Can anybody comment on this desaturation behaviour?

[Ratchick]

Are you using OSCAR to calculate your SpO2 drops or the Viatom software?

I only ask because most medical people seem to be interested in drops of 4% over 8 or 10 seconds. The Viatom software, however, calculates a drop of ANY length and doesn't "finish" the drop until the sats reach reaches 2% of the baseline.

I mean, it is possible that you have both things going on - some obstructive and some centrally-mediated. That's entirely possible too. But no, AFAIK it's not typical to have marked periodic breathing while awake, in the absence of other issues.

[desaturator]

Are you using OSCAR to calculate your SpO2 drops or the Viatom software?

I only ask because most medical people seem to be interested in drops of 4% over 8 or 10 seconds. The Viatom software, however, calculates a drop of ANY length and doesn't "finish"  the drop until the sats reach reaches 2% of the baseline.

That's a great question. It's probably difficult to compare the desaturations I have now on CPAP, with those that were measured on my sleep study, because I doubt they were calculated the same way. When  SpO2 is as erratic as mine (see attached), how do you even figure out what the baseline is, against which the drops are measured?

I suspect that any report of the number of desaturations will depend very much on the precise details of the calculation. I'm reasonably sure that CPAP improves my desaturations, just by eyeballing the graphs; but I don't know whether it's a radical or a modest improvement. In the sleep study, I don't know if my desaturations were obstructive, or with clear airways, or a mixture of the two as I seem to have now.

Is it bad for your heart (or other organs, for that matter) if your SpO2 oscillates with a 4%-6% amplitude for periods of 20-30 minutes at a time? Does it matter if this happens when your general SpO2 is 96%? What if it is 90%? What if -- as in my case -- the periodic breathing takes place against slower desaturations of 8-10 percentage points that are unrelated to ventilation?

My doctors don't know the answers to these questions -- I'm not sure anybody does.
Maybe ASV would fix the periodic breathing, whatever its origin? But that's a very expensive option and, at present, I have no reason to think it's necessary. Even if it worked on the OSA and the periodic breathing, it's not going to fix the desaturation that happens during periods of constant ventilation.

I remain baffled. I'm leaning towards getting the intracardiac shunt closed, just because I don't see any other way to exclude it as the cause of all this weirdness.

BW, DS

[SarcasticDave94]

Wouldn't an acceptable baseline be what your SpO2 measures with no assisted device(s)?

[desaturator]

Wouldn't an acceptable baseline be what your SpO2 measures with no assisted device(s)?

Sorry, I'm probably not explaining clearly what I mean by "baseline". I'm not talking about comparing one night with the next, but the process of determining what the actual number of desaturations actually is on a given night. If your SpO2 is basically constant all night, or for long periods of time, then it's easy to determine when a "desaturation" has occurred. If it wanders about all over the place, it's much less obvious. In the the attached (from last night) the red dotted line at about 98% was where my SpO2 was just before tonight's episode of periodic breathing started, and where it returned to afterwards. The green dotted line is what you get if you track the highest point of SpO2 over 30 seconds or so.

If you take the red line as the "baseline" from which to measure 4% drops, you get a very different number than if you take the green line.

My point is that I don't think there is any "standard" way to define exactly what a desaturation is, that all equipment manufacturers use. So, although I can compare the number of "drops > 4%" with and without CPAP now, using the same equipment, I have no way to know what that figure was before CPAP, measured using the same equipment.

In fact, if your SpO2 is all over the place, then I'm not sure it's even useful to talk about "desaturations" any more.

BW, DS

[desaturator]

Is it possible to diagnose sleep apnea, rather than treat it, based on the behaviour of a xPAP machine?

To be frank, I'm increasingly wondering whether I have "sleep apnea" at all in the conventional sense; even if I do, I wonder whether it's significant, compared to my other oddities.

I did have a sleep study, but it was only a home, WatchPAT thing. I really don't know how reliable those are. I was told I have AHT ~20, all obstructive. However, I have no usual symptoms of sleep apnea -- I don't snore, I don't wake feeling tired or with a headache, I don't have problems with concentration, etc., etc. I do have both long-term and short-term oxygen desaturations but, now I'm measuring this, I'm increasingly seeing that I have them when I'm awake as well.

My doctors say that, since I have a positive sleep study -- even if not particular reliable -- and because the APAP machine is detecting what it thinks are obstructive events and trying to control them by changing the pressure, these two things together are conclusive.

But is that really so?

On CPAP my AHI is usually reported as ~1. My doctors tell me that means it must be working. But the odd thing is that the machine settings make absolutely no difference to the AHI reported. It's still ~1 if I set it to a constant 4cm, which is sub-therapeutic for most people. Neither AHI nor SpO2 are affected very much whatever pressures I set, or whatever I set EPR to. What I mostly see in the OSCAR results is periodic breathing which may, or may not, be classed as a hypopnea by the machine. Usually it isn't classed as anything. My SpO2 isn't enormously different if I have a night without the CPAP at all.

I was advised to start CPAP because it "might" fix my cardiac arrhythmias, not because I have any other indication for CPAP. But if I don't actually have sleep apnea, and my SpO2 isn't really any different, it could be a waste of time.

I don't particularly like CPAP, and the thought that I might endure it for the rest of my life when I don't actually benefit from it -- well, that's a really depressing thought.

So -- is there any way to be sure, just from looking at data reported by OSCAR from the CPAP, that a person really does have a sleep apnea that can be fixed by CPAP?

With the UK NHS in its current, completely broken, state I'm not going to get a proper, laboratory sleep study unless I pay for it myself, and even then it will be difficult.

Best wishes, DS

[Ratchick]

OK, so this is the first I'm hearing about a watchpat test. They're not as good as ones with a chest/belly effort strap, and they only use indrect measure to guesstimate when apneas occur. It has no way to tell if your apneas are really obstructive or could be central, which is why they're an indicator. Generally speaking, though, the watchpat gives a reasonable correlation for OSA.

The fact that the watchpat decided you were having 20 obstructions or hypops an hour and on CPAP you have none? That means one of two things. 1) you don't have sleep apnea per se, but you have some other sleep-disordered breathing (maybe cardiac-related) and the watchpat was fooled by your periods of hypoventilation. but the CPAP is helping your ventilation or b) you actually DO have OSA, and the CPAP is helping.

The only way to be sure? Polysomnography. They can check for not just OSA and CSA, but other sleep disorders too.

There is a difference between OSA and OSAS (or CSA and CSAS). OSA is the presence or absence of 5 or more apneas or hypopneas an hour during sleep. OSAS is the SYMPTOMS associated with having OSA. Not all people who have OSA have OSAS. And some people with mild OSA have horrible OSAS, while there's at least one other member on this board who has very severe OSA (certainly high 2 digits, maybe even 3 digits for their OSA) but has zero symptoms of drowsiness, not feeling refreshed etc.

Sometimes, a very small magnitude of change in the airflow can cause a gradual decrease in oxygen levels. It doesn't have to be a huge crash down over a few seconds. That's how it normally is with apneas, yes, but as I've said all along, there are far more than just OSA and CSA that cause sleep-disordered breathing.

You don't especially have to go into a hospital for the sleep study (though that's better). If your doctor can provide you with a device that allows the measurement of airflow via nasal cannulas, effort belts. and perhaps even a built-in ECG, then you can do that at home. I can't imagine that would be as pricey as doing a full study in the hospital.

I mean, ultimately it's up to you. You don't HAVE to keep on CPAP if it's not really helping. What you really need, as I think I said way back the start of the thread, is to at least have an ECG Holter on for at least one and maybe a few nights of sleeping with the CPAP and see if that improves over your previous one in terms of the arrhythmias.

You would need to ask your doctors how THEY calculate the baseline figure to know if it's a fair comparison. Sometimes it's calculated from the top x percent of the whole recorded session, sometimes it's over just part of it, and the exact figure changes, so something like ODI is relative. That does mean that sometimes a 3% drop on one night is higher or lower than a 3% drop on another. It's to spot how variable your SpO2 is during a given timeframe.

That's why, ideally, you want to be using the same consistent pulse ox and software for all measurements, where possible.

[desaturator]

If your doctor can provide you with a device that allows the measurement of airflow via nasal cannulas, effort belts. and perhaps even a built-in ECG, then you can do that at home. I can't imagine that would be as pricey as doing a full study in the hospital.

I already failed that one, a long time ago :/ A nasal cannula is no good for somebody whose mouth falls open as soon as he falls asleep. I could have tried something to keep my mouth closed, had I known about this at the time. But this was right at the start of my apnea journey, when I was even more ignorant than I am now.

As it happened, the unit kept alarming all night, because the nasal sensor wasn't reading anything. So I don't think I actually slept. That's how I ended up with the WatchPAT thing. I'm not sure how accurate it is, because all the studies that seek to measure its correspondence with more establish methods were funded by the manufacturer. But at least it read something.

I've recently discovered -- or, rather, my wife has discovered -- that if I close my mouth with a chin-strap, I snore through my nose. I didn't know it was even possible to snore through your nose. I don't snore at any other time. In any case, I suspect that any test that required a nasal cannula would read something weird in my case.

I'm considering repeating the WatchPAT test whilst on CPAP, so I have something concrete to compare with my pre-CPAP records. This is, at least, comparatively inexpensive. I have to confess that I'm struggling a bit with the financial side of this. The NHS has done nothing for me. They wouldn't even sanction a sleep study because I have a zero Epworth score. I've been able to get my insurers to contribute a bit, but almost everything I'm paying for myself. Besides, the NHS has a protocol for dealing with unexplained cardiac arrhythmias, and it doesn't involve sleep studies. Basically it involves increasingly toxic drugs. I don't want to start down that road if there's any alternative. I'm already on all the "safe" drugs.

I can afford PSG if there's really no alternative. But it's going to be a substantial chunk out of my pension fund, which is already looking a bit depleted.

BW, DS

[Ratchick]

I mean yes, at least a watchPat while on CPAP would be measurable against the one before. If it shows no apneas this time, I guess it shows that something has changed for the better, at least.

I honestly didn't realise that not everyone snored through their nose at first. That was a surprise to me to find out. LOL I guess because I'm not a snorer in general.

I'm not so worried about the home apnea tests and their validity. They're basically just a smaller control box that records a subset of data that a PSG does. This is why they are primarily used to diagnose sleep apnea, not all sleep disorders because you don't (technically) need the more advanced data to see if someone isn't breathing. As long as they can be demonstrated to accurately capture that data, and it's being reviewed by someone who understands that data, I would trust it enough for a basic apnea diagnosis. But YMMV.

[pholynyk]

It hasn't occurred to me that someone could snore through their nose, but I guess it could be similar to the palatial prolapse that others have mentioned - but instead of a complete closure, it vibrates. Maybe due to different geometry?

Definitely an interesting case

[Geer1]

It seems counter intuitive to use arterial tone signals to try and diagnose if breathing issues are causing heart issues. Doesn't it?

I don't like watchpat because it doesn't directly measure breathing. I know there are studies supporting its accuracy but I don't know of studies indicating what other health issues are contraindications for its use. Do heart arrhythmias affect pat? I'd like to know that before giving someone with known arrhythmias a watchpat test.

You bring up a good question about nasal canula accuracy in mouth breathers. I did a google and found the below link for Resmed apnea link home studies and it mentions an optional mouth breathing canula.

https://www.virtuox.net/DynDocs/Document...N.pdf?v1.2