Target oxygen saturation in COPD

We have all learnt the target oxygen saturation for patients with COPD is 88-92%. This target was supported by a number of studies that found having high oxygen saturation without titration was associated with high mortality and complication rates. However, what was the mechanism behind this?

Initially this was attributed to the decrease in "hypoxic drive" when patient was on oxygen and having high oxygen saturation. The theory is by providing oxygen and increasing the oxygen saturation, the respiratory drive will be decreased, leading to hypercapnia. However, studies have shown that this is not the only mechanism. 

(VE = minute ventilation. CO2 = partial pressure of carbon dioxide)

Figure 1 was from a study conducted by Aubier et al. During 15 minutes of oxygen administration, there was an initial decrease in minute ventilation, but it recovered substantially after 5 minutes. However, the oxygen-induced hypercapnia did not recover. This suggested that minute ventilation couldn't explain the total increase in PaCO2 alone.

Now, with more evidence, an increasing number of physicians attribute the hyperoxic hypercapnea also to V/Q mismatch and Haldane effect. 

In normal physiology, low oxygen saturation is a potent vasoconstriction stimulus for pulmonary vasculature. Thus, poorly ventilated or damaged alveoli from COPD will have decreased perfusion (low V and low Q). Giving extra oxygen will remove the vasoconstriction effect. Thus, the alveoli will have an increased perfusion (low V and increased Q). This V/Q mismatch ultimately leads to an increased PaCO2. In computer simulation, this was found to be the main mechanism of oxygen-induced hypercapnia in COPD. 

The Haldane effect refers to the increased ability of deoxygenated hemoglobin to carry CO2. Thus, in the presence of high oxygen saturation, the dissociation curve for CO2 will shift toward the right, release CO2, and increasing the PaCO2. Normally, this can be compensated by increasing the ventilation, but that is more challenging in patients with COPD. Aubier et al estiamted that 25% of the oxygen-induced hypercapnia was caused by Haldane effect. 

In conclusion, V/Q mismatch, Haldane effect, and hypoxic drive all contribute to the oxygen-induced hypercapnia in COPD patients. 

-YZ-

Reference

Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial - PubMed (nih.gov)

Outcomes of acute exacerbations in COPD in relation to pre-hospital oxygen therapy - PubMed (nih.gov)

Oxygen-induced hypercapnia in COPD: myths and facts - PubMed (nih.gov)

Causes of hypercarbia with oxygen therapy in patients with chronic obstructive pulmonary disease - PubMed (nih.gov)

Oxygen-Induced Hypercapnia in COPD: What is the Mechanism? – Clinical Correlations