Using a Bipap Auto SV and using a Vpap Adapt SV

[-SWS]

When you suggest dsm have a cardiovascular work-up to assure he is not a transitional case of cardiac-related Cheyne-Stokes Respiration (CSR-CSA), are you suggesting that the Adapt SV might be better suited, if such was the case?

Banned, I think either SV machine is targeted for periodic breathing and CSR. Whichever happens to work best is the machine of choice.

DSM thinks his nights with nasal congestion may have made the VPAP Adapt SV harder to sleep with. The Resmed SV machine indirectly recent-averages minute volume while the Respironics machine recent-averages peak flow. So I suppose it's possible the latter algorithm happens to work out better with DSM's combination of breathing nuances.

I have seen a few examples of PB showing up in the Bipap SV charts.

If you really are experiencing periodic breathing, one possibility is that your PB is a slightly complex reaction to xPAP. Another possibility is that the PB is a transitional, slight, or intermittent symptom of cardiovascular problems.

I had a stress ECG a couple of years ago & came out of it very well. But, at the ages we are at, these need to be repeated.

Interesting story: Last summer my mother passed a fairly exhaustive suite of cardiovascular tests. The doctor ordered those tests because she had been having intermittent symptoms that might have reflected heart problems.

Unfortunately she was a transitional case, and wasn't manifesting any problems when she passed the gamut of tests. Two months later I took her in for cataract surgery. During routine screening that morning the staff discovered dangerously low blood pressures and a pulse rate bottoming out at 38. Instead of having cataract surgery that morning she took a two-mile ambulance ride down the road for a pace maker.

The problem with intermittent symptoms and transitional pathologies is that they don't always crop their ugly heads during diagnostic procedures. Again, I'll bet your PB is a slightly complex reaction to xPAP therapy (if you really experience PB that is). But just to be on the safe side... Please keep tabs with your doctor.

Then there is the indicator - snoring - the sound of an impending OSA event closing in & it may result in any of 3,2,1 depending on how far the snore leads. I am sure snoring can continue right through #3 & #2 until #1 kills the snore (and the air-flow). I think it is agreed that #1, #2 & #3 can occur without a snore.

My understanding is that obstructive types one, two, three, and four can occur in any concomitant or non-concomitant nightly distribution across the patient population.

More importantly, those are the four obstructive types that both SV manufacturers want to see manually addressed by the clinician during titration. Neither SV manufacturer currently wants to see obstructive types 1, 2, 3, or 4 automatically addressed by upward fluctuating PS.

I always get confused when you say 'obstructive hypopneas'

I refer to obstructive hypopneas in this discussion simply to distinguish those lesser flow-measured events from central hypopneas. The former occurs because of airway narrowing ("plumbing" problems). And the latter occurs because of dysregulated or lesser diaphragmatic effort ("electrical signal" problems).

Those two hypopnea etiologies are most often not differentiated during a routine PSG. Here's an interesting PSG scoring article that touches on hypopneas of obstructive etiology versus hypopneas of central etiology:
http://www.sleepreviewmag.com/issues/ar ... -04_07.asp

I always get confused when you say 'obstructive hypopneas' & 'obstructive flow-limitations'

My apologies about that truly redundant phrase "obstructive flow limitations". The central equivalent would be a marginal sequence of lesser central hypoventilation. It would fail to meet "central hypopnea" scoring criteria and it would fail to meet the more repetitious/cyclic and symptomatic diagnostic criteria of any given central hypoventilation syndrome.

It's entirely reasonable to assume this type of sporadic and lesser-severity central hypoventilation occurs across the patient population IMO. However, I would also suspect it would be virtually impossible to routinely differentiate/diagnose with today's methodologies. Whether those marginal central events really do occur or, more importantly, entail symptomology/pathology across the SDB or general populations is largely unknown.

But for the purposes of our SV discussions, I wanted to make it abundantly clear that the SV manufacturers intend (obstructive) flow limitations to be manually addressed by a clinician during titration---and not automatically addressed by Servo Ventilation's fluctuating PS.




The "fluctuating PS" responses administered by today's Servo Ventilation machines have not been algorithmically optimized to automatically address typical obstructive components of SDB. But someday...

[dsm]

SWS,

Aha I have it

There can be hypopneas & flow-limitations that are not 'obstructive' such as if they lead to worst case of zero air-flow and no thorcic effort.

Now I can follow the words

Thanks

DSM

#2

For future clarity when I talk of an obstruction that is a block (vs a partial block) I'll say air-way obstruction & when meaning a hypopnea or flow-limitation, I'll use the words partial obstruction.

This will completely eliminate one source of confusion for me (being, when is an obstruction not an obstruction - i.e. when it is a partial obstruction )

[dsm]

SWS,

Also on that matter of fluctuating PS (The tri-level setting).

It did occur to me that if the Epap is set to splint the airway open then the Bipap SV is going to treat a string of hypopneas or flow-limitations as a reson to increase pressure & is thus effectively applying treatment to what can be 2 of our obstructive components of OSA.

I know the PS was not specifically designed to treat OSA but by the way it works it was always going to do it.

I agree though that the manufacturers aren't selling this aspect & neither have they offered any testing in that regard.

Personally, I find the way these machines are heading, to be very interesting.

Thanks agin for your patient explanations - another good learning opportunity.

DSM

[-SWS]

Doug, that's it! Lesser airflow can occur in smooth gradations between "none" and "all" (or "normal"). And those gradations of lesser airflow can occur because of airway narrowing ("plumbing" problems) or because of incorrectly regulated diaphragmatic effort ("electrical signal" problems).

That makes for hypopneas that can be of obstructive etiology as well as hypopneas that can be of central etiology. Presently lesser flow limitations or FL are considered exclusively obstructive, and are scored based on obstructive-hinting wave shapes.

However, I'm convinced that sporadic lesser gradations of (central) flow limitations exist that aren't quite central hypopneas and aren't frank cases of repetitive/cyclic central hypoventilation. Who knows if they're innocuous or perhaps entail undiscovered symptomology/pathology in some unknown percentage of the population?

But for now all lesser flow limitations or FL are generally believed to be obstructive in etiology.

[Guest]

I know the PS was not specifically designed to treat OSA but by the way it works it was always going to do it.

I respectfully disagree there, Doug.

For a variety of reasons and physiologic scenarios Servo Ventilations' fluctuating PS won't always address obstructions correctly.

[dsm]

I know the PS was not specifically designed to treat OSA but by the way it works it was always going to do it.

I respectfully disagree there, Doug.

For a variety of reasons and physiologic scenarios Servo Ventilations' fluctuating PS won't always address obstructions correctly.

SWS,

But if the airway is held open by an adequate Epap (a splint) and a hypopnea or flow-limitation is taking place during inspiration and the SV uses its algorithm (as explained in the powerpoint charts) to determine in one breath that ...

'this inspiration cycle will not reach the projected target so I will boost it with added PS'

#3 (added directly from the pp)
(from the pp: "Just before the halfway point of the breath, Bipap AutoSV predicts if the patient will reach the flow target" - If - "will not reach peak flow target" - "additional pressure support given"). Also Page 7 of the pp states (I guess, in a contradictory manner) that the BipapSV will normalize complicated breathing petterns by - ventilating the patient appropriately during periods of apnea and hypopnea.

To me, the above looks like using PS to deal with OSA components !. I would make the case that such handling of OSA components is superior to what any other machine can do or can even try to do.


Surely that is the dream and the goal of all obstructive OSA therapy. To be able to do just that 'boost PS' within a single breathing cycle. It is an impressive algorithmic feat.

The titration method of eliminating such a situation is to manually raise pressure (Ipap) - surely the machine being able to do it right in the middle of an inspiration cycle, is even better than manually having to raise pressure.

If the sleeper is breathing in, then we can say this is not a central & the Bipsp SV is only going to boost PS whilst the sleeper is breathing in so there isn't the danger of using PS the wrong way - the Bipap SV machine will as I understand it, be quite able to recognize a central & use its PS + cycling capability to nudge a central away.

Once again, am impressed with what the algorithm designers are achieving.

DSM

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CPAPopedia Keywords Contained In This Post (Click For Definition): bipap, Titration, Hypopnea

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CPAPopedia Keywords Contained In This Post (Click For Definition): bipap, Titration, Hypopnea

[dsm]

SWS,

Thanks for that link you provided. I have extracted the following as it is actually the 1st time I have seen such a definition of an apnea and it clarifies for me, even further, why you have described hypopneas & flow-limitations as you do.

Again thanks

DSM

"While apneas have enjoyed a relatively solid consensus definition for many years, hypopneas have not. An apnea has traditionally been defined as “a cessation of airflow at the level of the nostrils and mouth lasting at least 10 seconds.”1 Many courses in sleep disorders medicine and many computerized sleep systems quantify the word “cessation” as meaning an 80% to 100% reduction in the airflow signal for 10 seconds or longer. However, in order for an apnea to be considered clinically significant, it must be followed by either an arousal of some sort and/or an oxygen desaturation.

In contrast, hypopneas have not been defined so precisely.2,3 Various authorities have defined hypopneas either conservatively or liberally. A conservative definition of a hypopnea (one that yields fewer hypopneas than a liberal definition) was defined in a paper by Gould et al.4 Their conservative definition was that a hypopnea was defined as a 50% reduction in the sum of thoracoabdominal excursion signal obtained from inductive plethysmography, lasting for >10 seconds. In contrast, Guilleminault1 initially proposed a liberal definition of a hypopnea as “a reduction—but not complete cessation—of air exchange.” More recent liberal definitions of a hypopnea have ranged all the way up to any visually discernible change in the appearance in the airflow signal or effort signals. This change may be a decrease in the amplitude or change in the shape of either the airflow signal (airflow flattening) or one of the two effort signals (abdominal or thoracic movement signals). Authorities2 agree that in order for a hypopnea to be clinically significant, it must be followed by either an arousal of some sort and/or an oxygen desaturation.

A recent slide show presentation produced by the American Academy of Sleep Medicine (and presumably approved by the AASM Board of Directors)5 defines a hypopnea as any visually discernible reduction in the amplitude of either the airflow or the effort signals. This decrease in airflow must last for 10 seconds or longer. Also, in order to be counted as clinically significant, either an arousal of some sort and/or an oxygen desaturation of three points or more must follow the hypopnea.

However, the issue of an apnea occurring within a hypopnea (an event that could be called an apnea/hypopnea) has not yet been addressed. Most experienced sleep technicians have seen an event that could be scored as a hypopnea based on the majority of the event but contains an apnea as well. That occurs at the beginning and/or the end of the event with airflow signals that are less than an 80% reduction (typically only about a 50% reduction) in airflow. However, somewhere within the apnea/hypopnea event (beginning, middle, or end), there exists a period of 10 seconds or more of 80% to 100% airflow reduction that is great enough to be called an apnea."

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CPAPopedia Keywords Contained In This Post (Click For Definition): Arousal, Hypopnea

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CPAPopedia Keywords Contained In This Post (Click For Definition): Arousal, Hypopnea

[dsm]

That link is full of gems - have extracted this as it is a great summary ...


Rule 1. Hypopneas (and at the discretion of the sleep laboratory medical director, also apneas) are to be counted or scored only if there is an arousal beginning at or near the end of the event and/or an oxygen desaturation within 30 seconds following the event. Importantly, the arousal may be either an EEG arousal or a cardiac arousal.

Rule 2. EEG arousals should be defined according to the ASDA10 or similar standard. Most authorities agree that an EEG arousal is defined by an abrupt change in the EEG amplitude, frequency, and/or synchronization. An example of an amplitude increase would be an increase in the voltage (amplitude) of the alpha activity. An example of a change in frequency would be a sudden increase in fast or very fast frequencies (beta or muscle artifact). An example of a change in EEG synchronization would be a paroxysmal increase in either alpha or theta activity. Such a change in the EEG pattern must have a duration of 3 seconds or longer. An increase in the chin electromyographic signal is required to score an EEG arousal during rapid-eye movement (REM) sleep. The main thing to look for is a visually discernible and abrupt change in the EEG pattern. In other words, a shift from the desynchronized EEG and mixed frequency pattern characteristic of stage 1 or stage 2 sleep to the synchronized or very fast, low voltage EEG pattern associated with a partial awakening (an EEG arousal).

Rule 3. A cardiac arousal is defined as either a mild increase in heart rate or a substantial increase in heart rate (called tachycardia, with a heart rate greater than 100 beats per minute). Alternately, cardiac arousals may be defined as a transient increase in blood pressure, though this is more difficult to measure on a routine basis.

Rule 4. An oxygen desaturation is defined as a three or more point decline in the local oxygen saturation level from the previous high to the subsequent low, as long as the nadir value reaches a low point of 90% Sao2 or less. This would correspond to a po2 level of about 60 mm Hg, and is usually considered to be a clinically significant drop in the blood oxygen level.

Rule 5. An apnea is defined as an 80% to 100% reduction in the airflow signal (thermistor, thermocouple, or nasal pressure transducer signal) for a duration of 10 seconds or longer, followed by either an arousal of some sort (EEG arousal or cardiac arousal) and/or an oxygen desaturation. Usually, this EEG arousal occurs with the coincidence of the first hyperpneic breath, but if it occurs later during the hyperpnea period, the apnea still should be counted.

Rule 6. A hypopnea is defined as any visibly discernible reduction in either the airflow or one of the respiratory effort or movement signals (in any one of three respiratory channels). Again, in order to be counted as a clinically significant hypopnea, either an arousal (EEG or cardiac) and/or an oxygen desaturation must follow the hypopnea. The EEG arousal for a hypopnea definition does not necessarily have to occur at the onset of hyperpneic breathing. It may occur one to several breaths later.

Rule 7. Events that contain an apnea within a hypopnea (apnea/hypopneas events) are to be scored as apneas for the entire duration of the event.

Rule 8. A central apnea is defined as an 80% to 100% reduction in both the thorax and abdominal effort signals, which are perfectly in phase before, during, and after the event. There can be no snoring, phase shifting, paradoxical breathing, or airflow flattening immediately before, during, or right after a central hypopnea. If even a portion of the event has no abdominal or thoracic airflow for 10 seconds or longer, according to Rule 7 above, the entire duration of the event, beginning and ending as defined in Rule 13 below, is scored as a central apnea.

Rule 9. An obstructive apnea is defined as an 80% to 100% reduction in the airflow channel only, which is usually (but not always) associated with either paradoxical breathing, slight phase shifts of the thoracic and abdominal movements, or evidence of airflow flattening. The beginning of the obstructive apnea should be identified as the airflow peak near the last in-phase breath (abdominal and thoracic movement signals indicating a simultaneous upward peak). The end of the obstructive apnea should be identified as the trough of the first airflow breath that is close to when the thoracic and abdominal movements both begin to move upward at the same time. It is also desirable to end the apnea event at or near the onset of an EEG arousal and/or at the beginning of the next very large, in-phase breath.

Rule 10. A mixed apnea is defined as an 80% to 100% reduction in the airflow channel during which time the effort (or movement) channels show one or more missed breaths. The mixed apnea must last for a duration of 10 seconds or longer and, of course, in order to be counted as clinically significant, it must be followed by either an arousal of some sort (EEG or cardiac) and/or an oxygen desaturation. The effort (or respiratory movement) channels must indicate one or more missed breaths that look like a miniature central apnea. The absence of breath may occur at the beginning, middle, or end of the mixed apnea.

Rule 11. A central hypopnea is defined (at the user discretion) as in-phase reductions in both the thoracic and abdominal efforts in which there is near perfect in-phase synchrony between the thoracic and abdominal movements before, during, and after the event. As always, in order to be considered clinically significant, the event must be followed by either an arousal of some sort (EEG or cardiac arousal) and/or an oxygen desaturation. The beginning of a central hypopnea should be the peak of inhalation (upward peak in which inhalation is up) of the last largest or second to the last largest breath as measured by the abdominal and thoracic movement channels (not the airflow channel). The ending point of a central hypopnea should be the low valley or trough point of the beginning of the next very large breath (again on the effort channels). If possible, this should be chosen as that point which is closest to the onset or immediately following the beginning of the EEG arousal.

Rule 12. An obstructive hypopnea should be defined as any visibly discernible reduction in either the airflow or effort channels, accompanied by phase shifts, frank paradoxical breathing, snoring, and/or airflow flattening. The beginning of an obstructive hypopnea should be the last largest or second largest peak of a full in-phase inhalation. The ending of an obstructive hypopnea should be the low valley or trough point representing the beginning of the next in-phase, very high amplitude inhalation. If possible, choose the ending point to coincide with the onset (or just after the onset) of the EEG arousal (increase in alpha, theta, or beta).

Rule 13. Apneas, hypopneas, and apnea/hypopnea events that contain apneas within longer events should have their beginning and end points scored as follows: the beginning of the event should be the peak of the last very large airflow signal that corresponds as much as possible to a large pair of in-phase effort (or movement) signals. The ending point of the event should be selected to coincide with as many of the event-end indicators as possible. The event-end indicators are the beginning of the next very large airflow signal; the beginning of the next very large pair of effort or movement signals; the sudden change from paradoxical to in-phase respiration; the end of the event should be scored as near as possible to the beginning of the EEG arousal; and the end of an event should be scored close to the low point of heart rate or at least near the beginning of heart rate acceleration (Figure 12).

Rule 14. Leg jerks that occur during the hyperpnea phase and are either coincident with or followed by an EEG arousal are not to be counted as leg jerks indicative of periodic limb movement sleep disorder. These are merely leg jerks associated with the hyperpnea/EEG arousal consequence of a previous sleep apnea or sleep hypopnea. Such leg jerks are to be considered part of the post-apnea or post-hypopnea arousal complexes and not causes of the EEG arousals themselves.

[-SWS]

SWS,

But if the airway is held open by an adequate Epap (a splint) and a hypopnea or flow-limitation is taking place during inspiration and the SV uses its algorithm (as explained in the powerpoint charts) to determine in one breath that ...

'this inspiration cycle will not reach the projected target so I will boost it with added PS'

Well, no, Doug.

Your description above kind of misses the fact that Respironics wants the entire obstructive component (apneas, hypopneas, and FL) completely taken care of (with EPAP and IPAP min) BEFORE the above PS flow targeting and automated response even occurs. The above targeting is for treating central events.

#3 (added directly from the pp)
(from the pp: "Just before the halfway point of the breath, Bipap AutoSV predicts if the patient will reach the flow target" - If - "will not reach peak flow target" - "additional pressure support given"). Also Page 7 of the pp states (I guess, in a contradictory manner) that the BipapSV will normalize complicated breathing petterns by - ventilating the patient appropriately during periods of apnea and hypopnea.

That's not contradictory. Those apneas and hypopneas are the central ones associated with periodic breathing. The obstructive ones are supposed to be manually addressed with EPAP and IPAP min---otherwise the obstructive component is under-titrated according to both Respironics and Resmed.

To me, the above looks like using PS to deal with OSA components !

To Respironics it's very explicitly PS used to deal with central components---with obstructive components titrated away with either fixed CPAP pressure or fixed BiLevel pressures (EPAP and IPAP min).

I agree though that the manufacturers aren't selling this aspect & neither have they offered any testing in that regard.

Doug, how many years has Resmed and Respironics been in possession of their SV algorithm by now? How many years has Resmed sold their various SV BiLevel machines already? Don't you think the manufacturers would have tested their own machines by now to discover OSA efficacy? And don't you think the manufacturers would have discovered already discovered if their SV algorithms adhered to your statement below:

I know the PS was not specifically designed to treat OSA but by the way it works it was always going to do it.

And if those SV machines could do that with OSA, don't you think they would have deployed those algorithms for pure cases of OSA by now (since CPAP, APAP, and fixed BiLevel can't cut the above mustard)?

It's not as if the manufacturers haven't had time to bring today's SV algorithms through the appropriate stages of FDA approval. Since the manufacturers have developed their SV machines, they have come up with yet other new AutoBiLevel platforms targeted for OSA. And they have brought those OSA AutoBiLevel platforms through the various stages of agency approval.

So are the manufacturers being tricky by withholding this "OSA superior" SV platform from obstructive patients? Are they keeping this modality as a secret silver OSA bullet for when they REALLY need a high revenue year? Or could it be that there are plenty of homeostatic/physiologic issues in epidemiology not even considered in this thread?




So far we have Resmed and Respironics telling everybody to manually address all obstructive events with their SV machines. Then we have Banned and dsm telling everybody that SV machines are going to "always" automatically treat obstruction.

Are you guys sure you have adequately considered all the relevant physiologic and algorithmic issues to override the manufacturer's recommendations? Because there are plenty of people here listening very carefully to your expert SV recommendations.

[dsm]

Some further thinking about differences between the Bipap SV and the Adapt SV.

One thing that really had me thinking was why the Vpap SV showed such high leaks (backed up by lots of annoying squeaks in the night) but the Bipap SV normally shows little to no real leak, or even when it does, I seem to blissfully sleep though the leak.

It has occurred to me that the restless I spoke of when using the Vpap SV, could explain why that machine shows the higher leak data.

Both machines were capped at 20 CMS, both machines show patterns of PS going to 20 CMS (or close) several times a night. The mask used was the same mask. But Adapt SV shows regular problematic leaks.

So whatever was causing the shallow restless sleep appears to have caused a lot of tossing & turning & that puts strain on the mask a lot more than keeping mostly still & thus the Vpap SV records more leaking.

The next issue to get to the bottom of is what causes the restlessness & shallow sleep when using the Vpap SV.

DSM

[Banned]

Then we have Banned and dsm telling everybody that SV machines are going to "always" automatically treat obstruction.

Are you guys sure you have adequately considered all the relevant physiologic and algorithmic issues to override the manufacturer's recommendations? Because there are plenty of people here listening very carefully to your expert SV recommendations.

ok. I will admit to one or two events in all the months I was on the 'old' Adapt SV that were not adequately addressed by the machine. I did wake up and had to take the mask off to breath. However, I didn't jump out of bed and tear the mask off gasping got air like I did with the Vantage. I have been using the 'Enhanced' Adapt SV for the past month with no issues. There seems to be less of the EPAP/IPAP switching that I used to experience with the 'old' adapt SV. I believe there maybe some improvements other than just raising the EEP 5cmH2O on the 'Enhanced' model.

Banned

[-SWS]

Banned, I'll admit that I've been wondering about your pull-the-mask-off events with the Vantage. Might those have been machine-induced periodic breathing?

[Banned]

Banned, I'll admit that I've been wondering about your pull-the-mask-off events with the Vantage. Might those have been machine-induced periodic breathing?

I don't think so. I was waking up with these fits prior to CPAP and going to the ER in the morning for chest pain. The Respironics CPAP Pro took care of things for awhile, than the Vantage took care of it for awhile 'til it came back with vengeance. Including the chest pain. I never bothered with Bi-levels, other than going straight to the Adapt SV. No more fits, chest pain, or ER visits since on the Adapt SV.

Banned

[-SWS]

Banned, I'll admit that I've been wondering about your pull-the-mask-off events with the Vantage. Might those have been machine-induced periodic breathing?

I don't think so. I was waking up with these fits prior to CPAP and going to the ER in the morning for chest pain. The Respironics CPAP Pro took care of things for awhile, than the Vantage took care of it for awhile 'til it came back with vengeance. Including the chest pain. I never bothered with Bi-levels, other than going straight to the Adapt SV. No more fits, chest pain, or ER visits since on the Adapt SV.

Banned

Okay, so let's forget about a machine-induced disorder or complication for the moment...

We can still presumably fit those pre-CPAP episodes as (respiratory-controller related) periodic breathing---with associated apneas and/or hypopneas. Then sub-optimally controlled with CPAP followed by APAP. Finally optimally controlled with VPAP Adapt SV.

How well/poorly does that theory seem to fit from your perspective, Banned? Somehow standard OSA just doesn't seem to fit the experiences you or DSM have described---including and especially that part about only finding suitable treatment with Servo Ventilation.

[dsm]

QUOTE SWS ...

"And if those SV machines could do that with OSA, don't you think they would have deployed those algorithms for pure cases of OSA by now (since CPAP, APAP, and fixed BiLevel can't cut the above mustard)?

It's not as if the manufacturers haven't had time to bring today's SV algorithms through the appropriate stages of FDA approval. Since the manufacturers have developed their SV machines, they have come up with yet other new AutoBiLevel platforms targeted for OSA. And they have brought those OSA AutoBiLevel platforms through the various stages of agency approval.

So are the manufacturers being tricky by withholding this "OSA superior" SV platform from obstructive patients? Are they keeping this modality as a secret silver OSA bullet for when they REALLY need a high revenue year? Or could it be that there are plenty of homeostatic/physiologic issues in epidemiology not even considered in this thread? Question "



But, SWS - the 2001 SV machine technology was primitive and very complicated as in the Autoset CS. Have you seen one of those early SV machines ? - guess what it weighed ? ans what it cost ?. - the therapist had to attach a computer to set the machine !!!. Back then neither Resmed nor Respironics had the blower technology nor mature microprocessor technology to exploit the SV concept in any economical way. They were still struggling with the humble Auto Cpap & look at the debates that have raged through 2005-today over how effective the Auto actually is and the algorithms used.

If the SV machine addresses the base OSA with Epap, & as much of the the other elements with Ipap then you have the classic Bilevel now becoming very popular. So where does the SV differ when it comes to OSA, it adds PS and a very interesting algorithm for determining when to apply it that is far more effective AFAICT that the average Autop Cpap. SVs can do now what we all dreamed Auto Cpaps might do.

So today we have a machine (currently very expensive) that adds a third level of breathing aid (PS) & as clear as the nose on my face, can raise PS to respond to me slowing my breathing to a point where Ipap is not effective enough.

Your comments seem to imply that the SV should not be providing me with effective OSA therapy because the manufacturers banned them from doing so - naughty naught SV machines. (but lucky lucky me )

DSM



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CPAPopedia Keywords Contained In This Post (Click For Definition): auto cpap, respironics, resmed, CPAP, auto, APAP