[Health] Interpreting sleep study results, EERS enhanced expiratory rebreathing space

[mper6794]

.....for nexts: It would help if you blow up a little TV and RR on the full nights.
All the best

[JoeyWallaby]

Min EPAP 7.4, PS 5.4, Ti Max 2.5, Ti Min 0.5, Trigger High, Cycle Med

EERS, mouth taped, chin strap, cervical collar and sleep positioner.
Sleep positioner stopped me rolling onto my back 100% but I still managed to roll onto my back 50% near the end of sleep, I was laying with head facing a 45 degree angle (if directly up is 0 degrees and on side is 90 degrees).

I feel moderately refreshed.

[JoeyWallaby]

Extra charts, I'll post these as well for the next night

[slowriter]

Nice.

I did want to mention something on masks and leaks:

I use the Bleep mask. One of the huge advantages of it for EERS purposes it that, so long as you attach it correctly, it basically doesn't leak; at all.

So then the only thing you need to worry about in terms of leaks is mouth leaks.

Its simplicity also makes it super easy to fashion the EERS mod.

[Sleeprider]

I'm sorry, but JoeyWallaby's therapy is totally inconsistent, and I for one don't see any progress from page one of this 18 page thread. Whatever is going on here is completely unpersuasive to me that it amounts to improvement. Given that we have tried various pressures, pressure support EERS and other variables, I think with AHI ranging from less than 1 to over 20 on any given night, we are no farther along the path to a solution than when this started. I'm not committed to it, but my opinion is turninging back to ASV as a better choice.

[JoeyWallaby]

Agree with the inconsistency! 


I do feel better than before, leaks are mostly managed now, flow limitations are basically gone. Main problem is the CAs. I'm hopeful that this is somehow caused by positioning, given that this night (http://www.apneaboard.com/forums/Thread-...#pid321964), every single time I had a CA was when I was laying on my back. I've only been using standard length EERS as well, it may not be sufficient to account for the increased efficiency of respiration with 5+ PS vs 3 EPR? My sleep schedule and hygiene has been pretty bad lately and my CAs seem pretty temperamental so maybe when I improve that, my CAs will improve.

[JoeyWallaby]

Same settings as before. EERS and mouth taped. No video recording, chin strap or cervical collar. I might try increasing EERS length.

I found this, it's interesting

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[JoeyWallaby]

Interesting

From "Principles and Practice of Sleep Medicine 6th Edition"

The key feature [of treatment-emergent central apnea] is NREM-dominant central hypopneas or periodic breathing with obstruction, resolving spontaneously during REM sleep

From this study https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5430122/

Physiologically, when PaCO2 is reduced, ventilation is inhibited centrally, thus allowing PaCO2 levels to rise globally. Yet, during wakefulness, an extreme reduction in PaCO2 is required to inhibit ventilation to the point of apnea. The central control of respiratory motor output prevents apnea when PaCO2 is physiologically reduced. However, during non‐rapid eye movement (NREM) sleep, central respiratory control is diminished, and a resulting apneic threshold of PaCO2 emerges. During NREM sleep, when ventilatory fluctuations occur that decreases PaCO2, the PaCO2 can easily fall below the threshold and provoke a central apnea. This situation can occur in the setting of OSA, where a high loop gain (i.e., a high ventilatory response‐to‐stimulus ratio, often seen in OSA) causes an exaggerated hyperventilation that drives PaCO2 beneath the apneic threshold. In the setting of a high loop gain, minimal reductions in ventilation and accompanying changes in arterial blood gas would be sufficient to activate chemoreflex control of ventilation to produce a large increase in ventilation sufficient to drive PaCO2 beneath the apneic threshold.

CSA also manifests itself in the context of OSA during Positive Airway Pressure (PAP) titration studies (and not during baseline polysomnography), which is termed treatment‐emergent or complex sleep apnea (CompSAS) and is thought to be related to Hering‐Breuer mechanisms via PAP‐mediated activation of pulmonary stretch receptors.

[JoeyWallaby]

More stuff about treatment-emergent central apnea

TECSA should be viewed as a dynamic polysomnographic phenomenon. The application of PAP promotes restitution of airway patency but at the same time suppresses the normal physiologic rise (2–8 mmHg) in PaCO2 that occurs during stage NREM, and may intermittently bring it below the apneic threshold creating episodes of TECSA. Overtime the apneic threshold which is a fluctuating value readjusts and resets itself making TECSA a transient process. The vast majority of patients will demonstrate the resolution of TECSA with continued CPAP or adaptive servoventilation use within few weeks to few months. While most patients demonstrate gradual resolution of central apneas over weeks to months, 1.5–3% of patients with TECSA may continue to exhibit central apneas on a chronic basis. Furthermore, some patients with sleep-disordered breathing who did not demonstrate TECSA on the first titration study may insidiously start showing TECSA when undergoing re-titration studies few months later. All these polysomnographic scenarios support the dynamic nature of TECSA.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4966223/

Ventilatory responses vary widely between the awake and asleep state, as well as between rapid eye movement (REM) and non−rapid eye movement (NREM) sleep. Ventilation during sleep is largely regulated by the same mechanisms that drive breathing while awake,  except that behavioral influences become suppressed in transition to, and during, sleep. Therefore central apneic events are rarely present during the awake state or REM sleep. During NREM sleep, however, changes in the respiratory pattern are primarily controlled chemically, being the result of a fine balance among a critical Paco2 level, below which there is a central cessation of breathing (i.e., apneic threshold); its triggering factors (mainly hypocapnia); and respondent receptors (i.e., central and peripheral chemoreceptors). Additionally, the level of ventilation in respiratory dysrhythmias is augmented by arousals from sleep, resulting in transient hyperventilation with hypocapnia below the apneic threshold and therefore initiation of central apneic events, primarily during NREM sleep.

The removal of most excitatory inputs to breathing that occurs with sleep onset is a feature of stable sleep as well. Respiratory load compensation also is reduced during stable sleep compared with wakefulness. Thus minute ventilation decreases during stable sleep, and the control of breathing becomes dominated by chemical input. However, downregulation in chemosensitivity is not isolated to the sleep-onset period. Ventilatory responses to hypoxia are reduced during stage 2 (N2) and slow wave sleep (N3), compared with wakefulness, such that major decreases in oxygen levels are required to stimulate breathing during sleep. Accordingly, CO2 is the main regulator of breathing during sleep. However, ventilatory responses to hypercapnia also are reduced during sleep compared with wakefulness, albeit to a lesser extent than for hypoxia. Consequently, people can tolerate lower levels of minute ventilation and higher levels of CO2 during sleep than in wakefulness. Typically, depending on the prevailing metabolic conditions, minute ventilation is reduced by 1 to 2 L/minute, and the partial pressure of carbon dioxide in the blood (Paco2) increases by 3 to 8 mm Hg during stable sleep, compared with wakefulness.

Principles and Practice of Sleep Medicine 6th edition, chapter 109

The appearance of central apnea is related to a patient's "apneic threshold." The hypocapnia-induced apneic threshold is a physiological state-dependent, nonconstant numerical value resulting from a drop in end-tidal PaCO2 (usually 3-4 mm Hg) below the eupneic PaCO2. Higher pressures lead to pressure intolerance and mask leak, contributing to sleep fragmentation. This could result in a drop of PaCO2 to a level below the apneic threshold, thereby triggering central apneas. Furthermore, in patients with obstructive sleep apnea the withdrawal of "wakefulness drive" precipitates decreased and fluctuating oscillatory muscle tone in the upper airway, leading to ventilator instability and central apneas.

https://www.ncbi.nlm.nih.gov/pubmed/26653197

[Sleeprider]

Have you considered volunteering as a wiki editor so you could put these gems into articles that won't get lost as forum posts? http://www.apneaboard.com/wiki/index.php...iki_Editor