Dangers of Oxygen

The primary reason you breathe is to get 02. Where did you read that about CO2?

Julie wrote:The primary reason you breathe is to get 02. Where did you read that about CO2?

The primary reason you breathe is to exchange O2 and CO2. The primary stimulus to breathe is build-up of CO2 in the bloodstream.

The primary reason I breathe is to stay alive!

Sorry, I just couldn't resist.

gvz is on the right track. Both absorption of O2 and removal of CO2 are necessary for life.

You can read more about it on Wikipedia; I've listed two links.

There are sensors for CO2 in the brainstem, and sensors for both O2 and CO2 in the carotid body (near the carotid artery in your neck)

But the CO2 sensors are more sensitive than the O2 ones, and under normal conditions CO2 drives ventilation. If you take five or so rapid deep breaths, you will notice that you don't have seem to "need" to breathe for longer than usual. That demontrates how sensitive the CO2 receptors are to pH changes.

At high altitudes, lack of O2 can become the principal driver of ventilation.

There is such a thing as oxygen toxicity, but at normal atmospheric pressure, it would require your breathing about 50% O2. I did a rough calculation on a previous post that suggests it's probably impossible to get that high an O2 concentration by bleeding O2 into a cpap mask (I haven't figured out how to link to a previous post):


"You need to know the volume your mask is designed to vent. For the following sample calculation I'm using 35 l/m:

Each minute the mask receives at least 35l of room air + 5l from the concentrator = 40l/m

5l from the concentrator @ 90% O2 = 4.5l of pure O2

35l of room air @ 20% O2 = 7l of pure O2

So, theoretically, if there are no other variables, the mask receives 40l of air, containing 11.5l of pure O2, or 29% O2."


http://en.wikipedia.org/wiki/Control_of_respiration

http://en.wikipedia.org/wiki/Oxygen_toxicity

I just wonder where in the body I store that liquid form of CO2, I hear it's very cold. I don't think you could live with any liquid CO2 inside your body, your freezer maybe.

As you cool CO2 it goes from a gas to a liquid, then into a solid (Dry ICE), as the DRY ICE warms it turns to a GAS CO2 directly. Jim

gvz wrote:So this is potentially why supplemental O2 infusion can be dangerous: If you happen to have a failure in expelling CO2 properly and then at the same time you inhale excess O2, you can get into a mode where your autonomous body is not breathing as much because the atmospheric O2-level is higher than normal,

Some respiratory therapists think this is actually untrue and that it needs to stop being taught. Most doctors and RTs still believe it, though, because that's what they were taught.

Very interesting article by an RT

Jeff Whitnack wrote:If this CO2 Retainer/hypoxic drive theory had any real merit, then where are the legions of patients arriving in ERs whom have turned up their home O2? Where are the episodes on "Murder She Wrote", as then home oxygen would be the perfect murder weapon (the evidence would disappear after the heinous crime) for any greedy relatives of a CO2 retainer? Has any malpractice suit ever been won on the grounds of giving a CO2 retainer too much oxygen? If so then that case should now be reviewed/reversed in light of recent studies and a newer approach which actually makes some sense.

Jeff Whitnack wrote:And some people say, "but I've seen it happen....No you didn't really see all that theory happen. You witnessed a series of clinical events interspersed with some lab data and then chose to invoke a certain theory to tie it all together. For eons people have believed that they've seen various unscientific superstitions come true and "happen" as lightning, thunder,and earthquakes have wreaked havoc with our psyche and compelled people to come up with some explanation for what they witnessed.

Where is the RT report room where stories don't echo off the walls--- telling the tale of the "stupid nurse who almost killed the COPD patient by turning up his oxygen"(notice that the patient is always "almost" killed). Or one of my favorites, "I couldn't wake him up after his O2 was turned up". Why did you need to wake him up? Perhaps his hypoxemia was finally relieved so the patient could get a good rest?

Jeff Whitnack wrote:I have asked local RT instructors their opinion. One said, "I don't believe in it (CO2 retainer/hypoxic drive theory), but I've got to teach it".

This theory causes clinical silliness as we try with oximetry to maintain CO2 retainers in some magic SpO2 range of 88-90%.

This theory causes clinical suffering as hypoxemic patients are often denied the very oxygen which would relieve their dyspnea.

The hypoxic drive theory is already dead. It's ghost still lives on in clinical practice. But the body is beginning to smell. Our profession was instrumental in bringing this theory to life. It is now our responsibility to drive the nails in the coffin, say a few words, and bury it.

[ emphasis mine ]

Six Part Series of Blog Posts

This is in 6 parts, but honestly, it's not difficult to read.

In Part 3, Rick Frea wrote: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.

In Part 4, Rick Frea wrote:So why do we make COPD patients suffer with a sat of 88%? It's because most of our doctors believe in the hypoxic drive theory.

In Part 5, Rick Frea wrote:And, even if they don't blow off that CO2, it will not be a big deal. All COPD patients have their CO2 levels rise from time to time. It does not kill them. What kills them is lack of oxygen.

Interestingly, the answer, he says, to high levels of CO2 in a patient is not withholding oxygen, but helping them expel CO2--through bilevel PAP or mechanical ventilation.

Goofproof wrote:I just wonder where in the body I store that liquid form of CO2, I hear it's very cold.

Funny, Goofproof! I'm sure you know CO2 in the body is dissolved as a gas in the blood.

Goofproof wrote:as the DRY ICE warms it turns to a GAS CO2 directly.

Solid CO2 ("dry ice") only sublimates under the right pressure and temperature conditions. Otherwise, it goes back through a liquid state before moving to the gaseous state.

Even H2O ice can sublimate under the right pressure and temperature conditions. Often in the winter around here when there is ice on the ground, it will sublimate and melt, both at the same time.

LoQ, the article is interesting (I couldn't get the blogs for some reason). The article is about RT in patients with COPD, and I don't know how that applies to people with SDB and healthy lungs.

I am supposing the reluctance to prescribe supplemental O2 to SDB patients is due to some concern it might be harmful. But it seems to me that if supplemental O2 has any dangerous effect on people with hypoxia due to SDB, it would be very easy to demonstrate that in clinical experiments. Maybe those studies have been done; I don't know.

But if supplemental is not dangerous, then neglecting to supplement O2 in people with SDB and desaturation, is irrational, and needs to be reconsidered.

I think you and I are on the same page.

M.D.Hosehead wrote:I am supposing the reluctance to prescribe supplemental O2 to SDB patients is due to some concern it might be harmful.

I am supposing the reluctance to prescribe supplemental O2 to SDB patients is due to the fact that the current protocols don't call for it, rather than some imagined harm. In fact, one article posted by someone on this board recently flat out said that one of the contraindications for supplemental O2 was that the patient did not meet the bloodwork guidelines--meaning their blood values weren't poor enough. That's a value judgment based on cost or something. A strange sort of "contraindication."

The articles I posted made clear to me at least that in all but the sickest patients, supplemental O2 is not harmful. Well, a more careful statement is that no harm has been shown, and with the lack of studies on the subject, it might also be fair to say that long-term use has not been shown to be either harmful or free of harm. It really hasn't been studied, I think. The articles in question were more about critical care, which is largely temporary.

My guess is that long-term use is unlikely to be harmful to a patient if all you are doing is maintaining at night their unsupplemented ability to oxygenate when awake. In other words, if they are capable, without supplementation, of maintaining 96%, then it is unlikely to be harmful to use supplementation at night to maintain that same value. We could call this the LoQ hypothesis. Anyone want to fund a study?

The real reason doctors won't prescribe it? Insurance probably won't pay for it, and physicians have not been taught to offer medical treatment that insurance won't pay for to patients, so it doesn't enter their thinking. I think that makes it of some value to at least ASK the physician if they would; they might not know you would be willing to pay for it without insurance. I asked my neurologist, and he wouldn't agree without a sleep study. He is by-the-book, and I don't know what the study will show. If he declines, I'll ask one of my out-of-the-box thinking doctors.

Did you see that frh asked two of his doctors, and the first said "no" and the second said "yes"? I hope I'm remembering that right. I have several doctors I could ask; I'm not sure which one I want to approach next if the neurologist says no. I'm afraid if I get too many "nos" and then I ask again, I'll get a "no" just because that's what everyone else said. Gotta consider their personalities carefully.