Monday, June 9, 2008

The hypoxic drive theory: Why do we breathe?

(This is part two of a six post series. To return to part one, click here.)

When you are thinking about it, you can control your breathing on your own. Most of the time you are alive, however, you will have other things to think about, yet your breathing continues.

So, how does this work?

(For further reading you can click here.)

There are basically two reasons for breathing. One is to maintain homeostasis (balance) within the body, and the other is for the exchange of gas. By homeostasis I mean maintaining a normal level of oxygen (PO2), carbon dioxide (CO2) and acid base balance (pH or hydrogen ions). By exchanging gas, I mean breathing in oxygen, and blowing out CO2.

According to Donald F. Egan's "Fundamentals of Respiratory Care", breathing is controlled by the Central Nervous System, and originates "in the brain stem, mainly from neurons located in the Medulla Oblongata. For the most part, and skipping a bunch of crummy detail, this gland controls breathing by messages it receives from Chemo receptors.

There are two sets of chemo receptors: the central and the peripheral. The central sit right on the Medulla, and the peripheral are located in the "bifurcations" of both carotid arteries and the arch of the aorta, or somewhere between your shoulders and above your heart.

These chemo receptors send messages to the brain (the Medulla) based on changes in CO2 and PO2. However, for the most part, the main driver of non-spontaneous breathing is carbon dioxide (CO2) way more so than oxygen (PO2).

Allow me to put it simple, when CO2 goes up above a certain point, your breathing speeds up. This is evident quite often in COPD and asthma patients who are suffering an exacerbation. They are having great trouble breathing, and ultimately they start to poop out, and their CO2 starts to build up. Thus, their breathing speeds up.

A normal CO2 is 40. Say it goes up to 100. By this point, when CO2 is 20% or greater above the normal value, CO2 starts to act like a sedative, and slows breathing down. Thus, as CO2 continues to rise, this is a sign doctors watch out for that a person is pooping out, and may need aggressive therapy.

The majority of the time, the central chemo receptors send signals to the brain that control breathing. The peripheral chemo receptors only have a minor roll during normal respirations, and only send a signal to breathe when the PO2 is less than 60. Either way, this response is far slower than the signal sent by the central chemoreceptors. Thus, the peripheral chemoreceptors only play a minor role in breathing, unless a patient is a chronic CO2 retainer (so the theory goes), of which we will discuss in a moment.

Thus, we will focus on the central chemo receptors for purposes of simplicity.

Let me confuse you a minute. The real drive of breathing is actually hydrogen ions . As hydrogen ions increase, your breathing speeds up. But, since hydrogen ions are not allowed to cross the blood brain barrier so that the pH of the brain can be different from the pH of the body, it cannot directly be used to stimulate breathing.

Thus, CO2 is used. CO2 is allowed to cross the blood brain barrier. Excess levels of CO2 arrive in the brain and are received by the Central Chemo receptors. Thus, "elevations in CO2... cause rapid diffusion of the gas into the CSF (Cerebral Spinal Fluid), where it dissociates into hydrogen ions and lowers the CSF, thereby stimulating the central chemo receptors. The central chemo receptors, in turn, signal the medulary centers to increase ventilation."

So you can see, CO2 "indirectly" causes changes in respiration's.

If the CO2 becomes chronic, or is still hanging at a high level after a day or two, according to Egan, the stimulatory effect of the high CO2 diminishes because the kidneys will try to compensate for the high CO2 by creating more buffers (bicarbonate or HCO3), thus causing the pH of the CSF to go back to normal. The medulla thus receives a signal that CO2 is normal, even though it is actually elevated.

It therefore is easy to tell which patients are chronic retainers because their HCO3 level will usually be high, and usually something greater than 30.

And, in Chronic COPD patients, this CO2 level may stay high while at the same time maintaining homeostasis (a normal pH), and, thus, CO2 has less of an effect on breathing as it would on a normal person (in theory anyway).

In effect, it may be normal for a COPD patient to have a CO2 of 50, and a PO2 of 50. We call these guys members of the 50/50 club, or chronic CO2 retainers or simply chronic retainers.

Changes in PO2 have no direct effect on Central Chemo receptors.

As anything in life, this process is far more complicated than I just explained, but you can see from what I have described here why in many COPD patients CO2 may lose its ability to stimulate a person's drive to breath, especially when CO2 is chronically elevated (or so the theory will have it).

And this is where the gold standard of RT comes into play. As, when a patient has a chronically elevated CO2, it is believed that it stops being the drive to breath. In these patients, it is believed that oxygen becomes their main drive to breath.

Thus, we must take a look at peripheral chemo receptors. According to Egan, "Peripheral chemo receptors are not very sensitive to CO2 changes... their primary role appears to be in response to hypoxia."

Normal PO2 is 104. It does not effect the peripheral chemo receptors until it is less than 60. To put this in perspective, a PO2 of 60 will usually generate a sat (SPO2) of about 90%. As the PO2 falls from 60 to 30 torr (SPo2 of 90% to 60%), the rate of breathing should be expected to be increased due to signals sent from the peripheral chemo receptors.

Now, as we've explained, CO2 is normally the drive to breath. But, if a patient with COPD is having so much trouble breathing that there is no way possible that he can speed up his breathing further to blow off that excess CO2 "regardless of patient effort," CO2 no longer is the drive to breathe, and PO2 becomes the drive to breathe.

This is called the hypoxic drive theory.

And this, my fellow readers, is why doctors soooooo do not want to put a COPD patient on more than 2LPM even though their oxygen levels continue to be low.

This is why many COPD patients are allowed by many doctors to have sats in the mid to low 80s even though low levels of oxygen may be deadly to the heart. This is why many doctors refuse to put many COPD patients on 100% oxygen, because they are afraid they will knock out their drive to breath. They are afraid the patient will become lethargic and die.

The hypoxic drive theory is the gold standard of respiratory therapy, but is it a fallacy or a reality? This is a debate that may be ending.

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

4 comments:

michelle said...

Interesting stuff! I've been looking forward to this.

Amy said...

So about that cat....when Mr. Asthma Mom and I were dating, he'd be allergic to cats at one person's house but not another's. I thought it was totally ridiculous until, years later, I found out it is possible to be allergic to one species of cat but not another.

So maybe you could give in, on the condition that you'll have to find a new home for it if anyone's health suffers?

Take what I'm saying with an enormous grain of salt, though--I have yet to break down and get a family pet, lol.

Anonymous said...

The problem though is that Dr's and RN's miss the point that it is not the Fi02 that matters. It is having the PO2=60ish. Even if you subscribe to this theory, any amount of FiO2 is acceptable (won't make the patient stop breathing) provided the PO2 is 60 (SpO2=90). It is completely unacceptable to leave patients with SpO2's in the low 80's because, well that will cause most of them to die.

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