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Can anybody comment on this desaturation behaviour?
#51
RE: Can anybody comment on this desaturation behaviour?
It would be based on my observations about members working with Central and some form of Obstructive events from FL up to Apnea, with review of action to result/subjective comments correlation. It is because of the opposing nature of CA to OA. Obstructive responds to more pressure, which can increase any CA, even treatment emergent.

Secondarily some had been via my own PAP usage. I am one that has a heavy bias towards pre-dominant Centrals, not the treatment emergent ones.
Dave

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INFORMATION ON APNEA BOARD FORUMS OR ON APNEABOARD.COM SHOULD NOT BE CONSIDERED MEDICAL ADVICE. ALWAYS SEEK THE ADVICE OF A PHYSICIAN BEFORE SEEKING TREATMENT FOR MEDICAL CONDITIONS, INCLUDING SLEEP APNEA. INFORMATION POSTED ON THE APNEA BOARD WEBSITE AND FORUMS ARE PERSONAL OPINION ONLY AND NOT NECESSARILY A STATEMENT OF FACT.
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#52
RE: Can anybody comment on this desaturation behaviour?
Pretty sure between Dave and myself we have seen hundreds of times where decreasing EPR has helped with treatment emergent centrals. You can find these same recommendations on at least two other online forums but yes for some reason is harder to find medical literature on the subject. Probably because most doctors don't look at OSCAR level data and haven't realized the connection. This correlation is so strong I would say that a good 95+% of patients with TECSA see at a minimum a noticeable improvement when reducing or turning off EPR. Usually when we see no improvement we find out the patient also had centrals pre cpap which of course can be for reasons other than TECSA and then not as easily effected.

Not only have we seen this numerous times but it also makes sense from a physical/mechanical sense. Pressure doesn't create flow, case in point a balloon or tire full of air. Pressure just expands materials/airways. Pressure differential on the other hand creates flow, for example blowing up a balloon or tire. EPR and PS are pressure differentials, they increase the pressure while you inhale and then decrease it when you exhale. The higher they are the faster the flow and the more efficiently CO2 is evacuated and replaced with fresh air.

Feel free to research mechanical ventilation and pressure support to further confirm the effects pressure support has and things like how too much pressure support will cause hypocapnia etc. A quick link to get started.

https://pubmed.ncbi.nlm.nih.gov/9230739/

If decreasing EPR from 3 to 0 doesnt create any noticeable difference I would lean away from TECSA as being the cause as TECSA is almost always responsive to EPR being reduce from 3 to 0.
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#53
RE: Can anybody comment on this desaturation behaviour?
@SarcasticDave94, @Geer1 Thank you. I'm not doubting your experience. It's just that my background in experimental medicine has made me acutely aware of the lack of published data in this area. In fact, the whole CPAP area seems to be poorly-supported by research, compared with the number of people who use it.

Anyway, I think what Geer1 is saying is that using EPR makes the CPAP machine more like a pressure-supporting ventilator, and less like a device that simply maintains positive EEP. The increased ventilation (IIUC) leads to an increased gas exchange, with decreased pCO2.

Fair enough, but... isn't CPAP all about improving ventilation? Why would the increased ventilation caused by differential pressure have a different effect on pCO2 than the improved ventilation caused by preventing upper airway collapse?

BW, DS
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#54
RE: Can anybody comment on this desaturation behaviour?
My take is this: CPAP is dealing with Apnea patients that have had respiration that's not ideal, as in the normal range of ventilation, inhale and possibly exhale had been suppressed or restricted for some time. Quite a lot of Apnea patients have endured Apnea and its effects for many months or years before Apnea is tested and the Apnea diagnosis discovered. Then add in time to get the PAP. The PAP tries to bring respiration aspects back to the normal range, and some patients need to return to that normal range more slowly. Years of poor ventilation and the body gets used to the poor state. Some bounce back quickly, while lots of others need to transition back a lot slower.

ResMed's EPR is actually BPAP Pressure Support in action. It does work well for comfort, but again its therapy value is equal to the BPAP PS.
Dave

OSCAR
Standard OSCAR Chart Order
Mask Primer
Dealing With A DME
Soft Cervical Collar Wiki
INFORMATION ON APNEA BOARD FORUMS OR ON APNEABOARD.COM SHOULD NOT BE CONSIDERED MEDICAL ADVICE. ALWAYS SEEK THE ADVICE OF A PHYSICIAN BEFORE SEEKING TREATMENT FOR MEDICAL CONDITIONS, INCLUDING SLEEP APNEA. INFORMATION POSTED ON THE APNEA BOARD WEBSITE AND FORUMS ARE PERSONAL OPINION ONLY AND NOT NECESSARILY A STATEMENT OF FACT.
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#55
RE: Can anybody comment on this desaturation behaviour?
(01-12-2022, 08:34 AM)SarcasticDave94 Wrote: Years of poor ventilation and the body gets used to the poor state. Some bounce back quickly, while lots of others need to transition back a lot slower.

ResMed's EPR is actually BPAP Pressure Support in action. It does work well for comfort, but again its therapy value is equal to the BPAP PS.

Sure, I get that. I suppose that, for most people the purpose of CPAP is to reduce awakenings. That it might improve ventilation is a sort of incidental bonus. But the CPAP must improve ventilation at least a little, at to the extent of preventing apneas. If you prevent an apnea then, I presume, you have improved ventilation at least a little, for at least a short time.

So, conceivably, using EPR improves ventilation all the time, by acting as a kind of intermittent-pressure ventilator, while positive EEP only improves ventilation at the times when apneas would otherwise occur. So (presumably) EPR improves ventilation more than is actually necessary to prevent apneas.

If either of us is right then, presumably, the total ventilation with EPR would be higher than without it. That hasn't been what I've found myself so far, at least when making a small change to EPR. I guess I need to try a larger change, to see what effect that has.

BW, DS
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#56
RE: Can anybody comment on this desaturation behaviour?
While yes, the primary purpose of CPAP is to treat obstructive sleep apnea, the pressure itself does increase ventilation beyond just reducing apneas. Simply by blowing air into your airway means you inhale more air for the same effort. It just so happens that the swing in pressure with PS increases ventilation more because, as has been explained, the change in pressure causes more movement of air than a single pressure. And that's why both increased pressure and use of EPR can affect the number of centrals negatively, by causing reduced carbon dioxide levels. Whether that's for someone like me who is genuinely hypercapnic and gets towards a more normal level with CPAP, or whether it's someone with treatment-emergent centrals, where they're at a more normal level then end up slightly hypocapnic to a level that their brain needs to adjust to (if it can), it doesn't really matter.

I mean, to me this seems fairly clear because this is precisely why they use xPAP (usually BiPAP) to manage conditions like COPD and why they have to be careful about giving patients oxygen without it. Because their carbon dioxide-based breathing reflex is basically ruined by the severe hypercapnia, the only thing pushing their breathing response is actually hypoxia and the difference between the hypoxic-triggered breathing reflex and the point where you fall unconscious is dangerously small (as freedivers who hyperventilate predive have found to their peril). Treat them with plain high flow oxygen and there's a significant chance they will go into respiratory arrest and stop breathing completely. So doctors use xPAP to increase ventilation and help them to blow off more CO2 to eventually sensitize their breathing reflex again, and reduce the symptoms of acidosis while supplementing with oxygen just below the point where it will stop their breathing completely. And it's a BIG balancing act.

I kept my pressure at 15 because if I let it get higher, my centrals could easily double, just with that extra 4cm of pressure. But at the same time, that 15 improved my ventilation enough that I no longer had crippling headaches, despite still having up to 60 centrals an hour. It's also why my sats are not great even though my apneas are now virtually nil on ASV, because I need to get the pressure and PS tweaked upwards to increase my overall ventilation on a par with at least the CPAP.
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#57
RE: Can anybody comment on this desaturation behaviour?
(01-12-2022, 03:26 AM)desaturator Wrote: Anyway, I think what Geer1 is saying is that using EPR makes the CPAP machine more like a pressure-supporting ventilator, and less like a device that simply maintains positive EEP. The increased ventilation (IIUC) leads to an increased gas exchange, with decreased pCO2.

Fair enough, but... isn't CPAP all about improving ventilation? Why would the increased ventilation caused by differential pressure have a different effect on pCO2 than the improved ventilation caused by preventing upper airway collapse?

It is the same idea as a pressure support ventilator with differences in wave shape (designed for comfort instead of maintaining life), venting and that they limit PS to 3 and call it EPR and treat it mostly as a comfort setting. The online community have noted that it still has therapeutic effects at these levels especially in the case of TECSA. A lot of doctors know this as well but it isn't really documented because it doesn't really warrant studies etc.

CPAP in its most basic form (pure pressure, no EPR) only has minimal effects on ventilation. The only thing it does is prevent airway collapse and air transfer is done via spontaneous breathing effort. CPAP in this form can actually hinder ventilation because it requires more effort to exhale and that is why some people must use EPR or a bilevel with higher PS to be comfortable. In rare cases just opening the airway can cause enough of an improvement in patients to cause TECSA.

CPAP with EPR/PS does all of that and then adds a differential pressure aspect pumping air in and out of lungs further improving ventilation beyond spontaneous breathing effort. The higher ventilation increases O2 levels and decreases CO2 levels and this increases the chances of causing TECSA. As noted above sometimes this extra ventilation support is necessary for people that struggle to breath out against pressure. Sometimes itis also necessary to help overcome flow limitations that pressure does not help (flow limitations caused by narrow airways or blockages that do not expand/respond to pressure). Then there are TECSA cases where the extra ventilation is an issue (or at least a temporary one). 

If I had to guess based on what I have seen probably 90% of TECSA cases are resolved using lower or no EPR (and many are able to eventually slowly increase it) and only 10% fail PAP or require treatment with ASV. That is just a rough estimate off the top of my head from cases seen on here.
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#58
RE: Can anybody comment on this desaturation behaviour?
(01-12-2022, 01:10 PM)Geer1 Wrote: In rare cases just opening the airway can cause enough of an improvement in patients to cause TECSA.
[...]
The higher ventilation increases O2 levels and decreases CO2 levels and this increases the chances of causing TECSA.

OK. So is it your view that anything that improves ventilation can potentially lead to TECSA? What would make EPR more of a risk than simply opening the airway?

BW, DS
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#59
RE: Can anybody comment on this desaturation behaviour?
(01-12-2022, 04:50 PM)desaturator Wrote: OK. So is it your view that anything that improves ventilation can potentially lead to TECSA? What would make EPR more of a risk than simply opening the airway?

BW, DS

I just explained that, to reiterate. In rare cases pressure alone seems to be enough to cause TECSA (higher EPR exaggerates it further though). CPAP with EPR acts as a pressure pump during inhale and vacuum pump during exhale. This washes out CO2 more effectively and worsens TECSA. 

I figured I would look at my uptodate documents to see if there was any good references. Here is one with a few good notes and some more references you can chase if desired.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2576324/

"With the application of CPAP, the upper airway is opened, making the arterial CO2 tension lower for any given set of ventilatory conditions. If the fall in PaCO2 yields a value below the so-called CO2 apnea threshold, then central apnea would be expected.7 Over the course of several days to weeks, the CO2 apnea threshold is known to change, resulting in resolution of the central apnea."

"With bilevel PAP, inspiratory positive airway pressure titration can lead to augmented tidal volumes, which drive down arterial CO2 tensions.12,13 If the resulting PaCO2 falls below the CO2 apnea threshold, then central apnea will occur.14,15 Thus, a variety of phenomena can theoretically contribute to fluctuations of CO2, all of which are easily treated with careful attention to mechanism; none require the development of new nomenclature."

EPR is a form of "bilevel PAP". What they don't specifically address is how bilevel PAP is a larger contributor than pressure alone. That is something we just know from experience on here. Lowering EPR usually helps, lowering pressure only occasionally helps. A couple examples, surprisingly doesn't look like we have had too many TECSA cases on here recently. 

http://www.apneaboard.com/forums/Thread-new-centrals


http://www.apneaboard.com/forums/Thread-...-Questions
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#60
RE: Can anybody comment on this desaturation behaviour?
@Geer1 Thank you. I had mixed results from reducing EPR to 1, at least on the first night.

On the one hand, my overall oxygen saturation was the best it's ever been -- average 98% and no time at all below 90%. It's not just a little better, it's way better than any previous night.

On the other hand, my AHI was 1.43, up from 0.2 the previous night. But what struck me most was that the weird periodic breathing was no better. In fact, it was slightly worse, both in duration and magnitude (see attached screenshot). These episodes can cause SpO2 swings of 5 percentage points, sometimes more.

I'm increasingly convinced that it is these periods of odd breathing that give me an AHI > 0 at all. I've looked back of the previous week's recordings, and almost every place the machine marks an apnea or hypopnea is preceded by a section of periodic breathing. I have sufficiently few of these marked events that I can check every one, but I have periodic breathing for at least an hour every night. It may, or may not, be accompanied my marked periods of flow restriction.

Sometimes the amplitude of the periodic breathing change is enough for the machine to mark an AH event, and sometimes it isn't. Last night several periodic breathing episodes were substantial enough to increase AHI; the night before they weren't; the before that they were.

I have no idea what to make of all this.

My original hope with CPAP was that it would improve my oxygenation well enough to figure out whether that was a cause of my night-time cardiac arrhythmias. But what if the problem is not the overall oxygen saturation, but the sudden desaturations? Of course, it could be neither. My point is that nothing I do seems to change the pattern of periodic breathing in the slightest.

Honestly, if it weren't for the cardiac problems, I would ignore this. I just don't know whether I can.

BW, DS


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