Mouth Breathing problem

As many of you know I have had a terrible time with breathing over the past two years. In January I had septoplasty and turbinate reduction to try and improve my nasal breathing. The results have been mixed. The good news is that the procedure has defiantly improved my daytime breathing. For the first time in two years I can breath fairly easily during the day. I recommend the procedure to anyone considering it (but make sure you get a good ENT!) The resulting improved airflow however seems limited to only my right nostril only (where they removed a septal spur)

On the down side however my night time breathing has not improved very much. Still get congested quickly after lying down and still can't use nasal CPAP.

I do however think I have made a bit of a discovery in the past few days. As those of you who know my story will remember I lost control of my apnea once the nasal swelling got bad. I eventually had to breath only though my mouth at night. However once I did regain control of my apnea I still continued to feel quite unwell. I have made slow improvements with the addtion of an ASV, etc but still have ever felt like I used to and in fact felt worse in respects different that just apnea symptoms.

One problem with breathing though my mouth is trying to keep it open wide during the night. As a mostly stomach sleeper I find it very hard to keep my mouth wide open. I usually wake up breathing though just a small slit by morning, often just between my teeth. I recently started wondering if I wasn't getting enough airflow and if this is a piece of the puzzle. To test my theory I used my Mandibular Advancement Device with my DYI breathing tube which forces my mouth open. Its a very unpleasant experience but it did seem to make a big difference. To be a valid test I will need to do it a few more times but I really don't want to. The MAD makes swallowing hard and my already GERD sore throat gets extremely sore. However I really think I might be on to something here.

Is it possible that I am rebreathing CO2? Is there someway to test for that? Would rebreathing CO2 mean low oxygen levels or are they independent? What are the symptoms of CO2 rebreathing?

Thanks for any ideas.

Hi James! So glad you can breath better during the day. I used a MADD for over a year and didn't like it either. I don't have GERD. The device made my lower jaw stay forward in the morning until it returned to a normal position. I slobbered like all get out during the night when using it - not fun. I didn't like the pressure on my lower jaw teeth long term. That said, that it led you to be onto something - yeah!!

Isn't the concern of not getting enough oxygen or rebreathing CO2 measured by a pulse ox? A meter would certainly tell you if that's happening.

I looked all over the internet trying to find devices that hold the mouth open and all I found is dental office appliances Maybe a dentist could suggest a device that would do the trick without causing structural damage!

Best wishes. Thanks for letting us know how you're doing. BTW, thank you for the umpteenth time for your fabulous Encore Pro Analyzer : )))

gasp wrote:Hi James! So glad you can breath better during the day.

Yes its an unbelievable relief. Its not perfect but soooo much better. Again I urge anyone thinking of this surgery to just do it (with the right surgeon). It really was only two days of pleasantness for a whole lot of relief.

gasp wrote:I used a MADD for over a year and didn't like it either.

I actually didn't mind using the MAD. In fact I think I would prefer it over CPAP if I wasn't congested and it was able to control my apnea enough. I think for mild apnea its a great option that is probably under utilized.

The problem for me was using MAD with CPAP. I have done this occasionally as a way of keeping my mouth open. You see when I was using MAD along I had to modify it to get enough air as my nose would congest and then I would be suffocating. I added a breathing tube that allowed air in (http://james.istop.com/apnea/reports/Device.jpg) Those where not good times.

gasp wrote: I slobbered like all get out during the night when using it - not fun.

Yes I agree that aspect was not great.

jskinner wrote:I actually didn't mind using the MAD. In fact I think I would prefer it over CPAP if I wasn't congested and it was able to control my apnea enough. I think for mild apnea its a great option that is probably under utilized.

To clarify, I totally agree with you about if the MAD actually worked as well as CPAP I'd prefer it (even with the slober - which by the way decreased markedly over time). Wouldn't it be nice to have it in my bag and be able to nap anywhere, anytime? Or just stay overnight at a friends house without having to come with machine in tow? Travel is so much easier with MAD. I'm just happy the XPAP therapy works so well for me - I'm very grateful.

James,

I have been interested in the PCo2 issue myself. We have some things in common - GERD (I take Pariet tabs), nasal congestion, use of SV.

Re Co2
- if you retain too much, the brain detects this and triggers hyperventilation in an attempt to reduce the co2 levels.
- if you retain too little, the brain shuts breathing down in order to allow co2 to build up in the blood. This is a cause of centrals in some people.

Cheynes-Stokes breathing is a pattern alternating between the two conditions & thus is a helpful way to explain it. Typically CSR (Cheynes-Stokes respiration) occurs with people who have CHF (Chronic Heart Failure) - they breathe slowly then rapidly then slowly then rapidly, the slow cycles typically end in a central (not enough Co2 in the blood) and the rapid breathing typically is in response to too much co2 in the blood & results in hyperventilation. The tidal volume goes up & down in this rhythm.

I certainly don't have CSR but my breathing will on occasions go into a sort of rhythm that is a bit like CSR. Very shallow then followed by a more rapid phase then shallow again. Far more variable than CSR which is usually a very regular pattern. Interestingly and when awake, most times I attend meetings this pattern also starts. I used to bite a finger to try to break the cycle - oddly it mostly passes by the middle of the meeting

DSM

James

Some useful info on CO2 ...
http://www.pubmedcentral.nih.gov/articl ... id=1872042

DSM
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Background.
All cells in the human body need oxygen (O2) to keep them alive. O2 is absorbed into the blood from the air by the lungs (which also release carbon dioxide [CO2], a waste product of cells, from the blood into the air). The blood then delivers O2 to the rest of the body. For healthy people, breathing air (which contains 21% O2) is sufficient to keep their tissues healthy. But there are medical situations in which O2 delivery to tissues needs improving. For example, during resuscitation or after a stroke when the O2 supply to a part of the brain is disrupted. Premature babies often need help with O2 delivery because their immature lungs don't absorb O2 efficiently. In situations like these, the O2 supply can be increased by providing an O2-rich gas mixture to the lungs—so-called “hyperoxic (i.e., high O2) ventilation.” But, paradoxically, hyperoxic ventilation can make matters worse. Hyperoxia increases the exchange of air between the lungs and the atmosphere (hyperventilation), which reduces the CO2 level in the blood. This “hypocapnia,” i.e. low CO2, reduces the blood flow to the brain by narrowing the blood vessels. Hyperoxia also alters the heart rate and blood pressure and the blood levels of some hormones. It probably causes these changes by affecting the brain regions that control autonomic functions (body functions such as heart rate, insulin and other hormone release, sweating and gland action that are not controlled by conscious thought). All told, although hyperoxic ventilation saves lives, it can also have serious adverse effects. In premature babies, for example, although it is often essential for their survival, hyperoxic ventilation can cause serious heart muscle and brain injury or lung problems (bronchopulmonary dysplasia) if it is not carefully monitored.

...

The addition of a little CO2 to the hyperoxic gas mix can reduce the adverse effects of hyperoxic ventilation on blood flow to the brain. However, it is unclear whether this alteration can also modify responses of brain areas that control autonomic functions and hormone release to hyperoxia. If it does, then CO2 supplementation could prevent those adverse effects of hyperoxic ventilation that affect the whole body. In this study, the researchers investigated whether hyperoxic ventilation increases neural responses in brain regions that regulate the activity of the hypothalamus (the part of the brain that controls autonomic bodily functions) and whether the addition of CO2 reduces these responses.

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http://www.talkaboutsleep.com/sleep-dis ... ract23.htm

Summary

Idiopathic Central Sleep Apnea Syndrome (ICSAS) is much less common than Obstructive Sleep Apnea (OSA) and less well understood. These apneas follow abrupt increases in breathing and reductions in arterial CO2, suggesting that they arise from hyperventilation. The authors have evidence that patients with ICSAS, compared to normal controls, show chronic hyperventilation and low blood CO2 both asleep and awake. Also the patients have increased sensitivity of receptors to blood oxygen and carbon dioxide, suggesting that this may underlie their hyperventilation. They authors propose that, in central sleep apneics, chronic hyperventilation keeps arterial CO2 close to the threshold for apnea, and acute episodes of hyperventilation drive it below this threshold, resulting in central apneas.

If this is true, raising the patients' blood CO2 and maintaining it above the threshold should prevent central apneas. They did this by having patients breathe a Co2-enriched gas or breathe through a face mask with added dead space during sleep to increase the amount of rebreathed CO2.

The authors studied six male patients, ages 54-71, with Idiopathic Central Sleep Apnea Syndrome, defined as apneas and hypopneas occurring at least 10 times per hour during sleep, of which at least 75% were central, along with at least two other symptoms of sleep apnea such as excessive daytime sleepiness or nocturnal choking.

All these patients received routine lab polysomnography, with added measurement of esophageal pressure during the first night to determine apnea type. Central apneas were defined by absence of breathing for at least 10 secs without esophageal pressure swings or thoracoabdominal movements to indicate respiratory effort. Central hypopneas were defined by a 50% or greater reduction in breathing under similar conditions.

Studies were conducted on four consecutive nights in the sleep lab. The first night, a control night, subjects breathed room air without a face mask. The second night, patients went to sleep wearing a face mask, at first breathing room air but once entering stage 2 non-REM sleep with the occurrence of central apneas, the Co2-enriched gas was given for 1 hour, after which room air and the enriched gas were alternated at 1-hr intervals for the rest of the night. The concentration of CO2 was gradually increased if apneas persisted. The third night, patients received an enriched gas mixture slightly higher than the threshold found the night before for suppressing apneas (1.5-2.3% vs. 1.0-2.0%). The fourth night, only four subjects agreed to breathe through a face mask with added dead space, increased gradually to increase the amount of rebreathed carbon dioxide.

The six subjects ranged in age from 54 to 71, averaging 60; in Body Mass Index from 223 to 37, averaging 29 (i.e., all were slightly overweight); in Apnea Hypopnea Index from 28 to 79/hr, averaging 44; in Movement Arousals from 17 to 29/hr, averaging 23. While awake, they had normal levels of blood oxygen (71-101, averaging 84) and mildly low blood carbon dioxide (35-38, ave. 36). While asleep, they had mild oxygen desaturation (minima 80% to 92%, average 86% and low carbon dioxide (37 to 43%, ave. 40%). Apneas and hypopneas occurred mostly in stage 2 sleep (80% of the time) in association with "periodic breathing," defined as at least three consecutive cycles of overbreathing alternating with central apnea or hypopnea. Reductions in carbon dioxide level always preceded central apneas. An apneic threshold was found to be 0.29% lower than baseline CO2; CO2 never fell lower than this without causing an apnea/hypopnea.

Inhaling CO2-enriched gas increased blood carbon dioxide and reduced its variability. This abolished periodic breathing and desaturations as well as central apneas and hypopneas. As a result, the proportion of time spent in stable breathing during stage 2 sleep was longer, significantly less fragmented than when breathing room air. These improvements were due entirely to reduction s in central apneas and hypopneas, not to obstructive apneas or hypopneas, which occurred mainly in REM sleep. Breathing through added dead space had similar effects on blood carbon dioxide and stabilization of breathing during sleep.

The authors found their results quite consistent with their initial theory, which had evolved out of related previous research. They had shown a therapeutic effect on sleep apneas of increased blood CO2. They noted that a similar measure had been used to relieve central apneas associated with neurological or cardiac diseases and after tracheostomy for obstructive sleep apnea, though these treatments were brief and documentation was minimal. The authors concluded that their findings with added CO2 and added dead space "point to their potential as treatments for this disorder. More studies over longer time periods will be required to test the therapeutic potential of these approaches."

Comments

Small as this study was, involving only six patients and, at times, only four, I nevertheless am impressed enough by their findings to consider it important for all patients with central sleep apnea to be aware of this line of research, which seems quite likely to eventuate in therapeutic uses, perhaps sooner for those patients who carry some knowledge of the potential for this approach to convey to their doctors. I recall one study of one patients with central sleep apnea who responded much more poorly to BiPAP, which had the push-pull effect of hyperventilation, than with CPAP. So far, chat discussion, bulletin board postings, and even this website have relatively neglected central sleep apnea, leaving it in a somewhat "mysterious" position of unknown cause and treatment. Yet I am aware of people with central sleep apnea, which may not so infrequently occur along with obstructive sleep apnea.

The different response of the central and obstructive sleep apneas to these measures to increase carbon dioxide indicate the likelihood of fundamentally different mechanisms underlying the two disorders, and different treatments necessary to control them. The fact that the vast majority of sleep apneics have OSA should not lead us to ignore those unfortunate people who suffer, perhaps in addition, from central sleep apnea--or from restless legs, periodic leg movements or sleep, or narcolepsy, all of which can coexist with OSA.

(#2 Added defs: hypercapnia = too much co2 in blood, hypocapnia = too little)


Here is another VERY interesting set of comments on hypoxia & hypercapnia.
http://answers.google.com/answers/threadview?id=197162

Note in particular the mention of the effect of hypercapnia on cooling rate in humans. - I have a real
problem in keeping the right temperature - I wear a wool pullover on hot days to stop cooling too quickly.
On cold days I often wear little much to wife's consternation.

EXTRACT :
1) Hypercapnia lowers the shivering threshold and increases core
cooling rate in humans. Along with eucapnic hypoxia, hypercapnia hence
has intense effects on human temperature regulation. Research work,
both current and past have been done on this subject. I have found
abstracts and mentions of such research here: .......

DSM