Why Aren't Doctors Paying More Attention to Oxygen Levels?

torontoCPAPguy wrote:Hello? Anyone out there? Is this not what I have been hollering for weeks and months now? Work with your blower's numbers but keep close track of your SpO2 because THAT is the single biggest indicator of what is going on inside you?

It is an important indication. But people can have horrid, health damaging sleep disruptions without low SpO2.

Oh. Just one other thing. Just saw a top pulmonologist and am scheduled for three pages of tests next week or so. I took in ALL of my blower data as well as my SpO2 graphs. Guess what she did? Threw the blower data back in my file folder and poured over the SpO2 graphs and then, after a cursory examination, ordered up three pages of every imaginable test known to man and mouse in the hospital ASAP, including a baseline arterial blood gas workup (I HATE those).

It bears remembering that you started your cpap treatmnent because of the major damage done to your lungs by pigs' flu. You pulmonologist is still concerned about that. This it not necessarily typical of the majority of people with Obstructive Sleep Apnea, for whom the major cause of desaturations is the obstruction, and not the lung function. It also bears remembering that your AHI with the blower is low -- and your oxygenation is still not too good -- an indication your lungs have healed enough and are not yet functioning as expected.

The pulmonoligist and sleep doc who viewed my "oxygenation without cpap" data both said "that's useless, I have to see how these desats are, or are not related to breathing interuptions!" and both sent me to have a PSG without CPAP before any other tests. Based on my medical history -- which is very different from yours -- they had no concern about my lungs at that point.

People have different medical reasons' for using CPAP, and we should not assume that what is right for one is right for the other.

O.

ozij wrote:

torontoCPAPguy wrote:Hello? Anyone out there? Is this not what I have been hollering for weeks and months now? Work with your blower's numbers but keep close track of your SpO2 because THAT is the single biggest indicator of what is going on inside you? Low SpO2 = Skyhigh BP = stroke, aneurism, heart attack, poor organ function, lack of REM sleep, etc., ad nauseum.

I will just get up on my soapbox for a moment here....

THE MOST IMPORTANT SINGLE NUMBER THAT YOU NEED TO BE RECORDING AND WATCHING CLOSELY IS BLOOD OXYGEN SATURATION!

Over and out.

Oh. Just one other thing. Just saw a top pulmonologist and am scheduled for three pages of tests next week or so. I took in ALL of my blower data as well as my SpO2 graphs. Guess what she did? Threw the blower data back in my file folder and poured over the SpO2 graphs and then, after a cursory examination, ordered up three pages of every imaginable test known to man and mouse in the hospital ASAP, including a baseline arterial blood gas workup (I HATE those).

ozij, did you have something that you wrote in this post, or is the forum software deleting people's comments again? I know that sometimes people write within the quotation instead of above or below it, but I can't find it if you did.


I'm feeling really dumb tonight. I keep seeing and reading things I don't understand that are apparently obvious to others, so please bear with me if this is a stupid question. I'm just not seeing it.

M.D.Hosehead wrote:All XPAP machines should have integrated oximetry monitors.

Regarding an xPAP machine as some sort of Silver Bullet that could/should address a wide range of Sleep Disordered Breathing (SBD) conditions that can lead to low blood O2 levels is just wrong

The purpose of any type of PAP treatment is to address a limited number of SBD issues which are primarily related to Obstructive Sleep Apnea (OSA) and a few somewhat related conditions such as Cheyne-Stokes respiration etc.

Its about keeping airways open so that the lungs can do their job of transferring oxygen into the bloodstream..... so it is explicitly and directly related to the management of airway conditions and air flow into the lungs (that is, delivering the raw material to the oxygen transfer factory) and only not explicitly and directly related to the management of blood 02 levels (that is, the operation of the oxygen transfer factory processes).

Some SBD sufferers using XPAP have other issues beside their airways which can/do impact their blood O2 levels, so that even if the airways issue are managed, they have other reasons why they may not be getting enough oxygen into their blood stream. For those users, appropriate management protocols need to be established, and it is the role of a sleep clinician to diagnose the particular condition, and then work with the patient to institute a sustainable clinical care plan appropriate to treating it. For those users xPAP treatment plus other appropriate treatments, which may or may not be concurrently in operation, are often indicated.

Such a sustainable care plan may well involve careful blood O2 level monitoring for those users that need it.

Cheers,

Bill

Well, assuming that you are reasonably healthy and most parts are in good working order - it seems that nightly O2 saturation charts are a good metric of how much you fail to breathe while you sleep.

You stop breathing, your O2 goes down, you breathe more - your O2 levels rise. So it's a pretty simple story for most people. If you have a complex situation, then of course things are not that simple. But, I betcha when machines routinely measure O2 levels - Dr's will be riveted to the graphs.

Well, according to my new pulmonologist Phd MD, a reasonable target line during sleep would be 95% SpO2. She seemed to pay a great deal of attention to the AMOUNT OF TIME that my SpO2 was below 90% and suggested that 2 - 4L/M of O2 infused into the CPAP line was minimal and 'should take care of the issue'. Having said that, she wanted a baseline with which to work and also wanted to check out any other preexisting conditions that contribute to the issue of desats during REM sleep when breathing tends to become shallow, SpO2 plummets and BP skyrockets (and we note pulse races quite often). Already aware that I have compromised lungs in terms of capacity and diaghragn strength we have a list of tests three pages long including a full cardiopulmonary efficiency workup and, interestingly, a full set of allergy testing (I believe not only to do with lung issues but more so to do with nasal, OSA issues).

The "magic number" seemed to be 90% as a minimum SpO2 at ANY GIVEN TIME.... but since my SpO2 was well maintained in the high 90's during the time I was awake and especially during the time that I was moving about at 'exercise', the issue only appeared during sleep and then only during what is believed to be REM sleep (can't tell with an EEG running), where my SpO2 would drop into the 70's without CPAP and O2 and was maintained generally above 90% WITH CPAP AND infused O2 at 2 - 4 L/M. Again, I got the very distinct impression that the magic number was 90% during conversation and all of the consequences of OSA and SpO2 desaturations in general as we have discussed on here and as are generally common knowledge amongst educated CPAP/OSA folks were discussed and assumed. (i.e. stroke, heart attack, major organ function, etc.)

For SpO2 to plummet into the 70's, even for a brief period of time should set off alarm bells as well - it is not only an indication of possible deeper underlying issues but more importantly greatly increases the danger from the desaturation(s) as it will drive up both BP and heart rate.

MY bottom line is that with infused O2 in the 2 - 4 L/M range my SpO2 tends to remain in the high 90's while at sleep, dropping as I fall deeper asleep and my breathing shallows out and finally bottoms out in the lower 90's during what is perceived to be REM sleep (again imporrible to confirm without an EEG running but 'somewhat obvious')

So, I take the articles with a grain of salt - I have seen some of the best respirologists and pulmonologists and cardiologists in the area and all seem to confirm the above.

For whatever it is worth I would repeat that I also brought a pile of charts and data taken from the S9 Auto which were not even glanced at but were returned to the file folder. It was the SpO2 that seemed to capture interest during this first visit.

Corrected OSA may or may not result in 'proper' SpO2 levels depending on the ability to take in sufficient air while in deep sleep/REM sleep and the body's ability to strip the oxygen out of it, etc. OSA sufferers need to keep in mind that simply eliminating the OSA issue may not give the desired end result of proper SpO2. In other words, one needs to be vigilant and a self advocate in ensuring that the end results are what they are seeking as often the sleep study will not disclose further issues and the patient may assume, albeit incorrectly, that their issues have been resolved by the use of the XPAP machine. A very dangerous assumption to make in this day of home sleep studies, split sleep studies, sleep studies where REM sleep is not achieved, etc.

billbolton wrote:

M.D.Hosehead wrote:All XPAP machines should have integrated oximetry monitors.

Regarding an xPAP machine as some sort of Silver Bullet that could/should address a wide range of Sleep Disordered Breathing (SBD) conditions that can lead to low blood O2 levels is just wrong

(/rant on)
I guess that's why most xPAP users are in the same state as myself. It's been 10 months, and 4 days since I received my CPAP.

I have YET to be contacted by the sleep center (a HOSPITAL RUN sleep center). I have YET to be contacted by a RT from the DME. I have YET to be asked to look at ANY data from my machine from ANY Doctor I have visited lately (including: Primary Phy., Cardiologist, and Psychologist).

As far as I can tell EVERY DOCTOR sees an xPAP as exactly that: A SLIVER BULLET. Put them on an xPAP and they are OK.

It has only been MY diligence at looking at the machine's data, and looking at my medicines (including the side effects) that have kept me from having major issues. I still have no idea what my SPo2 level is as I don't have a meter.

I think that's what makes many of us so frustrated about our treatment.....
(/rant off)

billbolton wrote:
Regarding an xPAP machine as some sort of Silver Bullet that could/should address a wide range of Sleep Disordered Breathing (SBD) conditions that can lead to low blood O2 levels is just wrong

The purpose of any type of PAP treatment is to address a limited number of SBD issues which are primarily related to Obstructive Sleep Apnea (OSA) and a few somewhat related conditions such as Cheyne-Stokes respiration etc.

Its about keeping airways open so that the lungs can do their job of transferring oxygen into the bloodstream..... so it is explicitly and directly related to the management of airway conditions and air flow into the lungs (that is, delivering the raw material to the oxygen transfer factory) and only not explicitly and directly related to the management of blood 02 levels (that is, the operation of the oxygen transfer factory processes).

Some SBD sufferers using XPAP have other issues beside their airways which can/do impact their blood O2 levels, so that even if the airways issue are managed, they have other reasons why they may not be getting enough oxygen into their blood stream. For those users, appropriate management protocols need to be established, and it is the role of a sleep clinician to diagnose the particular condition, and then work with the patient to institute a sustainable clinical care plan appropriate to treating it. For those users xPAP treatment plus other appropriate treatments, which may or may not be concurrently in operation, are often indicated.

Such a sustainable care plan may well involve careful blood O2 level monitoring for those users that need it.

Cheers,

Bill

I certainly agree xPAP isn't a silver bullet. However, oximetry was added to clinical PSG early on, because it is an additional (i.e., in addition to AHI) measure of severity.

One personal experience: I can remember, in 1972, being in an audience when Dement presented his findings (minus oximetry) about sleep apnea as a cause of insomnia, and the number of skeptical heads shaking. The general feeling was that insomnia itself was not a "serious" medical problem, and therefore SA, as a possible cause of some cases of insomnia, was pretty trivial. It was O2 desaturation that got people's attention, validated SA as a "genuine" disorder, and got sleep evaluations and PSG's covered by insurance.

And now that it's easily available, users here have found that our desats are an important measure to follow. It could be, as you suggest, that we have "other reasons" for our desats.

However, it could also be that SDB is a more complex problem than it seemed around 1970 when it was first being explored. That it's not just a malfunction of air tubing (trachea and nasopharynx) and pumps (diaphragm and chest muscles). And that SDB might have long-term consequences that aren't being addressed by current treatment protocols.

I can follow your argument, and respect your opinion because it is logical as it stands, but you haven't convinced me yet. I still think measuring SpO2, to verify that xPAP is effective, should be encouraged, and availble with every machine.

The point of the article in the OP, though, (and it is just one study that had its flaws) is that using 88% or even 90% as a criterion for desaturation may be disregarding desats that lead to some premature deaths. If that turns out to be verified, it would be anadditional reason to monitor SpO2 in every xPAP user.

Tielman wrote: (/rant on)
I guess that's why most xPAP users are in the same state as myself. It's been 10 months, and 4 days since I received my CPAP.

I have YET to be contacted by the sleep center (a HOSPITAL RUN sleep center). I have YET to be contacted by a RT from the DME. I have YET to be asked to look at ANY data from my machine from ANY Doctor I have visited lately (including: Primary Phy., Cardiologist, and Psychologist).

As far as I can tell EVERY DOCTOR sees an xPAP as exactly that: A SLIVER BULLET. Put them on an xPAP and they are OK.

It has only been MY diligence at looking at the machine's data, and looking at my medicines (including the side effects) that have kept me from having major issues. I still have no idea what my SPo2 level is as I don't have a meter.

I think that's what makes many of us so frustrated about our treatment.....
(/rant off)

Welcome to the 21st century in medicine! I'm afraid we are now into mass-produced diagnoses and treatment driven by costs and profits. "The system" is set up to diagnose a problem (by very stiff and inflexible means), and provide you with what is supposed to be a "solution". Whether the solution actually works is not really important to the system as we are long forgotten soon after we walk out the exam room door. Just give the patient an official diagnosis (with code) and send them to door #2.

It happens everywhere ... "take this course of antibiotics" and (very optionally) "see me in 10 days to make sure the infection has gone away". I guess what is lacking in general is follow-up.

This site has about 50,000 times as much information on treatment and ways to optimize treatment that anyone or anything I have ever seen or read about SA. I have not seen one book that talks about ways to adjust your XPAP machine for optimal performance, etc. - though there are millions of books on getting optimal performance out of your car. I suspect it all is about legal liabilities and the "sanctity" of medical advice and information- with a dash of indifference by the people we choose to take care of us medically.

For most of us, O2 levels are an important indicator of "fine tuning" or even the basic success of XPAP. But the system is all about diagnosing people and giving them machines (within guideline provided by insurers, not doctors). Just looking at the fact that the medical system requires several thousands of dollars of tests to get you a (several hundred dollar - max.) machine to help you sleep better is so counterproductive. To not follow up or help with efficiency is about par for the course.

Just think of all the people who could be helped with quick tests (or even judiciously used "medical suspicion") if the "long tests" were eliminated in patients with obvious OSA! Hell, just make people with telltale signs of OSA sleep with a home sleep monitor at home for one night. The system would be able to afford many times more machines for people who need them. Now how many percent of OSA patients remain untreated? Even with advances in awareness these days - many people remain untreated because of the prohibitive costs involved. And I suspect this will get worse in coming years, not better as most of the escalating costs of medical treatment are to absolutely prove - and not to treat.

I think premature death from untreated or under-treated medical conditions is a major problem in the western world. Lack of follow up is just a small fraction of that under-treatment.
[/rant]

I still have no idea what my SPo2 level is as I don't have a meter.

Check at your local Walgreens. I noticed yesterday that they now sell fingertip pulse oximeters. I did not check to see if it was recording or anything, but might we worth a look. It was out in the open area near the pharmacy with blood pressure monitors, etc., not behind the pharmacy counter.

jonquiljo wrote:Welcome to the 21st century in medicine!

Perhaps where you are, but no everywhere by any means.

jonquiljo wrote:I think premature death from untreated or under-treated medical conditions is a major problem in the western world.

If you look at the life expectancy at birth figures across Western nations you will see significant variations, which indicates its not a general problem for the whole Western world, just in some places.

Cheers,

Bill

I've said it before, and I'll say it again, AHI is not everything:

One of the most common neurobehavioral impairments
in OSA is sleepiness. In fact, two-thirds of adults
with OSA complain of significant sleepiness and/or fatigue
(100). When treated for OSA, patients typically report
less somnolence (153, 491). Despite marked improvements
in subjective sleepiness, randomized controlled trials
show small improvements in objective sleepiness (<1
min increase in mean sleep latency overall) despite effective
therapy for OSA (491). This objective measure is the
average latency to fall asleep during four or five nap
opportunities distributed across the morning and afternoon.
Thus falling asleep 1 min later across four or five
nap opportunities is not a clinically significant improvement
in wake function. Although apneic events result in
many physiological disturbances as reviewed in previous
sections, the oxygen desaturation indexes most strongly
predict sleepiness, relative to other polysomnographic
parameters, including sleep time, AHI, or arousal index
(42, 114, 153, 303, 678). While clinical studies show a
strong association with hypoxia/reoxygenation and sleepiness,
as discussed above for memory function, whether
hypoxia/reoxygenation can induce irreversible sleepiness
must be explored in animal models, without the confounds
of obesity, diabetes, and other comorbidities.

Taken from http://www.binarysleep.com/phpbb2/download.php?id=1316

In that same document:

Sleepiness has been assessed in mice 2 wk after
exposure to 8 wk of IH and resulted in marked reductions
in the average sleep latency across the day and reductions
in total wake time for 24 h (694). The magnitude of these
effects was similar to changes observed in humans with
sleep apnea. Most importantly, these wake impairments
in mice were not reversible, even after a 6 mo recovery
period in normal oxygen conditions (768). The Veasey
laboratory (768) has recently identified the groups of
neurons implicated in wakefulness (wake-active neurons)
injured by intermittent hypoxia. Forty percent of the noradrenergic
neurons in the locus coeruleus and dopaminergic
wake-active neurons in the periaqueductal grey
were lost in this model, and most remaining wake-active
neurons in these nuclei showed impaired wake responses
(768).

If that doesn't concern you, maybe this will:

Hypoxia/reoxygenation events increase the production
of angiotensin II peripherally or in astrocytes, resulting in activation of
angiotensin 1A receptors on catecholaminergic neurons. AT receptor
activation upregulates NADPH oxidase activity, resulting in oxidative
injury. Sleep apnea and intermittent hypoxia are associated with marked
inflammation in the brain including inducible nitric oxide synthase
(iNOS), cyclooxygenase-2 (COX2), and tumor necrosis factor-α (TNF-α).
Whether this proinflammatory response occurs in neurons or adjacent
microglial cells should now be advanced.

If you are just starting on PAP therapy, before irreversible damage is done, make sure you are getting enough oxygen at night, especially if you are a mouse. Seriously, for me this is a concern.