a slight rise in PaCO2. The slight rise in PaCO2 stimulates the respiratory centre in the brain, creating the impulse to take another breath. In some patients with a chronically high level of PaCO2, such as those with COPD, the stimulus and drive to breathe is caused by a decrease in PaO2. This is called a hypoxic drive. Thus, when oxygen is administered to patients with known CO2 retention, patients need to be watched for signs of hypoventilation, a decreased level of consciousness, and apnea.[5]
Mechanism
[edit]In individuals with chronic obstructive pulmonary disease who receive supplemental oxygen, carbon dioxide accumulation may occur through two main mechanisms:[6]
- Ventilation/perfusion matching: under-ventilated lung usually has a low oxygen content which leads to localized 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
[edit]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%.[7]
References
[edit]- ^ 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.
- ^ Young, IH (2007). "Revisiting oxygen therapy in patients with exacerbation of chronic obstructive pulmonary disease". The Medical Journal of Australia. 186 (5): 239. doi:10.5694/j.1326-5377.2007.tb00880.x. PMID 17391085. S2CID 27365725.
- ^ 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.
- ^ 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. Archived from the original (PDF) on 2015-09-22. Retrieved 2008-09-28.
- ^ Doyle, Glynda Rees; McCutcheon, Jodie Anita (2015-11-23). "5.7 Cautions with Oxygen Therapy". Clinical Procedures for Safer Patient Care.
- ^ Lumb, AB (2000). Nunn's Applied Respiratory Physiology (5th ed.). Butterworth Heinemann. p. 533. ISBN 0-7506-3107-4.
- ^ Abdo, Wilson F; Heunks, Leo MA (October 2012). "Oxygen-induced hypercapnia in COPD: myths and facts". Critical Care. 16 (5): 323. doi:10.1186/cc11475. PMC 3682248. PMID 23106947.