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Explanation of RE and RERA on Sleepyhead
Hi members, I finally got SleepyHead on my computer. I failed in a couple of attempts but then I got a new hard drive and it wasn't a problem. So happy to have it. Can't believe the amount of information it gives you.

I read over RobySue's Guide for Beginners and was amazed at her knowledge. So lucky to have her on the Board. She might have explained this, but I can't remember. But when they talk about the RE (respiratory effort) or RERA (respiratory effort related arousal index) what does it mean? Of course, the name gives me an idea, but would like an informed explanation from one of you people (like RobySue) who understands it all.

Thanks in advance.

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Good question! I'm interested too.

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(12-02-2016, 05:36 PM)sleepytimegal Wrote: But when they talk about the RE (respiratory effort) or RERA (respiratory effort related arousal index) what does it mean? Of course, the name gives me an idea, but would like an informed explanation from one of you people (like RobySue) who understands it all.

Thanks in advance.


In polysomnography, RERA is defined as a respiratory parameter that indicates an arousal associated with a respiratory event and an increase in respiratory effort. This greater respiratory effort occurs as a response to an increase in upper airway resistance, which is a factor present in the pathophysiology of sleep-disordered breathing, such as obstructive sleep apnea syndrome and upper airway resistance syndrome. https://www.ncbi.nlm.nih.gov/pubmed/20944976

Basically, it is telling you that your xPAP machine encountered airway resistance as derived from the flow data. This might be a partial obstruction which leads to snoring and/or to extra effort to breathe -- but the event does not rise to the scoring level of an apnea or hypopnea. RERAs are not standardized and some machines do not even count them.
"The object in life is not to be on the side of the majority, but to escape finding oneself in the ranks of the insane." -- Marcus Aurelius
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Allow me to hijack the thread Thanks

Is there anyway to reduce RERA's?

What is considered too many? I have from a couple events a night up to 17, max. I have tried to tie them in with flow limitations and or snoring but they do not line up on my graph.

By the way my AHI is usually below one. Feel like a champ the next day with high RERA's or just a few.

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Let's see if this helps. Although RERA is recorded by some CPAP machines, it is not well documented what exactly is being measured fas a surrogate for increased esophageal pressure which is the defining clinical measurement using PSG. This article touches on some of the questions being tossed around here. CPAP is sometimes used to treat UARS, but bilevel pressure seems to show better results. I'll need to do some more digging to find some references pertaining to treatment. Maybe we can use this thread to put together some information we can use to improve the current wiki on Apneaboard.

Source: Sleep-Disordered Breathing
Puneet S. Garcha
Loutfi S. Aboussouan
Omar Minai
Published: January 2013 http://www.clevelandclinicmeded.com/medi...breathing/

Upper Airway Resistance Syndrome

UARS can cause symptoms similar to those found in OSA, yet this syndrome is considerably different due to the absence of oxygen desaturation found during sleep studies. Upper airway resistance syndrome was a term first applied to patients who were found to have excessive daytime sleepiness without a clear cause on a multiple sleep latency test, which was further documented by an overnight polysomnogram.18 These patients were often said to have idiopathic hypersomnia. After many of these patients were further tested with invasive polysomnography (including an esophageal balloon transducer and full pneumotachograph), they were found to have increased upper airway resistance. Resistance manifested as increased negative esophageal inspiratory pressure.

UARS is characterized by repeated arousals, due to resistance to airflow in the upper airway, that lead to excessive daytime sleepiness and fatigue. Snoring has been noted to be present in association with these brief arousals, but snoring is not necessary for identification of UARS. UARS events are noted to be typically short: 1 to 3 breaths in duration. These events have been termed respiratory effort-related arousals (RERAs). In UARS, unlike in OSAHS, there is no evidence of oxygen desaturation. For the measurement criteria to be classified as a RERA, there must be a pattern of progressively increased negative esophageal pressure that is terminated by a sudden change in the pressure to a less-negative level and a sleep arousal. Furthermore, the event must last 10 seconds or longer.


In an epidemiologic study of sleep disorders in more than 1000 volunteers in Brazil, the prevalence of UARS in the general adult population was 15.5% UARS occurs in a less-obese, younger individuals and more commonly in women versus men than does OSAHS. The natural history of this disorder is not well understood.


Guilleminault and coworkers demonstrated that many nonapneic patients show a reduction in cross-sectional area of the pharynx during sleep. Reduction in airway area is sufficient to avoid hypopnea and apnea but enough to increase upper airway resistance. These patients also have increased airway collapsibility due to abnormal anatomy. Patients with UARS suffer from increased airway resistance, which leads to arousal episodes and ultimately to excessive daytime sleepiness. Nasal airway anatomic issues (ie, deviated septum, inferior turbinate hypertrophy, nasal valve collapse, or any combination of these) have been associated with UARS.

Signs and Symptoms

Clinical presentation of UARS can be varied, the cardinal symptoms of UARS are fatigue and excessive daytime sleepiness. Some patients also complain of difficulty with concentration, morning headaches, impotence, and difficulty with sleep onset and sleep maintenance (insomnia). Snoring is not a necessary feature of this syndrome because the upper airway resistance is due to a partial decrease in airway cross-sectional area and the airway walls do not have to vibrate to produce a snoring sound. It is now increasingly recognized that the clinical features seen in UARS overlap with functional somatic syndromes such as chronic fatigue syndrome, fibromyalgia, irritable bowel syndrome (IBS), chronic headache, and temporomandibular joint (TMJ) syndrome. Based on the signs and symptoms alone it can be difficult to distinguish the patients with UARS from those with mild OSAHS.


The diagnosis of UARS requires a high degree of clinical suspicion. Diagnosis of UARS requires symptoms (excessive daytime somnolence, fragmented sleep, fatigue), anatomic features consistent with upper airway narrowing, and supportive PSG findings.

UARS is present only if there are documented elevations in upper airway resistance, sleep fragmentation, and daytime dysfunction or excessive daytime sleepiness. The clinical complaint of fatigue or daytime sleepiness can be documented by an abnormal increase in the Epworth Sleepiness Scale (Table 1) score to a value greater than 10, or by use of another validated sleep questionnaire. A low respiratory disturbance index (RDI) is also needed to distinguish UARS from OSAHS. The elevated EEG arousal index related to increased respiratory efforts is the specific measurement that distinguishes UARS from idiopathic hypersomnolence. The clinical complaint of snoring (including crescendo snoring), increase in snoring intensity before EEG arousals, and clinical improvement with a short-term trial of nasal CPAP can be regarded as supporting a diagnosis of UARS.

The diagnosis of UARS requires full polysomnography. Although measurements of upper airway resistance were first used, based on the original definition of UARS, substitute measurements of effort and ventilation may be used as long as there is no evidence of hypopnea or apnea. A normal apnea-hypopnea index (AHI) of less than 5 events per hour of sleep should be seen on the polysomnograph. Additionally, EEG arousals should occur at a rate of more than 10 per hour of sleep and must be associated with increased respiratory effort (usually made by nocturnal esophageal pressure monitoring). Studies have shown an association of alpha-delta sleep pattern in the EEG of patients with UARS. Alpha-delta pattern is a nonspecific EEG finding in which there is intrusion of wake alpha pattern into the deep, slow-wave sleep. This is also seen in some functional somatic syndromes listed above but is not a feature of OSAHS.

The measurement of esophageal pressure is the gold standard for measuring respiratory effort and is the only consistent measurement reported for the diagnosis of UARS. Current literature supports that esophageal pressures more negative than 10 cm H20 are abnormal. Substitute measurements can include inductive plethysmography, strain gauges, oronasal temperature measurements, nasal pressures, and the carbon monoxide levels in exhaled gas. Arousals are documented from the EEG tracings and electromyography, although changes in heart rate, ventilation, and other measurements of autonomic activity may play some role in the future.


CPAP, surgery, oral appliances, and weight loss are possible treatment options for UARS. Ideally, the recommended treatment of UARS should be effective, relieve symptoms, and produce normalized studies after therapy. These therapies also should be covered by health insurance and have long-term effectiveness. Thus far, however, none of the proposed treatments has fully met these criteria.


Data in the sleep literature are not clear-cut regarding the efficacy, safety, and compliance of UARS treatment modalities, including weight loss, nasal CPAP, oral appliances, and surgery.

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Thank you sleeprider.
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Now I have understood the RERA very well
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