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Split-city

I am a fair example.

My titration originally was put to me as 15 CMS (but after some months on that setting & feeling as high as a kite, I dioscoved the lab tech had made a transcription error & that it should have been 13 CMS).

But for quite a while I ran a Bilevel & loved it & had it set to 8 epap and 15 ipap. This machine was a PB330 and I also had A/C mode (same as S/T) activated with a backup breathing rate of 6 BPM.

I was on that wrong setting for about 9 months.

2 years later I went in for a 2nd titration having lost a 20 kilos of weight (6ft tall - was 103 kg got that down to 83 kg b=ut today am at 89 kg).

With the 2nd titration, I was quite certain I would be told I was ok & no longer needed cpap but not so - the study tech told me he had to bump up cms to 12 . The doc then settled on my suggestion of 13/10 as he knew I used a PB330 Bilevel.

So I went home & using a new rule of thumb I largely adhere to now, set my PB330 with ipap to 13 & epap to 10 & have been on that for close on a year.

My readings were showing AIs lower than 0.5 and HIs varying from 3.0 to 7.0 (on a Resmed S8 set for CPR of 3 with cpap at 13).

Now I am using a Bipap AutoSV set
epap = 11, IpapMin to 14 and IpapMax to 20. This device now shows AIs around 1 or 2 and HIs of 0.

DSM

dsm wrote:Split-city

the study tech told me he had to bump up cms to 12 . The doc then settled on my suggestion of 13/10 as he knew I used a PB330 Bilevel.

So I went home & using a new rule of thumb I largely adhere to now, set my PB330 with ipap to 13 & epap to 10 & have been on that for close on a year.

My readings were showing AIs lower than 0.5 and HIs varying from 3.0 to 7.0 (on a Resmed S8 set for CPR of 3 with cpap at 13).

Now I am using a Bipap AutoSV set
epap = 11, IpapMin to 14 and IpapMax to 20. This device now shows AIs around 1 or 2 and HIs of 0.

DSM

Thanks for that. So your EPAP is close to your prescribed CPAP level. This is what I was informed to be the case.

I would be happy to hear if there is anyone with an EPAP much lower than their prescribed CPAP level. I guess it would be better if the time between the CPAP titration and BiPAP titration was kept relatively small given that therapeutic pressure can change over time.

split_city wrote:

dsm wrote:Split-city

the study tech told me he had to bump up cms to 12 . The doc then settled on my suggestion of 13/10 as he knew I used a PB330 Bilevel.

So I went home & using a new rule of thumb I largely adhere to now, set my PB330 with ipap to 13 & epap to 10 & have been on that for close on a year.

My readings were showing AIs lower than 0.5 and HIs varying from 3.0 to 7.0 (on a Resmed S8 set for CPR of 3 with cpap at 13).

Now I am using a Bipap AutoSV set
epap = 11, IpapMin to 14 and IpapMax to 20. This device now shows AIs around 1 or 2 and HIs of 0.

DSM

Thanks for that. So your EPAP is close to your prescribed CPAP level. This is what I was informed to be the case.

I would be happy to hear if there is anyone with an EPAP much lower than their prescribed CPAP level. I guess it would be better if the time between the CPAP titration and BiPAP titration was kept relatively small given that therapeutic pressure can change over time.

This is an answer I was given in regards to the BiPAP question:

It is used for people who have ventilatory insufficiency of some kind i.e are in respiratory failure. (neuromuscular weakness, severe COPD, obesity hypoventiliation etc) Usually the EPAP (and expiratory pressure) is set at the “CPAP” pressure required to open the upper airway (during inspiration) and the IPAP set at a higher level to provide additional ventilation by increasing tidal volume. The devices are usually set to trigger when they detect a drop in pressure at the mask (i.e go from EPAP to IPAP). If the airway is occluded during inspiration, then this drop in airway pressure is not detected at the mask and the device doesn’t trigger, hence need to treat UA inspiratory obstruction (with appropriate EPAP).

There are devices called C-flex or Expiratory pressure reduction (EPR) CPAP devices. They are essentially CPAP devices that drop the pressure (slightly) during expiration, then increases during inspiration. Only manufacturers have done studies on this type of device, so not clear what happens physiologically to UA. However one abstract did suggest slightly poorer control of SDB with this device possibly for the reasons you suggest.

I hope this helps.

NightHawkeye wrote:Many, perhaps most people who use Bi-level therapy have an EPAP setting substantially lower than their CPAP level.

Right. And that's because (as I understand it) in a CPAP titration, the single CPAP pressure is set to take care of EVERYTHING -- obstructive apneas, hypopneas, flow limitations, snores. But with a bilevel machine (and in a bilevel titration) there are TWO pressures to be set -- each with a different job to do.

As I understand it, in a bilevel titration EPAP is set to prevent obstructive apneas, which can be eliminated at a lower pressure than the higher pressure required to eliminate hypopneas, flow limitations, and residual snores. Odd as it sounds, it takes less pressure to prevent a complete apnea than it does to prevent hypopneas and flow limitations.

And when you look at it this way, it makes sense... if "some" pressure (the lower EPAP) can keep the airway from closing completely, there can be no "apnea." However, that "some pressure" might be allowing the airway to collapse "somewhat" -- partially -- as in a hypopnea or flow limitation. More pressure is needed to keep the throat well and truly open (preventing hypopneas) than is needed to keep the throat at at least "somewhat open" -- i.e., no obstructive apnea.

NightHawkeye wrote: Given that a patient's CPAP level is ostensibly the minimum required to maintain patency, how can an even lower EPAP level maintain patency if the airway collapse occurs prior to the end of the expiratory cycle? It would seem that the collapse would need to be delayed. Otherwise, a contradiction exists.

Well, if collapse is happening before the end of an exhalation, I would say that the EPAP is not set high enough. But that doesn't mean EPAP has to be set AS HIGH AS the single straight CPAP pressure, in order to prevent airway collapse during, near the end, at the end, or even during the pause following, exhalation.

If the airway can be kept even partially open (by EPAP) during exhalation, at the end, and during the pause after exhalation is finished...then it is open "enough" to allow the person to start the next inhalation. And that's when the higher IPAP kicks in. Voila' -- a patent airway for full inhalation.

As I understand it, the two separate pressures set in a bilevel titration in the sleep lab are to address two different things:

EPAP (if set right) handles preventing obstructive apneas, keeping the airway open "enough" at the end of exhalation or at the pause at the end of exhalation, to allow the person to START to inhale again. The instant the person begins to breathe in, the higher IPAP then takes care of opening the airway fully -- eliminating hypopneas, flow limitations and snores.

split_city wrote:
<snip>
The surprises keep coming RG . Snoring can occur during inspiration and expiration. Here's a snapshot from a subject showing expiratory snores

Snoredog wrote:

...with snore details omitted that model doesn't appear to accurately represent the vast majority of patients.

I haven't really concluded anything at this stage. I'm just stating that in my experience, collapse tends to occur in a passive manner. This supports data from other studies.

I still don't understand what you are trying to get at with the "snoring" side of things. How does it fit into the model?

Okay, now that snore graph was what I was wanting to see, unfortunately you didn't indicate on that graph where the end expiration collapse would occur in relation to that snore.

In previous post above, you asked about what preceded collapse at the end of expiration and I said "snore", meaning that if snoring is introduced into your model that it would precede the airway collapse. Because "where" we begin to snore and airway collapse occurs is closely related (in my opinion) to support your theory.

If I am understanding you correctly, collapse occurs at the end of expiration and precisely "before" inspiration begins or the lull between the two. Same point where "snore" is likely to begin or occur.

Now to me that makes sense, but that lull period has a timed value (Bill is suggesting it "shifts" further down the cycle w/CPAP and I agree with him on that).

Therapy wise that time frame seems critical as that time frame is included in rise time values input for bilevel therapy, however rise time extends/continues on up to peak of IPAP pressure.

What kind of throws this theory off is the graph Bill put up on Respironcis BiFlex, if you observe that graph for EPAP Respironics appears to lower pressure at the precise point you indicate collapse takes place.

The question is why would Respironics lower pressure with Biflex/Cflex at the precise point collapse is to occur?

Note: Cflex is technically identical to the EPAP shown below baseline in that graph, it also lowers pressure precisely where collapse is to occur.

That is what doesn't make sense to me. It appears that timing is somehow off in trying to correlate these events. By introducing snore into the picture that model now reflects a much broader audience (in my opinion).

I say that because if you have observed years of machine reports you know snore nearly always occurs or precedes an apnea event. If you could inverse releasing the air out of a ballon that is pretty much what is happening to the upper airway as you snore on inhale, apnea soon follows. If we attempt correlate that event to your charts, snore would occur immediately before the collapse and at the end as you suggest.

Note: This is also why nearly every CPAP manufacturer who produces autopaps chase snore so aggressively, splint the airway to eliminate snore (in this case EPAP pressure is what maintains that minimal splint). The higher IPAP pressure only compensates for the extra lung volume of inhale. EPAP pressure is the very bottom of that chart Bill put up. There should actually be another absolute zero baseline below that EPAP graph representing esophageal pressure, if EPAP=7 cm, then there is 7cm pressure between zero and the very bottom or lowest pressure of EPAP.

From your first graph, it appears the patient was getting up to 13 cm pressure when those end collapses took place? That would seem to skew or shift the point of collapse as Bill suggests and I agree with him on that.

Snoredog wrote:

Okay, now that snore graph was what I was wanting to see, unfortunately you didn't indicate on that graph where the end expiration collapse would occur in relation to that snore.

I didn't put in any markers for airway collapse in the above figure because the airway remained patent in this OSA patient.

Snoredog wrote: In previous post above, you asked about what preceded collapse at the end of expiration and I said "snore", meaning that if snoring is introduced into your model that it would precede the airway collapse. Because "where" we begin to snore and airway collapse occurs is closely related (in my opinion) to support your theory.

Not necessarily. A figure I showed earlier had no evidence of snoring prior to airway collapse.

Snoredog wrote: If I am understanding you correctly, collapse occurs at the end of expiration and precisely "before" inspiration begins or the lull between the two. Same point where "snore" is likely to begin or occur.

Now to me that makes sense, but that lull period has a timed value (Bill is suggesting it "shifts" further down the cycle w/CPAP and I agree with him on that).

Therapy wise that time frame seems critical as that time frame is included in rise time values input for bilevel therapy, however rise time extends/continues on up to peak of IPAP pressure.

What kind of throws this theory off is the graph Bill put up on Respironcis BiFlex, if you observe that graph for EPAP Respironics appears to lower pressure at the precise point you indicate collapse takes place.

The question is why would Respironics lower pressure with Biflex/Cflex at the precise point collapse is to occur?

I have to say I am a novice when it comes to BiPAP. I am getting a little confused with what you are saying and the graph Bill put up. Is EPAP pressure lower during early expiration and then rises towards the end of expiration? I see a downwards deflection followed by a rise towards the EPAP line.

I do agree re timing though.

Snoredog wrote: I say that because if you have observed years of machine reports you know snore nearly always occurs or precedes an apnea event. If you could inverse releasing the air out of a ballon that is pretty much what is happening to the upper airway as you snore on inhale, apnea soon follows. If we attempt correlate that event to your charts, snore would occur immediately before the collapse and at the end as you suggest.

We certainly could correlate whether snores precede apneas. While snores are commonly associated with obstructions, there are certainly times where there is an absence of snoring prior to apnea. I came across many examples of this in several patients. Nevertheless, the main aim of the project is to identify what caused the unstable breathing and ultimately, the obstruction. Snoring is part of the unstable breathing.

Snoredog wrote:From your first graph, it appears the patient was getting up to 13 cm pressure when those end collapses took place? That would seem to skew or shift the point of collapse as Bill suggests and I agree with him on that.

This 13cm isn't quite right. This pressure is actually elevated due to compression of the esophageal balloon by overlying medialstinal structures. I can't quite find the file where I found that data. However, just a look at some other files, Pes was around 6-8cmH20 at the point of collapse. Adjusting for the compression artifact, Pes would be around 1-2cmH2O

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

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

[quote="-SWS"]That pretty much settles the matter in my mind: "FOT is for naught" where A10 is concerned.

But I still wonder why Resmed has continued this highly basic FOT patent for so many years. Perhaps the decision is based on nothing more than a "FOT because we ought" philosophy.

I had better escape the "FOT light" before a well-deserved stage hook reaches out and...



<-SWS caught by FOT>

ozij wrote:

The three other devices, in addition to the analysis of the flow shape and snoring, included a simplified method of FOT for detecting increases in airway resistance.
The Autoset II Plus (Resmed) generated a small pressure oscillation (5 Hz) when no breathing flow was detected in the course of 8 s. This capability allowed the device to detect obstructions only during apneas. The SOMNOsmart 2 (Weinmann GmbH; Hamburg, Germany) and the AutoTREND (Hoffrichter GmbH; Schwerin, Germany) detected airway obstructions by continuously generating a small pressure oscillation at 20 Hz during the whole treatment. These three devices were identified as O1, O2, and O3, respectively. All devices were programmed with a minimum CPAP of 4 cm H2O, a maximum CPAP of 16 cm H2O, an initial CPAP level of 4 cm H2O, and the initial waiting time or the ramp period were set to 0 min (when possible). All the other parameters were set at their default value.

Being curious, I checked to find out what manner of device the Autoset II Plus is and here's the best description of its capabilities I found:

Reference=www.sleep-solutions.com/clinical_library/White_Matter_Disease_SDB.pdf wrote:Sleep studies. Studies were performed 7 to 14 days following stroke onset using the ResMed Autoset II plus system (Sydney, Australia) in diagnostic mode.9 This equipment records airflow by nasal cannulas, arterial oxygen saturation (SaO2) by a finger oximeter probe, chest movement by a thoracic resistance band, and body position. It was chosen because of patient tolerability and ease of placement/replacement of sensors in an acute stroke unit and because it permitted easy handling and pressure area care in hemiparetic patients. A number of studies have validated the Autoset device in comparison with polysomnography,9-11 and it has been used previously to diagnose SDB after stroke.12,13 Results were expressed as Apnea–Hypopnea Index (AHI), the frequency of apneas and hypopneas per hour of study. With the Autoset device, an apnea is recorded if the 2-second moving average ventilation falls to 25% of the recent average value (time constant 100 seconds) for at least 10 consecutive seconds; a hypopnea is defined as a decrease in nasal ventilation of at least 50% but 75% for at least 10 seconds; the level of oxygenation is not used in the definition. We also used the oximetry data from the device to determine the Desaturation Index (DI) for each subject. DI was defined as number of desaturations of 4%/hour of study.

That would seem to settle the matter then. The Autoset Spirit did NOT use FOM (simplified FOT) according to the researchers ozij referenced. Presumably, the newer S8 Autoset Vantage does not use it either. (Not a shred of evidence has been presented here to suggest its use.)

Thank you, ozij.

Regards,
Bill (glad we finally got that cleared up ... )

What great sleuth work.

Thank you ozij!!!

-SWS wrote:What great sleuth work.

Thank you ozij!!!

Indeed! Glad you're back "at work", ozij!

[quote="ozij"][quote="-SWS"]That pretty much settles the matter in my mind: "FOT is for naught" where A10 is concerned.

But I still wonder why Resmed has continued this highly basic FOT patent for so many years. Perhaps the decision is based on nothing more than a "FOT because we ought" philosophy.

I had better escape the "FOT light" before a well-deserved stage hook reaches out and...



<-SWS caught by FOT>

Split_City wrote:EDIT: I noticed something which contradicts what I said in my post after this. I stated that the airway would reopen following initiation of IPAP. However, I guess this wouldn't be true because if the airway has collapsed, IPAP would not be triggered because there would be no pressure change detected by the BiPAP machine. Please correct me if my thinking is wrong.

Speaking from experience, having used BiPAP, you are correct that IPAP would not be triggered, at least not with standard BiPAP. (Disregarding the inevitable variations in accuracy with which a machine can be set to detect the difference between inspiration and expiration.)

RG, as usual, you offered a different way of describing this than I've been using. Thank you for that. It completes the picture very nicely (at least how I think about it).

rested gal wrote:As I understand it, in a bilevel titration EPAP is set to prevent obstructive apneas, which can be eliminated at a lower pressure than the higher pressure required to eliminate hypopneas, flow limitations, and residual snores.
...
If the airway can be kept even partially open (by EPAP) during exhalation, at the end, and during the pause after exhalation is finished...then it is open "enough" to allow the person to start the next inhalation. And that's when the higher IPAP kicks in. Voila' -- a patent airway for full inhalation.

Voila indeed! The lower pressure used during expiration is insufficient to keep the airway open during inspiration. If pressure is not raised sufficiently as inspiration begins, then at some point collapse finally occurs.

This is the very shift I was getting at. Rather than collapse occurring during expiration, it would be shifted in time to inspiration. As the flow begins to increase during inspiration, at some point the airway finally collapses.

Thank you, RG, for graphically describing the underlying physical processes.

I suppose there's not been any fundamental shift in musculature as pressure increased from ambient to EPAP, CPAP or IPAP in our hypothetical individual though.

So, if I may be so bold as to make yet another observation which fits into the broader overall discussion ... If this time shift for airway collapse can occur in a single individual as a result of pressure changes, would not this also suggest, very strongly, that the timing of collapse varies among individuals as well.

For example, consider how an individual's apnea may progress. DSM has already commented about how his needs have changed over time. In the beginning phase of apnea perhaps, generally, airway collapse occurs during inhalation and only a slight pressure increase is needed to correct that. As an individual's apnea gets worse over time then more pressure might be needed which would correspond with collapse occurring toward the end of the expiration phase. (Now, I'm not saying that apnea progresses like this in everyone. However, we know from what has been posted on this forum that pressure needs do change, often considerably, over time. Usually, not always, required pressure increases over time.)

Just some more thoughts on the matter ...

Regards,
Bill

Snoredog wrote:So in the Chest bench test WHICH machine did they test?

The Autoset II Plus, Snoredog. that much is clear.

I get the impression that the Autoset II Plus is a quite different machine from either the Autoset Spirit or Autoset Vantage. Apparently, it is a lab machine which includes provisions for oximetry and thoracic measurements.

Regards,
Bill

snoredog wrote:The AutoSet Spirit and the Autoset II Plus are 2 totally different machines

Geez, snoredog, of course they are.

They tested the Autoset Spirit as one of a group of seven machines that "based their detection algorithms on the analysis of the flow shape and the high frequency vibrations produced in the airways during snoring."

And they tested the Autoset II Plus as one of a group of three other devices three other devices, that, "in addition to the analysis of the flow shape and snoring, included a simplified method of FOT for detecting increases in airway resistance".

What's so confusing about that????

O.