How to improve Snore Index?

General Discussion on any topic relating to CPAP and/or Sleep Apnea.
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Ric
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Post by Ric » Mon Feb 20, 2006 9:08 am

I guess I could have done the calculation, it looks like about 0.2 x 625 hours would make about 125 "Non Responsive" OA/H events. (sorry, i used the term "uncompensated", but I see you got the meaning). On the EncorePro "Summary of Daily Details, next to the last page, it gives the totals, but only for a limited time interval. On that line I have only seen zeros, ever.

I am not quibbling about your success, it's obvious that you get up early, (4:57 AM, WHOA!), pound your chest, and do a Tarzan yell, unashamedly. I could hear it all the way here in Southern Calif. Awesome!

I think you might be optimistic attributing the NRs to using the Australian heated hose as a lasso, and the bed for a trampoline, as you suggest. I think I worry more about those NRs or potential NRs just above some threshold, especially if they are the obstructive kind, those would probably be the worst. Maybe the added pressure of CPAP makes them shorter in duration, and therefore not that big a problem. Or maybe none of those are "obstructive". Without a few more wires here and there, and maybe an infrared camera, we may never know. I'm not sure how higher pressures would extinguish a central apnea. It doesn't seem like "air splinting" would be operative in that situation.

I'm glad yours works for you and that you have reversed the aging process. I say BRAVO!

He who dies with the most masks wins.

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Ric
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Post by Ric » Mon Feb 20, 2006 11:35 am

GLC wrote:Could someone explain how "Centrals" are associated with increased pressure? I understand that Centrals Apneas are caused by the brain not giving instructions to breath, I believe. However I do not understand this relationship to increased pressure. Does the increase pressure at some point cause the brain to think it does not need to give instructions to breath? If so, how do you interpet this on the graphical analysis? Therefore, not increasing your upper range to eliminate snores, or what ever. Thanks
The simple answer is that CO2 is a stimulus for breathing. If you breathe too rapidly, or breathe too much air volume in a short period of time you will "dump" too much CO2 and the sensors in the brain that measure CO2 will say "OK, enough breathing for now, try again later". The result is you stop breathing, which is by definition an apnea event. That has a built-in assumption that increased pressure equates to increased tidal volume, which is not actually obvious and may not always be correct.

It can be shown experimentally that by increasing the amount of ambient CO2, even in the presence of normal amount of oxygen, the urge to breathe is overwhelming and results in a panicky feeling of being suffocated. (DON'T TRY THAT AT HOME!). That is akin to what happens when the CPAP is not putting out air but one continues to breathe into a long tube, or when the exhaust vent on the mask fails. Same feeling of suffocating, which in that case would be actually true.

The CO2 sensors in the brain can fail for other reasons than hyperventilating, including trauma, brain damage, old age, infections, toxins and a long list of other (fortunately uncommon) things. And poor breathing ensues.

CO2 is mildly acidic, so when one hyperventilates, it can increase the pH in the body (respiratory alkalosis), and other symptoms may become apparent. (dizziness, etc.) That's an experiment too many people have done unwittingly. DON'T TRY THAT WHILE DRIVING! OR DIVING!. (We used to do that in my diving class, on purpose, while sitting in a classroom to show what can happen if you hyperventilate. If one should faint at 200' below it could have serious consequences!)

It has been argued on this forum and elsewhere that central apneas are not that big of a problem, since they represent over-breathing, and the apneas are just a way of "catching up" so to speak. The counter-argument to that is that when you stop breathing, the heart is the first in line to feel the effects of desaturation. Blood from the lungs goes directly to the LEFT heart, and that is where the coronary arteries derive their blood supply. For healthy people it is probably not a huge problem. For someone who is borderline or who has other heart problems, central apneas should be taken seriously.

He who dies with the most masks wins.

GLC
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Post by GLC » Mon Feb 20, 2006 12:02 pm

Ric,
Thank you very much for such a detailed and informative explanation. I would assume from your explanation that a central apnea would then display itself graphical the same as an obstructive apnea. If you take that one step further if pressures were being increased, an apneas events started increasing over where they were at with lower pressure, that most likely, not positively, that these apneas are central and not obstructive. It is like reaching a point of diminishing return for increase in pressure, your sweet spot, is right before these occur and obstructives are at their lowest. Maybe, not sure, but sounds feasible. Thanks, again Ric, so much. Just a new guy trying to educate himself.

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NightHawkeye
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Post by NightHawkeye » Mon Feb 20, 2006 1:12 pm

GLC wrote:Just a new guy trying to educate himself.
GLC, you might be interested to know then that one of the techniques now being used to combat centrals is to increase the percentage of CO2 one breathes. Two techniques are used - one increases the rebreathing percentage, and the other simply adds CO2 from a canister.

Interesting stuff, really. If interested, you can do a search in Google for Complex Sleep Disordered Breathing (CSDB) and you'll find a number of articles about it. Also there's an ongoing thread about it on apneasupport.org.

Regards,
Bill

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rested gal
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Post by rested gal » Mon Feb 20, 2006 7:02 pm

This might be the thread you're thinking of, NightHawkeye. A 14 page topic on the TAS message board:

November 06 2005 subject: Sleep Disordered Breathing - a New Category. Excellent artic