Resmed vs. Respironics - Help

ozij · Post by **ozij** » Mon Apr 14, 2008 12:08 pm

Maximum pressure for command on apnea:
Maximum pressure beyond which no pressure increase will be applied following the detection of an apnea in breathing

From PB's manual.

Till this thread, I thought "Maximum pressure for command on apnea" meant how hard you push against an apnea. On reading the thread, and re-reading the manual, this definitely has another meaning... probably did all along .

O.

rested gal · Post by **rested gal** » Mon Apr 14, 2008 4:09 pm

Got a hypothetical question...

IF -- in a sleep lab setting with a full PSG titration going -- a person had an obstructive apnea involving tongue, soft palate, and back of throat all collapsing on each other, but there was still a thread of air being breathed in and out, and IF the sleep tech did immediately raise the pressure a cm or two, would that additional pressure be more likely to:

1. open the airway a bit more?

2. close the airway more firmly?

3. do something else?

4. do nothing?

Then...same 4 questions if the obstructive apnea were a full occlusion -- no air, not even a thread, being breathed.

It's just a hypothetical question. Has nothing to do with how sleep techs actually go about a titration or how our treatment machines are designed to behave when presented with an obstructive apnea.

I realize the sleep tech doesn't sit there pouncing on each apnea as it happens, with more pressure. Nor do our autopaps jump in with more pressure when there's an apnea.

Just curious about what more pressure, if actually applied, might be expected to do against an almost full obstructive apnea, and against a full obstructive apnea.

Perhaps SAG could tell us if most obstructive apneas seen on PSGs show no airflow at all from the sleeper? Or do most of them fall into the "slight amount but not anywhere enough" airflow category?

Wulfman · Post by **Wulfman** » Mon Apr 14, 2008 4:18 pm

My guess would be that if it didn't open the airway at some point, the subject would have a choking reaction like most of us did pre-therapy and clear their own airway.

Den

rested gal · Post by **rested gal** » Mon Apr 14, 2008 4:33 pm

Wulfman wrote:My guess would be that if it didn't open the airway at some point, the subject would have a choking reaction like most of us did pre-therapy and clear their own airway.

Den

True, but I'm not asking about what happens if an apnea continues. I'm just curious about what would be most likely to happen IF more pressure were applied as soon as an obstructive apnea was seen on a PSG.

Not that more pressure should be applied if a single obstructive apnea were seen. Just...what would probably happen IF....

Would there be likely to be a little more improvement in air flow? Or would more pressure be likely to make the collapse even worse?

NightHawkeye · Post by **NightHawkeye** » Mon Apr 14, 2008 8:59 pm

Excellent questions, RG!

A recent modeling effort offers some insight toward answering your first question: http://www.angle.org/anglonline/?reques ... &page=0791
Customized Three-dimensional Computational Fluid Dynamics Simulation of the Upper Airway of Obstructive Sleep Apnea

The language is typical researcher-ese, but I'll quote it anyway:
"High airflow velocity predominated in medial and ventral nasal airway regions. Maximum air velocity predominated in medial and ventral nasal airway regions. Maximum air velocity (15.41 m/s) and lowest pressure (negative 110.8 Pa) were observed at the narrowest portions of the velopharynx.
...
Pressure becomes an important factor in mediating airway obstruction because reduced pressure in the presence of rapid airflow leads to adduction of the surrounding tissue."

According to these researchers the answer to your first question is that without additional pressure, the partially occluded airway collapses in on itself when the opening is narrowed (at least that's my interpretation of "adduction of the surrounding tissue".)

The APAP algorithms, of course, attempt to raise pressure quickly enough to keep the airway from collapsing. It's worth repeating that these researchers explicitly indicate the collapse is compounded as the airway becomes narrowed. Considering that these guys used 3-D modeling based on human physiology, I'd give their results more credence than the Starling resistor model discussed earlier (which didn't offer an answer to your question).

There would seem to be a logical extension to your second question as well, RG, but I know we don't all view things the same way.

Regards,
Bill

dsm · Post by **dsm** » Mon Apr 14, 2008 9:55 pm

RG / NHE,

A few thoughts (thinking aloud)...

If the airway collapse is where excess soft tissue in particular shaped throats narrows then because of the excess loose tissue occludes without the tongue falling back to create the occlusion then I can see that pressure from an external source could 'pry' the occlusion open.

If the occlusion is because the rear of the tongue has slipped back just as a breath inwards was starting to accelerate, I imagine the tongue could cause an occlusion that additional external pressure only reinforces. I think this has happened to me when sleeping on my back. I guess an ENT really is the person who could probably best add thoughts as to what types of occlusions can occur & what might be able to clear them.

An xPAP machine can't really guess at what the cause of an OSA occlusion is because there are so many different physiologys among us OSA folk.

DSM

rested gal · Post by **rested gal** » Mon Apr 14, 2008 10:21 pm

NightHawkeye wrote:"Pressure becomes an important factor in mediating airway obstruction because reduced pressure in the presence of rapid airflow leads to adduction of the surrounding tissue."

Ok, I understand that.

NightHawkeye wrote:According to these researchers the answer to your first question is that without additional pressure, the partially occluded airway collapses in on itself when the opening is narrowed (at least that's my interpretation of "adduction of the surrounding tissue".)

I agree. That would be my interpretation of that, too.

NightHawkeye wrote:these researchers explicitly indicate the collapse is compounded as the airway becomes narrowed.

Yes. I understand that.

That was an interesting simulation to read about. Thank you for the link.

NightHawkeye wrote:According to these researchers the answer to your first question is that without additional pressure, the partially occluded airway collapses in on itself when the opening is narrowed

So, if I understand you, the answer you're giving, NHE, is that more pressure applied by a hypothetical tech-with-a-triggerhappy-finger-on-the-button would likely open the obstructive apnea to at least some extent? If so, it looks like we're viewing the results of the researchers you quoted the same way.

rested gal · Post by **rested gal** » Mon Apr 14, 2008 10:30 pm

dsm wrote:If the occlusion is because the rear of the tongue has slipped back just as a breath inwards was starting to accelerate, I imagine the tongue could cause an occlusion that additional external pressure only reinforces.

Well, I think the additional (if by "additional" you mean increasing the cpap pressure -- the hypothetical finger on the button, remember) external pressure could push the soft tissues of the back and sides of the throat aside, and probably push the soft tissure of a relaxed tongue aside also. After all, it's that relaxation that could make the tongue "relax back" too far in the first place.

I don't mean the increase in incoming air would flop the tongue into the mouth into proper position. I just mean press vertically against it to push the back of the tongue toward the front of the throat.

I think a lot of soft tissue would "give"...get pushed aside...by an increase in the incoming cpap air rather than the back of a tongue (which is anchored) be pushed farther down. All dependent on IF the pressure were raised, of course.

I guess I think soft tissue would get moved aside before something as big as a tongue would be pushed farther down. IF pressure were raised.

-SWS · Post by **-SWS** » Mon Apr 14, 2008 11:12 pm

One thing that I liked about the single-patient model Bill just cited, is that it shows that high nasal impedance can contribute to an ordinary apnea occurring down at the pharynx.

More on the same topic from yet an additional source (bold emphasis mine):

J Am Board Fam Pract 15(2):128-141, 2002. © 2002 American Board of Family Practice wrote:Another cause of OSA is nasal obstruction. The nose, best viewed as a variable resistor, contributes to nearly 40% of total airway resistance.[23] This resistance is greatly influenced by the vasomotor reaction of the nose to several factors, such as hormonal effects, metabolic changes, and numerous pharmacologic agents.[23] Olsen et al[24] measured the respiratory effort in a patient during sleep and suggested that the oral airway resistance was greater than the nasal airway resistance. With the nasal pathway being the preferred route for nocturnal breathing, an increase in nasal resistance will invariably increase the possibility of collapse of the nonrigid portion of the upper airway, namely, the pharynx.

StillAnotherGuest · Post by **StillAnotherGuest** » Mon Apr 14, 2008 11:18 pm

ozij wrote:The FDA document.

Received: May 9,2003

Right. But SAG said:

StillAnotherGuest wrote:Further, given the timeline of the patent (1996-1998), the algorithm under consideration is undoubtedly the one in the 418P, and that machine was a slug when it came to returning to baseline.

relating to

ozij wrote:If you read US Patent no. 5803066, (also no. 5,546,933) given to Rapoport et. al. and later sold to PB, you will see that the PB auto algorithm assumes the existence of a prescribed pressure, a "preferred" pressure which is neither the min. nor the max. of the range. I'm adding emphasis to the quote, from pat. 5803066:

38. A breathing device for optimizing the positive airway pressure to a patient, comprising:

a source of breathing gas at controlled positive pressure to the airway of a patient;

a flow sensor configured to generate first data values representative of an inspiratory flow of breathing gas to the patient;

computer memory configured to store the first data values generated by said flow sensor;

a microprocessor including means for calculating the area of the inspiratory waveform from said first data values and calculating the area of a pure sine wave to generate a ratio of said areas and configured to generate a first signal when said ratio indicates a flow limitation in the patient; and

a pressure controller responsive to the first signal from said microprocessor and coupled to said source of breathing gas for increasing the positive pressure to the airway of the patient.

39. The breathing device of claim 38 wherein said micropressor is further configured to cause said pressure controller to increase the positive airway pressure to the patient at a greater rate when said positive airway pressure is less than a preselected prescribed pressure that (sic) when said positive airway pressure is greater than said preselected pressure.
40. The breathing device of claim 38, wherein said microprocessor is further configured to cause said pressure controller to decrease the positive pressure to the airway of the patient when said ratio does not indicate a flow limitation in the patient.

41. The breathing device of claim 40, wherein said microprocessor is further configured to cause said pressure controller to decrease positive airway pressure to the patient at a greater rate when said positive airway pressure is greater than a preselected prescribed pressure than when said positive airway pressure is less than said preselected pressure.

Those differing response rates would seem to relate only to 418P, maybe 418A. Rather than an asset, the early version of the algorithm gave the machine a slow return to baseline following an attack on events. In more recent Rapoport patents like US20050016536, reference to the differing increase/decrease rates is now gone, and coinincidently, the return to baseline in 420E is quicker.

But, again, who knows if any version of machine and patent really match up perfectly.

SAG

-SWS · Post by **-SWS** » Mon Apr 14, 2008 11:20 pm

Speculation from that same source about neuromuscular dyscontrol possibly contributing to airway collapse:

J Am Board Fam Pract 15(2):128-141, 2002. © 2002 American Board of Family Practice wrote:The primary force holding the airway open is the activity of the dilator muscles that give tone and tension to the pharyngeal muscles. One suggested mechanism that might be important in producing upper airway obstruction is a difference in timing between the hypoxic-hypercapnic drive to inspiration and activation of the dilator muscles.[21] If inspiration is initiated before there is any activation of the dilator muscles, the upper airway is at risk of closure by this suction effect.[22]

That theory gets into suction dynamics, very similar to the ones Bill and Doug were hypothesizing about.

ozij · Post by **ozij** » Mon Apr 14, 2008 11:47 pm

20050016536 is a patent application from Jan. 2005.

O.

rested gal · Post by **rested gal** » Tue Apr 15, 2008 12:12 am

-SWS wrote:Speculation from that same source about neuromuscular dyscontrol possibly contributing to airway collapse:

---snipped---

That theory gets into suction dynamics, very similar to the ones Bill and Doug were hypothesizing about.

Another good link with interesting material. Thank you, -SWS.

Again, this is talking about how an obstructive apnea can get started.

Which is actually more interesting to think about (I really mean that) than my question about what might happen if an obstructive apnea were already established...already happening... and MORE cpap pressure were applied right then and there to try to open the collapsed airway during the event.

dsm suggests that increasing the cpap pressure coming down from above might force the tongue into blocking the airway even more tightly... in large part due to suction force from below, while the sleeper tries unsuccessfully to breathe in.

My hypothetical question was (and still is)... is increasing the pressure from a cpap by one or two cms while the back of a relaxed tongue is obstructing the airway be more likely to shove the tongue into blocking the airway a bit more tightly? Or would increasing the cpap pressure by one or two cms be more likely to push the tissues of throat, tongue, and soft palate into a position that opens the airway a bit more?

Perhaps there is no answer. Perhaps...it "depends." Certainly could depend on the amount of pressure increase that was used. Maybe one or two cms more wouldn't do it. And then depends on the size of airway, the softness or elasticity of the tissues, the sheer amount of tissue, the amount of suction holding the blockage in place, length/thickness of tongue, exactly where the tongue is attached, are there tonsils involved, huge epiglottis, how pliable is that particular soft palate, etc., etc. I can think of a lot of factors for "it depends."

-SWS · Post by **-SWS** » Tue Apr 15, 2008 12:13 am

ozij wrote:20050016536 is a patent application from Jan. 2005.

Meaning the design contained in any 2005 application is submitted too late to represent what's inside any machine having received a May 2003 FDA approval.

However, I suppose there's a fair chance the 2005 application contains modifications that eventually went into the 420e after 2003.

Clincher is when the quick return to baseline first started to show up in SAG's radar. If it showed up in 2003, and if it's still observable in newly sold 420e's, then we might presume the patent description text ozij is citing (containing text about a "preferred-prescription" influencing "rate-of-change") is functionally embedded in the firmware.

Snoredog · Post by **Snoredog** » Tue Apr 15, 2008 12:33 am

-SWS wrote:
ozij wrote:20050016536 is a patent application from Jan. 2005.
Meaning the design contained in any 2005 application is submitted too late to represent what's inside any machine having received a May 2003 FDA approval.

However, I suppose there's a fair chance the 2005 application contains modifications that eventually went into the 420e after 2003.

Clincher is when the quick return to baseline first started to show up in SAG's radar. If it showed up in 2003, and if it's still observable in newly sold 420e's, then we might presume the patent description text ozij is citing (containing text about a "preferred-prescription" influencing "rate-of-change") is functionally embedded in the firmware.

Resmed vs. Respironics - Help

Resolving apnea on the fly - not.

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