Resmed vs. Respironics - Help

split_city wrote:

-SWS wrote:I was wondering specifically about these cases of expiratory-end-phase airway collapse. In these cases is there a frequent pattern of slight (respiratory cycle) sinusoidal decay leading up to that final expiratory cycle of obstructive collapse?

That hypothetical sinusoidal decay I am wondering about might be reflected by peak pressure and/or flow progressively diminishing (perhaps slightly or even moderately) in previous respiratory cycles.

First of all, I shouldn't really hijack this thread with data from my current project. I will add some results to an earlier thread I started which talks about my work.

However...

Yes, there is generally is a reduction in flow i.e. sinusoidal decay as you put it, leading into cyclical obstructions. The example I posted doesn't really show this but it is very common. Patients tend to hyperventilate i.e. ventilation is increased at the termination of an apnea as ventilatory drive is quite high at this time. Once CO2 levels decrease, flow slowly begins to fall back to "normal" levels. But for some reason, flow continues to fall until an apnea results.


In my current study, I'm attempting to identify what events lead into an apnea. Such events include:

1) Lung volume
2) Genioglossus activity
3) End tidal CO2
4) Diaphragm position (probably in the too hard basket with the equipment we have)
5) Ventilation
6) Airway resistance

Hopefully, we can sort out what factors generally precede an apnea. From my preliminary data, lung volume and genioglossus muscle activity significantly decrease prior to obstruction. There has been quite a bit of work looking at tongue muscle activity, but very little data concerning changes in lung volume.

how about snore? where does snore fall into that diagram?

Would seem to me the event would show up at the precise shift point between exhalation and inspiration or period before rise time.

Snoredog wrote:

split_city wrote:

-SWS wrote:I was wondering specifically about these cases of expiratory-end-phase airway collapse. In these cases is there a frequent pattern of slight (respiratory cycle) sinusoidal decay leading up to that final expiratory cycle of obstructive collapse?

That hypothetical sinusoidal decay I am wondering about might be reflected by peak pressure and/or flow progressively diminishing (perhaps slightly or even moderately) in previous respiratory cycles.

First of all, I shouldn't really hijack this thread with data from my current project. I will add some results to an earlier thread I started which talks about my work.

However...

Yes, there is generally is a reduction in flow i.e. sinusoidal decay as you put it, leading into cyclical obstructions. The example I posted doesn't really show this but it is very common. Patients tend to hyperventilate i.e. ventilation is increased at the termination of an apnea as ventilatory drive is quite high at this time. Once CO2 levels decrease, flow slowly begins to fall back to "normal" levels. But for some reason, flow continues to fall until an apnea results.


In my current study, I'm attempting to identify what events lead into an apnea. Such events include:

1) Lung volume
2) Genioglossus activity
3) End tidal CO2
4) Diaphragm position (probably in the too hard basket with the equipment we have)
5) Ventilation
6) Airway resistance

Hopefully, we can sort out what factors generally precede an apnea. From my preliminary data, lung volume and genioglossus muscle activity significantly decrease prior to obstruction. There has been quite a bit of work looking at tongue muscle activity, but very little data concerning changes in lung volume.

how about snore? where does snore fall into that diagram?

Would seem to me the event would show up at the precise shift point between exhalation and inspiration or period before rise time.

We did not use a snore sensor in the study but we have pretty sensitive pressure transducers which pick up snores.

How would you fit a "snore" into the story? Snoring represents unstable breathing. The same factors which contribute to snoring are also likely to lead to hypopneas/apneas. I guess snoring can be an outcome whereas we are interested in what caused the unstable breathing in the first place.

The original thought would be that airway collapse occurred at the beginning or during inspiration. Results from our work and work from others suggest that collapse occurs passively towards the end of expiration. This is certainly conceivable given that dilator muscle activity is lowest at the end of expiration, surrounding tissue pressure is highest at the end of expiration, airway size is smallest at lower lung volumes and the stretch on the airway is lowest at the end of expiration (our theory anyway).


We have pretty sensitive pressure transducers which should be able to pick out whether collapse occurs during late expiration or early inspiration. Unfortunately, we cannot determine if the airway has collapsed during the expiratory pause i.e. pause between end expiration and the beginning of inspiration. You would need to visualize this.

Split-city

This topic is one dear to the hearts of a few of us & RG in particular has mentioned previously favouring snoring occuring in the late exhalationperiod (good call RG )

I had commented that I thought their might be 2 types of sufferers, those whose apneas occur at exhalation & those whose apneas began with an inhalation & subsequently sucked their own airway shut.

I considered this from the point-of-view that the physiology of people differs & those with large necks with excess tiissue would probably be prone to the exhalation apneas whereas those people with less added weight but other factors such as relaxed musculature etc: would fall into the inhalation apneas type.

Do you see any possibility of two clear types of apnea sufferers ?

Tks

DSM

split_city wrote:The original thought would be that airway collapse occurred at the beginning or during inspiration. Results from our work and work from others suggest that collapse occurs passively towards the end of expiration. This is certainly conceivable given that dilator muscle activity is lowest at the end of expiration, surrounding tissue pressure is highest at the end of expiration, airway size is smallest at lower lung volumes and the stretch on the airway is lowest at the end of expiration (our theory anyway).

Assuming that, in general, collapse occurs toward the end of expiration (which seems entirely reasonable), then how might the timing of the airway collapse be affected by application of CPAP?

I'm not sure I've seen anyone list any basic assumptions about collapse, so allow me to list some assumptions (which I hope others will correct, or add to as appropriate).
1. Expiration flow pressure tends to keep the airway patent (at least through much of the cycle).
2. Inspiration flow pressure tends to close the airway.
3. CPAP maintains patency with increased pressure.
4. EPAP can be lower than IPAP because of assumptions 1 and 2 above.
5. Bi-level is useful for lowering average overall pressure.
6. EPAP can generally be lower than CPAP.
7. EPAP maintains patency by virtue of keeping the airway open throughout the entire expiratory cycle until the beginning of inspiration when pressure increases rapidly to IPAP. (OK, maybe this is less an assumption than my question.)

The reason I ask the question is because it does seem entirely reasonable, based on physics and flow dynamics, that collapse occurs during expiration. However, it also appears to me that applying CPAP (or BiPAP) would shift the timing of any potential collapse. Presumably, at titration pressure CPAP maintains patency throughout the entire cycle, so how could there not be a timing shift at pressures somewhat below the titration value, but still greater than ambient pressure?

Regards,
Bill

split_city wrote: Once CO2 levels decrease, flow slowly begins to fall back to "normal" levels. But for some reason, flow continues to fall until an apnea results.


In my current study, I'm attempting to identify what events lead into an apnea. Such events include:

1) Lung volume
2) Genioglossus activity
3) End tidal CO2
4) Diaphragm position (probably in the too hard basket with the equipment we have)
5) Ventilation
6) Airway resistance

Hopefully, we can sort out what factors generally precede an apnea. From my preliminary data, lung volume and genioglossus muscle activity significantly decrease prior to obstruction. There has been quite a bit of work looking at tongue muscle activity, but very little data concerning changes in lung volume.

Thanks for satisfying my own curiosity, split_city.

Your information most definitely doesn't hijacking this or any wildly "meandering" thread. And this fascinating thread sure seems to have taken a few interesting and interrelated side excursions. Your input just makes this thread that much richer IMO. Myself and others dearly appreciate what you and your team members are doing for us.

Cheers, mate!!! .

dsm wrote:Split-city

This topic is one dear to the hearts of a few of us & RG in particular has mentioned previously favouring snoring occuring in the late exhalationperiod (good call RG )

Doug, perhaps you meant to write "collapse" (as in collapsed airway) rather than "snoring." I don't think I've ever mentioned anything at all about "snoring" happening during exhalation... 'cause I've always thought snoring happens during inhalation.

I have written that I thought the collapse of the airway happens near the end of exhalation or during the pause just before a person was going to try to breathe in again, if that (instead of "snoring") is what you meant to say I've said previously.

I would also wonder about the epidemiology or statistical breakdown of expiratory-end-phase airway collapse.

Across the OSA population, for instance, how often does obstructive collapse occur at the end of expiration? How often does it occur at the beginning of inspiration? And how often does it occur during that interim pause between expiration and inspiration? I could be wrong, but I don't think there is adequate epidemiology just yet discerning phase-related distributions across the patient population.

I would personally expect a variety of combinational nuances (in etiology and pathophysiology) to skew that temporal distribution of airway collapse, in either direction of a hypothetical bell curve. Perhaps the center of a rather narrow hypothetical bell curve thus sits somewhere at the end of expiration for the OSA population.

As Rested Gal pointed out earlier, the premise of C-Flex is to return to CPAP equivalent pressure before expiratory end-phase apneas have a chance to become incipient.

-SWS wrote:Across the OSA population, for instance, how often does obstructive collapse occur at the end of expiration? How often does it occur at the beginning of inspiration? And how often does it occur during that interim pause between expiration and inspiration? I could be wrong, but I don't think there is adequate epidemiology just yet discerning phase-related distributions across the patient population.

But ..., ( ... the sheer audacity of someone willing to point out contradictions.)

... what difference does it matter, really, if application of CPAP shifts the timing of imminent collapse?

Regards,
Bill ( ... thinking that his point was entirely missed earlier ... )

NightHawkeye wrote:

-SWS wrote:Across the OSA population, for instance, how often does obstructive collapse occur at the end of expiration? How often does it occur at the beginning of inspiration? And how often does it occur during that interim pause between expiration and inspiration? I could be wrong, but I don't think there is adequate epidemiology just yet discerning phase-related distributions across the patient population.

But ..., ( ... the sheer audacity of someone willing to point out contradictions.)

... what difference does it matter, really, if application of CPAP shifts the timing of imminent collapse?

Regards,
Bill ( ... thinking that his point was entirely missed earlier ... )

Bill, my speculative pondering had to do exclusively with untreated apneas. I really intended that line of thought as separate but non-contradictory to your post.

I think your point about CPAP potentially shifting the timing of apneas is a good point. Along that same line of thought, I would expect some of those residual obstructive occurrences to be lesser flow-limited events than frank apneas, because of that static pressure support. And like you, I also expect at least some residual frank apneas to manifest as delayed because of CPAP's preliminary degree of pressure support.

I think your analysis was pretty much spot on, although I don't have a feel for just how often apnea latency may occur because of CPAP's preliminary pressure support.

Regarding physics and biophysics, though. One principle that seems to crop its ugly head again and again in SDB research: while physics is highly predictable, less-predictable biophysics deals wild card after wild card into the SDB equation.

NightHawkeye wrote:

-SWS wrote:Across the OSA population, for instance, how often does obstructive collapse occur at the end of expiration? How often does it occur at the beginning of inspiration? And how often does it occur during that interim pause between expiration and inspiration? I could be wrong, but I don't think there is adequate epidemiology just yet discerning phase-related distributions across the patient population.

But ..., ( ... the sheer audacity of someone willing to point out contradictions.)

... what difference does it matter, really, if application of CPAP shifts the timing of imminent collapse?

Regards,
Bill ( ... thinking that his point was entirely missed earlier ... )

-SWS wrote: Bill, my speculative pondering had to do exclusively with untreated apneas. I really intended that line of thought as separate but non-contradictory to your post.

I know, -SWS. That's why I confessed to rudeness in advance.

However, that timing shift, which we seem to be in agreement on, has an awfully important part to play in how one might achieve effective therapy. I just hoped the discussion would continue on with acknowledgement of the timing shift whether or not the specifics could be fully accounted for.

Without the occurrence of that timing shift, Bi-level therapy, C-flex, A-flex, EPR and EasyBreathe (? or whatever ResMed's calling their version of A-flex) get kinda nasty to analyze. Without that timing shift possibly they don't even work ...

It seemed like an important point ... worth emphasizing.

Regards,
Bill

rested gal wrote:

dsm wrote:Split-city

This topic is one dear to the hearts of a few of us & RG in particular has mentioned previously favouring snoring occuring in the late exhalationperiod (good call RG )

Doug, perhaps you meant to write "collapse" (as in collapsed airway) rather than "snoring." I don't think I've ever mentioned anything at all about "snoring" happening during exhalation... 'cause I've always thought snoring happens during inhalation.

I have written that I thought the collapse of the airway happens near the end of exhalation or during the pause just before a person was going to try to breathe in again, if that (instead of "snoring") is what you meant to say I've said previously.

RG,

You are quite right - I didn't mean snoring but collapsing

Sorry for that

Doug

dsm wrote:I had commented that I thought their might be 2 types of sufferers, those whose apneas occur at exhalation & those whose apneas began with an inhalation & subsequently sucked their own airway shut.

I considered this from the point-of-view that the physiology of people differs & those with large necks with excess tiissue would probably be prone to the exhalation apneas whereas those people with less added weight but other factors such as relaxed musculature etc: would fall into the inhalation apneas type.

Do you see any possibility of two clear types of apnea sufferers ?

Tks

DSM

While a majority of apneas I have seen occurred towards the end of expiration, I have no doubt that there are individuals out there where collapse occurs during the inspiratory phase. Your hypothesis might be right as I only recruited obese OSA subjects into my study. It would certainly be interesting to see the airway collapse timing in healthy-weight OSA individuals.

I also believe that there is some overlap within individuals i.e. combination of expiratory vs inspiratory collapse. It will be interesting to look at the events preceding each type of collapse. Nevertheless, I expect the same factors to be involved, but maybe the timing of these changes will be different.

NightHawkeye wrote: The reason I ask the question is because it does seem entirely reasonable, based on physics and flow dynamics, that collapse occurs during expiration. However, it also appears to me that applying CPAP (or BiPAP) would shift the timing of any potential collapse. Presumably, at titration pressure CPAP maintains patency throughout the entire cycle, so how could there not be a timing shift at pressures somewhat below the titration value, but still greater than ambient pressure?

Regards,
Bill

I'm not quite sure I follow but are you asking whether there is a timing shift in regards to airway collapse follow the application of subtherapeutic CPAP? Hhhmmm...I don't see how there would be much of a change in the timing. CPAP does "switch" off UA dilatory muscle activity which could mean the collapse might occur during inspiration. However, if CPAP is below the therapeutic level, the dilatory muscles would still be active due to higher negative pressure during inspiration. I still think that end expiration would be the optimal time for collapse. There would just be less periods of apnea during sub-therapeutic CPAP therapy given that airway pressure is maintained above atmospheric pressure.

rested gal wrote: Doug, perhaps you meant to write "collapse" (as in collapsed airway) rather than "snoring." I don't think I've ever mentioned anything at all about "snoring" happening during exhalation... 'cause I've always thought snoring happens during inhalation.

The surprises keep coming RG . Snoring can occur during inspiration and expiration. Here's a snapshot from a subject showing expiratory snores



I guess it doesn't help when you have two catheters down your nose though

-SWS wrote:I would also wonder about the epidemiology or statistical breakdown of expiratory-end-phase airway collapse.

Across the OSA population, for instance, how often does obstructive collapse occur at the end of expiration? How often does it occur at the beginning of inspiration? And how often does it occur during that interim pause between expiration and inspiration? I could be wrong, but I don't think there is adequate epidemiology just yet discerning phase-related distributions across the patient population.

I would personally expect a variety of combinational nuances (in etiology and pathophysiology) to skew that temporal distribution of airway collapse, in either direction of a hypothetical bell curve. Perhaps the center of a rather narrow hypothetical bell curve thus sits somewhere at the end of expiration for the OSA population.

As Rested Gal pointed out earlier, the premise of C-Flex is to return to CPAP equivalent pressure before expiratory end-phase apneas have a chance to become incipient.

I agree with all of this. I'm not concluding that end expiratory collapse is the norm. There are likely to be differences between individuals and also within individuals. It might be difficult to pinpoint the collapse of the airway during the expiratory pause without visualizing the airway.

Here are some data from previous studies looking at UA cross-sectional area during respiration.

Progressive Retropalatal Narrowing Preceding Obstructive Apnea
MARY J. MORRELL, YASEEN ARABI, BRIAN ZAHN, and M. SAFWAN BADR
AM J RESPIR CRIT CARE MED 1998;158:1974–1981

During expiration, for all breaths there was an initial significant increase in CSA compared with the nadir CSA during the preceding inspiration.... followed by a significant narrowing at end-expiration compared with the peak CSA during that expiration. These results show that expiratory narrowing produced a significant reduction of CSA at end-expiration prior to obstructive apnea

We have observed narrowing of the end-expiratory pharyngeal
CSA during breaths preceding an obstructive apnea and
on a number of occasions the airway occluded before the subsequent
inspiratory effort. The expiratory narrowing we observed
may have been associated with a decay of the positive
intraluminal pressure generated during early expiration.

They went on to talk about surrounding tissue pressure:

In our study, the occurrence of pharyngeal narrowing during
expiration, when intraluminal pressure was positive, suggests
that the surrounding extraluminal pressure was also positive
and higher than intraluminal pressure. Thus, our findings are
consistent with studies in anesthetized rabbits and dogs that
have demonstrated that surrounding extraluminal pressure,
applied by mass loading of the anterior neck and negative
pressure around the neck, respectively, can significantly influence
pharyngeal caliber

Here's an abstract from another study looking at airway collapse during central sleep apnea. It again confirms that collapse can occur in a passive manner.

Pharyngeal narrowing/occlusion during central sleep apnea.
Badr MS, Toiber F, Skatrud JB, Dempsey J.
J Appl Physiol. 1995 May;78(5):1806-15

We hypothesized that subatmospheric intraluminal pressure is not required for pharyngeal occlusion during sleep. Six normal subjects and six subjects with sleep apnea or hypopnea (SAH) were studied during non-rapid-eye-movement sleep. Pharyngeal patency was determined by using fiber-optic nasopharyngoscopy during spontaneous central sleep apnea (n = 4) and induced hypocapnic central apnea via nasal mechanical ventilation (n = 10). Complete pharyngeal occlusion occurred in 146 of 160 spontaneously occurring central apneas in patients with central sleep apnea syndrome. During induced hypocapnic central apnea, gradual progressive pharyngeal narrowing occurred. More pronounced narrowing was noted at the velopharynx relative to the oropharynx and in subjects with SAH relative to normals. Complete pharyngeal occlusion frequently occurred in subjects with SAH (31 of 44 apneas) but rarely occurred in normals (3 of 25 apneas). Resumption of inspiratory effort was associated with persistent narrowing or complete occlusion unless electroencephalogram signs of arousal were noted. Thus pharyngeal cross-sectional area is reduced during central apnea in the absence of inspiratory effort. Velopharyngeal narrowing consistently occurs during induced hypocapnic central apnea even in normal subjects. Complete pharyngeal occlusion occurs during spontaneous or induced central apnea in patients with SAH. We conclude that subatmospheric intraluminal pressure is not required for pharyngeal occlusion to occur. Pharyngeal narrowing or occlusion during central apnea may be due to passive collapse or active constriction.

Snoredog wrote: and I'd like to know how many patients were tested to conclude that model represents the vast majority of patients?

1, 10 or 100? and what percentage fall under that model?

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?

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CPAPopedia Keywords Contained In This Post (Click For Definition): bipap, C-FLEX, Titration, Arousal, CPAP, Hypopnea, CSA

_________________

CPAPopedia Keywords Contained In This Post (Click For Definition): bipap, C-FLEX, Titration, Arousal, CPAP, Hypopnea, CSA

split_city wrote:

NightHawkeye wrote: The reason I ask the question is because it does seem entirely reasonable, based on physics and flow dynamics, that collapse occurs during expiration. However, it also appears to me that applying CPAP (or BiPAP) would shift the timing of any potential collapse. Presumably, at titration pressure CPAP maintains patency throughout the entire cycle, so how could there not be a timing shift at pressures somewhat below the titration value, but still greater than ambient pressure?

Regards,
Bill

I'm not quite sure I follow but are you asking whether there is a timing shift in regards to airway collapse follow the application of subtherapeutic CPAP?

Correct.

split_city wrote:Hhhmmm...I don't see how there would be much of a change in the timing. CPAP does "switch" off UA dilatory muscle activity which could mean the collapse might occur during inspiration.

OK.

split_city wrote:However, if CPAP is below the therapeutic level, the dilatory muscles would still be active due to higher negative pressure during inspiration. I still think that end expiration would be the optimal time for collapse.

That fails to explain Bi-level therapy which generally applies lower pressure during the expiratory phase and then increases pressure during inspiration. Since a picture's worth a thousand words, I'll illustrate with one from the Respironics website:



At the top of the figure airflow is plotted, while on the bottom IPAP and EPAP are plotted. Note that the transitions between IPAP and EPAP occur at the same time airflow reverses, at least according to Respironics. Many, perhaps most people who use Bi-level therapy have an EPAP setting substantially lower than their CPAP level. 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.

It's a sincere question Split_City. There genuinely seems to be a contradiction here. It's an area I've had questions about for a while and there have also been arguments about this on the forum (but hey, we'll argue about nearly anything here).

Any light you might be able to shed on the subject would be appreciated.

Regards,
Bill

NightHawkeye wrote: That fails to explain Bi-level therapy which generally applies lower pressure during the expiratory phase and then increases pressure during inspiration. Since a picture's worth a thousand words, I'll illustrate with one from the Respironics website:



At the top of the figure airflow is plotted, while on the bottom IPAP and EPAP are plotted. Note that the transitions between IPAP and EPAP occur at the same time airflow reverses, at least according to Respironics. Many, perhaps most people who use Bi-level therapy have an EPAP setting substantially lower than their CPAP level. 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.

It's a sincere question Split_City. There genuinely seems to be a contradiction here. It's an area I've had questions about for a while and there have also been arguments about this on the forum (but hey, we'll argue about nearly anything here).

Any light you might be able to shed on the subject would be appreciated.

Regards,
Bill

Oh, I got ya now! The light just switched on . Very interesting question which I have passed on to my supervisor and also one of the sleep physicians here.

Before I answer this question, I need some help from people who had a CPAP titration study, but then went on to use BiPAP. For these people, can you please tell me what your therapeutic CPAP level was and what your IPAP and EPAP levels are.

EDIT: I have just been informed that BiPAP is generally used in patients who need assistance with inspiration such as patients with neuromuscular disease, COPD. I was also told that EPAP (not IPAP) = therapeutic CPAP. IPAP is actually > therapeutic CPAP. The person I spoke with wasn't completely confident with this so I'm happy to discuss further. If true, then this explains why the airway remains patent during BiPAP therapy.

However, for arguments sakes, lets assume that EPAP really is sub-optimal therapy. If low enough, the airway could potentially collapse at end expiration during therapy. However, the airway would pretty much reopen following initiation of rapid IPAP (as shown in your figure). This will depend on the surface tension forces acting on the walls of the airway though.

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.

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

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