Flow Limitation?

Jay Aitchsee wrote:

penuel wrote:About JNK post, imo, a lot of water came down to Jordan river since Jeff's reference to 1981 report...

Avi, your presentation of flow limitations is interesting. Thank you.

Let me ask you this, can you cite anyone on this forum who had successfully adapted to xpap, i.e., used it through the night with minimal leaks, and obtained a long term AHI less than 5, but still suffered from excessive daytime sleepiness (EDS), who then switched to a bilevel, or equivalent, as suggested by your references and overcame their EDS?

I see people switching to bilevel as a means to tolerate PAP, but I don't recall seeing any who switched after mastering PAP solely to overcome EDS who were successful. Have you?

The difference between EDS and RES is that RES = Residual Excessive Sleepiness, meaning that a CPAPER experiences EDS= Excessive Daytime Sleepiness. Using the word EDS by itself does not need to relate to CPAP. In your question, I think that you are relating to Dr Barry Krakow who himself suffers from FL. In the past, he used to post in this website. See in this WIKI what he posted about URS:

wiki/index.php/UARS
It's at the top of this Window

Upper Airway Resistance Syndrome
(Redirected from UARS)

Jay, in your question you start with one set which is this:

can you cite anyone on this forum who had successfully adapted to xpap, i.e., used it through the night with minimal leaks, and obtained a long term AHI less than 5, but still suffered from excessive daytime sleepiness (EDS), who then switched to a bilevel, or equivalent, as suggested by your references and overcame their EDS?

But next, you add: who then switched to a bilevel,


Dr Krakow switched to a BiLevel b/c he had to raise the pressures above 15 cm which calls for switching from CPAP or Auto CPAP to a BiLevel = BIPAP, in order to reduce the exhalation pressure.

Is this to what your' referring?

As to Jnk's posts I find him often to be a "shmearer" = a smudger, and of course he has buddies.

penuel wrote:Is this to what your' referring?

No, not exactly, Avi. Without quoting your whole post, let me just pull out some parts of it.

You say,

A Bipap would be the choice XPAP to deal with FL. By using a Bipap I should be able to reduce the FL considerebly more than by using APAP or CPAP

Dr K says,

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)...

I have treated thousands of patients with UARS who had either no apneas or hypopneas or an AHI less than 5. Nearly all these patients suffered sleepiness or fatigue from their conditions, and many suffered from insomnia and nocturia...

Along these lines, let me mention a working theory we have developed about UARS and why bilevel might be the best option for its treatment...

The reference material you provided implies SDB could be treated with C/APAP, reducing the AHI to less than 5, but the patient may still suffer from EDS because flow limitations (not included in the AHI number) haven't been fully treated - resulting in disturbed sleep and, therefore, EDS.

My question is, do you know anybody on this forum who outwardly seemed to have successful xpap therapy (compliant, low leaks, low AHI), but still suffered EDS who switched to a bilevel machine and overcame the EDS. Aside from Dr K, that is?

Jay

Jay, why do you start mixing EDS following a treatment when the subject is FL?


The following is the content of the article in Chest website from 2011, authored by the following:

Olukayode Ogunrinde, MD; Herbert J. Yue, MD; and Christian Guilleminault, MD, BiolD

Dr. Ogunrinde is Clinical Fellow, Department of Sleep Medicine, Stanford University; Dr. Yue is Clinical Fellow, Department of Sleep Medicine, Stanford University; and Dr. Guilleminault is Professor, Division of Sleep Medicine, Stanford University Medical School, Redwood City, California.
Drs. Ogunrinde, Yue, and Guilleminault have disclosed no significant relationships with the companies/organizations whose products or services may be discussed within this chapter.
Objectives
1.Identify the demographics of previously described patients with upper airway resistance syndrome (UARS).
2.Describe the polysomnographic findings in UARS, including markers of increased respiratory effort.
3.Discuss the clinical symptoms of UARS and their link to functional somatic syndromes.
4.Describe the EEG findings during a respiratory event in UARS.
5.Identify the current treatment options for UARS, as well as the benefits and risks of each.

Key words: cyclical alternating pattern; sleep-disordered breathing; upper airway resistance syndrome

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

Professional Practice Gap

Over the past few years, numerous articles have been published that have increased our understanding of the features of upper airway resistance syndrome (UARS). UARS has been previously described as a distinct clinical syndrome, although there is ongoing controversy and some consider it to be part of a spectrum of sleep-disordered breathing that includes primary snoring, obstructive hypopnea syndrome (OHS), and obstructive sleep apnea syndrome (OSAS). However, patients with UARS present with different polysomnographic abnormalities and do not meet generally accepted criteria for either apneas or hypopneas. The lack of education about UARS in the medical community has allowed these patients to go undiagnosed and untreated. Increased research into UARS will help us to identify the optimal treatment for these patients, as well as to educate clinicians about this relatively under-recognized population.

Introduction

UARS is characterized by abnormal respiratory effort, nasal airflow limitation, absence of obstructive sleep apnea, minimal pulse oximetry fluctuation with oxygen saturation nadirs ≥92%, and frequent nocturnal arousals or reflex brainstem activation.1 It was first recognized in children in 1982, although the term UARS was not used until the first adult cases were reported in 1993.2,3 The incidence and prevalence of UARS has been systematically investigated in a recent São Paulo epidemiologic study4 (discussed below in “Epidemiologic Studies of UARS”). Prior to the São Paulo study, some have reported prevalence rates of 8% to 20% in the literature.5,6 We now know that this syndrome has recognizable clinical and polysomnographic characteristics that differ from those observed in patients with OHS/OSAS. UARS occurs in all age groups without any clear sex preferences, although some studies suggest that women may be at increased risk. UARS has the potential for significant impact on the daytime functioning and quality of life in untreated patients and there is growing evidence to suggest that symptoms are progressive without treatment.

Pathophysiology

Sleep-disordered breathing affects multiple aspects of the upper airway and respiratory tract, including the nasal passage, nasopharynx, oropharynx, hypopharynx, and supraglottic larynx. In these patients (primarily those with OSAS), multiple changes to the control of the upper airway have been described, including development of lesions in the soft tissue and changes in the upper airway dilator muscles, all in response to repetitive airway obstruction.7 Histologic studies have demonstrated significant abnormalities in biopsy samples taken from the palate and posterior pharynx. The most consistent finding has been evidence of a neurogenic lesion, with progressive abnormalities identical to those associated with a polyneuropathy.8,9 In patients with OSAS, poor responses to airway collapse or instability are often seen and thought to be related to blunting of the afferent upper airway receptors. In contrast to patients with OSAS, similar lesions have not been described in those with UARS. In a study of 45 subjects evenly divided into one group with OSAS, one group with UARS, and a control group, no significant sensory differences in palatal two-point discrimination were seen between control individuals and those with UARS.10 Of note, those with OSAS were observed to have significant decrements in their palatal two-point discrimination, consistent with the prior findings of neurogenic lesions. Other contributors to the pathophysiology of UARS include an increase in airway collapsibility owing to abnormal inspiratory and expiratory airflow dynamics.11,12 Increased nasal airflow resistance has also been thought to contribute to the breathing impairment seen in UARS, with frequent clinical findings of collapsible nasal valves, enlarged nasal turbinates, a deviated septum, or a combination of these findings in UARS patients.13

Epidemiologic Studies of UARS

The only known epidemiologic study of UARS has been one performed as part of an epidemiologic study of sleep disorders in the city of São Paulo, Brazil, in 2007. The São Paulo Sleep Epidemiologic Study is a population-based, cross-sectional study of sleep disturbances and their risk factors.4 Methodological details of the São Paulo Epidemiologic Sleep Study are published. A total of 1,042 volunteers underwent polysomnography at the Sleep Institute of the Federal University of São Paulo; the refusal rate was a very low 5.4%. The criteria used for scoring for UARS were those described by Bao and Guilleminault.14 Polysomnography was performed according to American Academy of Sleep Medicine guidelines.15 The prevalence of UARS for the total sample was 15.5%. It was higher in women (21.87% vs 15.19%) and also in people aged <40 years (31.04% vs 5.49%).

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.16 In a separate study, upwards of 30% of subjects with UARS had abnormal sleep-onset latency on the Maintenance of Wakefulness Test.17 Individuals with abnormal airway anatomy are at increased risk, including those with a decreased retrolingual space, narrow nasal passages, or a small neck circumference.6 Patients are typically not obese, with a mean BMI often <25 kg/m2.3 They are also usually younger than those in whom OSAS is diagnosed, with a mean age of approximately 38 years.3 Snoring is not a requisite symptom, with 10% to 15% or more of patients having never or only intermittently snored.3,18

Patients with UARS are also more likely to report symptoms of frequent nocturnal awakening with difficulty falling back to sleep.19 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.20 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%).21 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.22 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.23 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.24 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.25 Table 1 lists symptoms associated with UARS.



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Tables and other illustrations are not included
Table 1—Clinical Features Associated With UARS


Daytime symptoms Excessive daytime sleepiness
Fatigue
Morning headaches
Myalgias
Difficulty concentrating
Sleep disturbances Frequent nocturnal awakenings
Difficulties initiating sleep
Insomnia
Bruxism
Restless leg syndrome
Unrefreshing sleep
Autonomic nervous system Hypotension
Orthostasis
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
Alpha intrusion during sleep

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Diagnosis

Patients with UARS can present with a constellation of generalized and/or specific symptoms and a clinical examination often demonstrates craniofacial abnormalities. As noted previously, many of the prior difficulties in making a diagnosis of UARS arose because these patients do not meet polysomnographic criteria for OSAS. In the original description of UARS back in 1991, repetitive increases in upper airway resistance associated with arousals were observed in 15 subjects, defined as an increase in the peak inspiratory esophageal pressure that immediately preceded a transient arousal.3 A diagnosis of UARS requires patient symptoms, evidence of upper airway narrowing or craniofacial abnormalities, and appropriate associated polysomnographic findings. When an overnight polysomnogram is performed on a patient with UARS, there are no apneas with a hypopnea index <5, the oxygen saturation is usually >92%, and there is evidence of respiratory effort-related arousals (RERAs). Flow limitation can also be present, identified as an abnormal contour in the nasal pressure transducer signal waveform.3,14 Other techniques have been used to detect the subtle changes in respiration, such as the oral/nasal thermistor, pneumotachograph, quantitative respiratory plethysmography, and nasal cannula/pressure transducer, although measurement of esophageal pressure (Pes), or esophageal manometry, remains the gold standard.26,27

Typically, a pediatric feeding tube is used in the measurements of esophageal pressure during sleep. A number of characteristic Pes patterns associated with RERAs have been described.28,29 Pes crescendo (Fig 1) is a progressive increase in negative peak inspiratory pressure with each breath that terminates with an EEG arousal, typically a burst of alpha or delta activity. Other changes include sustained continuous respiratory effort; the Pes tracing shows a stable and persistently abnormal negative peak inspiratory pressure, different from the baseline pressure and present for more than four breaths. In both instances, the increase in respiratory effort is not usually associated with oxyhemoglobin desaturation and there may be a flattening in the nasal pressure transducer waveform, consistent with flow limitation (Figs 2, 3). The termination of both Pes crescendo and flow limitation is called Pes reversal, which is a decrease in respiratory effort indicated by a less negative peak inspiratory pressure, often without an associated EEG arousal (Fig 4). Heart rate variability is often seen during events of increased respiratory effort. Patients with UARS may also have more negative peak inspiratory pressure during nonrapid eye movement (NREM) sleep, especially slow-wave sleep, as compared with rapid eye movement sleep.30 Patients with UARS have also been described to have less NREM (both stage 1 and stage 2) sleep and more slow-wave sleep when compared with other patients with sleep-disordered breathing, although no significant difference in arousal threshold was seen.31

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Figure 1. Pes crescendo. Note the esophageal pressure recording at the bottom of the tracing.
L13Fig2

Figure 2. Flow limitation on a polysomnogram. Note the association between CAP, with phase A2 and A345 indicative of sleep disruption, and the continuous flow limitation seen on the nasal cannula recording (duration of sample, 5 min).
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L13Fig3
Figure 3. Flow limitation on polysomnogram monitored at slow speed (duration of sample, 30 s) Note the abnormal shape of the nasal cannula pressure transducer flow curve, with disappearance of the normal “round” curve with each breath. Note also the downward movement of the finger plethysmography (finger PPG) over-curve indicating sympathetic brainstem activation. Simultaneously, the EEG (right side of figure) changes to lower amplitude and faster frequency, indicative of a short arousal response.
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L13Fig4

Figure 4. Pes reversal. Note the esophageal pressure recording at the bottom of the tracing.



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Patients with UARS may also have characteristic changes in their EEG patterns during sleep. As noted previously, prior studies have shown that subjects with UARS have increased amounts of alpha frequency on EEG when compared with patients who have either OSAS or OHS.32,33 Other investigations using power spectrum EEG analysis have demonstrated that UARS patients have more theta and low alpha powers (7 to 9 Hz) during NREM sleep and more delta power during rapid eye movement sleep.29 Although an arousal is frequently seen following termination of an event associated with increased respiratory effort (ie, Pes crescendo or continuous increased respiratory effort), studies have shown that Pes reversal can occur in the absence of any clear arousal. In a study of 15 patients with UARS, a spectral analysis was performed on EEG data from central leads. The authors noted EEG changes in association with Pes events, including an increase in delta frequency activity prior to Pes reversal, and with increases in other frequencies after the event, suggesting that significant EEG changes are occurring with Pes events, even when an arousal is not visible.29

Lastly, patients with UARS have evidence of increased rates of the cyclical alternating pattern (CAP) on EEG. CAPs are a well-described pattern of NREM sleep, defined as electrocortical events that are distinct from background EEG activity and occur with a periodicity.34 An increase in CAP frequency is generally associated with sleep instability/disturbance and CNS hyperactivity and has been observed in a number of conditions, including sleep-disordered breathing, restless leg syndrome, and insomnia.31 In a study of 30 patients with UARS, increased CAP rates were seen in addition to more EEG arousals and higher markers of sleep disruption and transition (A2 and A3 indices of CAP).35 More importantly, the CAP rate was correlated with daytime symptoms of sleepiness and fatigue. This finding suggests that normalization of the breathing events in patients with UARS/sleep-disordered breathing may not be sufficient to fully treat their daytime symptoms and that addressing EEG abnormalities is important as well.

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.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

Conclusion

Although UARS has a symptomatology close to the one seen in patients with OSAS, there are distinct clinical differences between the two syndromes. In clinical studies, it is seen more in younger, slim subjects and in premenopausal women; it is more commonly associated with an increase in vagal tone during sleep than with sympathetic hyperactivity (as seen in association with apnea and hypopnea and oxygen desaturation).21 Can individuals with UARS become patients with OSAS? Guilleminault and colleagues1 suggested that weight increase (with development of a chest-bellow problem related to abdominal obesity) and the association of the supine position and sleep (leading to a restrictive impairment and secondary oxygen saturation drop and sympathetic hyperactivity) will lead to passage from one presentation to another with different complications; but more data are needed from additional systematic, longitudinal studies.1 UARS is underdiagnosed owing to unfamiliarity with the syndrome and the lack of polysomnographic criteria for either hypopneas or apneas that are associated with other types of sleep-disordered breathing. The advent of use of an esophageal catheter for esophageal pressure measurement (Pes) has allowed clinicians to more clearly identify patients with UARS. Although Pes measurement is the most sensitive method available to detect the abnormal respiratory events in UARS, it has not been used widely for several reasons, including lack of clinician experience and patient reports of discomfort. Usage of the nasal cannula pressure transducer allows recognition of flow limitation.43 But guidelines on how to tabulate the amount of flow limitation during total sleep time are lacking. Patients with UARS have significant impairment in their daytime functioning, with reports of sleepiness, fatigue, and sleep disruption. A follow-up study of these patients has shown that they often go untreated and experience progressive worsening of their symptoms. Among those patients who have been treated, typically with CPAP therapy, many have experienced symptomatic improvement. The current fund of knowledge regarding UARS has been growing, and we are beginning to understand the underlying pathophysiology.

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Jay, about the daytime excessive sleepiness vs UARs this may answer your question:

It's an older post than the long one which I posted above from 2011.

As to your question if I know anyone who reached an adequate treatment on a CPAP but suffers from Excessive Daytime Sleepiness, well there are hundreds of ex-posters who don't show up anymore. Who knows how are they doing? A survey done in 2009 in France discovered that about 12% of CPAP users were suffering from daytimes sleepiness. Most were at a younger age. Excluding depression, RLS, and COPD, the percentage drops to 6%. About the BiLevel that should be effective to treat FL, I don't know. Dr Krakow talks about it may be b/c he himself has UARs and uses a BiLevel with hi inspiratory pressure but a reduced expiratory pressure.
While going over the above mentioned report from 2011 Chest Journal I am going to try going to sleep without my upper removable denture and see if it makes a difference in the FL. BTW, it was very difficult to post the above LONG post which I had to do b/c there is no free access to it anymore. I had to fill out all kinds of questions including deciphering " are you a person"words. Is it something new? I don't think that I ever going to repeat here such experience.


See if you can access this report which might answer your question:

A cause of excessive daytime sleepiness. The upper airway resistance syndrome. FREE TO VIEW

C Guilleminault; R Stoohs; A Clerk; M Cetel; P Maistros

Author and Funding Information

Chest. 1993;104(3):781-787. doi:10.1378/chest.104.3.781

http://journal.publications.chestnet.or ... id=1044407

Hello Avi,

Thanks for going through the work to post the 2011 article from Chest. It is quite informative.

In response to your question,

penuel wrote: Jay, why do you start mixing EDS following a treatment when the subject is FL?

I don't feel I'm mixing anything.The clinical portion of the above paper you provided says, in part,

Typical symptoms reported by patients with UARS include excessive daytime sleepiness, fatigue, difficulty concentrating, morning headaches, and unrefreshing sleep.

Additionally, your previous citations imply UARS (FL) may exist independent of OSA further implying that successful treatment of OSA by C/APAP may result in a low AHI, but significant UARS may remain, thus contributing to disturbed sleep and EDS.

Both you and Dr K imply UARS may be best treated by BiPAP. See previous quotes.

I was simply asking for anecdotal evidence of the superiority of BiPAP treatment over C/APAP in treating UARS when I asked if you knew anyone who had successfully adapted to C/APAP, resulting in a low AHI but their EDS remained, but by switching to a BiPAP, overcame the EDS as well. Apparently not.

Thanks for the discussion.
Jay

Jay,

I appreciate how your questions get to the heart of the matter.

For an adapted CPAP user, FL/UARS/RERA only matters in the context of residual symptoms. And if there are residual symptoms, they can be addressed with a change of pressure or modality to see if the symptoms improve, and that can be done without getting distracted with what the home machine reports as possible precursors that may or may not be related to arousals or the symptoms. Docs are more likely to respond well to "I am still tired and sleepy" than to respond well to "my machine says I have FLs." The first statement makes sense to the doc who might then recommend bilevel (especially if the patient hints stongly at that, asking if it might help). The second statement sounds like a patient obsessed with data he misunderstands.

I have no anecdotal evidence for your question. Part of the reason is that someone who has "successfully adapted to C/APAP" is generally someone with improved EDS, or else he often has little motivation to continue. After all, it was likely the symptoms that took him to the doc office; the numbers/data were just what were used by the doc to show payers that PAP might help the symptoms. There are exceptions to that, of course. But I believe that is the most common scenario of how someone makes it to PAP therapy.

That said, my understanding of the way it works is that if someone continues to be excessively tired and sleepy, the next step is to help the doc document that fact in a way that shows that the patient has "failed CPAP." In that case, payers may pay for a bilevel trial. Added comfort can alleviate the PAP-related arousals that plague some who have trouble feeling rested on PAP. Especially when pressure above 15 cm is needed.

Problem is, most patients give up before that point, since most patients don't realize that bilevel is an option for those who are not sufficiently helped by CPAP/APAP.

An addded aspect to this is to keep in mind that bringing up UARS to a doc can sink your own ship. Some docs aren't on board with it, since some payers consider UARS to be an interesting theory that never quite made it mainstream in its efforts to circumvent the criteria for qualifying for PAP. Dr. K has a room full of financially-minded nerds who find ways to get around that little hurdle. Many docs don't have the personnel for that.

Not a doc. Just opinionated.

Hope that helps.

-Jeff

Yes, thank you , Jeff.
I think, perhaps because I didn't use the term "residual", Avi didn't grasp the essence of my questions, which were motivated by his references to bilevel in his posts.
I understand that bilevel may allow adjustment and adaptation to the therapy in those that are struggling, but I couldn't recall anyone on this forum who moved on from "successful adaptation" of CPAP with residual EDS to bilevel without EDS, though there are many who have "successfully adapted" by my definition meaning they are compliant, have low leaks, low AHI, and "on paper" should not be suffering residual symptoms, but they do. It is these people Avi's posts hint may be helped by bilevel and I was curious to know if there were any.
Thanks for your comments.
Jay

jnk wrote:Jay,

I appreciate how your questions get to the heart of the matter.

The second statement sounds like a patient obsessed with data he misunderstands.

Problem is, most patients give up before that point, since most patients don't realize that bilevel is an option for those who are not sufficiently helped by CPAP/APAP.

An addded aspect to this is to keep in mind that bringing up UARS to a doc can sink your own ship. Some docs aren't on board with it, since some payers consider UARS to be an interesting theory that never quite made it mainstream in its efforts to circumvent the criteria for qualifying for PAP. Dr. K has a room full of financially-minded nerds who find ways to get around that little hurdle. Many docs don't have the personnel for that.
Jeff

+1to both of you guys!! I just want to add that try as I did and with lots of cooperation from my Dr and his staff,insurance, as well as the DME(might have been financially motivated but very kind nevertheless) , I could not get Mike a new 5-year replacement with a Vpap unless he underwent another sleep study which we weren't willing to do at this time. I can't really prove that he NEEDS bipap since we never had a problem with FL and his AHI stayed below <5.0 on Autoset, although RDS was and still is a problem which Drs believe is caused by hip pain and some age-related medical issues. I bought my own used Vpap and use it almost like Autoset with very narrow range but somehow he sleeps better and longer, the PS seems to agree with him which is the only difference I can discern, his data is better and he's a little less sleepy during the day after his morning nap. Our real problem is with mask leaks which could probably be solved if he was aware of it during the night and could make some slight adjustment after turning over. I'm still trialing the Air and Simplus, the leaks are better with both, but he takes them both off during the night, "something doesn't feel right"?? Trying to figure it out.

In general, I believe that simply increasing pressure is the first step in preventing arousals that come from less-than-hypopnea changes in the airway. And if that takes a person over 15 cm, there is definitely an argument for bilevel.

Other than that, bilevel would be for comfort reasons in someone who may be having arousals as much from PAP discomfort as from airway trouble--the airway may be reacting to the discomfort.

That is my understanding as a patient, based on my personal take on the following practice suggestions about decisions made by a sleep tech during a titration:

CPAP exploration does have utility; upper airway resistance can be four times normal despite selection of a pressure that eliminates apneas and hypopneas, and this residual high airway resistance can lead to repetitive arousals and insomnia. Reduction of this resistance has been demonstrated by increasing pressure until . . . the shape of the inspiratory flow limitation curve are normalized, or by increasing pressure by 2 cm H2O but no higher than by 5 cm H2O.

. . . 4.3.1.1 If the patient is uncomfortable or intolerant of high pressures on CPAP, the patient may be tried on BPAP. If there are continued obstructive respiratory events at 15 cm H2O of CPAP during the titration study, the patient may be switched to BPAP (Consensus).
This recommendation is based on consensus agreement by the PAP Titration Task Force and Option-Level evidence (1 level IV study and 1 level V study). However, this recommendation does not imply that BPAP is more effective than CPAP at maintaining upper airway patency. Additionally, efforts should be made to explore why the patient is uncomfortable or intolerant of high pressures on CPAP and to remedy the situation before trying the patient on BPAP.

--http://www.aasmnet.org/Resources/clinic ... 040210.pdf

My personal experience was that the tech who did my titration found that I "fought" the pressure and did not react well to it until bilevel was tried on me. Of course, that may have had something to do with the fact that the last words I said to the tech as he headed to the booth for the night were, "How do you feel about bilevel?"

I believe the same principles apply over time with treatment.

I presently use an S9 APAP, because I find that using 3 cm EPR on it feels very nearly as comfortable to me as true bilievel.

DoriC wrote:I bought my own used Vpap and use it almost like Autoset with very narrow range but somehow he sleeps better and longer, the PS seems to agree with him which is the only difference I can discern

jnk wrote:I presently use an S9 APAP, because I find that using 3 cm EPR on it feels very nearly as comfortable to me as true bilievel.

Interesting, thanks to you both.
J

jnk wrote:In general, I believe that simply increasing pressure is the first step in preventing arousals that come from less-than-hypopnea changes in the airway.

CPAP exploration does have utility; upper airway resistance can be four times normal despite selection of a pressure that eliminates apneas and hypopneas, and this residual high airway resistance can lead to repetitive arousals and insomnia. Reduction of this resistance has been demonstrated by increasing pressure until . . . the shape of the inspiratory flow limitation curve are normalized, or by increasing pressure by 2 cm H2O but no higher than by 5 cm H2O..

I presently use an S9 APAP, because I find that using 3 cm EPR on it feels very nearly as comfortable to me as true bilievel.

So would "nearly" be the operative word here since I have no way of knowing what "nearly" means? Thanks for that article, it made me review the last 2 months of data and it's clear that his 95% is mostly in the 12.5 range which I kind of knew but was reluctant to increase the pressure because of leaks but I'm thinking now that perhaps if I can get the min pressure closer to his 95% that in itself might help with the leaks. So I'm going to just increase the Epap 1cm from 10 to 11 and leave everything else the same for now. Reading about arousals and your explanation really encourages me, so maybe it's the pressure and not the mask!There should be a lightbulb smilie! Thanks.

Many docs routinely prescribe 2 cm above titrated pressure. That may cover the need to keep the airway stable beyond apnea and hypopnea.

By "nearly" I mean that if I consciously think about it, I can tell a slight difference. Fortunately, I'm very good at keeping myself from consciously thinking. My wife says it's a talent that only males possess.

I would say an S9 with 3 cm EPR feels like about 95 to 97 % bilevel. It may not help work of breathing all that much, I don't know--but it has that same smooth rock-a-bye lulling-to-sleep sensation to me that bilevel offers.

Is Bilevel the Answer?

{to UAR, taken from CPAP Wiki at the top of this page. Most likely posted by Dr Barry Krakow}

Why bilevel works so well is still a puzzle. But, what’s so intriguing is that the subjective and objective findings match. That is, nearly all patients who switch from CPAP to bilevel state that it is easier (subjectively) to breathe out with bilevel. And, during their titrations, the ratty airflow signal disappears on expiration (objectively) and is replaced by a smooth and rounded curve indicating normal expiration.

Should you be able to produce the same results with CFLEX, APAP, etc? Presumably so, except for one “large” difference. You cannot generate the same gradient or gap between IPAP and EPAP with any of the other devices. And, in our clinical and research experience, we are using gaps of 4 to 12 cm of water in our patients. My personal bilevel settings are 21/12.5 for a gap of 8.5.

In our prescriptions for bilevel, I would venture that the average gap is in the 5 to 6 range with tremendous variation, including some with a gap of only 2 or 3. Those with a lower gap requirement would likely do as well on FLEX or APAP, but to repeat, the large majority of our patients have a gap of 4 or greater.

Still, it would be nice to have a respiratory physiologist explain to us why the larger gap is so effective. As an internist and sleep medicine physician, there are only two obvious theories that stand out. First, what if we’ve always assumed, mistakenly, that airway pressure had to be constant for both inspiration and expiration? I think it has already been proven by other researchers that you actually need higher pressure to keep the airway pinned open on inspiration and a lower pressure on expiration. If that’s so, then is bilevel the best system because it provides the exact pressure you need (not too much and not too little) during expiration.

The second idea relates more to the psychophysiological response to PAP therapy. Maybe the larger gradient simply gives the patient a distinctly more comfortable feeling, because the lower pressure creates a feeling so much closer to breathing normally (without PAP). If this theory were accurate, though, it would imply that over time as you get used to any sort of PAP therapy, then perhaps the gap would narrow and eventually you could use fixed CPAP again. If this were true, I would expect more people to eventually adapt to fixed CPAP pressure, and I don’t believe that’s occurring.

Summing Up

Last and not least, 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.

I\'ve lived through this problem and I've breathed through it, and no other single factor enhanced my sleep quality to the level I currently enjoy and am eternally grateful for experiencing.

Surely, this is something to sleep on. I do, night after night.

I'll try to word my question without confusing you...does anyone know the average measurements of inhale/exhale that occurs with normal breathing at rest without cpap?

I don't know the answer.

EPAP fixes apnea. IPAP helps the other stuff. As I understand it.

Comfort is a matter of subjectively balancing all the factors to make the patient as comfortable as possible as often as possible without needlessly allowing increase of reported apnea/hypopnea.