As you guys know I do not believe in the Hypoxic Drive Theory, which I refer to as the Hypoxic Drive Hoax. I remind nurses, doctors and other Respiratory Therapists of this from time to time, and I get the usual, "Well, I've witnessed it a few times. I've seen it with my own eyes, oxygen knock out a person's drive to breathe."
Ah, I say, surely you witnessed a COPD patient from time to time become lethargic and lose his drive to breathe, but it had nothing to do with the hypoxic drive, which does exist by the way. The hypoxic drive does exist, but it is not knocked out just because someone is a CO2 retainer. It's a theory. It's a myth, just like it's a myth that too much salt makes you develop high blood pressure. It's a myth just like carrying a dried rabbits foot will give you good luck.
Too much oxygen does not knock out the hypoxic drive. There is no evidence that it does. I repeat: there is not, nor will there ever be, any study to prove the hypoxic drive theory. However, there are many theories that disprove it. I wrote about those theories in this post.
The reason CO2 rises is due to V/Q mismatching and Haldane Effect. V/Q mismatching causes less oxygen to get to the lungs, and this results in less oxygen in the blood attaching to hemoglobin molecules. With less oxygen in the blood, the body naturaly produces more red blood cells because it thinks this will remedy the situation. Yet the result is the same amount of oxygen and more red blood cells. This results in an SpO2 that is lower than normal. This means that a COPD patient may live with an SpO2 around 88-92%. This means a normal PO2 of around 55-65.
This brings me to the Haldane Effect. The law was created by John Haldane, one of the pioneers of oxygen therapy, which states: Deoxygenation of the blood increases its ability to carry carbon dioxide. This means that the less oxygen in the blood, the higher the CO2 will be. Since COPD patients normally have polycythemia, and they also have some permanent V/Q mismatching, PO2 will generallty be low, and CO2 will generally be high. Since they have a limited capacity to increase their respiratory rate, their bodies will simply get used to the high CO2. It's not unusual for a COPD patient to have a PO2 of 50 and a CO2 of 50. We call these patients members of the 50-50 club. They are also often called blue bloaters, because many are overweight and cyanotic (when not on supplemental O2) due to the general nature of their disease. Usually these patients respond well to 2-3 LPM of oxygen.
Now, so what happens when these patients have an exacerbation? You will have increased V/Q mismatching. This will cause PO2 to drop, and CO2 to rise. Since these patients have a limited breathing capacity, they will be unable to blow off the excess CO2. These patients are hypoxic, and they are hypercaptic, and it has nothing to do with oxygen because you're not oxygenating them yet. But as these patients enter the emergency room, you put a pulse ox on them that reads 80%. So you do an ABG that gives you a PO2 of 45 and a CO2 of 75. You put that patinet on a 50% venturi mask to get the PO2 to a life sustaining level. Now you do another ABG and you get a PO2 of 60, SpO2 of 90, and a CO2 of 85. This looks good except for the CO2.
Some of these patinets will continue to poop out, and they will become lethargic, and they will require a ventilator. The original theory was that the oxygen knocked out their drive to breathe. But this is not true. The truth is the Haldane Effect happened. You added more oxygen molecules to the blood stream, and this knocked CO2 off the hemoglobin and into the blood stream. This is why the CO2 goes up when you give the patinet oxygen. The trick is here that if you give too much oxygen you might cause the CO2 to rise too much, and this may cause lethargy. However, most COPD patients (and I've seen this a gazillion times) can tolerate these higher CO2s because they are generally used to it. A CO2 of 90 may kill you or me, but to a COPD patient its tolerable. You'll can have a discussion with a COPD patinet with a CO2 of 90.
Yet those who believe in the hypoxic drive theory will panic and take away a person's much needed oxygen. Those who believe in the Haldane Effect as the cause of rising CO2 will monitor the person's oxygen level, and maintain a livable oxygen level, of around 88-92% SpO2. If maintaining that oxygen level knocks out their drive to breath, it's due to V/Q mismatching and the Haldane Effect, and not the hypoxic drive being knocked out. If the hypoxic drive theory were true, all of these COPD patients we oxygenate would drop off the earth, but you rarely see it. I have been giving breathing treatments with oxygen for 15 plus years, and not one COPDer ever stopped breathing during a treatment. The reason you don't see it is because the hypoxic drive theory is a hoax.
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