Supplemental oxygen can sometimes cause carbon dioxide to increase to dangerous levels, usually in patients with chronic lung diseases like COPD. I was originally taught that this was due to the extra oxygen blunting their respiratory drive, but it turns out that’s not the whole story. The mechanisms, in order of importance:
- V/Q mismatch: Lungs autoregulate their circulation to match ventilation, so that low-oxygen blood only goes to the parts of the lung that have oxygen, which are usually the well-ventilated parts of the lung with lots of air moving in and out. If there’s extra oxygen diffusing to places that are poorly ventilated, it can cause vasodilation within that poorly-ventilated lung. As a result, blood is going to parts of the lung that aren’t well ventilated and can’t blow off CO2. Basically, it increases perfusion to physiologic dead space. Not good for getting rid of carbon dioxide.
- Haldane effect: hemoglobin binds both oxygen and carbon dioxide in order to deliver oxygen from the lungs to the tissue and take CO2 from the tissue to the lungs. Unfortunately, when there’s high O2, the Haldane effect means that hemoglobin isn’t as good at carrying CO2. When there is also poor ventilation, this causes CO2 to build up in the blood.
- Blunting of respiratory drive: respiratory drive is controlled by oxygen-sensing parts in the periphery and pH-sensing parts in the brain. It was once thought that chronic CO2 retainers lose their pH-based respiratory drive, and require their hypoxic drive to be working well in order for them to blow off any CO2. It turns out that this isn’t the case.
Read more: Abdo WF, Heunks LM. Oxygen-induced hypercapnia in COPD: myths and facts. Critical Care. 2012;16(5):323. doi:10.1186/cc11475.