frequenseeker wrote:
The patent text clearly says that if the airflow signal is of "poor quality" then a predetermined fixed rate of ventilatory assistance will be provided (i.e. that "permeating 15" back up rate) .
My PFTs indicate inflexibility in my lungs. Just putting aside the Swift question for a moment, might there be an influence from the quality of my respiratory response?
I thought your other respiratory issues had cleared up by what you posted back when you requested a BiPAP ST, or even if they are not, I would expect one would need very advanced lung disease before it could possible affect the Adapt more so then a non-compatible mask.
I was hoping for a VPAP III ST because I seemed to get great results for my hypopneas with the timed respiration when I tried it. But my pulmonologist sleep doctor won't prescribe it now, not having enough medical necessity. There is a big danger she says with the ST, it is a ventilator and has the risk of building up the wrong gas balance and causing alkalosis.
I don't have central apnea, which is the usual necessary diagnosis.
I thought I had respiratory conditions bad enough to justify it. And I once did....until recently! I had full respiratory testing a couple weeks ago and arterial blood gases and everything came out great! Which is puzzling since I had been told I had early emphysema and other problems not likely to improve.October 06 2005
frequenseeker wrote:All the data records from my year and a half of VPAP III indicated RR of 10-12.
But was this influenced by your unconventional IPAP & EPAP spreads and min/max time settings? Which may not reflect a true reading since an unusually long IPAP & EPAP would have limited the number of breaths per minute?
..Readers may remember that I
set the IPAP max and min on the VPAP to as long as it would go, to get to the better results. Different from usual guidelines. Looking back I think that worked because it minimized the amount of CO2 washout..
May 21 2006
Then I decided to
depart from the conventional wisdom of maintaining 4 points of pressure between max and min paps. I put the exhale up to 12, only 1.5 between. But oh what a difference! AHI went to 2, apneas to .2, and I feel so much better. The kind of clear, alert, energetic, able to act spontaneously instead of thinking about it and never getting around to it - being HERE!
September 14 2004
From BI first PSG: The patient has
self titrated pressures of 11.4 cm over 9.6 cm of water in the BiPAP mode.
Wed Aug 02, 2006
frequenseeker wrote:
Ok, fine by a technical standard, but it resulted in the autonomic reactions of anxiety, chills, shivering, GI motility that woke me and kept me from going back to sleep. I did not feel well. Maybe it is possible to get to and be in deep levels of sleep despite things that are not good for one's well being, or simply that we learn to submit to or comply with.
Just from my personal experience, my sleep studies have been fairly accurate in when I wasn't sleeping well because of chronic GI issues (gastroparesis), and any resultant nausea, chills, anxiety, etc. If anything, there were times I thought I slept better then the results indicated. But that's just me.
frequenseeker wrote:My initial study showed complex problems including cyclic patterns.
I thought you said it didn't show any cyclic SDB? And even the report from BI noted that.
I got my results, and once again my REM-related apnea was confirmed.
It did not show any cyclic SDB. But - there is a problem - they read the study as if I had no deadspace used
since they did not see the pattern to put it into use.
From the first BI PSG report:
***
She had no evidence of periodic breathing or complex sleep-disordered breathing
***There were
some episodes of waxing and waning of airflow with pressures of 13/10 centimeters of water which is suggestive of
possible destabilizing effect of BiPAP on the respiratory control system.
***These findings were all consistent with
REM dominant obstructive sleep disordered breathing. There is
no clear evidence of sleep fragmenting respiratory dyscontrol noted and CPAP would be the preferred mode of support over that of BiPAP.
***She is unstable on BiPAP during unstable NREM sleep. This is her
best indicator of instability. (note, from the CSDB article from your doctors, it states: Under description of OSA “With a focus on unstable NREM sleep, typically characterized by unstable breathing + low-frequency coupling + CAP EEG...”)
***Arousals are vigorous for visually subtle
airflow obstruction.Wed Aug 02, 2006
frequenseeker wrote:The EERS for the CO2 needs made a big difference in how I feel and function. It was monitored and provided for in the sleep studies. I understand that it can be sensitive to alot of influences. Right now it seems to fit as a help for me.
But does it show you really need it? They never tested you with the 50cc EERS they prescribed. And what is the EERS fixing? Mild instability during nonstable NREM sleep? It sounds like they were aware they had tried EERS on you by the technicians notes, but that it wasn't needed. I don't know what transpired between the original report and the addendum, other then I know you contacted them when you were frustrated with the original results, but it doesn't sound like they were totally convinced you needed EERS to me.
The patient did have end tidal CO2 evaluated with a nonvented mask alone and it was 43-44 and with 70 cubic centimeters of enhanced end expiratory rebreathing space it was 47, with 140 cubic centimeters it was 50.
I don't understand end tidal CO2 measurements, I'll defer to SAG on these, but the 50 definitely looks high, possibly the 47...but his alter ego SD posted in TMOAT about CO2:
“Just for laughs, I put on a mask, ran the CPAP at about 5 cmH2O and occluded the exhalation ports. Monitored FECO2. It went from 40 to 51 in 3 minutes. That's bad. That's bad. If you don't how how bad that is, then you shouldn't be playing around with this. If you do know how bad this is, then you won't be playing around with this.”
frequenseeker wrote:My problem also involves the two different types of apnea I have.
REM obstructive events are the norm of OSA, which is what SAG has been trying to tell you since you started TMOAT over at TAS.
FQ: Could we generalize to all the folks here who have persistent hypopneas who have responded in the past to the description I have posted about such, who have said they had similar? In other words, if someone is on PAP and not feeling well and has a high hypopnea rate, or has to use a high pressure to prevent it, could they likely be in this category of CO2 problem?
SAG:If you're using a high pressure but have an acceptable AHI, then that's probably not CSDB. CSDB starts out with an abnormal AHI, and then gets worse or at least does not improve.
Unless the patient has a bunch of CA, this mode is probably not for them.
Then who? It seems to me that you need at least 3 things in order to be considered for this therapy:
1, Central apneas, and probably a lot of them;
2. Low pCO2 levels as a major contributor to the CA; and
3. The CA is insufficiently treated or made worse by conventional CPAP/BiPAP.
Unless you have a refractory AHI, you really don't fit in here.
FQ posts reply "...I propose that it be considered that there is relevance to a different group. People like me who have "good" AHIs, who feel lousy if it goes over 3-5, and who have not found anything that solves the problem. We are in new territory here.....I will also suggest that the REM events could be described as central events. They occur with certain brain wave activity, not obstructive anatomy I believe."
SAG: What is particular about these [CSDB] events is that they are NOT a REM phenomenon:
From BI article: A characteristic feature of control dysfunction-related disease is a dramatic improvement during REM sleep, which is the reverse of the pattern seen in dominantly obstructive disease
&
[Complex Sleep-Disordered Breathing has] stage-dependent variability (periodic breathing during non-REM (NREM) sleep and severe obstructions during REM sleep)
Therefore, respiratory events during REM are almost certainly obstructive in nature.
frequenseeker wrote:The search is for a machine that could make responses to address the REM related ones as the others are more easily dealt with.
I believe that is called a CPAP, and autoPAP at the most, since its been well established you do not respond well to BiPAP by multiple PSG's and have REM dominant OSA. Nothing unusual there, just standard fare when it comes to OSA. With as close as you had your IPAP & EPAP set, you really were not using that aspect of a BiPAP- a ResMed CPAP with EPR would give you the same spread.
frequenseeker wrote:Maybe the discussion here could explore possible other options.
It has been explored over and over ad nauseaum, but you have never wanted to consider any of our suggestions that did not fit your limited construct of having some sort of unusual & unique type of apnea.
Start over with non-treatment PSG to see what you are treating
....without all the layers of complexity- BiPAP set at very unorthodoxed settings, homemade mouth guard, EERS, etc.
What was your original PSG AHI? Was it 7.4 that BI stated it had been? Even you said your AHI was mild early on at TAS, but it seems to have gone up with treatment instead of down. That's a big sign something is wrong with the treatment itself, not the underlying problem. Adding more & more complex treatment does nothing, and can even harm, if you don't know what you're treating in the first place.
Did your earlier studies note the AI your first BI study showed? I commented on that several months ago as a possibility of why you continued to have excessive symptoms, but you never seemed to consider it and SAG has noted it again in your recent PSG raw data. BI suggested a Dx of primary disorder of hypersomnolence if you continued to not do well & had good compliance, but you never follow up on that. TAS has a wonder Idiopathic Hypersomnolence board you may want to visit.
I had "mild" OSA on my initial sleep study but my sleepiness scale rating was so high and I had such bad daytime symptoms, my board certified sleep doc had no hesitation in putting me into cpap therapy. The study results are not the only criteria for decisionmaking.
May 12 2004
Geez,
I get AHIs 13-25 regularly (AI 1-2)..I better get in touch with the doctor.
June 09 2004
I had
AHI 46 at my first sleep study, 26 at my next one on cpap, couldn't get it down below 15-20 on cpap/bipap until I got my third machine, VPAP III adjusted so that my results look so good now. But remember, this is average for a night, so HI of 2 can mean 12 in a 6 hour night. [url=ttp://
www.talkaboutsleep.com/message-boards/v ... ght=#39371]February 22 2005[/url]
BTW for those who don't know my history, I went from AHI 45 to 3 progressing through several machines until I got to the VPAP III with my customized settings. But - had huge hypopneas that the AHI was counting as 1 each but duration of many minutes each seen on the graph. And did not feel really right still. If AHI went above 3 I would feel really bad....
September 26 2006
Through heroic manipulation of my 4th machine, a ResMed VPAP III (bipap)
I was able to reduce my 45 AHI to less than 3 most of the time. But if it went over 3, even just a point, I felt way more awful than the routine awful I felt otherwise.
Mon Jan 01, 2007
Have you even looked back over the CSDB article to see what their other recommendations were, besides EERS that could possible apply? One thing it sounded like they tried doing with the original recommendations from the first PSG was 'permissive flow limitation' - allowing some obstruction to persist and thus avoiding the worsening of control dysfunction, but you never gave it a chance. You pushed that you needed the EERS and higher pressure- "Strategies include using the lowest pressure that allows reasonable control, avoiding modalities that destabilize (continuous and bilevel pressure may be less or more effective in individual patients; automatic continuous pressure machines should be avoided)"