Dr. Krakow, salesman extraordinaire? UPDATED

Indeed the data I have presented does not substantiate any increase in the AUC for my MAP. I was making the assumption (yikes – that horrible word again!) that any increase in overall pressure(s) would inherently increase MAP. Inhalation and exhalation time are (now) obviously a factor in determining MAP. Time to eat more crow? The fact is that my EEP is somewhat lower than my previously titrated CPAP pressure, but when you add the minPS the result is much higher. And if I am subjected to maxPS for any substantial length of time during the night… well, the simple math doesn’t turn out to be so simple. And that was the basis of my (flawed?) logic. Pass the salt, please.

Either way, if the lower EEP (compared to CPAP pressure) is a contributory factor in eliminating aerophagia (despite the influence of minPS), the Easy Breathe Waveform is still potentially an additional factor. But the end result for me is STILL a remission of aerophagia symptoms. And we should not forget about the RERA's that have been resolved by use of the ASV unit. Although the end result is what we care about, a clear understanding of WHY things are the way they are would be MUCH better from a curiosity & clinical point of view - but perhaps this is all WAY above my head!

As for the cardiac signal: Perhaps we should explain this for anyone that’s not familiar with that phenomenon. DeltaDave, please correct me if I’m wrong about this (again, I am just a layman trying to learn & understand things.) The cardiac influence (the small ba-bump, ba-bump, ba-bumps) on the flow tracing are actually a pressure waveform caused by a person’s heartbeat. The heartbeat pulses are being transferred into the airway via the lungs (acting much like a drum converts a physical strike into an acoustical signal.) My old PB 420E used a small diameter hose that ended near the mask interface, and this hose was used to supply a more accurate pressure signal to the machine’s pressure transducer. This allowed it to score central apneas due to “seeing” those cardiac signals via an open upper airway while a cessation of breathing occurred. But after looking at the graphs in the thread you linked – hmm. The low frequency oscillations not lining up with the EKG signal. Hmmm…

Now, the thought that Dr. K’s techs are “titrating to the cardiac bumps” is a frightening prospect IF that is true. However, it seems that any half-baked brain-dead hack of a practitioner would know about artifacts such as this, and account for this in their methods accordingly. So that brings up the question of IF that assertion is true.

I cannot attest to the filtering settings that Dr. K uses in his PSG software, but I can attest to what I did see in the PSG data stream. I clearly saw where there was “pressure intolerance” (“pressure instability”?) towards the end of exhalation phase, and it was also clear that incremental changes in the pressure settings smoothed out the waveform. If the adjustment were an increase in pressure, would it therefore mean that the additional pressure is enough to suppress the cardiac signal by partially inhibiting the lung tissue from beating in harmony with the pressure spikes created by the heart? Given the pressures that the heart generates, it seems unlikely, but again in all deference to your expertise, I’d love to know if that is a possibility! (Again, I recognize that I suffer from the “a little knowledge is a dangerous thing” phenomena.)

But what happens if the pressure adjustment is a decrease, and the waveform smoothes out in response to the decrease in pressure? Following the above logic, wouldn’t decreased pressure allow the cardiac signal to increase in amplitude? Or maybe I am just WAY off base on this entire subject and oversimplifying it - as once again, simple logic can lead one astray. And again, my knowledge base is probably on the order of 3% compared to what you’ve accumulated. (Speaking of accumulations, you should see MY garage!)

Please tell us what your thoughts are! (I’d buy you lunch as compensation for sharing your knowledge, but I don’t know where you are. Should I just send you a Subway gift card instead?)

ignorant1 wrote:SleepingUgly - Regarding adjusting the rise time: Your equipment is listed as an S9 Auto, not a bilevel. Unless you’ve found something in the menu’s that I’m not familiar with...

You are right... I've changed my profile to reflect the change in equipment.

ignorant1 wrote:The cardiac influence (the small ba-bump, ba-bump, ba-bumps) on the flow tracing are actually a pressure waveform caused by a person’s heartbeat. The heartbeat pulses are being transferred into the airway via the lungs (acting much like a drum converts a physical strike into an acoustical signal.) My old PB 420E used a small diameter hose that ended near the mask interface, and this hose was used to supply a more accurate pressure signal to the machine’s pressure transducer. This allowed it to score central apneas due to “seeing” those cardiac signals via an open upper airway while a cessation of breathing occurred.

Yeah, except that Mary Morrell showed 4 years before the Norman-Rapoport paper that cardiac oscillations can occur essentially anytime, even when the airway is closed:

http://www.journalsleep.org/ViewAbstract.aspx?pid=24522

ignorant1 wrote:Now, the thought that Dr. K’s techs are “titrating to the cardiac bumps” is a frightening prospect IF that is true. However, it seems that any half-baked brain-dead hack of a practitioner would know about artifacts such as this, and account for this in their methods accordingly.

You'd think so.

ignorant1 wrote:Please tell us what your thoughts are!

I think they need to objectively show that Expiratory whatever-the-heck they're looking at is a problem and not a benign curiosity, and if it is a flow-based phenomenon, that it is able to even exist once pressure therapy is initiated (i.e., it would seem to me to be highly pressure-responsive. The act of exhalation alone has the ability to overcome occlusion as it generates it's own PEP).

The paper by Morrell is interesting. I really like the subject whose (patent) airway did not transmit a signal at all. (!) So the study effectively calls the methodology of cardiogenic oscillation as a diagnostic tool into question. So much for my beloved old PB 420E. Yet I digress away from the main subject…

ignorant1 wrote:Now, the thought that Dr. K’s techs are “titrating to the cardiac bumps” is a frightening prospect IF that is true. However, it seems that any half-baked brain-dead hack of a practitioner would know about artifacts such as this, and account for this in their methods accordingly.

deltadave wrote: You'd think so.

Are you inferring quackery (or perhaps chasing ghosts) on the part of Dr. K and his techs? Your expertise is obviously multiple orders of magnitude beyond mine, and I sincerely value your willingness to share your knowledge with us plebes.

I think they need to objectively show that Expiratory whatever-the-heck they're looking at is a problem and not a benign curiosity

I agree that it would be preferable to have objective & irrefutable proof. However, phenomena are oftentimes observed, yet no explanation (currently) exists for the observed phenomena. The “scientific method” leaves a time gap while hypotheses are researched & debated until disproven. Is there any possibility (in your mind) that perhaps Dr. K and his team may have stumbled onto something significant, even IF their reasoning and/or explanation may be eventually be proven wrong?

if it is a flow-based phenomenon, that it is able to even exist once pressure therapy is initiated (i.e., it would seem to me to be highly pressure-responsive. The act of exhalation alone has the ability to overcome occlusion as it generates it's own PEP).

In my particular case (which is again only a sampling of “1”) the “phenomena” definitely existed after pressure therapy had already begun. If I remember correctly, as the pressures were titrated to where the phenomena was mitigated/eliminated, there was a significant decrease in the number of EEG arousals (including subcortical, IIRC). Thus, elimination of the phenomena (“normalization of the curve”) resulted in less sleep fragmentation. So there does appear to be a cause & effect relationship.

I recognize the maxim that “correlation does not necessarily imply causation”. My single individual case would be insignificant by itself. However Dr. K has had these results with other patients too. One basic principle of the Scientific Method requires repeatable results. While I am ill-equipped to explain the cause & effect, perhaps time will reveal all? Copernicus was not well received in his day...

josh816 wrote:

ignorant1 wrote:...

How do I know so much about this particular subject? Because I am living proof of the effectiveness of Dr. K’s methodology. And ASV. Enough said.

My AHI is near 0, but my RERAs are 50-60/hr on the "right" BiPAP pressure 20/16. But my local sleep dr's say that I'm treated, RERAs don't fragment your sleep (even though the sleep tech told me the next morning that my sleep was the most fragmented she's ever seen) and no need to try anything else. But...over the last year, I've spiraled downhill and the last 6 weeks I haven't been able to function, work, drive, etc. I've tried Nuvigil, Adderall, Dexedrine, Daytrana Patch, Ambien, Ambien CR, Sonata, Xyrem, septum repair, a dozen+ masks, 5 PSGs and 2 MSLTs this year, and things continue to get worse.

We fly out to NM in a few weeks and pray that Dr. K's method helps me also.

Be sure to let us know how it goes. I will be very interested. Good luck!!

ignorant1 wrote:Is there any possibility (in your mind) that perhaps Dr. K and his team may have stumbled onto something significant, even IF their reasoning and/or explanation may be eventually be proven wrong?

Easy enough to find out. Ask them to send you the raw data disc, noting the "phenomenon", titration steps and where/what the positive response is.

DeltaDave: While I have nothing to prove, I’m starting to feel like a shill for Dr. K. If you are seriously interested in looking at the data from the PSG's (which I acknowledge is a lot of work) I’d be happy to get it for you. A second opinion from a neutral third-party would be great. The question I must raise however is would you feel that you can be truly objective, neutral, and unbiased? I ask that not as an affront to you whatsoever, but just because of the seemingly contentious nature of the subject matter.

I don’t know if Dr. K’s staff would go through the data again to mark off the points that you are seeking, however the changes to the airflow signal should be apparent wherever the pressure changes occurred. The number of arousals after “normalizing” the airflow should diminish on the datastream – that’s what we are seeking to validate, correct?

I’ll feel a bit awkward asking for the data, but if you are sincere in your quest for getting to the bottom of this particular issue, I’m in!

WTF?

I go away for a few days of sun and debauchery, and come back to see that some of y'all have defaced my glistening, pristine thread with "raw data"?

deltadave wrote:Easy enough to find out. Ask them to send you the raw data disc,

Hi Dave. Agree with you so far, I'll even volumize your request to say that I believe that a CD (or DVD) copy of "the raw data" (and it's never truly the raw, not the 1s and 0s) is something everyone should demand whenever they do a diagnostic test.

Even X-rays are digital these days.

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But I fear, y'all might (and I could be wrong on this, often am) be missing the larger point:

The current "standard" SDB diagnostics simply aren't sophisticated enough to make a "scientific" decision.

Yeah, they stage sleep, so what?

If I, as the patient, tell you that I "sleep better" or "feel better" with K's ASV, how are you going to scientifically prove me wrong?

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You say "placebo", or "anecdotal", and I say: "See me in 5 years, when your sleep architecture diagnostics come into the 21 century."

ASV-bees don't have to cost $7000+, imho, that's just what today's market will bear.

But tomorrow, or maybe next month, I might just bring over a boatload of <$1000 ASVs from China, coded with their own proprietary code, and then lets see if "off the shelf" becomes:

"Oh that? ASVs?

Yesterday's news, my friend, yesterdays news."

Just a thought.

.

rocklin wrote: ...
Hi Dave. Agree with you so far, I'll even volumize your request to say that I believe that a CD (or DVD) copy of "the raw data" (and it's never truly the raw, not the 1s and 0s) is something everyone should demand whenever they do a diagnostic test.

Even X-rays are digital these days.

Agree 100%. And it's a crock when dr's claim that it costs them $25+ dollars per disc to copy the data. And that MSLT data takes up one disc (80% empty), PSG data takes another (60% empty), and the videos take another (nearly full). Doesn't seem reasonable to me.

ignorant1 wrote:The question I must raise however is would you feel that you can be truly objective, neutral, and unbiased?

Absolutely. The data should speak for itself.

Dave, I can see you need a project, and my aerophagia is a great candidate. It's frustrating to have finally been diagnosed correctly after TWO DECADES, feel better from the treatment and yet not quite good enough because I can't get to my titrated pressure. I have a big birthday coming up in less than a month, and it's important that I be cured by then. Or at least see hope that I will be before I die. Menopause isn't that far off, and then things are going to tank, so I'd like to enjoy a few years of my adult life not tired. Short of that, could you at least go over to the other thread and pay me a nice compliment, or maybe blow me a few xoxoxos like you did for Dori?

SleepingUgly wrote:This does not bode well for my overcoming aerophagia.

SleepingUgly, could it be your blind focus on passive "solutions", and bootlicking those who make a dollar off your pain that doesn't bode well for your overcoming aerophagia?

Just a 3 am-sh sleep-deprived thought, whateverz.

SleepingUgly wrote:I have a big birthday coming up in less than a month, and it's important that I be cured by then.

Apparently, the Big Secret will be revealed in a couple of weeks, so try to hang on till then.

SleepingUgly wrote:..could you...blow me a few xoxoxos like you did for Dori?

Sure.

oxox

ignorant1 wrote:I don’t know if Dr. K’s staff would go through the data again to mark off the points that you are seeking, however the changes to the airflow signal should be apparent wherever the pressure changes occurred. The number of arousals after “normalizing” the airflow should diminish on the datastream – that’s what we are seeking to validate, correct?

I was thinking more along the lines of comparing multiple sleep studies. The total number of variables is probably in the 4-6 range anyway (sleep stage, body position, xPAP mode, pressure, acclimatization period, unknown knowns (like of pile of heretofore undisclosed assorted pharmaceuticals) and unknown unknowns (like LA is in the ocean (or deserves to be) and Maimonides is on top of a mountain. That could create a significant first night confound).

deltadave wrote:

SleepingUgly wrote:I have a big birthday coming up in less than a month, and it's important that I be cured by then.

Apparently, the Big Secret will be revealed in a couple of weeks, so try to hang on till then.

SleepingUgly wrote:..could you...blow me a few xoxoxos like you did for Dori?

Sure.

oxox

SU, sure hope it does for you what it did for me!