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:
