Does supplemental oxygen cause loss of respiratory drive in COPD patients?

It is common to set the O2 saturation goal for hospitalized patients with COPD exacerbations at 88-92%, and patients without COPD to 94-98%. This is in accordance with British Thoracic Society guidelines. The O2 sat goals are lower for patients with COPD because of the risk of hypercapnenic respiratory failure.

I’m not questioning the O2 sat goals. What I do want to discuss is one of the oft-cited mechanisms for this respiratory failure: that a higher O2 sat will depress the respiratory drive in these patients. Is this true?

Not really. The explanation is very well stated in LITFL.  Patients with COPD suffer from parenchymal damage that increases V/Q mismatch. To compensate for this, those smart pulmonary arterioles vasoconstrict to deliver O2 preferentially to the parts of the lungs with the least damage. Giving someone supplemental O2 in this scenario causes the pulmonary arterioles to dilate, causing increased blood flow to the damaged parts of the lungs, too, which increases V/Q mismatch again. See this article for helpful diagrams and more detailed explanation. In addition, due to the Haldane effect (=introducing more O2 will cause CO2 to dissociate more readily from hemoglobin), adding supplemental O2 theoretically causes COPDers’ CO2 levels to increase. I’m not sure that anyone has actually demonstrated this experimentally, but it makes sense.

This review from Respiratory Care on the use of supplemental O2 cites a 2010 study of about 400 patients with COPD exacerbations. They were randomized into a 88-92% O2 sat group and a non-titrated group (so presumed >94%); each group could get as much supplemental O2 as needed to reach those goals. The titrated group had a 58% reduction in hypercapnea and respiratory failure compared to the non-titrated group.

In conclusion: patients with COPD exacerbations should have a lower target O2 sat, but the justification for this is not that it will affect their respiratory drive–instead, think about V/Q mismatch and CO2 dissociation. 

What if a patient has COPD but does not have an exacerbation while they’re in the hospital? I couldn’t find a clear answer but would assume that since the same physiologic properties above are in play, it makes sense to continue the lower O2 sat goal.

Tangent: oxygen has traditionally been recommended as standard management of MI. However, this 2017 Swedish RCT showed that putting patients who had an O2 sat >90% on supplemental O2 did not change outcomes. The British Medical Journal shows that maintaining very high O2 sats does not improve mortality and has a great infographic on why maintaining an O2 sat between 90-94% is appropriate for most patients.


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