definition of flow limitation

[kaiasgram]

oak: Yes. The PR machines show RERAs -- in that case RERAs are inferred from breathing patterns with some sort of algorithm. The only way to identify RERAs definitively would have to involve an EEG.

[kaiasgram]

My Sleepy Head graphs don't show a separate flow limitation graph. It is checked under graphs in preferences.

Stormy, I'm not sure, maybe it's something about your particular machine?

There are two places you can check to display a graph, in Preferences (Mac -- Settings for PC?) and down near the lower right corner of your screen. I think really that either one of those should work, i.e., I don't think you normally have to select the graph in both places. But you could experiment and check it out.

I'm assuming that graph is not just "hiding" down below the visible area of your screen and you just need to scroll down to see it!

[Stormynights]

It just isn't there for some reason with any of the 3 machines in our house. I am not really worried about it but just curious.

[kaiasgram]

It just isn't there for some reason with any of the 3 machines in our house. I am not really worried about it but just curious.

Hopefully someone will come along who knows the answer.

[Pugsy]

My Sleepy Head graphs don't show a separate flow limitation graph. It is checked under graphs in preferences.

It just isn't there for some reason with any of the 3 machines in our house. I am not really worried about it but just curious.

The Flow limitation graph is specific to the ResMed S9 machines...won't show up at all on the Respironics machines as a graph. Instead FL shows up as a specifically flagged event only when the PR S1 is in auto mode.
It should show up on your S9 AutoSet reports though.

Not sure why your S9 Adapt isn't offering you the Flow limitation graph....Have you checked ResScan to see if it is offered there?

[Stormynights]

Right now I am doing an experiment with the PR1 machine before my appointment with my sleep doctor. She wants me to try a new pressure on my old machine. I am very reluctantly doing it and feeling like crap but I just have to jump through all of these hoops trying to get approved so I can get permission to use and get supplies for my ASV machine. With the back pain and headaches it is rough. I am wondering if 100% coverage is worth all this rather that just buying out of pocket.

[jnk]

Here is the way I understand it in my overly simplified mind as a patient:

A flow limitation in this context is short for inspiratory flow limitation and has a lot to do with the shape of the flow curve when it comes to defining it. Machines have proprietary ways of defining it, and not all sleep researchers define it exactly the same way either, I don't think. And docs don't always agree on the significance. And testers don't always agree with whether there is a clear arousal accompanying instances of flow limitation.

For people who lean toward the UARS end of things, even slight narrowing of the airway can distrub their sleep and make them feel lousy the next day. For them, flow limitations can be particularly clinically significant, even when the limitations don't lead to hypopneas or apneas.

For those solidly in the OSA camp, their bodies/brains have basically learned to sleep through almost anything but a full-blown lengthy apnea. For them, flow limitations don't appear to mean much clinically in and of themselves.

Home treatment machines that record flow limitation generally do so, not so much for the purpose of treating it, but for the purpose of using that information for trending purposes and to indicate the possibility of approaching significant events. The auto-titrating machines can use that information to raise pressures preemtively in the interests of preventing obstructive apneas and hypopneas.

[Papit]

. . . Home treatment machines that record flow limitation generally do so, not so much for the purpose of treating it, but for the purpose of using that information for trending purposes and to indicate the possibility of approaching significant events. The auto-titrating machines can use that information to raise pressures preemtively in the interests of preventing obstructive apneas and hypopneas.

Hi jnk, nice write-up, thanks. Do you use an ASV? Re. your last paragraph, is that input you picked up from ResMed or from a specific ResMed or Respironics reference? If so, I'd sure like to see the link or text. I've gotten in touch with ResMed, but they won't be explicit with me (a patient rather than a Dr.) as to how the Flow Limitation graph can be used to help refine treatment on their S9 VPAP Adapt (newer model, same name), but they tell me it is useful for that purpose. Can anyone on this board get this info from them? My FL's are high and frequent every night since switching to the Adapt and my OA and CA are usually about 0.1 with AHI averaging 1.4. On the other hand when I was on their S9 AutoSet, my FL's were infrequent and very low, but my AHI averaged over 17.0. So you can see why I'm interested in learning what's up with the FL's. See my FL graph at bottom of second image below.



Typical Flow Limitation graph (at bottom of set below)

[avi123]

Reports on Flow Limitation (FL) from my archive:

Introduction


In recent years, there has been increasing recog-
nition that abnormal respiratory events other than
apnea can occur during sleep. These include hypop¬
nea, snoring, elevated upper airway resistance
events, and flow limitation. This expansion of what
is considered "abnormal" has implications for the
therapeutic titration of continuous positive airway
pressure (CPAP). While all CPAP treatment proto¬
cols are directed to the elimination of apnea and
hypopnea, there is less agreement on the goals of
therapy when applied to more subtle indicators of
upper airway dysfunction. Many clinical protocols
quote the need to eliminate snoring, and this has also
been used as a feedback signal to control some
"auto-CPAP" devices. We have established that
the presence of an abnormal contour on the inspira¬
tory airflow waveform is indicative of flow limitation
and noninvasively identifies increased upper airway
resistance.

Both flow limitation and snoring identify behavior
of the airway thought to be related to collapsibility,
and thus share several characteristics. Both have
been proposed to identify elevated upper airway
resistance events missed by standard monitor¬
ing. Both are often seen in the same patients
who elsewhere have apnea/hypopnea and both tend
to precede these frank reductions in airflow. Fur¬
thermore, arousals can occur after either snoring or
flow limitation, even without the occurrence of
frank apnea or hypopnea. During CPAP titration,
both flow limitation and snoring persist at pressures
that have obliterated apnea and hypopnea, and both
may appear and disappear with small changes in
CPAP {pressure}.

Our clinical experience suggests that
some patients exhibit both flow limitation and snor¬
ing simultaneously, while others exhibit only one or
the other with similar consequences.
Both flow limitation and snoring were present long after all
apneas and hypopneas had been obliterated, but our
data show that flow limitation appears to be more
sensitive overall than snoring. Thus, flow limitation
may be the best single feedback variable on which to
perform a therapeutic titration, while snoring may
play a complementary role if multiple signals are
used.

Source: https://journal.publications.chestnet.o ... 28/685.pdf

Dated 1998

Next report:

Dr Barry Krakow about Flow Limitation,

As of Dec 2007

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. "

The following is from a 2011 report in the chestnet.org that I can't provide a link to:

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 of UARs:

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.3,36 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.3 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.42


Abbreviations:

CAP = cyclical alternating pattern; CPAP = continuous positive airway pressure; LAUP = laser-assisted uvuloplasty; MSLT = multiple sleep latency testing; NREM = nonrapid eye movement; OHS = obstructive hypopnea syndrome; OSAS = obstructive sleep apnea syndrome; Pes = esophageal pressure; REM = rapid eye movement; RERA = respiratory effort-related arousal; UARS = upper airway resistance syndrome


Source:

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

{need subscription to enter}

But see the same content here:

http://www.apneaboard.com/forums/Thread ... e-Syndrome


________________________________________
This is my own report:

Measuring Flow Limitation (FL).

Resmed way:

Assign a weight to the flatness of the respiration waves:



Example from my own respiration waves:

FL rises when the respiration waves become flat on top.




On ResScan, some waves are rounded on top and some are flatter. The rounded are good and the flatter are bad:

[jnk]

Sorry. Had a busy few days.

. . . Home treatment machines that record flow limitation generally do so, not so much for the purpose of treating it, but for the purpose of using that information for trending purposes and to indicate the possibility of approaching significant events. The auto-titrating machines can use that information to raise pressures preemtively in the interests of preventing obstructive apneas and hypopneas.

Hi jnk, nice write-up, thanks. Do you use an ASV? . . .

No. I was on autobilevel for about 5.5 years, but recently switched myself to an S9 AutoSet.

Re. your last paragraph, is that input you picked up from ResMed or from a specific ResMed or Respironics reference? If so, I'd sure like to see the link or text. . . .

This presentation is the most comprehensive treatment of ResMed's thoughts and approaches to SDB, including flow limitation: http://www.resmed.com/us/multimedia/und ... 40x380.swf

Here are some recent words in connection with the S9:

AutoSet treats and prevents apneic events. Because AutoSet responds to flow limitation, and flow limitation often precedes snoring and apneas, AutoSet is able to preemptively treat apneic events and prevent more serious, subsequent events from occurring.--http://www.resmed.com/us/assets/documen ... er_eng.pdf

The following explanation is older, but it gives an idea of the foundations of the AutoSet algorithm and the ideas behind it:

AutoSet device's Three Lines of Defence

1. Flow Limitation
What is flow limitation?
-A physiological change in the status of the upper airway
-Causes a spectrum of closure, from subtle narrowing to partial collapse

What is the significance of flow limitation?
-It usually precedes snoring and apnea. It is therefore, usually, the earliest sign of impending airway collapse
-Airway changes limit flow despite respiratory effort and in fact, cause increased respiratory effort. This may lead to arousal

How do I observe flow limitation?
-The inspiratory flow time curve represents inspiratory flow limitation
-The shape of the curve indicates the status of the upper airway. A normal upper airway is observed as a bell-shaped curve. The curve flattens with increasing flow limitation and airway narrowing/ closure

How does a ResMed AutoSet device measure flow limitation?
It calculates flow limitation on a breath-by-breath basis, detecting and responding to subtle changes

How does a ResMed AutoSet device respond to flow limitation?
If flow limitation is detected, AutoSet Spirit responds by gradually increasing pressure to bring the airway back to normal. Typically, this helps prevent snoring and apneas
If no further events occur, AutoSet Spirit gently decreases the pressure, towards the minimum set pressure

http://www.resmed.com/au/clinicians/com ... clinicians

That information refers to this 1998 study: http://journal.publications.chestnet.or ... 28/685.pdf

Another older reference showing how flow limitations are responded to in order to preemptively prevent events:

The foundation of the technology in VPAP Malibu is the AutoSet algorithm. This algorithm has been specifically designed to preemptively respond to flow limitations, often preventing airway closure before it occurs.-- http://www.sleepdt.com/articles/2-5/

[hobbs]

http://www.resmed.com/us/multimedia/und ... 40x380.swf

[Papit]

My Sleepy Head graphs don't show a separate flow limitation graph. It is checked under graphs in preferences.

Stormynights, when did you get your VPAP Adapt? Only the more recently made units of the same model name offer the FL graph for real.

[Papit]

Thanks, jnk and avi, for the very thorough reply posts. They were good on-topic readings and I get that ResMed's algorithm jumps quickly to pre-emptively treat apneas and hypopneas. I have a recently produced S9 VPAP Adapt so I can see the FL graph (see below at bottom of second image). With my AHI reduced to almost nothing, what I still don't understand is why my FL graph is showing so many and such strong flow limitations throughout my sleeps every night since June when I got the machine. (I also notice a great amount of continuous "ragged hairy" fluctuations in both the Flow and Pressure graphs that suggest the Adapt is working hard continuously all night long.)

Neither do I understand why I saw only very few and very weak flow limitations all year before when I was using the S9 AutoSet which achieved an average AHI of about 17.0. Am still waiting for my doc's response after about a month now. ResMed tells me that the FL graph/data does offer treatment-related information, but they won't forward it to me as I'm a patient, not a doctor or medical professional. Can you or anyone else here get a copy of the relevant FL graph/data treatment guidance?



Typical Flow Limitation graph (at bottom of set below)
[/quote]

[barbaraz]

Flow limitation, when constant as it is for me, can be almost as bad as my having more apneas. I have very few apneas, but constant hypopneas or flow limitation. I cannot raise the pressure as my sinuses have a fit... even when using the Oracle (the only mask I can use and I have tried over 15) My sinuses despise having that air forced through them via CPAP.

My answer, discovered on this forum just recently, was to wear that awful thing called a c-collar. I am awake during the day! I feel as if I have really slept for the first time in decades. Been a faithful but disappointed CPAPer since 2007 and it was a fight to get that sleep study done. I knew I had a sleep problem. Had to go to a psychiatrist before my primary would write the script and he did so most reluctantly.

Thanks to Sheffey who brought up the subject of the collar. Finally, I am getting real sleep. Now to undo the damage that constant low oxygen levels have done to my energy and to my physical and mental being. I have been dragging myself along, thinking I was doing all I could. Now I see there is more I can do and want to do. Thanks again, Sheffey!

[NeedHelp2]

Barbaraz, where can I learn more about how this c collar could help my flow limitations?