Resmed vs. Respironics - Help

Velbor, you are very welcome at this cocktail party. You truly are!

Your long, limp balloon model is the closest approximation. Think about blowing that long, limp balloon only half way up, or a little more. Then hold that pressure for a few moments. That sustained pressure is just like CPAP's static pressure. That sustained pressure dilates the balloon via static pressure's inflation. Consequently clearances and diameters throughout are now greater. You can still move a breathable volume of air in and out despite that static pressure delivered by CPAP. And ideally that inflationary static pressure will nicely compensate for apneas by providing greater clearances.

The human airway, of course, isn't equally elastic throughout as in the case of the balloon. Some areas are more inflation prone while other areas are less. The elastic soft-tissue portions of our airway thus tends to dilate with CPAP's inflationary static pressure. These areas that inflate nicely tend to enjoy much improved clearances because of CPAP. However, the more rigid and dense parts of our airway do not move out of the way so easily, regardless of CPAP's inflationary pressure.

The question, then, is why you have a residual AHI around 10 or so on xPAP, and why a dental device seems to treat you better? My understanding is that you are not the only one. My guess is this just may have to do with exactly where your occlusion tends to occur. As an example, if your dense, muscular tongue tends to occlude opposite the rigid palate, then that type of occlusion is going to be much harder to resolve with airway inflation (than had it occurred where soft-tissue inflation is accomplished much easier). And yet pulling the mandible forward with a dental device just may resolve that type of occlusion much better than airway inflation. One of those two sides meeting or joining in occlusion must be capable of easy inflation in order for CPAP to properly do it's job. For most people, that seems to be the case, which is why CPAP serves as a gold standard: usually the soft palate pushes out of the way nicely because of CPAP. Of course, to simply say that CPAP is a gold standard and that it works well for most people fails to mention all the various exception cases in which CPAP does not work so well. You seem to be one of those cases, if indeed, you achieve better results when using your dental splint.

That's only my take. So please bear in mind that none of us are truly experts. I am certainly not an expert of any kind. We just like to talk, analyze, and sometimes speculate at our cocktail parties toward the common goal of learning, sharing, and, of course, helping others. .

Velbor, great questions.

And -SWS, great analysis, as always!

I hear clinking glasses!

ozij wrote:

so she is looking at getting a Hybrid so she can drive it in the HOV lane.

Wouldn't a Swift be faster?

O.

rested gal wrote:Velbor, great questions.

And -SWS, great analysis, as always!

I hear clinking glasses!

Thanks, RG. But I have to confess... IMHO the above is a nicely over-simplified balloon analogy. I also happen to think that kind of balloon analogy works absolutely great for newcomers. In my view there's "inflation" and there's also similar "stenting". I think of those two as being different. And yet they both utilize CPAP's static pressure to keep tissue or mass out of the way.

I'll demonstrate two hypothetical cases: one that I think of as "stenting" and another hypothetical case that I like to think of as "inflation". These two hypothetical cases might be thought of as "The Tongue Slider versus the Palate Sagger". These are hypothetical cases only, because most of us probably fall somewhere in the middle of those two etiologies. But here goes... for purposes of hypothetically demonstrating inflating versus stenting.

"The Soft Palate Sagger"- In this hypothetical case the obstructive culprit is a soft palate that occasionally sags down during sleep, for lack of neuromuscular airway maintenance. CPAP's static pressure to the rescue---but ideally to stent or hold up that soft palate in it's original non-sagging position. I tend to think of that as stenting rather than inflating. Stenting ideally holds the airway open to it's original contours and diameters (in reality static-pressure doesn't work out so perfectly).

"The Tongue Slider"- In this hypothetical case the gravity-prone tongue tends to fall back (gravity-assisted neuromuscular lack of airway maintenance is our culprit). In this entirely hypothetical "opposite-side" problem, lets say the soft palate tends to stay nicely in place. A CPAP titration would have to literally inflate or dilate the airway at that occlusive point---not simply stent the soft palate into its original position. Here CPAP needs to compensate with greater than normal clearance to accommodate that tongue sliding back a bit. If pressure can't dilate the airway wide enough to compensate for this scenario, then you may be better off with a dental appliance that pulls the mandible and/or tongue forward. After all, you can only compensate at any given occlusive point so much with inflation.

In both cases soft palate meets a dense, muscular tongue. In both cases static pressure holds the airway open. In that latter case the airway is dilated more than baseline. In reality everybody probably falls somewhere along various middle points on that continuum (between needing to merely stent versus needing to inflate). And in reality, at any given moment on CPAP, parts of the airway happen to be stented, while other parts happen to be inflated, with yet other rigid parts completely unaffected by pressure (regarding contour).

And Velbor, IMO you're right about blowing through a balloon being easier than drawing air through a sagging or near-flaccid balloon. Think of a paper milk shake straw. If the milkshake is too thick the straw starts to collapse as you draw fluid. That failing dynamic is called transluminal collapse. Yet, you can blow endless mouths full of milkshake through that straw in the opposite direction without ever suffering straw collapse. But what if you had a miniature "milk-shake assist pump" sitting near the bottom of your milkshake glass---helping you by sourcing milkshake as your also drew that same fluid in? The straw would be much less inclined to collapse, and that's truly what CPAP does for us as well.

On that same note of transluminal collapse, earlier we talked about nasal impedance contributing to an apnea way down in the pharynx. We can simulate that by partially pinching our nostrils closed as we draw in a very deep breath. You can literally feel an apnea in the making. And that experimental apnea has absolutely nothing to do with (neurologically) non-vigilant airway muscles or a sliding tongue. My take is that there are a variety of ways to both cause and/or contribute to obstructive apnea.

Velbor, how is our cocktail party going so far? Relevant I hope.

[quote="-SWS"]

<snip>

On that same note, earlier we talked about nasal impedance contributing to an apnea way down in the pharynx. We can simulate that by partially pinching our nostrils closed as we draw in a very deep breath. You can literally feel an apnea in the making. And that experimental apnea has absolutely nothing to do with (neurologically) non-vigilant airway muscles or a sliding tongue. My take is that there are a variety of ways to both cause and/or contribute to obstructive apnea.

Of course you're welcome, Velbor!

As for uninvited - invtitaion to all coctail parties in this forum are issure en bloc with the registration. It's there on the regisrtation screen...

O.

Velbor wrote:Being of limited imagination, I am having trouble visualizing OSA as a pressure-caused radial collapse of the upper airways, and therefore I am having trouble visualizing CPAP working as a radially-oriented "splint". If the airway "collapse" of OSA is due to the physical movement of "attachments" inside an otherwise relatively rigid tube (from the perspective of external pressure), i find it hard to see how CPAP, viewed as operative radially, can "expand" anything, whether immediately or preemptively.

Velbor, here is a figure which may be of some use in visualizing.



This image is from: http://www.aana.com/uploadedFiles/Resou ... 33-138.pdf

Velbor wrote:So .... if not radially (assuming that anything I have expressed above makes any sense at all), does CPAP work by exerting its pressure "axially," along the length of the upper airway? Here, at least, I can find pressure differentials, with respect to the flexible-walled chest and the lungs. Does CPAP work, then, by its pressure differential (with respect to the negative pressure within the thorax on inspiration) "pushing axially downward" (i.e., toward the lungs)? Would loose floppy tissue, or tongue protuberances, be "bent" (rather than "lifted") out of the way, because their bases are "fixed" to the "rigid" upper airway wall? (The vectors of such movement would have a radial component! But not due to a radial "pressure" differential!) And once air is moving, would the dynamics of the "wind" play a role?

Forgetting this entire paragraph, for the sake of discussion, the "expansion" you are questioning results from the pressure of the gas operating equally in all directions, not merely radially or axially. Hopefully, the illustration clarifies things a little.

The forces at play are sufficient to "splint" the airway open when the "titration" pressure is reached, but once the airway has become obstructed and the diaphragm subsequently moves downward attempting to fill the lungs with air, then a quite different set of forces come into play. The forces below the obstruction begin to draw the soft tissue further into the windpipe.

As an experiment, in case you doubt the strength of the force exerted when the diaphragm expands, simply push the back of your tongue toward your throat while inhaling. Next, simply imagine what chance a slight increase in CPAP pressure would have in clearing that obstruction which has already been pulled into your throat.

Hope this helps clarify, rather than confuse.

Regards,
Bill

I have to say I am mighty impressed with the content of this thread! I have only skimmed over it but most of it is very interesting. I'll have to take some time to read it in more detail.

Velbor wrote:
So .... if not radially (assuming that anything I have expressed above makes any sense at all), does CPAP work by exerting its pressure "axially," along the length of the upper airway? Here, at least, I can find pressure differentials, with respect to the flexible-walled chest and the lungs. Does CPAP work, then, by its pressure differential (with respect to the negative pressure within the thorax on inspiration) "pushing axially downward" (i.e., toward the lungs)?

Velbor: You raise some interesting points. I'll focus on the above point as it kind of relates to my work. While CPAP is thought to maintain airway patency by "splinting" the airway via positive pressure, axial tension is also likely to prevent collapse. The airway is connected to several intrathoracic structures. These structures are pulled downwards during inspiration along with the diaphragm. This action helps to stretch the airway, reducing airway collapsibility.

There have been several studies conducted in animals showing an inverse relationship between the degree of axial tension on the airway and airway collapsibility. This effect is independent of the influence of airway dilator muscles.

Van de Graaff also demonstrated the importance of axial tension (known as caudal traction) on upper airway resistance. Resistance is related to the radius of the "tube." The smaller the radius, the higher the resistance (actually resistance is inversely proportional to the radius^4). In this study, Van de Graaff showed that airway resistance went down during inspiration, indicating that the airway was getting bigger. It was throught that the increase in airway size was due to the actions of the dilator muscles. Therefore, Van de Graaff hyperventilated the dogs to apnea, thus "switching" off the dilator muscles. The dogs were then mechanically ventilated. Again, airway resistance decreased during inspiration, thus indicating that the dilator muscles were in fact not solely involved in increasing airway size. Van de Graaff then went on to cutting all cervical structures which linked the thorax to the airway. This resulted in airway collapse. These data suggest that axial tension generated by the descending diaphragm helps to maintain airway patency during inspiration.

Van de Graaff WB.
Department of Medicine, Stritch School of Medicine, Loyola University, Maywood, Illinois 60153.

Patency of the upper airway (UA) is usually considered to be maintained by the activity of muscles in the head and neck. These include cervical muscles that provide caudal traction on the UA. The thorax also applies caudal traction to the UA. To observe whether this thoracic traction can also improve UA patency, we measured resistance of the UA (RUA) during breathing in the presence and absence of UA muscle activity. Fifteen anesthetized dogs breathed through tracheostomy tubes. RUA was calculated from the pressure drop of a constant flow through the isolated UA. RUA decreased 31 +/- 5% (SEM) during inspiration. After hyperventilating seven of these dogs to apnea, we maximally stimulated the phrenic nerves to produce paced diaphragmatic breathing. Despite absence of UA muscle activity, RUA fell 51 +/- 11% during inspiration. Graded changes were produced by reduced stimulation. In six other dogs we denervated all UA muscles. RUA still fell 25 +/- 7% with inspiration in these spontaneously breathing animals. When all caudal ventrolateral cervical structures mechanically linking the thorax to the UA were severed, RUA increased and respiratory fluctuations ceased. These findings indicate that tonic and phasic forces generated by the thorax can improve UA patency. Inspiratory increases in UA patency cannot be attributed solely to activity of UA muscles.

So, CPAP certainly may help to prevent airway collapse by stretching the airway as speculated by yourself. This axial tension is likely due to the caudal displacement of the diaphragm and other intrathoracic structures caused by CPAP.

Another process which helps prevent airway collapse is lung inflation. This process is likely to work via axial tension forces. Heinzer et al undertook two studies looking at the effect of lung volume on AHI and also CPAP requirements to prevent flow limitation.

Effect of increased lung volume on sleep disordered breathing in patients with sleep apnoea.Heinzer RC, Stanchina ML, Malhotra A, Jordan AS, Patel SR, Lo YL, Wellman A, Schory K, Dover L, White DP.
Sleep Medicine Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. rheinzer@post.harvard.edu

BACKGROUND: Previous studies have shown that changes in lung volume influence upper airway size and resistance, particularly in patients with obstructive sleep apnoea (OSA), and that continuous positive airway pressure (CPAP) requirements decrease when the lung volume is increased. We sought to determine the effect of a constant lung volume increase on sleep disordered breathing during non-REM sleep. METHODS: Twelve subjects with OSA were studied during non-REM sleep in a rigid head-out shell equipped with a positive/negative pressure attachment for manipulation of extrathoracic pressure. The increase in lung volume due to CPAP (at a therapeutic level) was determined with four magnetometer coils placed on the chest wall and abdomen. CPAP was then stopped and the subjects were studied for 1 hour in three conditions (in random order): (1) no treatment (baseline); (2) at "CPAP lung volume", with the increased lung volume being reproduced by negative extrathoracic pressure alone (lung volume 1, LV1); and (3) 500 ml above the CPAP lung volume(lung volume 2, LV2). RESULTS: The mean (SE) apnoea/hypopnoea index (AHI) for baseline, LV1, and LV2, respectively, was 62.3 (10.2), 37.2 (5.0), and 31.2 (6.7) events per hour (p = 0.009); the 3% oxygen desaturation index was 43.0 (10.1), 16.1 (5.4), and 12.3 (5.3) events per hour (p = 0.002); and the mean oxygen saturation was 95.4 (0.3)%, 96.0 (0.2)%, 96.3 (0.3)%, respectively (p = 0.001). CONCLUSION: An increase in lung volume causes a substantial decrease in sleep disordered breathing in patients with OSA during non-REM sleep.

I want to focus on the LV1 result. Basically, the authors measured the change in lung volume caused by therapeutic CPAP. They then increased lung volume up to this volume via negative extrathoracic pressure. The patients were allowed to fall asleep at this lung volume without CPAP. As you can see, AHI decreased from ~62 events down to ~37 events. Not really treated hey? BUT the point was that increasing lung volume does indeed reduce airway collapsibility. The authors went on to state:

Because the subjects we studied were overweight or obese
(like most patients with OSA), we suspect that their
diaphragm was pushed upwards (cranially) when lying on
their back. The negative extrathoracic pressure applied in the
lung almost certainly pulled the diaphragm and trachea to a
more caudal position, thereby increasing the traction on the
upper airway and making it less collapsible.

And this....

In the present study we have shown that an increase in lung volume
alone (without CPAP) is able to decrease the apnoea and
hypopnoea frequency significantly, which supports this
hypothesis. The rest of the effect of CPAP is probably due
to a splinting effect of positive airway pressure on the upper
airway, maintaining a positive transmural pressure throughout
the respiratory cycle.

This is an abstract from their other study:

Lung volume and continuous positive airway pressure requirements in obstructive sleep apnea.Heinzer RC, Stanchina ML, Malhotra A, Fogel RB, Patel SR, Jordan AS, Schory K, White DP.
Division of Sleep Medicine, Sleep Disorders Program @ BI, Brigham and Women's Hospital, 75 Francis Street, Boston, MA 02115, USA. rheinzer@rics.bwh.harvard.edu

Previous studies have demonstrated that lung volume during wakefulness influences upper airway size and resistance, particularly in patients with sleep apnea. We sought to determine the influence of lung volume on the level of continuous positive airway pressure (CPAP) required to prevent flow limitation during non-REM sleep in subjects with sleep apnea. Seventeen subjects (apnea-hypopnea index, 42.6 +/- 6.2 [SEM]) were studied during stable non-REM sleep in a rigid head-out shell equipped with a positive/negative pressure attachment for manipulation of extrathoracic pressure. An epiglottic pressure catheter plus a mask/pneumotachometer were used to assess flow limitation. When lung volume was increased by 1,035 +/- 22 ml, the CPAP level could be decreased from 11.9 +/- 0.7 to 4.8 +/- 0.7 cm H(2)O (p < 0.001) without flow limitation. The decreased CPAP at the same negative extrathoracic pressure yielded a final lung volume increase of 421 +/- 36 ml above the initial value. Conversely, when lung volume was reduced by 732 +/- 74 ml (n = , the CPAP level had to be increased from 11.9 +/- 0.7 to 17.1 +/- 1.0 cm H(2)O (p < 0.001) to prevent flow limitation, with a final lung volume decrease of 567 +/- 78 ml. These results demonstrate that relatively small changes in lung volume have an important effect on the upper airway in subjects with sleep apnea during non-REM sleep.

Again, this indicates that lung volume, and likely axial tension forces, helps to maintain airway patency.

Snoredog wrote:
I'm sure Split_City would beg to differ with logic and our way of thinking, however I will say with "nasal" pressure being applied it should have enough leverage to dislodge a tongue (e.g. cork as it was referred to), this unless the persons anatomy is so screwed up that doesn't happen.

but an excellent post and all good questions, I refer to that tube as a firehose on the asphalt with not much pressure behind it, cpap cranks up the pressure and that firehose becomes nice and round.

I have no objection with the point about dislodging the tongue. I just say that the tongue is only part of the puzzle. The firehose analogy is acceptible but not complete. The action of the water is predominantly acting radially whereas I believe (and speculated by Velbor) that axial forces are at work as well. My abdominal compressin study and work by Heinzer and colleagues certainly does support this notion.

Another area of interest in this thread. I read up about whether the initial collapse occurs via suction pressures i.e. during inspiration, or passively during expiration. I am currently looking at this in my current study. From what I have seen, collapse predominantly occurs towards late-to-end EXPIRATION and NOT during INSPIRATION. I will attempt to paste in some examples when I get a chance.

This is not surprising given that the activity of the airway dilator muscles decreases during expiration and surrounding tissue pressure increases at the same time. Increased tissue pressure will likely lead to passive collapse of the "flaccid" airway during/at the end of expiration.

_________________

CPAPopedia Keywords Contained In This Post (Click For Definition): CPAP, AHI

Thanks for coming to our cocktail party, split_city!

Velbor's also trying to understand why his dental device seems to work better for him than CPAP. I took some purely speculative attempts at answering that question. If you had thoughts toward that question, we would love to hear those as well.

This is some cocktail party

Just when I feared it was losing steam (& focus) another party minded soul turns up and adds a new line of vigour.

Thanks Velbor & welcome Split-City



DSM

PS S-C - wife & I were in Rowland Flat near Tanunda early last week as part of a national car rally great week - Barossa towns are more magical than ever.

Hope the weather there has settled

Thank you for joining the party, Split!

split_city wrote:From what I have seen, collapse predominantly occurs towards late-to-end EXPIRATION and NOT during INSPIRATION.

I've thought that for a long time, just by "feeling" what the back of my throat does if I deliberately relax it as much as possible while awake. The total collapse of mine definitely happens as the exhalation dwindles down and is already in place well before I try to inhale. Of course, not being asleep when I try to deliberately let the blockage happen...not make it happen..let it happen, I don't know if it could also happen suddenly (when going into REM, for example) at some point during an inhale too. I'd suspect it could.

But by and large, I think what you're saying is on target...that the collapse of an obstructive apnea does "predominately occur towards late-to-end EXPIRATION and not during INSPIRATION.

Which is exactly why, imho, C-flex (and A-flex) were designed to let the regular pressure come back in BEFORE exhalation was finished. So that the necessary splinting pressure would already be in place by the time the exhale was dwindling and WELL BEFORE the person started to inhale again.

With bipaps, of course, if the EPAP (the exhale pressure..."expiratory positive air pressure) is set high enough to prevent apneas (which is all that EPAP needs to do) the apneas are... well prevented during and after exhaling.

I think you nailed WHEN the obstructive apnea is most likely to occur, Split.

*clink*

-SWS wrote:Velbor's also trying to understand why his dental device seems to work better for him than CPAP. I took some purely speculative attempts at answering that question.

-SWS, those were some of your best and easiest to understand explanations ever:

"The Soft Palate Sagger"

"The Tongue Slider"

You need to trademark (I wanted SO BADLY to say "patent 'em" LOL!) those two phrases, along with your explanations of them.

I agree with RG,

that data provided by split-city - who is a cpap researcher, is very very informative.

DSM

Glad to have you in the party - split-city! And thanks for the info about living systems.

O.

Hi,

Can I join the party?
All indulges in xpap, uars......anyone knows how to reduce the fats of pharlyngel?

Mckooi