Medical Rationale for CPAP over APAP?

Vicki wrote:True Liam, my APAP is an older model ResMed Autoset T. But the sleep labs I've spoken with recently still aren't satisfied with APAPs. Just a little clarification, the reflex to breath is actually not a decrease in O2 sat., but a rise in CO2. A moot point since none of the autoPAPs measure either, but other responses like vibration, etc. Therefore, an apneic event has to be started for an APAP to recognize the need for increased pressure.

Vicki

I haven't had a chance to read this whole thread yet, but wanted to join in the fun. Vicki, just a little clarification. The reflex to breathe is determined by both blood gases mentioned. When O2 factors in as liam correctly stated, the "hypoxic ventilatory drive" is at play. When CO2 comes in to play the "hypercapnic ventilatory drive" is triggered. Some patients' respiratory drives are thought to be primarily hypoxic while others are thought to be primarily hypercapnic.

"AutoPAPs requiring an apnea to prevent yet another apnea" is actually a myth. AutoPAPs can and will trigger on residual apneas to prevent subsequent obstructive events. However, snore in and of itself and even slight non-apneic flow limitation are used as precursor indicators toward determining proactive AutoPAP pressure response strategies. In addition, AutoPAPs tend to perform airway collapsibility tests using correlations between slight pressure deltas and patient air flow. All of these latter methods are proactive and none entail an apnea. Without them so many patients wouldn't be able to achieve their nighly AHI indices of under 1 or 2. The bottom line is if these proactive airway gauging techniques result in neither cortical arousal nor appreciable SpO2 drop, then there is no inherent physiological risk or problem. Any given AutoPAP algorithm will fall short for some patients---but so will fixed CPAP pressure leave more than just a few patients with unsatisfactory treatment (many of which are now happy AutoPAP patients on these message boards)!

Guest, Resmed has published the A10 algorithm as specifically holding a pressure response "command on apnea" at 10 cm or less to avoid what they term "runaway central apneas" (which specifically refer to pressure-induced occurences). The other AutoPAP manufacturer's also take great care (expressed in great detail in their patent descriptions) to avoid the pressure-induction of cental apneas as well. However, none of these manufacturers give us patient-based probabilities or statistics relative to the pressure induction of central apneas. Yet, if the rate was not significant across the SDB patient population, why would all of the manufacturers devote so much development cost and effort toward avoidance of pressure-induced central apneas?

That's the -SWS we know and love! ...and you didn't have to use the word "thingy" once!

Vicki wrote:Just a little clarification, the reflex to breath is actually not a decrease in O2 sat., but a rise in CO2.

Yeah, that's true, and why it's very dangerous to work around high concentrations of Nitrogen or Helium or other inert gasses: You can literally suffocate to death and never notice any change in respiration.

But I still think my point was valid: If the Auto can notice and fix the problem (not prevent it, but still...) fast enough that the O2 sat never drops significantly, and before the event can cause an arousal, then where is the harm? And meanwhile, the therapy is more comfortable on nights where you don't really need it to be as high, thus allowing better levels of compliance. (And I think we can all agree, being compliant with a 90% treatment is better than not using a 100% treatment. It may not be the "better" treatment, but if you'll use one and not the other...)

Just my thoughts this morning.

Liam, who should know better than to think before he's had his morning coffee.

wading thru the muck! wrote:That's the -SWS we know and love! ...and you didn't have to use the word "thingy" once!

Hell yeah. I didn't realize there was a new page yet. -SWS said essentially what I wanted to say, but he said it so VERY much better.

Way to go!

Liam, who really needs to read ALL of a threads responses BEFORE writing his.

Guest, Resmed has published the A10 algorithm as specifically holding a pressure response "command on apnea" at 10 cm or less to avoid what they term "runaway central apneas" (which specifically refer to pressure-induced occurences). The other AutoPAP manufacturer's also take great care (expressed in great detail in their patent descriptions) to avoid the pressure-induction of cental apneas as well. However, none of these manufacturers give us patient-based probabilities or statistics relative to the pressure induction of central apneas. Yet, if the rate was not significant across the SDB patient population, why would all of the manufacturers devote so much development cost and effort toward avoidance of pressure-induced central apneas?[/quote]

I am thinking that if resmed and the other companies are concerned with Pressure induced apneas over 10 cm of pressure they are just being overly careful because there is a slight possibility there machine could be used on a child or very small person. (Get it pass the FDA or Sued). I have been in the 20's on patients with Bad OSA on pure CPAP before I switched them to BIPAP and did not cause true Pressure induced Apnea. The leaks alone at that pressure LOL keep the patient from it. Oh well I guess will agree to disagree that Pressure induce Apnea is Rare and not to worry about it on an Auto Pap. I never said that an Auto is programmed to induce pressure Central Apnea. I was saying that there is nothing to worry about even if it screwed up it takes allot of pressure to cause one. Not that you still will not get Centrals for other reasons all night long. Now if you have been doing titrations SWS how many pressures induced Centrals have you caused? If you have caused allot below 10 CmH2o do you live in the land of little people?

Ok cya all later keep up the good work of the misinformed leading the misinformed. Nah we don't need no Stinking Professionals in here LOL .

No we need more arrogant condescending professionals...

Hey, I'm an arrogant, condescending professional. It's just that I'm a professional computer programmer, which is not strictly relevant to the topic at hand.

But I'm definitely arrogant and condescending.

Liam. Better than you.

Guest,

I would think that in a population of patients requiring high pressures near 20 cmH2O to maintain open airways, runaway centrals caused by pressure would not be common. But what about people (like me) with relatively low titrated pressures (mine was 7 cmH2O)? My guess is that you have no experience in whether or not high pressures in this population group will cause apneas, because you probably stop before such a pressure is reached. Could that be why you think they're so rare?

I can tell you from my own experience with the 420E, that runaway pressures did induce central apneas until I set the max pressure limit to below 10 and turned off the IFL1 setting.

In fact, I calculated and plotted my central apnea index over a range of 5 to 14 cmH20, and the increase in centrals was exponential with pressure (with an R-squared > 0.9!) As an engineer, I can tell you that without a doubt, this is a statistically significant statistic.

Now I'm not saying that this will happen to everyone, but like SWS said, it must be relatively common. I'd even be willing to bet that the lower one's titrated pressure is, the more common it is.

If one's titrated pressure is say 18 or 20 cmH20, then you are probably correct in saying that APAP poses little risk to inducing central apneas, but I would be willing to bet that for those of us who have low to moderate titrated pressures, you're way off base.


-John

Guest (and maybe even Vicki), I have to apologize. I did not mean my own statements in any way to make you feel chased. Specifically with my central apnea statement, I ended with a question as if to imply "Let's interleave these two contrasting clues or pieces of information and see if we can make them fit together so that they both stand up to reason." Once again I think I failed to properly convey the spirit of my own words.

My own background is as a patient who also happens to be a technology consultant---not as a health care professional. If you feel barraged with questions don't feel alone, my friend! I was besieged with questions and analytical argument when I first came to this board as well. As it turns out there are people from all walks of life and professions on this board----including more advanced degrees than you might ever guess. Those are the kinds of patients who will ask plenty of hard hitting and hard driving questions. We do appreciate professionals with relevant anecdotes and especially data. Please accept my apology if you felt "dogged" by my questions. I honestly didn't intend that.

On the topic of how rare/common pressure-induced central apneas happen to be, I still consider the topic to be open for lack of data (I hope I didn't state that in a bad way). Here's my thought relative to the great deal of development cost and effort that AutoPAP manufacturers invest toward the avoidance of pressure-induced central apneas: in light of all the AutoPAP manufacturers' heavy R&D costs toward avoidance of pressure-induced central apneas, the occurence of pressure-induced central apneas across the SDB patient population must therefore be significant, indeed. However, let's not confuse the concept of statistically "significant" with the concept of "common". The example of significant I have in mind is when those AC or DC power adapters that plug into the wall get recalled. In the recall notice we will read that maybe five or ten house fires were caused because of manufacturer defects. Yet there were tens of thousands of those potentially defective power adapters placed in the homes of consumers. The occurence of fire outbreak in this example is clearly "significant", yet not "common" by any stretch of the imagination.

We are not at all the misinformed leading the misinformed here, Guest. We are, for the most part, simply trying to get at the facts because as it turns out those facts are extremely relevant to us. If you can still help us out with data, I for one would be very appreciative. In lieu of data, I for one have not dismissed your anecdotes. Rather I have tucked them away in my hip pocket to help me piece this big mystery together. Thank you for helping us guest, and please don't leave. Most of all please don't feel as if we intended any ill will with our line of questions.

JRM made a very good point, imho:

But what about people (like me) with relatively low titrated pressures (mine was 7 cmH2O)? My guess is that you have no experience in whether or not high pressures in this population group will cause apneas, because you probably stop before such a pressure is reached. Could that be why you think they're so rare?

I can tell you from my own experience with the 420E, that runaway pressures did induce central apneas until I set the max pressure limit to below 10 and turned off the IFL1 setting.

Just to add another anecdote to the mix, I had much the same experience as JRM.

I've used three different brands of autopaps with all of them treating me well at pressures of 12 and below, rarely ever hitting 13 briefly. The "90%" pressure that for months has handled me fine is usually 9, 10 or 11. I've had virtually no centrals show up on the software data - except:

During the month or two of first using the 420E before I turned off IFL1, the machine was bumping the ceiling of whatever high pressure I set. I kept resetting the high pressure up and up, thinking, "Well, I must actually need more pressure." Finally had the range set for 7-19 and was hitting 19 even!

During this month or so of experimentation, centrals were showing up consistently for me beginning at 15 cm H2O. As I increased the pressure every few days, the occurrence of centrals increased on the data reports.

Maybe they were pressure induced centrals, maybe not.

I spent enough nights on each upper pressure I selected to have given my body time enough (I believe) to adjust to the pressure. If the centrals at any given high pressure I was using were going to be transitory and subside as my body got used to that pressure, I think I gave each pressure change enough nights for that to happen. The centrals persisted for me at any pressures 15 and above. And became more numerous, the higher I set it.

I don't doubt there are people using 20 cm H20 and above with no centrals. Or that there are some who experience centrals at much lower pressures.

SWS makes a wonderfully clear distinction between an occurrence being "significant" vs "common".

I've always considered myself "significant". I try not to be "common" - although IFL1 was making me wonder.

A very well informed non-medical poster on the message boards helped me make the 420E behave perfectly, btw.

Ok Sorry about that comment it was uncalled for my aplogies.
Let’s get back to the business at hand. I talked with 2 other Clinicians today. Both agreed that the only time they have witnessed Centrals caused by pressure below 20 CMH20 is when some one was compromised with another problem besides OSA. Both agreed a true definition of a Pressure induce central is Rare.

So after reading the last post about where you’re coming up with all this central apnea DATA it sounds like it’s not off of Sleep lab titrations but off the down loads your getting from your APAP. Well it seems that your right as well as am I. One of the reasons you may see more centrals on mid to higher pressure with your APAP is there is the possibility that your not comfortable on the higher pressure and you do some Breath Holding. That’s much different then your brain shutting down breathing because your lungs are over extended. I know it sounds like the same thing but its not. I can see were you could call that a pressure induces Apnea. If that’s what you’re talking about then yes that’s possible on lower pressures. The reason I did not think of it that way is it's handled differently in The Lab. When I was talking to one of the other clinicians they mentioned it might be Breath Holding you’re talking about.

In a real Sleep study we would just watch you do a few centrals lower the pressure down and then if you stilled need more pressure put the pressure back up slowly. We could tell your doing breath holds rather then true centrals because you would take a few regular breaths in-between the centrals. When you raise a pressure to fast sometimes you get Breath holds. It’s a comfort thing the back pressure bothers you so you hold your breath. If I left you on that long enough you may stop doing it.
So in conclusion if the APAP wanted to give you more pressure for an apnea but when it did you had a breath hold (Central Apnea) but instead of waiting you out reduced your pressure are you not still have that apnea it was trying to fix but was stopped? If there was no OSA to fix why was it rtying to raise in the first place? Again is is very unlikely for a pressure that fixes your OSA to be the pressure that overloads your lungs.

There are reasons why most of the SLEEP doctors I know of do not like the APAP for long term use. I am going to start asking them why.

Well, perhaps, but I think you're getting into semantics AND missing the point...

Whether it's a "true" central apnea or merely a "breath hold", if I am wakened fully from trying to fall asleep, panting because I haven't been breathing, and I know that my throat wasn't closed, I just WASN'T breathing, then it really doesn't matter if the pressure induced a "central" or induced a "breath hold". Either way, it made me stop breathing (dangerous), woke me up (detrimental), and made the therapy not work properly.

And the point you're missing is still one of comfort. Again, a 75% treatment is better than a 100% treatment, if the 100% treatment is so uncomfortable or difficult that one doesn't follow it.

I know this point very well. I'd gladly take a 75% solution to my apnea problem, if it would WORK for me. The close-to-100% solution (positive pressure) does NOT work for me, because something about it (the mask on my face perhaps, or the sound of the machine, or the pressure) prevents me from ever getting to sleep at all.

Do I know that an APAP would solve all of those problems? No, and the reason I don't know is I was never given the chance to find out, because my idiot sleep doctor would rather have me quit entirely than prescribe me an APAP or give me my prescription so I can buy one on my own.

(For the record, I suspect an APAP would not solve these problems, because my trouble is not pressure-induced discomfort, so I doubt the pressure reduction an APAP might allow would solve it... But I think it's worth trying to find out, and it borders on criminal that my sleep doctor thinks that it's worth holding to his principles against APAP (because it's "not as good") even in the face of my quitting the CPAP entirely because I can't sleep at all.)

It's about comfort and compliance. If you can't be comfortable enough to be compliant, then the treatment is 0% effective, and can not be called "better" than a 75% effective treatment that's used with 100% compliance.

Liam, still pissed at the idiocy of Dr. Park.

Hello Guest
I'm glad you're back, we want and appreciate your info.
I don't think the disinction between "central apnea" and breath holding is "merely semantic" - many of us want to know and understand exactly the ins and outs of our problem, and treatment - few of us have met professionals who take the time to explain with the thoroughness we want.
As patients - or clients - we here are concerned with our health and comfort.

For some of us, the necessary treatment is very uncomfortable and unlike other therapies, this discomfort itself goes against the treatment's aim. Some therapies are temporary, and very uncomfortable - surgery, chemotherapy, etc. But any therapy can't be therapy if it works against itself: If it raises sugar, it can't be for diabetes, if it causes pain it can't be a painkiller, if it disturbs sleep, it can't be therapy used for a person whose sleep is interrupted, and if it causes breath holding it clearly can't be for a person whose breathing interruptions are disturbing his sleep.

Liam, your doctor sounds like a fool. If he knows he's right, he should let you try what you want, because reality will prove him right. He sounds like he doesn't trust reality, nor does he trust yot to be able to care for yourself and has made this into a power struggle. No need to waste your time struggling with him - find another doctor, who will treat you as an intelligent human being, his ally in finding the right treatment for you. A doctor whom you too can treat as an intelligent human being and ally...
O.

I have seen pressure induced central apnea in the sleep lab. That is why you must go very slow, no matter if the person stops breathing or not. 15 minutes at each pressure may settle out this if they are pressure sensitive.

I have seen breath holding that looks like central apnea. The chest belt and the diaphram belt stop making the nice curve and flatten, as breathing stops. Everyone does that from time to time. I do it when I roll over in bed.

Liam, you may verywell may be having hypopnea when you wake up gasping. Hypercapnia can make your body react to low oxygen levels and high CO2 levels. So what you think is a central or an obstructive apnea that forces you to wake even with cpap, could be something completely different.

I wish that I could take every one of you into a sleep lab and let you watch a sleep test. It would be benefitial for all the people who are majorly proactive in their therapy.

Ted

Titrator wrote:I wish that I could take every one of you into a sleep lab and let you watch a sleep test. It would be benefitial for all the people who are majorly proactive in their therapy.

Perhaps this would be good thing for the ASAA to suggest to their sleep lab sponsored AWAKE affiliates. Dave Hargett.... are you there?