Resmed VPAP Adapt SV - for Central Sleep Apnea

[StillAnotherGuest]

Lotta stuff here, but briefly (HAH!):

1) what your clinic's patient criteria is for your ASV trial

Actually, we're a "center" rather than a "clinic." We're picky about that.

There were criteria/recommendations that were given us at ASV start-up:

Indications
CHF NYHF Class III/IV with LVEF <40%
+/- Atrial fibrillation
pCO2 <38 mmHg
CSR by history or PSG
Cyclic hypoxia

Contraindications:
Chronic hypoventilation
Moderate-to-severe COPD (pCO2 >45 mmHg)
Restrictive thoracic or neuromuscular disease

We have added:

Central-oriented AHI refractory to traditional pressure therapy

to address CSBD.

The concept of using ASV for everything is VERY recent, hence my earlier comments, which I still stand by. There's "approved uses", "anecdotal evidence", and "hybrid mask" philosophy.

2) why your clinic's ASV patient-trial criteria is implicitly such an extremely narrow subset of patients targeted by Resmed for ASV?

It's a center!! Anyway, ya gotta learn to walk before you can run. The real question is as long as CS-2 and BiPAP-SV have been out, why are almost all the reports still anecdotal? Why didn't they include CS-2 in the CANPAP trial? That would have been the ideal study. I mean, even if SAG is dumber than dirt, what's the hold-up with everybody else?

The reason I suspect there are likely several CSA etiologies relates to a multitude of ways in which the human respiratory drive can be dysregulated if genetic diversity is simply parameter-remiss in one of many possible regulating mechanisms. Mother nature's rule is that if it is a physiologic mechanism, it is virtually guaranteed to fail in a certain percentage of humanity. Take any chemoreceptor, and neurological process, any organ and devise a physiologically reasonable way for it to fail. That reasonable model of physiologic failure is almost guaranteed to manifest in some epidemiological percentage IMHO. If you can devise multiple highly reasonable physiologic respiratory drive failure scenarios, there is a better than fair chance more than one CSA etiology exists. Haven't noticed too many physiologic traits that don't manifest with both diversity and failure.

This sounds like an NMI argument coming down the river. And that's one leaky boat.

Now, you can point to triggers, and you can look at the components that perpetuate periodic breathing. The perpetuators compose a short list, namely, the 3 "gains" (plant, feedback, and controller) and circulatory delay (yeah, I'm gonna die with that one). The way I see it, fix CT and you fix half the problem. Fix a gain and you fix all the problem. And in my mind (such that it is), ASV works not because of the effect it has on the apnea, but what happens in the resulting hyperpnea. The "loop" isn't a constant, it oscillates.

OLT, the concept of ASV has similarly been around a while, under a variety of names. It might be a good idea to start out with the basic concepts of ASV, and then we can apply this to what these "servo" machines pick and choose:

Adaptive Support Ventilation
• If no spontaneous effort to breathe, machine delivers required minute ventilation (VE) as pressure control, comprised of pressure support (PS) and rate (f).
• If patient starts to breathe spontaneously, machine reduces f and lowers PS to keep VE above set minimum.
• If spontaneous tidal volume (VT) is > target and f <target, PS is reduced and f is increased.
• If VT > target and f > target, PS is lowered and f is reduced.
• If VT < target and f > target, PS is increased and f is lowered.
• If both VT and f are < target, machine increases f and PS.

Gotta run, a trophy striper is calling me ("SAAAAG, SAAAAAG!")
SAG

[frequenseeker]

Just a note here to say last night I switched back to cpap at a lower pressure, 11.4, to try to reduce the aerophagia without using bipap (which had given me increased AHI the previous day of 4 along with slightly reduced aerophagia). Last night the aerophagia was significantly reduced and so far I feel okay in general, and my numbers were AHI 1.4, AI .2.
Also I am down another nearly 2lb and can tell the edema is less.

I wonder if the higher pressure in my respiratory system might force the edema mechanism into play?? Since my kidneys have checked out okay in every way except we haven't done biopsy yet (and probably won't at this point). Also the chronic kidney failure level of proteinuria appears to be cleared up as long as I take milk thistle (liver support) It came back in a day or two when I didn't take it...

[frequenseeker]

I have now a sleep study scheduled for August 18 at Beth Israel (Framingham). It will be a trial of the ResMed ASV, first half of the night with vented mask, second half with nonvented. Unless my data shows I need the nonvented sooner.

Since I am more representative of a larger SBD population than those with full blown CHF, this will be a good opportunity. This group includes: anyone who is not feeling well despite pap compliance, those who have trouble being compliant, those pappers who put off going to sleep and therefore are sleep deficient, those who have good AHI numbers but feel bad, those with aerophagia, and those who have persistent hypopneas. Maybe a few other types too!

[-SWS]

Wow, Frequen... that is extremely exciting news. As you might have guessed from reading the Apnea -v- Hypopnea thread, I am extremely interested in the margins and gradients of CSDB. And you would seem to fall in that category. I can't tell you how extremely interesting it will be to receive your AVS report.

I'll come back to SAG's most recent post in the next day or two, but I am admittedly curious if he managed to catch any trophy stripers (it's a good thing there's only one "p" in that word). If you ever make it down to Chicago, SAG, I'd love to take you out on the big MI pond for some nice post-glacial fish. Just arrange it through our mutual friend. And the boat won't leak, either... .

[frequenseeker]

I'd be glad to host both of you on the coast (or lakes) of Maine too, anytime!

[neversleeps]

I've got a fishbowl with a couple of guppies.... Give me a call, we'll set something up.

Do they make 1/64th pound test?

[rested gal]

ROTFL!

ok, gotta quit chuckling about the guppies...

frequen, I was looking back through the "MOAT" on TAS as I couldn't remember exactly what you had posted about the results from the deadspace study you had had earlier this year. Found this in your March 7th post:

I got my deadspace setup a few days ago. If readers recall, I had a sleep study at Beth Israel but they misinterpreted my results as if I was wearing a vented mask. I was wearing a non vented Swift with the holes all plugged up according to plan, but they forgot this in the interpretation.

So they read it again and decided I did have some CSDB after all.

It would be very interesting (to me, anyway) if you could post the study results here. I'd love to see both interpretations that you received...the first interpretation as if a vented mask had been used and the subsequent one where the plugged Swift was accounted for.

When you say they decided you had some CSDB, what did they mean by "some?"

Will look forward to hearing about your upcoming sleep study with the AdaptServo machine. I know you must be looking forward to getting a try with that. Do please let us know how it goes!

[frequenseeker]

Rested, here is my study they had emailed it to me, so I had it handy. BI has a very helpful email communication system for ongoing assistance, especially for people who live at a distance from Boston.

They had me on the vented Swift for an hour or two I think, then they changed it to a nonvented one for the bulk of the night. This is not well detailed in the study report...

Date: 03/05/06
Signed by GEOFFREY S. GILMARTIN, MD on 04/11/06 Affiliation: BIDMC

STUDY DATE 3/5/06

PSG #: G00245235

STUDY SITE: Beth Israel Deaconess Hospital, Needham Campus Sleep
Lab.

Study Type: CPAP and BiPAP titration.

INTERPRETING PHYSICIAN: Geoffrey S. Gilmartin, M.D.

TECHNICIAN'S NOTES: The patient had a home designed dental
device in place for the study. Alpha intrusion was noted as
prominent throughout sleep. She had no evidence of periodic
breathing or complex sleep-disordered breathing and nonvented
mask was not used. The patient used a Swift nasal mask
throughout. 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. The patient did
have prominent vivid dream recall after the night of the study.

CLINICAL HISTORY: Patient history of sleep
disordered breathing. She had REM dominant mild obstructive
sleep-disordered breathing diagnosed in the February 2004 with an
AHI of 7.2 and a low sat of 87%. She had CPAP treatment with
CPAP from 8-10 cm of water with a relative minimum change in her
daytime symptoms. She had BiPAP titration concluding that 14/8
was an optimal treatment pressure and despite those multiple
manipulations she has had no sustained substantial improvement in
her daytime symptoms. Polysomnography is repeated to allow
evaluation of optimally therapeutic pressures for future
treatment. The patient has self titrated pressures of 11.4 cm
over 9.6 cm of water in the BiPAP mode. She currently uses a
Swift nasal mask.

MEDICATIONS: T3, T4, estradiol, progesterone, molybdenum, chromium, Maxair and
Intal.

POLYSOMNOGRAPHIC SUMMARY:

SLEEP CONTINUITY AND SLEEP ARCHITECTURE: The patient's study
began at 11:33 p.m. Sleep latency was normal at 9.3 minutes as
was REM latency at 103.5 minutes. The study was conducted during
a total sleep period of 381.2 minutes with total sleep time of
359 minutes with sleep efficiency of 91.9%. Sleep architecture
was notable for some increased percentage of slow wave sleep on
the study and slow wave sleep distributed in the latter portion
of the night. Sleep was divided between stage I of 6.5%, stage
II of 42.9%, stage III of 14.3%, stage IV of 20.6% and REM 15.6%
of the total sleep time on this study. The increased percentage
of slow wave sleep is consistent with enhanced homeostatic sleep
drive. This may be attributable to a decreased sleep time,
partial sleep deprivation, and is consistent with hypersomnolence
described.

RESPIRATORY MEASURES:

CPAP TITRATION: The CPAP was titrated between five and nine
centimeters of water. In the supine position during stable
non-REM slow wave sleep seven appeared to be an adequate pressure
to eliminate significant airflow obstruction. However, during
REM sleep this pressure was obviously inadequate and pressure was
increased to 9 cm of water. Nine cm of water did allow rare
discrete hypopneas during REM sleep, although significant
desaturations were not seen. During unstable light non-REM
sleep, CPAP at nine centimeters of water appeared adequate to
eliminate significant airflow obstruction and no discrete events
were identified. The patient remained supine throughout.

BiPAP TITRATION: The BiPAP was titrated between 9/7 to 13/10
centimeter of water. The patient did have obvious flow
limitation seen at pressures of 10/8 centimeter of water that led
to the subsequent increase in pressures to 13/10 cm of water
during REM sleep. 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. This will make BiPAP a second choice
to CPAP for therapeutic intervention. The BiPAP response at
pressures of 12/9 cm of water during REM and non-REM sleep should
be noted to be quite good overall and oxygen saturations remained
greater than 95% throughout.

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.

PERIODIC LEG MOVEMENTS: There were no significant limb movements
seen leading to independent arousals.

EKG/HEART RATE: Heart rate is notable for sinus rhythm
throughout with rare PVCs noted.

EEG: Waking background rhythm is a healthy-appearing 10-11 Hz
alpha activity. There was an alpha delta pattern seen during
slow wave sleep and an alpha intrusion was notable during REM
sleep.

IMPRESSION: Successful CPAP titration with CPAP likely at 10 cm
of water, representing a reasonable therapeutic pressure. BiPAP
in the range of pressures of 12/9 would be a reasonable
therapeutic alternative, although CPAP did appear to have
adequate control of airflow limitation in the supine position
throughout light non REM and REM sleep. Residual symptoms of
daytime somnolence should they be substantial may well represent
a coexisting disorder of hypersomnolence as sleep-disordered
breathing does appear to be well treated. Followup evaluation
with a home device to allow CPAP use monitoring as well as
documentation objectively of adequate sleep time would be
important in the future diagnostic evaluations prior to
consideration of a primary disorder of hypersomnolence.


Geoffrey S. Gilmartin MD

eScription document:1-7998845


Addendum by GEOFFREY S. GILMARTIN, MD on 05/17/06:
Upon further consultation with Dr. Robert Thomas the following
modification to the study interpretation is suggested-->She is
unstable on BiPAP during unstable NREM sleep. This is her best
indicator of instability. She has fairly substantial obstruction
in REM - will need 12+ cm of H2O for treatment. She has periodic
breathing during unable NREM on CPAP. Reasonable to tolereate if
the clinical response is OK. Arousals are vigorous for visually
subtle airflow obstruction.
So I would recommend CPAP=12 with NV mask and 50 EERS given that
she has not done well clinically with conventional therapy.
Repeat study may be needed.

[dsm]

Just thought I'd point out that someone seems to have requested the Australian Design Awards website to remove the link I 1st posted (see 1st 5 posts in this thread) that showed a simple explosion diag of the new ASV-CS2 machine.

Seems it may have been giving away too much ?

DSM

[-SWS]

Since that diagram is a matter of public record, DSM, I suspect the issue might not relate to revealing intellectual property (or proprietary design). My guess is that the hot link just may have chewed up a little too much bandwidth on the host server. Could be wrong, though.

I still want to get back to talking about both Adapt-SV relative to algorithmic considerations and real-time constraints, as well as the topic of CSDB itself. Both of those are sufficiently deep technical topics from which some readers, myself included, very likely needed a breather. But we'll go deep and technical again, on both topics, for those who happen to enjoy those kinds of discussions.

[dsm]

SWS,

I just posted an attempt at a laymans's explanation of Adaptive Servo-Ventilation.

Cheers DSM

[-SWS]

Thanks for pointing it out, DSM. Let me place a link to your thread here as well:
viewtopic.php?t=11935

I will very specifically add to the topic regarding how real-time constraints necessitate a pattern-and-prediction approach to achieve a timely response. Instantaneous measured and target-achieved ventilatory values are not necessarily easy to attain in real time without pattern and prediction. I'll also link to the patent, explicitly citing fuzzy logic as being employed toward that crucial pattern recognition.

In short, adaptive servo is not simply adaptive servo. Rather, there must be a highly skilled driver behind the machine---and that driver is the algorithm itself. An adaptive servo analogy might be two Porsches: one with a highly skilled professional driver and the other Porsche with a novice behind the wheel. In that example one Porsche is not the same as the next toward accomplishing objectives that are largely about instantaneous precision---let alone with multiple highly-intricate road patterns that are analagous to multiple central SDB breathing patterns (each posing its own unique set of pattern and prediction challenges).

As it turns out, adaptive servo development still likely has a ways to go. I still hold great optimism for adaptive servo, which does not mean the majority of SDB patients will need it. I simply think it's going to nicely solve quite a few problems for some central apnea patients. I also still think it's one heck of an engineering feat!

[Snoredog]

boy I tell ya, I wouldn't mind trying out that ASV machine what do you think SWS?

Think it would help? I seemed to have a few CA and MA's on my psg:

[StillAnotherGuest]

Gotta run, a trophy striper is calling me ("SAAAAG, SAAAAAG!")

Well, that Trophy Striper turned out to be a Virginia Spot. Must've been a screen name. When are we gonna do something about these anonymous guest fish, errr, posters?

OK, if you wanted all the options associated with Adaptive Support Ventilation:

• If no spontaneous effort to breathe, machine delivers required minute ventilation (VE) as pressure control, comprised of pressure support (PS) and rate (f).
• If patient starts to breathe spontaneously, machine reduces f and lowers PS to keep VE above set minimum.
• If spontaneous tidal volume (VT) is > target and f <target, PS is reduced and f is increased.
• If VT > target and f > target, PS is lowered and f is reduced.
• If VT < target and f > target, PS is increased and f is lowered.
• If both VT and f are < target, machine increases f and PS.

Ok, so let's see what Adapt SV uses:

To determine the degree of pressure support needed, the ASV
algorithm continuously calculates a target ventilation. Based on
respiratory rate and tidal volume, the target is 90% of the
patient’s recent average ventilation—that means that ventilation
can vary gradually and naturally over the course of the night.

The algorithm uses three factors to achieve synchronization
between pressure support and the patient’s breathing.
1. The patient’s own recent average respiratory rate—including
the ratio of inspiration to expiration and the length of any
expiratory pause.
2. The instantaneous direction, magnitude, and rate of change of
the patient’s airflow, which are measured at a series of set
points during each breath.
3. A backup respiratory rate of 15 breaths per minute.

To ensure ventilatory support is synchronized to the patient’s effort,
the VPAP Adapt SV relies on factors one and two. When a central
apnea/hypopnea occurs, support initially continues to reflect the
patient’s recent breathing pattern. However, as the apnea/hypopnea
persists, the device increasingly uses the backup respiratory rate.

I know you guys are all enamored with this part:



And maybe someday being able to do this in OSA may be slick.

But here's the problem. If you DO have OSA, maybe like a little flow limitation, if this thing works absolutely flawlessly, then what do you think it's going to duplicate? Exactly! Flow limitations! The management of the obstructive component with Adapt SV is right now limited to manual control of obstructive events, then off it goes to address central events.

BTW, I did try this machine on for size (NB=normal breathing, CA=central apnea):


Do you think it makes me look fat?
SAG

[tomjax]

Very immpressive report by the doc.

My question is why an APAP was not mentioned or considered.
Seems to me APAP would be the answer to the variying pressures required, particularly with REM stages.

Why is APAP not even considered?