10 sec apneas on ResScan?

[rada]

My ResScan reading from last night shows multiple 10 second apneas. My understanding is that my machine is set to not record as apneic something less than 10 seconds, and thus I could see why there would be nothing less than 10. However, I don't understand why there would be a large number of 10s (about twenty-five 10s), about fourteen apneas at 19 or more seconds, but only about 4 apneas between 10 and 19 seconds. Does anyone have any insight as to why 10s would be common in such a graph? Thank you.

[packitin]

deleted

[rada]

About the duration of the apneic events, particularly the many 10 second ones, my doctor's response yesterday was that she cannot make adequate sense of my apnea and hyponea data because the respirator company keeps secret its algorithm and because the data analysis is based only on airflow from the respirator. I have, however, had an interesting experience last night. Last night I took a nap and put on a full-face mask. I slept well for one hour. When I checked the LCD on the respirator, I was surprised to see an apnea index of 35. I loaded the data onto my computer and saw that essentially all the 35 apneas were 10-second apneas. My nap was peaceful. Although I have no oxygen saturation data to coincide with my feeling, my guess is that those 10-second apneas in my case sometimes represent a long, restful pause at the end of expiration and before the next inspiration.

[jnk]

What are your latest sleep-study results? Does your doc say you are having obstructive events (that may respond to higher pressure) or central events (that may mean you might do better on an ASV machine)? What are your docs' exact words about what is in your present tagline: "neuropathy conflicts with OSA"?

[-SWS]

My ResScan reading from last night shows multiple 10 second apneas. My understanding is that my machine is set to not record as apneic something less than 10 seconds, and thus I could see why there would be nothing less than 10. However, I don't understand why there would be a large number of 10s (about twenty-five 10s), about fourteen apneas at 19 or more seconds, but only about 4 apneas between 10 and 19 seconds. Does anyone have any insight as to why 10s would be common in such a graph? Thank you.

Given all the 10s events, there's a distinct possibility that you are also experiencing a fair number of events @ <10s.

Last night I took a nap and put on a full-face mask. I slept well for one hour. When I checked the LCD on the respirator, I was surprised to see an apnea index of 35. I loaded the data onto my computer and saw that essentially all the 35 apneas were 10-second apneas. My nap was peaceful. Although I have no oxygen saturation data to coincide with my feeling, my guess is that those 10-second apneas in my case sometimes represent a long, restful pause at the end of expiration and before the next inspiration.

Well, post-expiration pauses are, indeed, very common. However, long 10s post-expiration pauses would not be common. Given the medical history on your profile page, my layperson's hunch is that uncommon airway dynamics should probably be in the realm of consideration.

I don't know much about the possible role that a damaged CN XI or accessory nerve might play with respect to perhaps spastic or reflexive type airway occlusions. But my hunch tells me that might be a possibility---especially if you did not present sleep-onset and other central apneas during a PSG sleep study.

[scrapper]

These could also be caused by too wide of a range for therapy........your machine cannot respond fast enough. You've probably got room for tweaking.

[-SWS]

These could also be caused by too wide of a range for therapy........your machine cannot respond fast enough. You've probably got room for tweaking.

I think that's a good comment---especially when looking at prolific 10s events while suspecting plenty below 10s as well.

Constant pressure high enough to stent fast obstruction might be the way to go here. Alternately, if that 35 AI during the hour nap were sleep-onset central apneas instead of obstructive, then again, fixed pressure just might work out better.

If airway closure is "fast and heavy" at the end of expiration, then be careful about not endeavoring too much EPR (expiratory pressure relief). Suboptimal pressure at the end of expiration would essentially allow fast-acting apneas to steadfastly set in before inspiration ever gets going. If those are all obstructions, they're probably mostly "fast and heavy", considering so few (inspiratory phase) hypopneas.

[-SWS]

...cannot make adequate sense of my apnea and hyponea data because the respirator company keeps secret its algorithm and because the data analysis is based only on airflow from the respirator.

There are three types of sleep-event signals your algorithm uses to trigger or commence a pressure increase: 1) snore signals, 2) flow-limitation signals (a.k.a. wave-flattening signals), and 3) apnea signals. In this case the algorithmic term "signal" can be thought of simply as "a detected occurrence".

If your pressure happens to already be at 10cm or above, then your algorithm will rely on those first two signal types when deciding whether to raise the pressure. If your pressure happens to be sitting below 10cm, then your algorithm will utilize all three signal types as a basis to raise pressure. In either case, the pressure increase is very, very gradual---and is really to prevent subsequent obstructive apnea type events.

So we can see two potential caveats for at least some unusual obstructive apnea cases: 1) if a patient does not present those first two types of apnea-hinting signals, then apneas can quickly occur before the algorithm has a chance to prevent them, and 2) if that same "snore remiss" and "flow-limitation remiss" patient just so happens to already be sitting above 10cm when apneas occur, then that algorithm will not raise the pressure in direct response to those detected apneas (that third decision-making signal type is not used above 10cm).

That last condition, in somewhat uncommon epidemiological occurrence with the first, essentially means that the algorithm ceases to function because it is not a good match for that particular kind of "unusual patient". In that case, fixed pressure CPAP is the next best thing to try IMHO. Again, that's all assuming that you DO NOT have a central apnea problem---in which case an ASV machine or BiLevel S/T (both having a backup rate) would be a better machine to try.

Good luck.

[rada]

Dear JNK,
In response to your question: "What are your docs' exact words about what is in your present tagline: "neuropathy conflicts with OSA"?"
As regards my tagline "neuropathy conflicts with OSA", what I meant to capture by that was the following. I was diagnosed with OSA in 2004 but have largely dealt with it by sleeping on my side, waking several times during the night and going to the bathroom, being sleepy throughout the day, and taking naps in the middle of the day. However, after I was diagnosed with progressive, irreversible radiation neuropathy in early 2009, my view changed. The conjectured pathophysiology of radiation neuropathy is that damage to the capillary endothelium gradually over the years increases blockage which leads to death of the tissue that the capillaries feed -- death by anoxia. While no treatment is known, my doctor has prescribed for me a treatment that Dr. Delanian reported using successfully recently on two patients with radiation neuropathy (successful in the sense of slowing progression of the disease). The treatment is 4 drugs of which one is 800 mg pentoxifylline per day which is meant to deform red blood cells to help them travel through constricted blood vessels. Another drug is 1000 mg Vitamin E per day. An adequate intake of Vit. E is 15 mg so that 1000 mg is 66 times over the normal recommended amount and may have adverse effects itself. The reason to give the Vitamin is partly this function of Vitamin E (from http://ods.od.nih.gov/factsheets/vitamine.asp): "Vitamin-E–replete endothelial cells lining the interior surface of blood vessels are better able to resist blood-cell components adhering to this surface. Vitamin E also increases the expression of two enzymes that suppress arachidonic acid metabolism, thereby increasing the release of prostacyclin from the endothelium, which, in turn, dilates blood vessels and inhibits platelet aggregation". Vit E thus might help oxygen get to the nerves. Vit E also has an antioxidant effect which involves protecting against free radicals and that also may help. If my nerves are dying due to lack of oxygen, and I am also suffering through anoxic events throughout the night secondary to OSA, then I am highly motivated to deal with my OSA which may be treatable. What I meant by "neuropathy conflicts with OSA" is that OSA would seem to make neuropathy worse. Additionally, the neuropathy may also make the OSA worse. My neuropathy is particularly present in my neck and could interfere with breathing (as SWS suggested).
Thank you, Roy

[rada]

This message replies to JNK, Scrapper, and SWS as follows:
1 Table of Contents
2 CPAP versus ASV for Central Apneas (from JNK)
3 Range of Therapy (from Scrapper and SWS)
4 Spastic Airway Occlusions (from SWS)

2 CPAP versus ASV for Central Apneas (from JNK)
JNK said:
What are your latest sleep-study results? Does your doc say you are having obstructive events (that may respond to higher pressure) or central events (that may mean you might do better on an ASV machine)?
I had one sleep study in 2004 and another in 2009. Both showed moderate obstructive sleep apnea. They did not show central apneas. Perhaps I also had a sleep study with CPAP in 2004 but I don't recall. When my sleep specialist raised the possibility of central apneas, she was speaking hypothetically about what might be happening as I attempt to interpret my ResMed data. I have been running my ResMed S8 Autoset II System largely in autoset mode with a minimum of 8.4 and a max of 12.8 pressure. I have also set EPR to 3. My sleep specialist had suggested switching to CPAP mode with pressure at constant 10. When I use the CPAP mode with pressure 10, my results are not better than with autoset.
You suggest that I consider an ASV machine. How different would an ASV be from my ResMed Autoset? Is that the ResMed has less flexibility in its response than the ASV?

3 Range of Therapy (from Scrapper and SWS)
Dear Scrapper, You said:
These could also be caused by too wide of a range for therapy........your machine cannot respond fast enough. You've probably got room for tweaking.
Are you referring to the settings on my autoset? I currently am using something in the 8s for low and 12s for high. Are you suggesting that I switch to something in the 9s and 11s. If I went to 10 at minimum and maximum, then I would return to CPAP. Or are you meaning something different by range of therapies?
Dear SWS, You said:
If airway closure is "fast and heavy" at the end of expiration, then be careful about not endeavoring too much EPR (expiratory pressure relief). Suboptimal pressure at the end of expiration would essentially allow fast-acting apneas to steadfastly set in before inspiration ever gets going.
Last night, in response to your suggestions, I returned to CPAP mode at a pressure of 10 and terminated EPR. I did not have a good sleep. Maybe tonight I will try a reduced EPR but not none. Maybe I'll also reduce the range of my autoset.
Your last note of 10:19 a.m. on Jan. 14 goes into further detail on the settings matter. In trying to understand your explanation of the operation of my machine, I have returned now to the manual entitled "ResMed S8 AutoSet II System Clinical Guide". On pages 9-12 of that manual attempt to explain what you have well explained but the manual gives more text which helps me. Those 4 pages which your text well summarizes, seem to give a rather complete description of the ResMed algorithm to me. I wonder why my sleep specialist tells me that the machine manufacturers keep their algorithm secret. I understand that with only the flow and pressure data that the ResMed has that the apneas or hypopneas might be incorrectly labelled, but the algorithm used seems clear enough. Anyhow, back to your point, I will try again tonight to modify my setting -- this time rather than switching abruptly from maximum EPR of 3 and CPAP of 8.4 to 12.6, I will switch to an EPR of 1 or 2 and reduce the autoset range.

4 Spastic Airway Occlusions (from SWS)
Dear SWS, Your suggestion about spastic airways is interesting. You said:
I don't know much about the possible role that a damaged CN XI or accessory nerve might play with respect to perhaps spastic or reflexive type airway occlusions. But my hunch tells me that might be a possibility---especially if you did not present sleep-onset and other central apneas during a PSG sleep study.
When the airway narrows, at some point it can stick together because the mucosal folds start sticking together. Maybe spasms bring a new kind of apnea that would be distinct from the typical OSA that is caused by excessive fat around the throat leading to an occlusion once the muscles relax during sleep. I will think on this further and what it might suggest about changing my treatment. If you have any further insights about this, then I'd be glad to know them.
Thank you again,
Roy

[-SWS]

I will try again tonight to modify my setting -- this time rather than switching abruptly from maximum EPR of 3 and CPAP of 8.4 to 12.6, I will switch to an EPR of 1 or 2 and reduce the autoset range.

Good luck!

I don't know much about the possible role that a damaged CN XI or accessory nerve might play with respect to perhaps spastic or reflexive type airway occlusions. But my hunch tells me that might be a possibility---especially if you did not present sleep-onset and other central apneas during a PSG sleep study.

When the airway narrows, at some point it can stick together because the mucosal folds start sticking together. Maybe spasms bring a new kind of apnea that would be distinct from the typical OSA that is caused by excessive fat around the throat leading to an occlusion once the muscles relax during sleep. I will think on this further and what it might suggest about changing my treatment. If you have any further insights about this, then I'd be glad to know them.

I see exactly what you're speculating---especially in light of your following apnea distribution:

a large number of 10s (about twenty-five 10s), about fourteen apneas at 19 or more seconds, but only about 4 apneas between 10 and 19 seconds.

So you're wondering if perhaps your 10s and any unrecorded shorter occlusions might be short-term surface-tension type "stick"----after what might be spastic upper airway muscle activity based on CN XI neuropathic damage. I'm thinking anti-snore spray is a surfactant that just might help in that situation... if that's REALLY what's happening with those 10s occurrences.

Then, there's always the banana smoothie approach: http://sleepeducation.blogspot.com/2009 ... -cure.html .

P.S. A "surfactant therapy" and "apnea" search on Google Scholar: http://scholar.google.com/scholar?hl=en ... =&as_vis=0

[rada]

Dear SWS,
I read the article now about banana smoothies that you suggested, and I found it interesting. I also followed the Google search page as you suggested and appreciated that too. Currently I sometimes put Biotene mouth gel in my mouth before sleep in order to provide some lubrication in my mouth. My radiation treatment has given me dry mouth (xerostomia). My radiation affects the particular distribution of mucins and other content of the saliva in ways that seem to me could account for some of the OSA. Having been concerned about this for several years and being an avid reader and writer, I wrote a literature review on this subject which was published in a journal in 2005 and then reappeared in a book in 2008 as follows:
1. Roy Rada (2005) "Obstructive sleep apnea and head and neck neoplasms" Otolaryngology - Head & Neck Surgery, Vol. 132, Issue 5, pp 794-799.
2. Roy Rada (2008) "Sleep and Quality of Life in Head and Neck Neoplasm" Sleep and Quality of Life in Clinical Medicine edited by J.C. Verster, S.R. Pandi-Perumal, and D.L. Streiner, Humana Press: Totowa, New Jersey, pp. 461-468.
(I could send anyone a pdf version, should anyone want). In 2004 my interpretation was that the xerostomia was the primary cause of my OSA. At the time, I had no evident muscle spasms or nerve death. Now with my marked spasms in my neck and shoulder, I can see that neuromuscular problems secondary to radiation may also contribute to my OSA.
Following your lead now, I've read further about the anti-snore spray. That reminds me that in 2004 I tried various lubricants. My sleep specialist had noted at the time that something simple like olive oil swished in the mouth before bed might help and I tried that. The biotene mouth gel seemed easier to handle. The problem to my mind in part with the banana smoothie is that I have periodontal problems secondary to radiation and need to be vigilant about dental hygiene. To leave my mouth coated all night long with a banana smoothie would seem to work against tooth and gum cleanliness and antibacterial activity. The irony of getting older and having these progressive, irreversible problems comes particularly when the treatment for one problem makes worse another problem.
Last night I did use the lower EPR and tightened the range on my autoset. My night was a so-so night -- woke a couple times over 6 hours and finally removed the mask and slept another 2 hours without it. The AHI was about 10 but most were 10 second and I feel slight progress is being made. I had trouble with my nasal pillows the first time I awoke so tonight I will keep the pressure settings (which are following your guidance about making the pressure setting more constant) as they were last night but switch the mask.
Thanks again,
Roy

[-SWS]

Currently I sometimes put Biotene mouth gel in my mouth before sleep in order to provide some lubrication in my mouth. My radiation treatment has given me dry mouth (xerostomia). My radiation affects the particular distribution of mucins and other content of the saliva in ways that seem to me could account for some of the OSA.

In light of that, I can understand your thoughts about your prolific 10s apneas in relation to mucosal folds:
http://scholar.google.com/scholar?hl=en ... =&as_vis=0

Having been concerned about this for several years and being an avid reader and writer, I wrote a literature review on this subject which was published in a journal in 2005 and then reappeared in a book in 2008 as follows:
1. Roy Rada (2005) "Obstructive sleep apnea and head and neck neoplasms" Otolaryngology - Head & Neck Surgery, Vol. 132, Issue 5, pp 794-799.
2. Roy Rada (2008) "Sleep and Quality of Life in Head and Neck Neoplasm" Sleep and Quality of Life in Clinical Medicine edited by J.C. Verster, S.R. Pandi-Perumal, and D.L. Streiner, Humana Press: Totowa, New Jersey, pp. 461-468.

I will look for those interesting papers. Thank you for listing them!

Last night I did use the lower EPR and tightened the range on my autoset. My night was a so-so night -- woke a couple times over 6 hours and finally removed the mask and slept another 2 hours without it. The AHI was about 10 but most were 10 second and I feel slight progress is being made. I had trouble with my nasal pillows the first time I awoke so tonight I will keep the pressure settings (which are following your guidance about making the pressure setting more constant) as they were last night but switch the mask.

I hope you can find a comfortable pressure that manages to treat your airway obstruction. I suppose if those 10s and shorter hypothetical "surface tension" type apneas caused neither hypoxic damage nor significant sleep deterioration, then it might not be worth stenting those with high and uncomfortable pressures. However, that would still leave the question of what treatment pressure might be required to treat the longer apneas. They might require more stenting pressure than the shorter apneas.

My hunch is that you have probably already investigated the feasibility of using a dental appliance. A few patients here have used them exclusively. And other patients have used dental appliances as adjunct treatment along with CPAP. A dental appliance can conceivably lower required CPAP pressure in some cases if not obviate CPAP.

I'm getting ready to head off to warmer climes for vacation, Dr. Rada, but should be back the first week of February. I wish you the very best of luck with your upcoming treatment experiments! Hope to see you when I get back.

[-SWS]

And a bump for additional thoughts from other posters....

[Muse-Inc]

For the periodontal concern, might consider adding Xylitol to your regime. It kills the pathogens that contribute to dental-gum as well as sinus issues. Maybe Xylitol added to the banana smoothie...would one cancel the effect of the other ? In sufficent quantity, it might have a laxative effect; although I am extremely sensitive to this effect with the other -itols (sugar alcohols), I find a several pieces of gum or the spray doesn't cause this...at least for me YRMV. Good luck and keep us posted!

Did I miss your posting what sort of insulation from Home Depot you're using?