Questions for UARS collected wisdom

I have been reading through the old UARS threads viewtopic/t34912/search.php?keywords=ua ... mit=Search. People mention things like "UARS is different from OSA, CPAP is trickier", but I haven't seen a compendium of collected wisdom on treating UARS with CPAP. I saw some really helpful advice like "you might need to set your min pressure a few points above where AHI = 0.0 to get rid of all your UARS events". But no collection of that kind of advice - the collective wisdom page only has one piece by Dr. Krakow, which is excellent but far from complete.

Here are some of my questions:

What metrics do UARSers use, since AHI doesn't capture all our "events", and ResMed "Flow Limitation" doesn't have a summary stat. Could SleepyHead calculate some kind of average flow limitation? My approach so far has been to try to get AHI as low as I can (averaging about 1.2 after 3 weeks) before worrying about UARS events. But that's partly because I don't have high-res data yet, so I don't have any Flow Limitation to target.

What difference have UARSers found in what kind of CPAP works for them? Does BiPAP work more often? ASV?

What kinds of setups work better for UARSers?

What machine settings do UARSers use, and what is different about how they select them?

Do any UARSers consider themselves "cured", or is UARS more stubborn?

How can we calm our hypersensitive nervous systems?

Please chime in with your questions and answers. Thanks!

patrissimo wrote:What difference have UARSers found in what kind of CPAP works for them? Does BiPAP work more often? ASV?

From a thread last summer:

jnk wrote:Here is something on the shape of the flow-signal squiggly thingies, especially flow limitations, with pictures and all:

http://journal.publications.chestnet.or ... id=1079416

Some docs, by the way, seem to think that pressure that is a little higher than what might normally be considered therapeutically sufficient for treating OSA in a particular patient may sometimes round the inspiratory flow curve and give better sleep.

The pressure changes of APAP (especially pressure "tests") can disturb the sleep of sensitive UARS-ish patients, I believe.

Finding one straight CPAP pressure (or two bilevel pressures, not autobilevel) high enough to round the curves might be better than APAP modality for some, from what I understand.

How would I figure out if I am disturbed by the pressure changes if they don't wake me up? The pressure changes will be correlated with flow limitations, hence how do I know which is waking me up? I suppose if there are completely treated events, where the machine ramps up pressure and there is no flow limitation, and I leave deep sleep anyway (from Zeo data), that would show it. I guess I could also just try CPAP and see if it feels better.

This is my latest on it:


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


Source: http://www.chestnet.org/accp/pccsu/uppe ... e?page=0,3


Check also this older stuff by the sleep specialist Dr Barry Krakow (Kraiko):

Dr Barry Krakow about Flow Limitation.

A reminder that for all practical purposes, the following three terms are interchangeable:

• UARS (upper airway resistance)
• Flow limitation
• RERAs (respiratory effort-related arousals)

UARS as Mini-Suffocations :

First and foremost, let's look at an analogy in cardiology to put to rest the nonsense that UARS does not exist or is somehow not important. We all know that asystole (heart stops) is bad, just as we know apnea (breathing stops) is bad. But, in cardiology, for decades we've known there are many other cardiac arrhythmias producing irregular heart rhythms, and we don't sit back and say, "well it's not asystole, so it must be OK." For decades, unfortunately, that practice is in fact what many physicians were taught or conditioned to believe, "it's not apnea, so it must be OK." Indeed, to this very day, I still see patients who have been to sleep doctors who told them their sleep study was OK because it didn't show apneas.

But, as we like to say, “a little choking is still choking,” therefore I think it is reasonable to state that each of the various forms of sleep-disordered breathing (apneas, hypopneas, UARS) reflects some degree of “suffocation.” Apnea is the most concrete form as the patient awakens choking or gasping, whereas UARS is probably equivalent to a “mini-suffocation,” which while asleep I imagine produces an unpleasant sensation but not choking.

UARS is not Mutually Exclusive of Hypopneas or Apneas

Please appreciate then that UARS is simply on the continuum of breathing events. To complete our analogy, UARS represents a more subtle form of breathing irregularity (or as some say pulmonary dysrhythmia). It is not mutually exclusive of apneas or hypopneas. You can have all three types of events when you are diagnosed with sleep-disordered breathing (SDB). In fact, the most common type of SDB shows all 3 components in varying proportions during the sleep study.

You would think though that apneas are more important than UARS events, right? Well, maybe. Don’t forget that UARS events, like apneas, are also frequently associated with sleep fragmentation and therefore unequivocally associated with daytime sleepiness and fatigue. We have seen patients with severe UARS (e.g. RDI > 40), who unequivocally have more sleepiness than say a patient with a moderate degree of apneas and hypopneas (AHI =20). That is why RDI (apneas + hypopneas + UARS) is more valuable when diagnosing and treating your condition than AHI.

To repeat, it is critical to realize that nearly all patients with OSA also have a UARS component on their diagnostic sleep studies, but if the sleep lab doesn’t use the proper respiratory sensors, they will not see it: "what you don't look for, you will not see!"

Good FL numbers. It's not so much good numbers; it's normalized airflow, because it is not so easy to count UARS events. Still, you can find a way to count flow limitation events, and you certainly want to reduce them as much as possible. There are data from Rapoport's group that suggests that an RDI consisting only of UARS (FLs, RERAs) in the range of 15 to 20 is clinically significant, so a number lower than this level should be and usually is the minimum to shoot for. In our lab, we occasionally get some patients below 5, but it's the lab environment, which I think in and of itself prevents the "perfect" titration.

UARS is one of the primary reasons that many SDB patients do not achieve an optimal response. As I describe at length in my book, it is a human tendency to "normalize" behaviors, which over time prevents us from obtaining the best possible response to PAP Therapy. If you are so used to fatigue and sleepiness, having suffered for so many years, then how could you possibly discern what a normal level of sleepiness and fatigue should be? Instead, (and I know this from my own trials from CPAP to APAP and finally bilevel), when you experience some improvement, the tendency is to create a new "normal" and wrongly assume that this is "as good as it gets."

Well, it's not as good as it gets if the UARS component of the SDB hasn't been treated, because there is still more to treat. Undoubtedly, most of the members of this forum recognize the fine-tuning and tweaking that's needed to manage mask leaks, mask comfort, mouth breathing, humidifier settings, and nasal congestion, just to name a few of the issues that must be regularly attended to enhance the PAP response.

Notwithstanding, in my clinical experience, I have found that resolving the UARS component of SDB is in the top tier of factors that frequently must be addressed to achieve optimal results, especially so among patients whose regular use of PAP therapy has not yielded the desired effects. "

patrissimo wrote:What metrics do UARSers use, since AHI doesn't capture all our "events", and ResMed "Flow Limitation" doesn't have a summary stat. Could SleepyHead calculate some kind of average flow limitation? My approach so far has been to try to get AHI as low as I can (averaging about 1.2 after 3 weeks) before worrying about UARS events. But that's partly because I don't have high-res data yet, so I don't have any Flow Limitation to target.

Everyone, not just UARS-ers, need to look at FLs/RERAs (whatever their machine reports) because apneas/hypopneas can be treated but leave residual RERAs. Depending which machine you get, you'll either get numbers for those values or you'll get graphs.

What difference have UARSers found in what kind of CPAP works for them? Does BiPAP work more often? ASV?

I haven't noticed any pattern from what I've seen on this board. Then again, I'm not a big believer in there being an appreciable difference between UARS and mild OSA. I think one lab's "mild OSA" is another labs "UARS" is another labs "negative study".

What kinds of setups work better for UARSers?

Not sure what you mean by this.

What machine settings do UARSers use, and what is different about how they select them?

There should be nothing different about how they are selected. You have to decide what your "dependent/outcome variable" is. RDI? EDS?

How can we calm our hypersensitive nervous systems?

I am still waiting for research/information other than by Dr. Park that shows that UARSers have more hypersensitive nervous systems than say someone with OSA who got the diagnosis by virtue of hypopneas with associated arousals as opposed to desaturations.

Hi,

I suffered from UARS for a while during a period when I was on a medical weight loss program. I stopped having OSA events and started waking up feeling like a zombie. What I found by experimentation is that CPAP machines, at least the two that I own, don't record any events for UARS. As a result, they cannot auto adjust. What I ended up doing is setting the machines to fixed pressures, and then tweaked the pressure day by day until I woke up feeling good. I ended up at pretty high pressure levels, so I am glad that I own BiPAP machines.

Insurance companies might consider that you are cured if you are no longer having OSA events. In fact, my insurance company wanted to cut me off from getting new CPAP supplies, but my sleep doctor used the phrase "medical necessity", and they continued to cover me with no issues.

Once I hit my target weight, both my OSA and UARS appears to be largely cured, but yet another breathing issue has emerged, so I still need CPAP to sleep. When it comes to sleep disorders, I am apparently trying to collect the entire set.

-john-

jweeks wrote:Once I hit my target weight, both my OSA and UARS appears to be largely cured, but yet another breathing issue has emerged, so I still need CPAP to sleep. When it comes to sleep disorders, I am apparently trying to collect the entire set.

Curious as to what kind of sleep related breathing issue other than OSA and UARS would require CPAP?

BTW, here's the biggest old UARS thread I could find:

General UARS Discussion - 2009 - viewtopic.php?p=349759#p349759

Question: why do you believe you have UARS / how were you diagnosed?

Dr. Guilleminault diagnosed me based on my symptoms, as did Dr. Li, because I had a small airway, low AHI (11 before MMA surgery, 5 after, all hypnopneas, no apneas), desats weren't very low, I'm young and thin and hyper, but felt tired all the time, had very unrefreshing sleep. But looking back at my sleep studies, none of them measured RERAs. So it hasn't really been shown that I have UARS, rather I fit the profile and it would explain why I have such EDS when my AHI isn't bad. When my S9 comes and I finally have full-night data, I will try to match up my flow limitations with my Zeo data to see if periods of FL correspond with light sleep, which would be evidence of UARS. Even better evidence would be to achieve a CPAP setup that results in minimal flow limitation and have that cure my EDS.

I am curious how, without esophageal manometry, we can accurately self-diagnose UARS.

patrissimo wrote:I am curious how, without esophageal manometry, we can accurately self-diagnose UARS.

You can't. That's a very important point.

There are a lot of people who think they have UARS on here and elsewhere, but the bottom line is that self-diagnosing UARS is generally impossible. With apneas, you can see desats with a recording pulse ox and at least get a general idea if they're present even if you don't know why they are (e.g. self-diagnosing anything more than a vanilla OSA diagnosis is playing with fire without a sleep study), but you can't see pressure differentials outside a lab.

It's one reason why I am not particularly hot on machine data suggesting RERAs and such; the diagnostic tools that can make a differential diagnosis on UARS for the home user simply aren't available. You can see flagged and untreated possible respiratory events, you can hear complaints about EDS, you can look at Zeo data suggesting something's screwy with someone's sleep stages, but none of this results in a solid diagnosis since all of it can be potentially attributed to something else.

The good news is self-treatment outside a clinic is pretty much as effective as what you get by going inside a clinic for said diagnosis. You can do so more or less the exact same way the medical community often does, which is to not bother with differential testing and just outright see if a patient's collection of medical complaints can be helped via xPAP. In practice, a differential diagnosis of UARS is only really helpful for someone in your situation, where it's a question of whether or not you should drop (and/or start) xPAP because xPAP treatment isn't otherwise indicated.

A diagnosis also helps for insurance purposes, but since treatment devolves in both OSA and UARS to xPAP it's usually a lot more cost effective to just get someone with UARS symptoms a machine to see if it helps, since a machine costs a bunch less and they're almost certainly going to end up trying one at some point anyway. There's also a point to be made for treating anything that could cause the pressure differential like allergies or nasal structure, but again short of exploratory surgery for the latter you're not gaining anything by having the formal diagnosis as opposed to just starting up on a nasal steroid and allergy shots.

Where all this becomes more complicated is when you have to tweak the treatment significantly. There are some UARS patients who just don't do well on bilevel, for instance, and that's just hard to gauge without trial and error as it varies dramatically from patient to patient. Unlike diagnosis, getting proper pressure settings for someone with UARS may sometimes genuinely require that they do go into a lab since you can't really tell if you're properly treating UARS with machines the way you can with apneas. That's when esophageal manometry becomes important, since you'll want to see if pressure x corresponds to RERA and hypopneas being smoothed out. If someone's still having problems after xPAP treatment such testing makes a whole lot of sense.

Hope that helps.

SleepingUgly wrote:

jweeks wrote:Once I hit my target weight, both my OSA and UARS appears to be largely cured, but yet another breathing issue has emerged, so I still need CPAP to sleep. When it comes to sleep disorders, I am apparently trying to collect the entire set.

Curious as to what kind of sleep related breathing issue other than OSA and UARS would require CPAP?

Hi,

Low respiratory effort. I have a paralyzed diaphragm (since birth), so I breathe with my upper chest. In the daytime, when I do cardio stuff, I can use some of my core muscles to assist with breathing more deeply. At night, that doesn't help since I have to think about it to do it. It appears that at night I go through periods where my brain doesn't send strong enough signals to my upper chest for a lengthy period of time. It isn't enough to register as an OA or hypo, it isn't periodic, and the desats are not that deep, but it does lead to me waking up. Running on BiPAP at a pressure of 8/13 seems to give me really good treatment. It sort of acts like a breathing amplifier...when I breathe in just a little, the BiPAP goes to the higher pressure, and I get a good breath of air.

-john-

jweeks wrote:I have a paralyzed diaphragm (since birth), so I breathe with my upper chest.

Fortunately, that should only be a problem if you fall asleep and REM:

http://jap.physiology.org/content/43/4/ ... l.pdf+html

I assume that my Flow Limitation level includes my UARs and RERA. So I check it with ResScan graphs from my S9 Autoset (in APAP mode) and try to minimize it.

In these graphs I can see that the my Flow Limitation started to rise at the same time that the shape of my respiration waves became flattened,
the pressure also started to rise because of it:





The following is another example that the FL rises when the shape of the respiration waves are flat:





An example of BAD FL graph that I had at the beginning of 2012:




So I started to rinse my nose and also raised the inhale pressure somewhat but not above 15 cm. If I needed higher pressure than 15 cm then I would be a candidate
for a BiPAP (= BiLevel). I also stopped using full face masks b/c of leakes and changed to my present setup.


The results:


Pressure and Events graphs:

(Data for APAP= AutoCPAP mode is shown)



This set-up took me some time to arrive at by following the pressure graph in Rescan. I started with the first set- up by using the optimal CPAP pressure from my latest sleep study. But later, I fine tuned the setup, by changing the limit pressures gradually as to have the pressure graph only "kiss" the two limit lines of max and min pressures. See the graph above. The idea was to set the limits so that the machine should not 1) Waste time responding to events, and 2) Run the pressure up, suddenly, and cause new Emergent Central Apneas and also cause the ingested air to rise.

Leak and Snore graphs:



Flow and Flow Limitation graphs:

(the Flow graph will be needed to show detailed graphs in the double panels)




And my recent Stats:





But, I still suffer from some RES (Residual Excessive Sleepiness) in the mornings.