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Results: All patients had an initial drop in minute ventilation (Ve) once placed on supplemental O2 but Ve then recovered to near baseline levels. Effect of minute ventilation during oxygen-induced hypercapnia. Methods: Minute ventilation and PaCO2 were measured in all patients first while breathing room air and then while breathing supplemental oxygen. Population: 22 ICU patients with known COPD in acute respiratory failure Effects of the administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure. The first study to really investigate this theory was done in 1980. Supplemental O2 removes a COPD patient’s hypoxic respiratory drive causing hypoventilation with resultant hypercarbia, apnea, and ultimate respiratory failure. Because COPD patients spend their lives chronically hypercarbic they no longer respond to that stimulus, and their only trigger for respiratory drive is the level of oxygen (or lack their of) in their blood.

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There are two central drivers of respiratory drive, hypercarbia and hypoxemia.

One commonly cited theory goes like this: Well lucky for you we sifted through the primary literature to bring you the myths and facts, and the short answer is…it’s complicated. If you’re like me then you’ve probably heard a number of conflicting theories as to WHY overzealous supplemental oxygen leads to bad outcomes in these patients.ĭoes hyperoxia suppress a COPD patient’s respiratory drive? Does it cause V/Q mismatching? Does it change the chemistry of the patient’s blood through the Haldane effect? It’s enough to make you want to give up and page respiratory therapy. We give enough O2 to prevent hypoxemia, but not so much that it causes hypoventilation or dangerous hypercarbia. Background: It’s common practice to give carefully titrated supplemental oxygen therapy for patients in COPD exacerbation.