CPAPtalk.com

Brian, you wrote:


That article went on to note that there are two primary treatment methods (see the subsection titled "Management of CompSAS) -- BiPAP S/T, which did not work well in my case, and ASV, for which the jury is still out. I think your confusion may be stemming from the fact that the only PSG results I pasted in this thread were from my ASV titration, which was my fourth sleep study in the past year. There were three prior studies: the initial diagnostic study, which showed over 30 obstructive events per hour (which qualifies as moderate OSA); the CPAP titration, where centrals were emergent and frequent ; and the BiPAP S/T titration, where the pressure of 20/16 appeared to control both the obstructive events and iatrogenic centrals in the couple hours of lab testing. Because my BiPAP S/T results at home were exceptionally poor both quantitatively (AHI around 35) and qualitatively (I felt like dung using it), I was sent in for an ASV titration. Hopefully that clears things up.


Do you have any evidence, which you can post, relating your case to ComplexSAS by a test or a Doc saying it?

About "the CPAP titration, where centrals were emergent and frequent", that you mentioned above, I see this:


Excerpt :

"If we were to limit the definition of complex apnea to treatment-emergent central apneas, the bulk of the evidence suggests that this “disease” is transient and inconsequential. The use of expensive new generation devices is currently unproven in such cases"

Source:

Complex Sleep Apnea: It Isn't Really a Disease

Atul Malhotra, M.D., Suzie Bertisch, M.D., M.P.H., and Andrew Wellman, M.D.Sleep Medicine and Pulmonary & Critical Care Divisions, Brigham and Women's Hospital and Harvard Medical School, Boston, MA

June 2008; Accepted July 2008.

Link:

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

About "the initial diagnostic study, which showed over 30 obstructive events per hour (which qualifies as moderate OSA); ", that you mention above, was it before or after CPAP treatment?

Yes, the doctor specifically used the word "complex."

I'm not sure if you're aware, but the article you linked is basically part of a Pro/Con series that you'll find on the NIH web site.
* The pro piece (which I cited earlier), written by Peter Gay, was titled Complex Sleep Apnea: It Really Is a Disease and is at http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2576323/
* Your con piece is -- aptly -- entitled Complex Sleep Apnea: It Isn't Really a Disease.

Most of us on this board don't have M.D.s, so our qualifications for weighing in on this debate (which, quite frankly, seems pretty semantic in some places) are poor. However, I think you'll find a fair number of people here who would take issue with your article's premise. If we feel like exhausted garbage while being treated on CPAP, despite CPAP successfully treating the obstructive apneas, then labeling those treatment-emergent centrals "innocuous" -- as the article does in its first sentence -- seems premature. Any of the dozens of people who comment on these boards every day who have found restful sleep with an ASV that they did not have while on CPAP due to emergent centrals would, I think, concur. Would there be long-term direct medical consequences from leaving treatment-emergent centrals alone? I have absolutely no idea. However, while on the BiPAP S/T, I did things like make wrong turns on the street and almost fall asleep at the wheel a couple times. And I don't feel like that on the ASV like I did on the BiPAP.

As for your final question: the 30+ events per hour was before CPAP. The CPAP eliminated nearly all of the clearly obstructive apnea events, although as you may know, classifying the remaining hypopneas as central or obstructive in nature is actually not straightforward. (Courtesy to -SWS who provided me with that information some weeks ago.)

ozij and I had a separate discussion via PM about a couple things, and she and I both thought it would be a good idea to paste most of the relevant sections of it here for people who might stumble across this thread in the future. I had misunderstood part of what she had been trying to say, but upon re-reading her posts pieced it together.

BrianinTN wrote: Re-reading your later posts though, I think what you were trying to say was that they should have used the information from my CPAP and BiPAP titrations as the starting point for EPAP -- not that the machine was configured improperly by the DME. Is that an accurate and fair characterization?...can I ask what you were suggesting? Do you think I should set my minimum EPAP higher as a trial?

ozij wrote: That is very accurate. If I were in your shoes, that's what I would do; I would set the EPAP at 6 or 8 and see what impact that had on my sleep and events. I would also open leave the IPAP to as wide as it was originally set...

The main problem for people with COMPSAS is is that once pressure is high enough to keep them from obstructive events, they start having central apneas. The aim of the advanced ASV is to autotirate the EPAP for obstructives, and then respond immediately when a central apnea occurs. Your machine will hover at the lowest pressure it is set on, until something triggers it to raise its EPAP pressure. That trigger could be a hypopnea, arousing you from sleep. By setting a somewhat higher EPAP - which is still far less the than the lowest you had on either CPAP or BPAP - you get a chance of having less arousals.

BrianinTN wrote:... Any of the dozens of people who comment on these boards every day who have found restful sleep with an ASV that they did not have while on CPAP due to emergent centrals would, I think, concur. ...

Though I do not suffer from CompSAS, I do have the central apnea portion of it. Mine is due to degeneration of my brain stem. There are many doctors out there, who ignore the central apneas as "inconsequential". I had one idiot doctor tell me that central apnea is very rare, so I could not have it. I asked him if the data showed that I had an AHI with 5 of more and that 5 of more of those apnea events were central. He hemmed and hawwed. He finally stated that it did not matter. He thought they were not as bad as obstructive. *WRONG!!* Ignorance (on the part of the doctor) CAN hurt.

I finally had a HORRIBLE sleep study where my current doctor attempted to retitrate me on BiPAP alone. I was so sleep deprived that I finally broke down in tears and anger asking what yet another BiPAP sleep titration study would accomplish. He *FINALLY* heard me that I had LOTS of profound problems with sleep onset central apneas. Some is normal. Stopping breathing for more than one minute is *NOT* normal. Yet because they were "sleep onset" central apneas the sleep studies had ignored them for years.

He recommended an ASV sleep titration study. While "bumpy", it was much better than the BiPAP sleep study. I wanted to take a unit home right away.

BrianinTN wrote:... Would there be long-term direct medical consequences from leaving treatment-emergent centrals alone? I have absolutely no idea. However, while on the BiPAP S/T, I did things like make wrong turns on the street and almost fall asleep at the wheel a couple times. Being utterly exhausted is far innocuous. And I don't feel like that on the ASV like I did on the BiPAP. ...

Besides the clear and present danger from poor sleep, the answer is an emphatic *YES!!* If left untreated (as was my case) central apneas can cause uncontrolled hypertension. This increases cardiac and vascular problems (heart attacks and strokes). It can also lead to kidney damage. Making it worse, Ibuprofen - which was the only pain medication that would touch my headaches from O2 desaturations during the night - in conjunction with the hypertension did lead to kidney damage. I know first hand that central apneas - if untreated - can result in irreparable harm.

I tell people not to "panic" if they see a few central apneas. A few is normal. But people should NOT leave a large number of them untreated.

[quote="JohnBFisher
Besides the clear and present danger from poor sleep, the answer is an emphatic *YES!!* If left untreated (as was my case) central apneas can cause uncontrolled hypertension. This increases cardiac and vascular problems (heart attacks and strokes). It can also lead to kidney damage. Making it worse, Ibuprofen - which was the only pain medication that would touch my headaches from O2 desaturations during the night - in conjunction with the hypertension did lead to kidney damage. I know first hand that central apneas - if untreated - can result in irreparable harm.

I tell people not to "panic" if they see a few central apneas. A few is normal. But people should NOT leave a large number of them untreated.[/quote]

John, I kept asking Brian if he knows of any underlying conditions that he might have and he answered None.


In my case I do see my Central apneas rising over time since I strated CPAPing.

For example, from 3 months ago the CA rose


From a lower pressure setting of:

Therapy Mode: CPAP Set Pressure: 7.4 cmH2O EPR: Off
EPR Level: 2.0 cmH2O

AHI & AI - Events/hr
Apnea index: 9.7 AHI: 11.6 Obstructive: 5.4
Central: 3.4 Unknown: 0.8 Hypopnea index: 1.9

To a more recent at a higher pressure setting of:

5/1/2011 - 5/1/2011
Device Settings
Therapy Mode: CPAP Set Pressure: 9.0 cmH2O EPR: Full_Time
EPR Level: 2.0 cmH2O

To:
Apnea index: 15.5 AHI: 19.4 Obstructive: 7.8
Central: 7.6 Unknown: 0.0 Hypopnea index: 3.9

But it improved at a bit higher pressure on the APAP:

5/14/2011 - 5/14/2011

Minimum Pressure: 8.0
cmH2O
Maximum Pressure: 12.0
cmH2O

AHI & AI - Events/hr

Apnea index: 9.2 AHI: 11.2 Obstructive: 4.6
Central: 4.4 Unknown: 0.1 Hypopnea index: 2.0

But still, the CAs are less than 50% of the AHIs, meaning it's too soon to call it a CAS or ComplexSAS.


It would be nice if I could distinguish between Central hypopneas and Obstructive hypopneas like these guys did:


viewtopic.php?f=1&t=48877&start=0

and

viewtopic.php?f=1&t=29851&p=258347&hili ... ea#p258347

JohnBFisher: Thank you so much for weighing in again. You also told me something that I had no idea about (the interaction between ibuprofen and hypertension) -- yikes! I've had hypertension ever since I was a kid, but only got it treated within the last 8 years or so, and I've been taking anti-inflammatories my whole life. So far all my workups haven't shown anything problematic, so if there are any additional non-standard tests you think I should request, please let me know.

I'm hoping to hear back from my doctor tomorrow or some time this week. I'm probably going to ask if I need to see a "specialist among specialists."

In the meantime while I'm in limbo, though, am I right that you would agree with ozji that an experimental increase in EPAP might be helpful?

BrianinTN wrote:JohnBFisher: Thank you so much for weighing in again. ..am I right that you would agree with ozji that an experimental increase in EPAP might be helpful?

JBF will suggest you consult your medical team. But you and Ozji, in your clandestine pms, maybe onto something. You may want to trial EPAP 5, PS Min 2, and PS Min 3. You may not want too exceed EPAP 5.

I'm hoping to hear back from my doctor tomorrow or some time this week. I'm probably going to ask if I need to see a "specialist among specialists."

[/quote]


I would trust your sleep doc JJT b/c he went to Duke, near me. Unless you can get to see Peter Gay.

In a test done in Dec 2007 by Peter Gay and others, they set the ASVs end-expiratory pressures at a range of 5 to 10 cm H20 and a median of 8 cm H2O.

Obstructive sleep apnea syndrome was diagnosed if AHI was ≥ 5 events per hour, or if the patient complained of sleepiness and the number of RERAs per hour was > 10 and CPAP titration was successful in eliminating the RERAs. CSA was diagnosed if the number of central apneas per hour was ≥ 5 and at least 50% of the total AHI was central in origin. CompSAS was diagnosed if CPAP titration eliminated obstructive sleep apnea syndrome but the residual central apnea index (CAI) was ≥ 5 or the CSR pattern became predominant. CSA/CSR was diagnosed if patients showed both CSA and CSR patterns on diagnostic polysomnography.

They concluded:

ASV is a new treatment modality that has been shown effective in treating CSA, CSA/CSR, and CompSAS. Our findings clarify and extend prior observations, and suggest that ASV is an appropriate consideration to other positive airway pressure treatments and is effective for most patients with these nonobstructive sleep-related breathing disorders.

One of my worst docs ever was my shoulder doc who did his undergrad at Princeton and his residency at Vanderbilt.

I picked the guy because he came highly recommended by my PCP who I like a lot and he has domain experience, and he definitely seems nice and helpful. CompSAS is so comparatively rare versus regular OSA that it's entirely possible he's on relatively unfamiliar ground with me. I don't know if that's the case or not, but even if so, it certainly wouldn't be a knock on the guy.

Like I said, we'll see what he has to says. Hopefully he'll have some ideas.

Just to make things clear:
PM-ing was initiated by Brian.
From my response:

I'm responding to all your points in what follows - I hope you don't mind quoting that part of your questions and my response in public - it is always better to have therapy related discussions in public: we all learn from them, and someone may correct something wrong I say.

Nothing at all calndestine about that exchange.

Yup, I'd PMed to apologize for the miscommunication that had transpired and raised the rest of the discussion (that I later pasted and you all now see) at the same time.

Thanks for making that clear, Brian.

Update: The nurse called back this morning. She said the doc isn't too concerned about the numbers I was reporting, so he'd simply see me six weeks after I began treatment, which is what we originally discussed. That'll put me in to see him around mid to late June.

BrianinTN wrote:JohnBFisher: ...You also told me something that I had no idea about (the interaction between ibuprofen and hypertension) -- yikes! I've had hypertension ever since I was a kid, but only got it treated within the last 8 years or so, and I've been taking anti-inflammatories my whole life. So far all my workups haven't shown anything problematic, so if there are any additional non-standard tests you think I should request, please let me know. ...

Nope. Standard blood work to provide information about kidney function is all that is needed. It's pretty standard for anyone during an annual physical.

StillAnotherGuess wrote:... JBF will suggest you consult your medical team. ...

Bingo!

Dependent on the type of underlying problem, I make that absolute or flexible. If the person with the ASV unit is in relatively good health, then they can experiment with their settings. But if there are heart issues (which does not appear to be the case here), then I am pretty emphatic that the doctor should be consulted first before fiddling with the dials. The cardiac patient runs the risk of unintentionally increasing their cardiac load, leading to a catastrophic problem. But even if someone does experiment with their settings, they should keep their doctor in the loop.

JohnBFisher wrote: Bingo!

Dependent on the type of underlying problem, I make that absolute or flexible. If the person with the ASV unit is in relatively good health, then they can experiment with their settings. But if there are heart issues (which does not appear to be the case here), then I am pretty emphatic that the doctor should be consulted first before fiddling with the dials. The cardiac patient runs the risk of unintentionally increasing their cardiac load, leading to a catastrophic problem. But even if someone does experiment with their settings, they should keep their doctor in the loop.

So, for me as a 31 year old guy with nothing going on other than (medicine-controlled) hypertension, and my doc preferring to let things ride, can I get a hall pass here? I ended up reverting back to my "Auto" settings a few days ago, just to collect some more data over time due to the high variance in my readings. For those of you with statistics backgrounds, you can feel more comfortable with consistent averages with little deviation than with an average that's derived from a wide range of numbers -- which (in addition to people pointing to EPAP more than PS) is why I cut short my home experimentation.

Quantitatively speaking:
* I have nights like last night, where my HI was 8 and my pressures stayed pretty low (Avg PS 3, 90% EPAP 6)
* I better nights like the two before (HI 5, Avg PS 2, 90% EPAP 9; and HI 4, Avg PS 3, 90% EPAP 7)
* I have some even better nights like three ago (HI 3, Avg PS 5, 90% EPAP 10).

I've also tried to "line up" the hypopneas on the charts with my pressures. Boy do I sure wish I had waveforms on these (now-old) ASVs; it would make things a lot easier! It sometimes seems hypopneas are more common at lower pressures, which would match what I would expect based on my reading here, but it's really really hard to tell.

All of the above would point to the suggestion given by ozij that I experimentally increase EPAP. However, I have also noticed something a little paradoxical: my best nights quantitatively tend to be followed by worse days qualitatively. And, I certainly have a harder time falling asleep at higher pressures too.

I'll add that I have a little bit of a time crunch. I took a year off before starting grad school precisely to get my apnea under control first. Because of the glacial speed of the medical process, the ASV that I really should have been starting with last summer is only now in my hands. Add my PLMD to the equation, and I simply cannot afford to play this slow. I need to get some resolution by late August, because there's absolutely no way I'm going to be able to be a lab rat or even think about this stuff come the brutal schedule that I'll face this fall.