REM SLEEP Faud

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REM SLEEP Faud

Postby somnonaut » Wed Apr 02, 2014 1:43 pm

Is it a kid of fraud for an HST vendor to claim they stage REM SLEEP when they do not record eye movement, nor the other defined characteristics of REM SLEEP?
This, I believe is the same as the Champagne wars in the wine industry. What weight does the copyrighted definition of REM SLEEP carry? Should the HST "surrogate" recordings be called something different, such as sREM (surrogate REM)?

I ask this for the sake of consumers. They must be completely baffled by this duality of REM SLEEP.
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Postby Water Boy » Wed Apr 02, 2014 7:45 pm

Absolute fraud, and yet HST manufacturers seem unscathed by any pushback, regulations or liability. More disturbing is how many clinicians accept stats and graphs on the HST reports without due diligence or even a trace of sketicism, even boarded sleep docs! But then I still can't get past how they can legally/ethically use the term "home SLEEP test", is there any analogous agressive diversion/redirecting by payors in any other medical specialities? I know Carecentrix cut their teeth in Imaging arena and expanded into sleep, but I don't hear of them forcing patients to an x-ray instead of a MRI via use of a qx the patient filled out.
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yes

Postby zack » Thu Apr 03, 2014 1:30 am

Maybe not technically, but it should be. There should be a standard for sleep/wake detection and sleep stage detection with the channel guidelines, and the pay for Type 2 tests should be greater. I don't even like Type 3 and 4 devices that estimate sleep time in general.
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Postby somnonaut » Sat Jun 07, 2014 5:37 am

[Its a long post, just so you know ahead of time]
So, Watch-Pat now contends that they can determine REM sleep as good as PSG.
Image

Using this atlasof the signals from Itamar, we find the description of their technology and depictions of the signals.

What I find of interest was looking up how the heart uses beta receptors for modulation of sympathetic tone, while the vasculature uses alpha receptors for their modulation to sympathetic tone. All of this is supposed to be in tandem with the vasculature opening and closing based on heart pumping capacity, which makes the picture of a system working together.
All well and good....as long as the system works, which is my point.

I have asked for years, and as recently as in May on a Linkedin Forum where I asked the question Is it a kind of fraud for an HST vendor to claim they stage REM SLEEP when they do not record eye movement, nor the other defined characteristics of REM SLEEP?
But then I found this little snippet in the Atlas above.
Image

So finally, someone tells us that the Watch-pat EXPECTS there to be an increase in Heart Rate to detect a respiratory event. My long standing question has been: "If a device relies on cardiac changes as a measure of "sympathetic tone", how does such a device function when the cardiac system does not respond to sympathetic changes, such as in non-compensating patients, (those that do not have cardiac changes to frank respiratory events?) This has always puzzled me.
Since in many OSA patients we see broken cardiac systems (non-compensating, no brady-tachy response to severe obstructive apnea), how can we trust devices that are designed to use this expected cardiac response as its main measure for sleep correlation?
Could you tell us what the inclusion/exclusion criteria were for the Itamar sleep correlation proving studies?"

As I asked Maya Pachter-Tal Director, Global Marketing at Itamar-Medical Ltd. on Linkedin, but alas have still not received a reply.

My point (long winded at that) is...What does Itamar do with patients whose symapathetic cardiac response is broken? Of which there are quite a few patients with this condition and one would expect there to be since years of severe OSA can lead to overtaxing said sympathetic responding systems (aka broken cardiac systems), or even young patients such as this 16yo female with OSA.

Image

So A few questions:
If Itamar EXPECTS this HR change for their device to work properly, why do they not SCREEN their patients for proper EKG functioning system PRIOR to device usage to make sure they have said response?
And does NOT having said response lead us to believe that the Itamar device is not capable of working correctly within this sub-group of possible OSA patients?
And if Itamar does screen, but cannot determine Apnea or Hypopnea without this response, should Itamar be forced to take their product off the market?
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Postby zack » Mon Jun 09, 2014 3:04 am

Is it a moot point if a proper eval is done prior to HST , and there is a current H&P and no commodities...or no?

Should be a rule about a recent full workup prior to testing. " Pt has no comorbidities, we just checked only 11 years ago..."
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Postby Hypnagogic Hal » Mon Jun 09, 2014 8:24 pm

Digital vasoconstriction and increase in heart rate can occur from any arousal from sleep; not just from arousals due to apneas/hypopneas. Apparently Itamar is unaware of PLMS (or wishes to pretend they are).
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Postby somnonaut » Wed Jun 11, 2014 6:16 am

I ask a favor of all.
If you have a sleep system that can show the pulsatile waveform from the oximeter on your PSG, please include it, and then screen capture records of the HR and pulsatile waveform for both Frank OSA patients, and OSA patient with non-compensating hearts (no HR change.)
When I had such a sleep system, I recall that the pulsatile waveform did not change when the Heart rate did not change from a non-compensating system. Unfortunately my present system (XLTEK) does not depict the pulsatile waveform.
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Postby Hypnagogic Hal » Wed Jun 11, 2014 7:18 pm

What would WatchPat do with this?

Image[/img]
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Postby somnonaut » Wed Jun 11, 2014 8:10 pm

Hal great pic.
Can you show again in smaller timeframe? Maybe 30 sec so we can truly appreciate the non-HR involvement.
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Postby somnonaut » Wed Jun 11, 2014 8:11 pm

Hal great pic.
Can you show again in smaller timeframe? Maybe 30 sec so we can fully appreciate the non-HR involvement. And did you have to dig and dig for this kind of patient (non-compensating) or is it fairly common?
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Postby somnonaut » Wed Jun 11, 2014 8:14 pm

Seeing minimal to non Pleth involvement can lead us to ask...is the cardiac system broken OR...is the sympathetic system broken?
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Postby Hypnagogic Hal » Wed Jun 11, 2014 8:30 pm

Despite the many PVCs, there is no heart rate change and no change in peripheral arterial tone with this hypopnea; therefore no detection with a PAT device.

Image[/img]
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Postby Hypnagogic Hal » Wed Jun 11, 2014 8:43 pm

This, on the other hand, would be counted, even though the arousal is clearly a result of the legs, not respiratory.

Image[/img]
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Postby somnonaut » Wed Jun 11, 2014 10:41 pm

Not sure if it would be counted as there is no desaturation.
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Postby somnonaut » Wed Jun 18, 2014 6:08 am

Still puzzled by Watchpat and their mysterious black box technology. So, I had to seek other sources for an explanation to the digital photoplethysmographic technology as used in something like Watchpat.

http://www.dantest.com/dtr_pwv_overview.htm

A physician was telling me that Watchpat uses an electric signal across the finger to gauge arterial tone. This sound specious. Does anyone know exactly how Watchpat is doing its magic?
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