The hypoxic drive theory: The CO2 retainer

(This is part three of a six post series. To go to part one click here.)

Today I would like to add to our discussion of why people breath. In particular, today's post will delve further into the topic of oxygen induced hypoventilation.

As we described earlier, the body will continually try to make sure that gases in the body are balanced in order to maintain a normal pH, and in this way maintain a certain level of homeostasis within the body.

Usually, increases and decreases in carbon dioxide levels detected by the central chemo receptors is what causes people to breath. When a person is in respiratory failure, and the carbon dioxide level is high, decreasing levels of oxygen as detected by the peripheral chemo receptors then takes over as the drive to breath.

Thus, if a person has a chronically high carbon dioxide level, and you give this person 100% oxygen, you knock out their drive to breath. This, my friends, is what we call the hypoxic drive theory. Actually, this is the gold standard of respiratory care. It is what helped to establish us as a profession.

According to Donald Egan's "Fundamentals of Respiratory Care," when a healthy person "breathes 100% oxygen, the peripheral chemo receptors remain essentially inactive. However, because blood oxygen levels are high, there is less reduced hemoglobin available to carry carbon dioxide. This causes a slight rise in (carbon dioxide) CO2, which in turn stimulates the medullary respiratory center (at the base of the brain)." This in turn causes a person to breath faster.

Now, if you have a patient who has a chronically low level of oxygen and high level of CO2, breathing high levels of oxygen (FiO2) can cause a person to slow down his breathing (per the theory). In essence, the "high blood O2 (oxygen) levels suppress these peripheral chemo receptors, thereby depressing ventilatory drive."

Since a person's breathing is how they blow off excess CO2, you can see how this could be detrimental to a person who already has a high CO2 level.

Thus, since the high FiO2 (say 100%) is signalling the peripheral chemo receptors to slow down breathing, a person with a chronically high CO2 may end up with a critically high CO2. In cases like this, I've seen CO2s in COPD patients as high as 110. This is not good. And usually these patients become lethargic. Yet many times they surprise us and they do not lose consciousness.

Usually, according to William A. French, "Hypoxic Drive Theory Revisited," rtmagazine.com (Issue: February/March 2000), CO2 must generally reach a level above 90 mm Hg for" a patient to become lethargic.

However, sometimes these patients are so used to high CO2 levels, that they remain conscious even with a high CO2 level. If you have ever seen a COPD patient in this situation, you will observe that they are usually blue, and this is where we get the term blue bloaters from. The patient is blue due to low oxygen.

And they also are jittery or shaky. That is the high CO2 at work. If they are lethargic, that is usually due to the high CO2 level, but as the hypoxic drive theory states, it may also be due to the high level of oxygen the medical staff provided to the patient.

That is the theory. Keep in mind it is a theory that doctors believe in to the point of ad nauseam. I personally think it is inhumane to allow a person's oxygen to stay low, when this could kill them. However, that's just my opinion.

This brings me to my next point. According to Egan himself, right in his book. And I think it is these next two paragraphs that will help me disprove the hypoxic drive theory, of which I will attempt to do in my next couple posts.

Egan writes that "the rise in PaCO2 that is observed in some patients is due mainly to impaired gas exchange, not depression of ventilation."

And, he writes:

"Regardless of mechanism then, hyperventilation is a potential hazard of O2 therapy in patients with chronic lung disease, however, this harmful effect should never stop us from giving oxygen to a patient in need. Preventing hypoxia should always be the first priority."

Thus, according to Egan, "in order to prevent hypoxia but avoid hypoventilation (breathing to slow down) in these patients, we should aim for an arterial PO2 between 50 and 60 torr. Generally, this approach provides adequate oxygenation, while minimizing the likelihood of hypoventilaiton."

In layman's terms, a normal blood PO2 is over 100. A PO2 of 100 would usually generate a sat (SPO2) of about 98% (this is the % of oxygen in inspired air that gets to the arteries). A PO2 of 50 to 60 would therefore generate a sat of 80 to 90%. So, if you werent' familiar with these medical terms, now you are. And now you know what to look for on the monitor besides heartrate, respiratory rate and blood pressure.

To maintain a sat of 80 to 90%, usually we RTs use 2-3 LPM via nasal cannula. Or, if a patient needs more oxygen, or is breathing laboriously, we will use a venti-mask at no more than 30 to 40% FiO2 (oxygen). (For the record, there is 21% oxygen in the air you breath).

However, what happens if a chronic COPD patient is on a 40% venti-mask and the sat on the monitor still reads 70%? Now what do you do. You give them more oxygen. You give them 100% oxygen if they need it.

Or, as I've seen many times, you walk up to the doctor to get an order for more oxygen, and he says, "keep it right where it is. We don't want to knock out his drive to breath." And he looks at you like you are an idiot.

Or, another scenario is you do a blood gas that shows a PO2 of 45 and a CO2 100. The patient is awake and alert and talking to you just fine. The doctor says, "decrease the oxygen. We need to see if we can get that CO2 down."

This is where you roll your eyes in frustration.

(To view part four click here. To return to part one click here.)