UARS, Flow Limit, and Flow Rate graphs

My doctor did not diagnose me with OSA. I had 207 RERAs in just over 5 hours of sleep, but only 10 apnea/hypopnea events. With an RDI of 40 my sleep doctor believes that I would benefit from CPAP treatment. I have done extensive reading on the subject of UARS (a good bit of it here in the archives) and I am becoming a believer.

I know there is a lot of confusion even in the medical community about UARS. Is it a form of OSA or a syndrome all to itself? Can it be treated with CPAP or should a dental device be used? I really don't care so much about all that academia; what I care most about is getting better and while on that journey posting my findings and progress so that others may benefit as well. To that end, that is why I am posting today.

It seems the APAP machines are designed primarily for OSA patients, in that, in the end they are attempting to apply an air stint to keep the airway open and to preemptively prevent apnea/hypopnea events from occurring. The end result being more uniform sleep architecture and a better rested patient. However, individuals who exhibit high frequencies of RERAs do not necessarily see many apnea or hypopnea events. There are many theories for this, the most notable that I have seen is that UARS patients have a more sensitive nervous systems and exhibit an arousal earlier in the cycle before the apnea/hypopnea event can occur. This usually results in oxygen desaturation that is not as low as that which occurs with apnea/hypopnea events. In my sleep study my desats never when below 91%, for example.

Back to the APAP machine, what I have observed is that the ResMed AutoSet increases pressure for flow limits, snores, hypopneas, and obstructive apneas. In my experience so far, the apnea/hypopnea events and major snores result in the most dramatic increases in pressure while flow limits and mild snoring result in very minor increases in pressure (usually around .25cm to.50cm). Since flow limitation is believed to be the precursor to a RERA, it is the basis of my former statement that (at least my) APAP machine seems to be optimized more for the treatment of OSA than UARS and probably for good reasons (that I won't go into here).

Because my condition concerns a high frequency of RERAs I have focused my energy on flow limitation. Inspiratory flow limitation reveals itself in the Flow Rate graph as a non-rounded shape to the upper half of the flow rate sine wave. I do not know how the ResMed algorithm calculates flow limit, only that it scores it on a scale of 0.0 to 1.0. It seems to be doing this on a range of respiratory cycles since flow limitation can be seen on a breath by breath basis with no or very minor change in the flow limit graph.

Now onto my personal observations over the last 11 days on the machine. The following graphs are typical. These patterns exist on every single day of my treatment thus far. While I can find exceptions to these patterns, they represent the majority of respiratory behavior at the given pressure.

Since we are working outside of insurance, my sleep doctor is using the APAP to dial in the pressure by using a rather wide range of 5cm to 15cm. Look at these first two graphs. They are typical of what I see when my pressure has dropped back down to the minimum area around 5cm. Notice the shapes of the tops of the inspiratory curves:




Compare those graphs to the next two where due to flow limits and/or apneic events the pressure was raised to around 7cm:




The 7cm curves are more sinusoidal and exhibit less erratic noise than those on the 5cm curves. What a difference a couple of cm's makes!
Also note this graph where I had an OA following by a rather significant snore resulting in my pressure approaching 12cm:



If we assert that rounding out the tops of the inspiratory curve does in fact correlate with reduction or elimination of flow limitation (there is plenty of literature backing up this assertion) and flow limitations lead to RERAs in UARS patients then it seems that a higher minimum pressure will work for me. I can further conclude that my pressure requirements should not be relatively high. This is good news since it means I may be able to continue treatment with the APAP without having to result to needing a BiPAP.

I also would like to share something I learned along the way looking at these graphs. Initially I thought that inspiration started at the bottom of the curve and ended at the top of the curve with expiration being the other half (from top to bottom). With this false understanding I never understood why I saw that brief pause in the middle of what I thought was inspiration. The lights came on when I realized these are rate graphs. As long as the value being graphed is above zero is represents inspiration. Whenever the value drops below zero (goes negative) it represents expiration. This is significant to the understanding of flow limitation since the non rounding of the tops of the curve represents that moment in the respiratory process when the rate of flow is at its maximum.

I am interested in your thoughts. If I have overstated the obvious or made any blunders please forgive and/or correct me. I admit that I am new to this whole thing, but it has become a very exciting journey so far!

Based on my understanding, I am considering raising my minimum pressure by 1cm per week until I see the majority of these flow rate graphs rounding out at minimum pressure. However, since I am still acclimating myself to having an alien on my face all night, I may delay those changes for a week or more.

Welcome!

NotLazyJustTired wrote:My doctor did not diagnose me with OSA. I had 207 RERAs in just over 5 hours of sleep, but only 10 apnea/hypopnea events.

Depends on how they score hypopneas. One lab's hypopnea is another lab's RERA.

I know there is a lot of confusion even in the medical community about UARS. Is it a form of OSA or a syndrome all to itself?

True there is controversy about that.

Can it be treated with CPAP

I don't think there's any controversy about that. Yes, it can.

or should a dental device be used?

I wouldn't say "should", but "could". Yes, it could, just as it could be used for OSA.

I really don't care so much about all that academia;

Me either.

what I care most about is getting better

Me too!

It seems the APAP machines are designed primarily for OSA patients, in that, in the end they are attempting to apply an air stint to keep the airway open and to preemptively prevent apnea/hypopnea events from occurring. The end result being more uniform sleep architecture and a better rested patient.

Not sure I've read anything that would make me think that APAPs are more suitable for OSA than UARS.

However, individuals who exhibit high frequencies of RERAs do not necessarily see many apnea or hypopnea events.

True (for some labs anyway).

There are many theories for this, the most notable that I have seen is that UARS patients have a more sensitive nervous systems and exhibit an arousal earlier in the cycle before the apnea/hypopnea event can occur.

I would think that would also be true of those with OSA who have hypopneas associated with arousals and not desaturations (i.e., AASM alternative criteria for scoring hypopneas rather than AASM recommended criteria).

This usually results in oxygen desaturation that is not as low as that which occurs with apnea/hypopnea events. In my sleep study my desats never when below 91%, for example.

Same comment as last. For example, my SaO2 is 92-93% at its lowest, yet I have OSA by virtue of hypopneas associated with arousals primarily.

Since flow limitation is believed to be the precursor to a RERA,

I thought a RERA was a FL with an arousal, no?

it is the basis of my former statement that (at least my) APAP machine seems to be optimized more for the treatment of OSA than UARS and probably for good reasons (that I won't go into here).

I'll let someone else field that... Again, I haven't read anything to that effect.

then it seems that a higher minimum pressure will work for me.

Agreed (although this is true for everyone, not just UARS).

I can further conclude that my pressure requirements should not be relatively high.

Who knows (yet).

Based on my understanding, I am considering raising my minimum pressure by 1cm per week until I see the majority of these flow rate graphs rounding out at minimum pressure. However, since I am still acclimating myself to having an alien on my face all night, I may delay those changes for a week or more.

Sounds like a plan!

NotLazy, do you have Upper Airway Resistance Syndrome (UARS)?


Clinical Features

Patients with UARS have symptoms similar to those seen in OSAS, although there are some distinct features. Much of the research performed has attempted to identify and describe a group of patients with significant daytime sleepiness and disrupted sleep, but without the other dominant clinical features seen in OSAS. Typical symptoms reported by patients with UARS include excessive daytime sleepiness, fatigue, difficulty concentrating, morning headaches, and unrefreshing sleep. There can be also be a significant impairment in daytime functioning; a recent study demonstrated that subjects with UARS performed worse than patients with obstructive sleep apnea hypopnea syndrome and normal control individuals on different aspects of the Psychomotor Vigilance Task. In a separate study, upwards of 30% of subjects with UARS had abnormal sleep-onset latency on the Maintenance of Wakefulness Test. Individuals with abnormal airway anatomy are at increased risk, including those with a decreased retrolingual space, narrow nasal passages, or a small neck circumference. Patients are typically not obese, with a mean BMI often <25 kg/m. They are also usually younger than those in whom OSAS is diagnosed, with a mean age of approximately 38 years. Snoring is not a requisite symptom, with 10% to 15% or more of patients having never or only intermittently snored.

Patients with UARS are also more likely to report symptoms of frequent nocturnal awakening with difficulty falling back to sleep. This is thought to be a potential reason for increased complaints of insomnia amongst patients with UARS, including sleep onset and sleep maintenance problems. In addition to difficulties with acute insomnia, patients with UARS also have an increased likelihood of carrying a diagnosis of chronic insomnia. Other notable complaints include parasomnias, especially sleepwalking, sleep talking, and sleep terrors. Patients may also have symptoms of abnormal autonomic function, including lightheadedness or dizziness on rising from a supine or sitting position, cold hands and feet, and low resting blood pressures (defined as a systolic BP <105 mm Hg with a diastolic BP <65 mm Hg). In a study of 400 patients with UARS, more than 20% met criteria for low BP, a significantly higher prevalence when compared with people who have OSAS (0.6%) or insomnia (0.9%). Interestingly, all subjects in the study had evidence of a small oral cavity on examination with a narrowed airway space dimension on cephalometric radiographs, consistent with other reports. Lastly, patients with UARS have increased rates of symptoms such as gastroesophageal reflux, muscular pain, diarrhea, abdominal pain, depression, and anxiety. This has led some authors to suggest a link between UARS and functional somatic syndromes, such as irritable bowel syndrome, chronic fatigue syndrome, and fibromyalgia. In a study of 75 subjects equally divided into three groups (UARS, mild to moderate OSAS, and severe OSAS), those with UARS were more likely to report symptoms of headache, irritable bowel symptoms, and sleep-initiation insomnia. Subjects with UARS were also more likely to have alpha intrusion during slow-wave sleep, a polysomnographic finding described in a number of fatigue syndromes. In children with UARS, symptoms consistent with attention deficit disorder or attention deficit hyperactivity disorder may be present, with behavioral changes leading to poor school performance.


________________________________________
Clinical Features Associated With UARS

Daytime symptoms:

Excessive daytime sleepiness
Fatigue
Morning headaches
Myalgia’s [muscle pain]
Difficulty concentrating


Sleep disturbances:

Frequent nocturnal awakenings
Difficulties initiating sleep
Insomnia
Bruxism [teeth clenching]
Restless leg syndrome
Unrefreshing sleep

Autonomic nervous system:

Hypotension
Orthostasis [maintenance of an upright standing posture]
Cold hands and feet

Functional somatic syndrome associations:

Depression
Anxiety
Chronic fatigue syndrome
Irritable bowel syndrome
Fibromyalgia

Polysomnographic abnormalities Increased RERAs:

Increased nocturnal arousals
Increased CAP rate [cyclical alternating pattern in EEG]
Alpha intrusion during sleep

Treatment

The optimal treatment for patients with UARS is not currently known. Continuous positive airway pressure (CPAP) has been quite useful in the treatment of sleep-disordered breathing and there are some notable positive results in CPAP treatment of UARS. In a study of 15 heavy snorers with clinical evidence of UARS, treatment with nasal CPAP was associated with decreases in observed nocturnal arousals on polysomnography and decreases in mean sleep latency times on multiple sleep latency testing (MSLT) after several nights of treatment. A follow-up study of 15 subjects (in the original description of UARS) with daytime sleepiness and fatigue and who had undergone a therapeutic trial of positive pressure therapy reported similar findings. After treatment with approximately a month of nasal CPAP, significant improvements were seen in mean sleep latency times on MSLT (5.3 minutes vs 13.5 minutes), Pes nadir pressure (–33.1 cm H2O vs –5.3 cm H2O), amount of slow-wave sleep (1.2% vs 9.7%), and EEG arousals (31.3 vs 7.9 events/hour of sleep). Along with an improvement in sleep latency times on MSLT, there were subjective reports of improved daytime symptoms. Lastly, in a study of 130 postmenopausal women with chronic insomnia and evidence of UARS (n=62) or normal breathing (n=68), treatment with either nasal turbinectomy or nasal CPAP was associated with improvements in subjective reports of sleep quality as measured with a visual analog scale as well as mean sleep latency times on polysomnography.19 Despite the growing body of evidence supporting the use of positive pressure therapy for UARS patients, it remains difficult to obtain therapy. In a follow-up study of more than 90 patients conducted 4 to 5 years after the initial diagnosis of UARS was made, none of the subjects were receiving CPAP treatment; the main rationale given was that their insurance provider declined to provide the necessary equipment.1 Formal follow-up clinical evaluations of these patients noted significant worsening in their sleep-related complaints, with increased reports of fatigue, insomnia, and depressive mood. More disturbingly, prescriptions for hypnotics, stimulants, and antidepressants increased more than fivefold.

Other interventions, such as surgery or oral appliances, have also been used with some success in the treatment of patients with UARS. Procedures such as uvulopalatopharyngoplasty, laser-assisted uvuloplasty (LAUP), septoplasty with turbinate reduction, genioglossus advancement, and radiofrequency ablation of the palate have all been described in the literature.37-40 A study of LAUP in nine patients with UARS who underwent uvulopalatopharyngoplasty (n=2), multilevel pharyngeal surgery (n=1), or LAUP (n=6) reported improvements in subjective daytime sleepiness as measured with Epworth Sleepiness Scale scores.37 In the two patients for whom postoperative polysomnographic data was available, significant improvements in Pes nadir pressures were seen. But patients had several interventions and it is difficult to assess which one was successful. A study of 14 patients with UARS who underwent radiofrequency ablation of the palate also reported improvement in subjective sleepiness, with concurrent improvements in Pes nadir levels and reports of snoring.40 However, prior reviews of the available literature have noted that many of the studies evaluated small numbers of patients, consisted of uncontrolled case reports or series without clear characterization of the subjects enrolled, and had no consistent end points for an adequate evaluation of efficacy.39 Further investigation is required to determine the specific role for surgical intervention in these patients. Other authors have also reported successful treatment of UARS with use of oral appliances, although these studies suffer from the same limitations as the surgical literature.41 In children, orthodontic approaches, such as maxillary distraction or use of expanders, have also shown promising results

Source: http://69.36.35.38/accp/pccsu/upper-air ... e?page=0,3

Thanks for those responses.

SleepingUgly,

I do not mean to imply that APAP cannot be used for effective treatment of UARS, just that the out-of-the-box algorithms seem to be more focused on lowering the AHI. To treat UARS more effectively I propose that the algorithm would be more sensitive to flow limitation than it seems to be. Or perhaps use an alternate algorithm that holds the higher pressure longer, I dunno. It's just a little disturbing to see the machine raise pressure eliminating the flow limitation only to regress to lower pressure and start the cycle all over again. The simple fix is just to raise the minimum pressure, so I don't know why I am harping on this, just an observation I guess.

AVI,

Yes, I do remember reading that text, perhaps you posted it in another thread that I came across in my research. I have many of those symptoms described and while I don't exactly meet the profile described now, I did when I was much younger. I was 150 lbs. dripping wet when I graduated from high school and had slightly low blood pressure. I have never been a person of high energy. Yep, cold hands too. Fast forward 35 years later, I am 60 lbs. heavier, have high blood pressure, acid reflux and extreme fatigue. Morning headaches have always been my bane. My theory is that I have suffered with UARS all my life and now in my later years with weight gain and other effects of the aging process I am developing a mild form of OSA on top of that. As SleepingUgly points out, the sleep labs have some discretion as to how they score hypopneas. My lab used rule 4A which does not count hypopneas with arousal only desat and airway restriction are important. Perhaps a percentage of my RERAs could be scored as hypopneas using rule 4B. Also, the sleep lab did not instruct me to sleep on my back so I spent most of the night sleeping on my side. It really doesn't matter, I am paying for the machine out of pocket and I am most interested in using it to get better. Thanks again for taking the time to respond.

NotLazyJustTired wrote: Because my condition concerns a high frequency of RERAs I have focused my energy on flow limitation.

The RERA etiology for classic UARS entails near-constant high upper-airway resistance. Essentially UARS patients must exert extreme inspiratory effort to draw adequate inspiratory volumes because of that high resistance. Extreme inspiratory effort during peak draw, in turn, is thought to trigger the arousal. Thus the classic UARS associated RERA tendency is correlated with flattened or distorted inspiratory peaks on the flow graphs as you mentioned. So it's a good idea to try and correlate your own subjective assessment of sleep and daytime symptoms with flow limitations manifesting during inspiratory peaks. Your RERA etiology might very well be based in near-constant upper-airway resistance attributable to narrow diameter typical of classic UARS.

However, your flow curves also manifest some "squiggly" lines just as inspiratory draw gets started---right after exhalation. That post-expiratory squiggly line might represent partial airway collapse as static pressure wanes between exhalation and inhalation. This is a common airway-collapse dynamic in OSA patients, as opposed to narrow-diameter/high-resistance based FL manifesting during inspiratory peaks. Your RERA etiology is probably based in stifled peak inspiratory effort----reflected by those distorted peaks at the tops of your inspiratory curves. However, there's a chance that at least some of your arousability is based in the effort necessary to begin your inspiratory draw. If so, then those squiggly lines immediately after exhalation are worth keeping an eye on. Good luck with this!

Thank you very much, SWS! I recognize your screen name from many of the posts I have encountered while researching UARS here. I recall one very long and lively discussion from about 4 years ago in particular. It was very helpful to my understanding.

Regarding the "post-exipiratory squiggles", I've noticed these on many flow graphs I've looked at and just assumed it was some normal pause between breaths. But I also realize that when I do have the occasional OA, it is a much longer pause ending in arousal. This is interesting in that I have been thinking that my UARS may be evolving into mild OSA and this post-expiratory collapse may explain that as well. It makes me wonder. I currently have EPR set at 3. I wonder if lowering this or turning it off would help with this post-expiratory collapse since it would maintain higher pressure. Raising the minimum pressure of the APAP would also likely help since the EPR pressure will increase in lock step. It is also interesting to note that with a minimum pressure of 5 my pressure needs to go above 8 to realize the full benefit of EPR=3; I rarely go that high. My FL seems to diminish around 7cm where I linger for a while and the pressure drops back down into the 5-6 range where FL rears its ugly head again and the cycle repeats.

Does anyone have opinions/experience to suggest where to start?

At any rate, it is something I will keep an eye on eliminating. I am very ingratiated for your help.

NotLazyJustTired wrote: I currently have EPR set at 3. I wonder if lowering this or turning it off would help with this post-expiratory collapse since it would maintain higher pressure.

As a side note, your flow curves above are shifted slightly down. You can adjust for that downward shift in flow-curve by comparing each inspiratory volume (area underneath the positive-value curves) with each expiratory volume (area underneath the negative-value curves). Generally each expiratory volume needs to break even with that immediately-prior inspiratory volume, since we exhale the same volume of gas that we just inhaled. Once we make that adjustment, we can see those squiggly lines occur during your expiratory-to-inspiratory transition---about the time you are getting ready to commence inspiratory effort.

Still, we don't know how much, if any, of your arousability is based in that portion of the breathing curve. A post-expiratory pause not based in obstruction tends to be flatter. I'm thinking that up-and-down fluttering you present might represent slight obstruction-based effort to begin some of those breaths. If so, some of those obstruction-based efforts might be associated with arousals. I'm merely speculating. So please take my conjecture with some healthy skepticism.

Anyway, to answer you question above, yes. If you need more static pressure during that part of the breathing phase, then it must be delivered with EPAP, since IPAP has not yet commenced. So reducing EPR is one way to present more airway stenting pressure during that part of the breathing phase.

NSJT,
Great post. You just increased my understanding of FL and RERA's exponentially. I'll use this information in my own treatment. Keep us posted on your progress.

Again, much appreciated. I did notice that shift in the rate curves and wonder if the machine is out of calibration. I will mentally adjust for the offset.

I realize you are speculating, but the information and the possibilities are vastly important to me. It is good to have experienced folks here to offer that speculation as starting points for improving treatment! In the end, the real answer will be to correlate how I feel with changes made and what I see in the data. I realize that may be a slow process, but now I am armed with some lucid ideas of what to try and that is immensely comforting to this newbie!

I am just now getting to a point where I am not seeing so much "equipment arousal". Once I am certain that it is the SDB that is primarily arousing my sleep, I will start to experiment. I will, of course, share any results in the hopes that others may benefit as well...

NotLazy, also check this:

https://www.youtube.com/watch?v=JWm7tT-ZNzE

Thanks AVI. That was good. Only bit I disagree with is the notion that you have to cycle back through to a sleep center to get your pressure dialed in.

-SWS wrote:

NotLazyJustTired wrote: Anyway, to answer you question above, yes. If you need more static pressure during that part of the breathing phase, then it must be delivered with EPAP, since IPAP has not yet commenced. So reducing EPR is one way to present more airway stenting pressure during that part of the breathing phase.

Both of your posts were very enlightening, SWS. Now I have to go back and look at my flow lines more critically, maybe even experiment further. You're on fire today Keep the good stuff coming Thanks also NotLazyJustTired for opening the conversation.

It seems to me that trying to deal with Flow Limitation (including UARS and RERAS) by adjusting a CPAP or APAP pressures by looking at the changes in the respiration waves curves is quite involved even for the experts in the field.

http://jap.physiology.org/content/68/3/1075.abstract

There is not much that I could do when I see on my APAP's data that my respirations waves are becoming flat top:



The flattening of the respirations wave cause the pressure to rise but only somewhat:




But Obstructive Apnea events cause the pressure to rise much higher:



But there are nights when the respiration waves are more top rounded:



BTW, my Stats are:

I am going to out on a limb here and suggest something that may or may not be true.
I have this working theory that much of the controversy/confusion surrounding UARS may be that UARS seems to be a grab bag of OSA "leftovers". "Your AHI is under 5, but you are fatigued. You must have UARS."
High pressure may not work for everyone to remove flow limitation. I am thinking it depends on the root cause for the limitation. It is also important to remember that not everyone that exhibits flow limitation necessarily has arousals as a result of it.

-SWS wrote:Anyway, to answer you question above, yes. If you need more static pressure during that part of the breathing phase, then it must be delivered with EPAP, since IPAP has not yet commenced. So reducing EPR is one way to present more airway stenting pressure during that part of the breathing phase.

I'm definitely going to be the first to take the plunge and try to get rid of my "squigglies", that is, by turning off my PR's EPR feature (my auto relief pressure, A-FLEX PR calls it, was set at 3). I've never had the slightest problem breathing without it before, so why not give it a try? Tho it should be noted to like minded people that my current pressure settings are 8/12, not very high thankfully.