In medical school, we learnt that oxygen administration in patients with chronic obstructive pulmonary disease (COPD) induces hypercapnia through the 'hypoxic drive' mechanism. I had talked about this in my previous blog here.
Today, I found out that it is a myth. Well, sort of. It has a minor role. At least, in COPD.
Studies found out that the minute ventilation had a limited effect on PaCO2 :/
The MAJOR mechanism on why you get hypercapnia due to oxygen administration is ventilation perfusion mismatch.
Normally, alveolar ventilation and perfusion are well matched.
Two extremes of ventilation-perfusion (V/Q) mismatch may occur:
1. No ventilation of an alveolus but adequate perfusion, resulting in shunting
2. Adequate ventilation but no perfusion, resulting in dead space ventilation
The body has protective mechanisms to optimize the V/Q ratio.
When alveolar oxygen tension decreases (for example, in bronchoconstriction), local mediators induce vasoconstriction of pulmonary capillaries supporting this particular alveolus, counteracting possible shunting, a mechanism called hypoxic pulmonary vasoconstriction.
(So areas that don't work, don't get blood. The lungs are pretty smart and don't pour blood in places where gas exchange can't occur.)
The strongest mediator for hypoxic pulmonary vasoconstriction is alveolar pO2 (partial pressure of oxygen). Therefore, a high fraction of inspired O2 (FiO2) will increase O2 tension in alveoli with a low level of ventilation, inhibiting hypoxic pulmonary vasoconstriction. As a result, alveoli with relatively impaired ventilation are well perfused, leading to an increase in V/Q mismatch.
(Now the areas that don't work are unnecessarily getting the blood causing a waste of everybody's time and increasing CO2 in blood.)
In short, the increased physiologic dead space through worsened V/Q accounts for the oxygen-induced hypercapnia.
Another minor mechanism is Haldane effect:
Hemoglobin combines with CO2 to form carbamino compounds.
The ability of deoxygenated hemoglobin to bind CO2 is much higher than that of oxygenated hemoglobin.
Thus, oxygen induces a rightward shift of the CO2 dissociation curve and this is known as the Haldane effect. (I talk about it in this blog post.)
A rightward shift in the CO2 dissociation curve will increase PaCO2, which normally is excreted through elevated minute ventilation, normalizing PaCO2.
However, in patients with severe COPD, who are unable to increase minute ventilation, the Haldane effect will increase PaCO2.
Interesting, isn't it?