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

[Gideon]

a step ahead of you, part of the plan  http://www.apneaboard.com/forums/Thread-...-the-group

[JoeyWallaby]

Ok I thought I'd post more interesting stuff I found and give a positive update.
With my improved CPAP titration, I no longer need to take any medication for acid reflux and my sleep bruxism seems to be gone when using CPAP (returns without CPAP). I say seem to be because I can't 100% sure but when I use CPAP, my jaw and teeth aren't sore in the morning (without CPAP, they're often at least a bit sore).

Also... I have many of the craniofacial anatomical features which are mentioned as often occuring in patients with UARS (high palate, narrow palate and small intermolar distance).


Everything bolded is bolded by me

Study on increased CO2 in air on cats
https://www.fasebj.org/doi/abs/10.1096/f....6.A1295-a

Carbon dioxide is a known respiratory stimulant. The effects of different CO2 concentrations on sleep have not been determined, although we demonstrated previously that hypocapnia reduces the amount of REM sleep. In this study, we sought to determine the effect of hypercapnia on sleep architecture and breathing. Three cats were studied during 3-hours sessions while breathing carbon dioxide added to room air. The animals breathed different concentration of carbon dioxide (0%, 2%, 4% and 6% CO2) each day over 4 weeks according to a 4 x 4 Latin Square design. Respiration was measured using pneumatography, and electroencephalograms and pontogeniculo-occipital waves were recorded from implanted electrodes to discriminate states of sleep and wakefulness. When breathing 2% inspired CO2, total sleep duration increased by 16% compared to control. Both NREM and REM sleep increased in duration (15% and 19%) and frequency (7% and 23%). Sleep latency decreased by 47%. However, when breathing higher levels of CO2 (4% and 6%), total sleep duration decreased. Both NREM and REM sleep decreased in duration and frequency. Tidal volume, minute ventilation, effort (tidal volume/duration of inspiration) and inspiratory duration increased proportionally in all states with increasing levels of CO2. Tidal volume increased by 52.9%, 133.2% and 196.2% with 2%, 4% and 6% inspired CO2, respectively. We conclude that a mild hypercapnic stimulus can stimulate breathing and sleep.

Don't know what to make of this
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2576324/

Several other hypotheses have also been proposed for the emergence of central apnea following the initiation of CPAP therapy. First, overtitration of CPAP is thought to lead to central apnea, although the mechanisms are poorly understood. One factor may be the activation of lung stretch receptors, which may inhibit central respiratory motor output. Another possibility is that washout of CO2 from the anatomical dead space may occur if mask leak or mouth breathing develop at high CPAP levels. However, dead space could increase on CPAP by raising the transmural pressure across the trachea and pharynx if no leak is occurring. Such CPAP overtitration may occur if there is an overreliance on nasal pressure flattening as the impetus for raising CPAP level. Nasal pressure flattening is a good surrogate for inspiratory flow limitation during spontaneous breathing, but it is poorly validated and potentially misleading during CPAP delivery. Second, initiation of CPAP can worsen sleep quality, and transitions from sleep to wake to sleep can contribute to central apneas associated with state instability. In such cases, the ventilatory response to arousal can drive the PaCO2 below the CO2 apnea threshold, yielding central apnea during subsequent sleep. This sleep disruption at the initiation of CPAP and the associated CO2 fluctuations also tend to resolve over time as patients habituate to the interface and the application of positive pressure. Although sleep is also fragmented prior to initiation of CPAP, presumably it is the application of CPAP that exaggerates the overshoots in ventilation by reducing pharyngeal resistance and augmenting the ventilatory response to arousal. Third, despite the lack of evidence for the superiority of bilevel positive airway pressure compared with standard CPAP for treatment of OSA, many laboratories use bilevel quite frequently. With bilevel PAP, inspiratory positive airway pressure titration can lead to augmented tidal volumes, which drive down arterial CO2 tensions. If the resulting PaCO2 falls below the CO2 apnea threshold, then central apnea will occur. Thus, a variety of phenomena can theoretically contribute to fluctuations of CO2, all of which are easily treated with careful attention to mechanism; none require the development of new nomenclature.

A second hypothesis is that over-titration with CPAP will lead to the development of central apnoeas. How this process exactly takes place is not well understood, but a potentially important factor could be the activation of stretch receptors in the lungs. When these receptors are activated due to an excessive expansion of the lungs, they send signals to the breathing centre along the vagal nerve, which inhibits the central motor output. Hence, this will result in an interruption of inspiration. This mechanism protects the lungs against overexpansion, and is called the Hering–Breuer reflex.

They reference this study for their claim that "Nasal pressure flattening is a good surrogate for inspiratory flow limitation during spontaneous breathing, but it is poorly validated and potentially misleading during CPAP delivery". I don't see how this study validates their claim?
https://www.atsjournals.org/doi/full/10.....5.9708008

In our data the flow/time contour was generally rounded and did not exhibit flattening during quiet breathing while awake. At sleep onset resistance increased in both symptomatic and asymptomatic subjects as has been reported by others. This occurred in breaths of all shapes and the rise in resistance was significantly greater in the symptomatic group. Both symptomatic and asymptomatic subjects showed some breaths with flattened flow/time contours during sleep and these were associated with further increases in resistance. This may reflect the changes in collapsibility of the upper airway during sleep. In general, the asymptomatic subjects showed both less flow limitation and less increase in resistance during abnormal shaped breaths than the symptomatic subjects. However, when present even in these asymptomatic subjects, the flattened flow/time curve identified the periods of highest resistance in both non-REM and REM sleep.

Acetazolamide, interesting.
https://www.atsjournals.org/doi/full/10....1410-469BC

Our study identified a group of patients with more significant control system instability (higher loop gain) who do not experience resolution of all their respiratory events on CPAP. In addition, the number of residual respiratory events is predicted by how unstable ventilation is on the CPAP titration night. These patients may respond to other therapies like adaptive/auto servoventilation (ASV), O2, oral appliances, or combinations of therapy including acetazolamide, and further studies are necessary. Recent findings regarding concern for safety of ASV in patients with congestive heart failure may encourage alternative strategies to avoid ASV in complex sleep apnea unless necessary.

Several limitations of this pilot study deserve mention. Loop gain may change from night to night, for example, based on fluid shifts or changes in medications. Thus, our finding that loop gain explains some proportion but not all of the variance in residual apnea is not surprising. Individual differences regarding the size of the reduction in loop gain over time may explain further variability in residual AHI. Possible mechanisms include the following:
1. Improved oxygenation may reverse the effects of apnea-induced intermittent hypoxia on chemoreflex sensitivity
2. Reversal of apnea-induced sympathoexcitation with CPAP may also contribute to reducing chemoreflex sensitivity
3. Patients may adapt to CPAP over time and achieve a greater sleep depth during the night and may therefore be less susceptible to the effects that lighter sleep and arousal may have on ventilatory instability
4. Changes in plant gain or circulatory delay could also occur, for example, with reduced circulatory delay or reversal of edema-related reduction in lung volume and thus oxygen/CO2 stores. These effects may be more important in some patients than others.

https://www.atsjournals.org/doi/full/10....507-1035OC

Central apnea is a temporary failure of the generation of breathing rhythm. Central apnea occurs when the level of Pco2 falls below the apneic threshold, a Pco2 level below which breathing ceases. Polysomnographically, central apnea is recognized by the absence of naso-oral airflow and by thoracoabdominal excursions that reflect the failure of activation of inspiratory pump muscles. Episodes of central sleep apnea (CSA) associated with periodic breathing (Cheyne-Stokes breathing) occur in severe heart failure with systolic dysfunction. CSA also occurs in an idiopathic form and at high altitude.

Few studies have reported on the use of acetazolamide to treat CSA of high altitude as well as idiopathic CSA. In six patients with idiopathic CSA, White and colleagues showed significant improvement in sleep apnea after 1 wk of drug therapy. A similar finding was reported by DeBacker and coworkers after chronic administration of acetazolamide.

The mechanism of therapeutic action of acetazolamide has been elucidated in a study (10) of normal subjects with induced periodic breathing during sleep. Nakayama and coworkers showed that because of metabolic acidosis induced by acetazolamide, the difference between the prevailing Pco2 and the apneic threshold Pco2 increased. As a result of this, acetazolamide decreased the likelihood of developing sleep apnea.

From the results of this prospective, randomized, placebo-controlled, cross-over, double-blind study, we conclude that among patients with stable heart failure (NYHA class II and III), before-bedtime administration of a single dose of acetazolamide improves sleep-disordered breathing and associated arterial blood oxyhemoglobin desaturation. This is reflected in patient perception of improved sleep quality and daytime function. 

Although no studies in heart failure have ever been reported, acetazolamide has been shown to alleviate idiopathic central sleep apnea and central apnea at high altitude. The present study shows that acetazolamide is also effective in heart failure. Acetazolamide decreased the apnea–hypopnea index in each subject, and the reduction in the apnea–hypopnea index occurred mostly because of a reduction in central apneas.

Another important finding of this double-blind study was the significant improvement in patient perception of improved sleep quality, waking up more refreshed, with less daytime fatigue and sleepiness while taking acetazolamide, compared with placebo. These results are in agreement with those of White and associates in patients with idiopathic central sleep apnea. The reduction in periodic breathing, perhaps via the combination of improved oxygen saturation and a trend toward diminished arousals, contributed to patient perception of improvement.

The mechanism of action of acetazolamide is related to metabolic acidosis, which stimulates chemoreceptors. It is noteworthy that in spite of the fall in PaCO2, central apneas improved, emphasizing that it is not the absolute value of steady state PaCO2 that increases the likelihood of developing central apnea. Rather, it is the difference between the prevailing Pco2 and apneic threshold Pco2 that is important. As noted earlier, in the face of background increased stimulus to breathe, the apneic threshold Pco2 decreases considerably (more than the fall in PaCO2) such that there is a widening of the difference between the prevailing Pco2 and the apneic threshold Pco2. This widening decreases the likelihood of developing central sleep apnea.

One important feature of this study was to administer acetazolamide as a single dose at night. In this way, the long-term side effects of frequent administration of acetazolamide could perhaps be minimized. In the present study, none of the patients complained of paresthesias, which occur with large doses of acetazolamide. One patient developed shortness of breath, which was probably mediated by acetazolamide-induced increased ventilation. However, in clinical practice, when the initiating dose could be less than in the present study and dose titration could be done gradually, such side effects may be further minimized, and gradually the maximum dose resulting in the least periodic breathing could be achieved.

Meanwhile, we were happily surprised that in spite of the short duration of the study and modest reduction in periodic breathing, patient perception improved. We hypothesize that with long-term therapy, as sleep-related breathing disorders improve, it may be reflected in an improvement in cardiac function that will further improve periodic breathing, resulting in a positive feedback cycle. Improvement in sleep apnea may improve cardiac function by a variety of mechanisms such as improved oxygenation. Use of acetazolamide in patients with heart failure may have the additional benefit of mild diuresis and the combating of metabolic alkalosis (induced by use of other diuretics), which may promote periodic breathing. Meanwhile, potential long-term deleterious effects of acetazolamide in heart failure are not known. It is conceivable that metabolic acidosis and chemoreceptor stimulation by acetazolamide increase sympathetic activity, and studies investigating this important issue are needed. However, studies by Teppema and Dahan show that a clinical dose of acetazolamide does not significantly change chemosensitivity. Furthermore, with single-dose nocturnal use of acetazolamide, metabolic acidosis is mild and mostly overnight. On the other hand, by decreasing sleep apneas and improving oxyhemoglobin saturation, acetazolamide should decrease sympathetic activity. The second potential deleterious effect of acetazolamide relates to respiratory muscle stimulation and hyperventilation, which could result in respiratory muscle fatigue in patients with heart failure. In this context, because acetazolamide was administered as a single dose before bedtime, its respiratory muscle stimulation should be diminished by daytime. Furthermore, it is also conceivable that the overall ventilation during sleep at night could have been similar in comparing acetazolamide with placebo because of reduction in the hyperpneic episodes of Cheyne-Stokes breathing by acetazolamide. Further studies monitoring nocturnal ventilation should shed light on this issue.

https://journals.plos.org/plosone/articl...ne.0093931

Since mountain tourism has increased during the last decades, it is nowadays popular to spend weekends and holidays at mountain resorts or lodges located at moderate altitudes between 1500 and 3000m. Sleep at altitude is altered in healthy individuals. A shift towards lighter sleep together with an increase in central apneas has been observed at altitude. Compared to the obstructive apneas observed at baseline in OSAS patients, central apneas induced by an ascent to altitude are characterized by the intermittent absence of the drive to breathe and are generated by the brainstem respiratory center as a response to changes in blood gas concentrations. One treatment for central apneas at altitude is acetazolamide, a carbonic anhydrase inhibitor frequently used in the treatment of acute mountain sickness. Acetazolamide prevents central apneas at altitude through metabolic acidosis by its diuretic effects. Sleep of OSAS patients at 490 m and at 1630 to 2590 m with and without CPAP treatment was investigated in three previous studies, in which acetazolamide was shown to reduce central apneas compared to placebo during sojourns to moderate altitude. In addition, as observed in healthy subjects, acetazolamide in OSAS patients reduced the apnea/hypopnea index compared to placebo and increased oxygen saturation and improved sleep quality (sleep efficiency, arousals, slow-wave sleep).

Independent of the dose, acetazolamide reduced the total AHI, by abolishing central apneas, increased SpO2 and reduced PCO2 in both studies. In terms of sleep architecture, waking was reduced and percent of non-REM sleep and sleep efficiency were increased with acetazolamide.

Acetazolamide is a carbonic anhydrase inhibitor used to treat multiple medical conditions. One of them being increased intracranial pressure (IIH), I found this post on Reddit on the IIH subreddit about thiamine being potentially effective for IIH through the same mechanism as acetazolamide (not medical advice, etc. don't do anything without consulting medical professional).
https://www.reddit.com/r/iih/comments/cb...e/ethepb1/







UARS and craniofacial anatomy
https://www.karger.com/Article/FullText/335839

Regarding clinical examination, some craniofacial characteristics were reported as being specific to UARS. These patients exhibit the classical long face syndrome with a short and narrow chin and reduced mouth opening. There is classically a ‘click’ and a subluxation when opening the temporo-mandibular articulation, which may be evidenced by palpation. The mandible is in the back position and the palate is high and narrow.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4608900/

Craniofacial abnormalities that may increase upper airway resistance are often present in UARS. Dental malocclusion and elevated ogival hard palate as well as a narrow posterior airway space can be frequent findings in upper airway examination. Surgical treatment were studied as an option for patients who cannot tolerate or are unwilling to adhere to CPAP therapy. Some authors studied UARS patients that preferred surgery (such as septoplasty, turbinate reduction, laser-assisted uvuloplasty – LAUP, uvulopalatopharyngoplasty, genioglossus bone advancement, mandibular osteotomy with tongue advancement and hyoid miotomy with suspension) rather than CPAP. Sleep studies were performed from 3 to 6 months after treatment. The only outcome evaluated in these studies were subjective sleepiness and snoring and the follow-up was not long enough to consider surgery a long-term effective management for this group of patients.

https://aadsm.org/docs/JDSM.03.01.21.pdf

Cephalometry has revealed craniofacial abnormalities in the upper airway anatomies of many UARS patients, including the presence of a long face, short and narrow chin with reduced mouth opening, retrolingual narrowing, increased overjet, high and narrow hard palate.

UARS, craniofacial anatomy and arousal threshold
https://www.atsjournals.org/doi/full/10....1.5.16158a

In our series of 400 cases of UARS, 93 have “pure” UARS. These patients frequently complain of insomnia, sleep fragmentation, and fatigue. Their mean age is 38 ± 14 yr; 56% are women, and 32% are of east Asian origin. Hence, their sex, age, and racial distribution are different from those with OSAS. The mean body mass index is ⩽23.2 ± 2.8 kg/m2, the mean respiratory disturbance index is 1.5, and oxygen saturation is ⩾95%. Their craniofacial anatomy reveals a predominantly high and narrow hard palate, an abnormally small intermolar distance, an abnormal overjet ⩾3mm, and a thin soft palatal mucosa with a short uvula. In 88% of the subjects, there is a history of early extraction or absence of wisdom teeth. Their psychological profile shows a high anxiety score. Other clinical features are cold extremities, postural hypotension, history of fainting, and low blood pressure. In a subgroup of 15 subjects, between 20 and 30 yr of age, orthostasis is present by tilt testing, and is associated with a low mean systemic arterial blood pressure. Four breathing patterns are noted with repetitive transient arousals: (1) “Pes crescendo”: progressively increasing esophageal pressure (Pes), terminated by reversal of the Pes to baseline; (2) increased Pes, without crescendo, terminated by a Pes reversal; (3) one or two breath increases in Pes preceding a Pes reversal; and (4) tachypnea with normal Pes, abruptly terminated by a normal breath. At the beginning of the sleep study, the average peak inspiratory effort during NREM sleep is low (mean Pes, −2.5 cm H2O). Typically, the events are terminated at low negative peak inspiratory pressure (−6 cm H2O).

In contrast, in OSAS, collapse of the upper airway typically occurs when the intrathoracic pressure falls to −20 to −30 cm H2O. The arousal threshold is at inspiratory pressures of −40 to −80 cm H2O, thus indicating that the arousal threshold for increased inspiratory effort is elevated in OSAS.

In UARS, the arousal threshold is lower. The recognition of the internal respiratory load is exquisitely sensitive, therefore allowing the patient to wake up in response to small increases in inspiratory effort. The sleep EEG in UARS shows an increase in alpha rhythm. There is a relative increase in delta sleep, which persists in the later cycles of sleep.

We believe that distinct functional arousal reflex pathways originating from peripheral mechanoreceptors exist in these two groups. The subjects with UARS have intact, sensitive receptor function while the subjects with OSAS have primary receptor dysfunction. In other words, subjects with blunted mechanoreceptor responses would develop OSAS, while those with intact or hypersensitive responses would develop UARS. This would explain our group of untreated patients whose UARS did not evolve into OSAS over time. Central nervous system responses to respiratory effort, mediated by these mechanoreceptors, have been investigated by studying respiratory related evoked potentials during sleep. Preliminary data from patients with OSAS indicate that these are blunted compared with normal controls.

In summary, the data suggest that a fundamental difference exists between patients with UARS and patients with OSAS. This difference is determined by the different mechanoreceptor function in the two groups, which is, presumably, genetically predetermined and environmentally altered. This might explain why subjects with a hypersensitive response pattern will develop UARS, whereas subjects with a dysfunctional response pattern, modified by factors such as chronic respiratory allergies, postpubertal tongue enlargement, etc., will directly develop OSAS. In addition, it is interesting to note that the autonomic nervous system responses are also polar opposites in the two groups (9, 17). We believe that two different “brain” responses best explain the two different syndromes. If appropriate physiologic investigations had focused more on nonobese subjects, these differences would have been observed much earlier.

a step ahead of you, part of the plan  http://www.apneaboard.com/forums/Thread-...-the-group

Can't access.

[JoeyWallaby]

Not embedded, image is really long
Central Sleep Apnea, An Issue of Sleep Medicine Clinics, Volume 9-1, 1st Edition, Page 31 and 32

All bold added by me

https://www.atsjournals.org/doi/full/10....cm.2203016

The pathophysiology of central sleep apnea (CSA) syndromes is fraught with paradoxes that have perplexed clinicians and physiologists alike. Central apneas during sleep arise when the summation of respiratory stimuli fall below a threshold level required to generate ventilation. Accordingly, all forms of CSA have the same “phenotypical” appearance: cessation of airflow in the absence of respiratory efforts. However, they may arise from diametrically opposite “genotypes,” which has been a source of confusion.

The central paradox of nonhypercapnic CSA is that the withdrawal of respiratory drive that causes apnea is a consequence of an abrupt increase in respiratory drive that forces PaCO2 below the threshold. This observation suggests that when ambient PaCO2 is close to the apneic threshold, it destabilizes the respiratory control system by making it more susceptible to the development of central apneas following relatively small increases in ventilation.

In this issue of AJRCCM, Nakayama and coworkers investigated conditions that alter the difference in end tidal PCO2 (PetCO2) between spontaneous breathing and the apneic threshold (ΔPetCO2) in dogs on pressure support during nonrapid eye movement sleep. Apneas were induced by increments in pressure support and ventilation. The apneic threshold was defined as the PetCO2 on the breath just before the onset of at least three cycles of apnea-hyperventilation. Two conditions narrowed ΔPetCO2 from 5mm Hg during control conditions to approximately 4mm Hg and reduced the pressure support required to induce central apneas. The first was a primary metabolic alkalosis induced by bicarbonate that reduced ventilatory drive. This increased PetCO2. The second was a primary hypoxia-induced increase in respiratory drive with respiratory alkalosis. This reduced PetCO2. These findings confirm that a narrower ΔPetCO2 increases the susceptibility to central apnea. They also establish that alkalosis is a factor that narrows ΔPetCO2 and strongly suggest that changes in hydrogen ion or pH are the intermediaries through which PaCO2 influences ventilation under these experimental conditions.

During metabolic alkalosis, PaCO2 rises in compensation for alkalosis, but as this compensation is never complete (pH was 0.129 above control), PaCO2 and hydrogen ion will remain close to the apneic threshold. Therefore, the magnitude of the fall in PaCO2 required to lower ventilation to zero is reduced. Similarly, in the case of respiratory alkalosis, metabolic compensation by retaining hydrogen ion is incomplete so that the change in PaCO2 or hydrogen ion required to induce apnea is reduced. Why then did the peripheral chemoreceptor stimulant almitrine have the opposite effect to hypoxia and widen the ΔPetCO2? The most likely explanation is that hypoxia is an inconstant and nonlinear respiratory stimulant. The definition of the apneic threshold in this study was the PetCO2 that precipitated three consecutive cycles of apnea hyperventilation. During hypoxic exposure, PaO2 was low and on the steep portion of the oxyhemoglobin dissociation curve. Therefore, during apnea, PaO2 would fall further, providing an increase in respiratory drive that could provoke postapneic ventilatory overshoot. This would tend to drive PaCO2 below threshold, facilitating periodic breathing. However, the degree of reduction in PaO2 during apneas was not reported. In contrast, almitrine probably provides a more constant ventilatory stimulation that is linear. Accordingly, almitrine-induced increases in ventilation would have raised PaO2 to supranormal levels on the flat portion of the oxyhemoglobin dissociation curve. When the first apnea was triggered, hypoxia would not have developed and would not have provided an additional stimulus for postapneic ventilatory overshoot. This would dampen oscillations in PaCO2 and stabilize breathing. Similarly, acetazolamide induced-metabolic acidosis, which also widened ΔPetCO2, would provide a relatively constant central stimulus to breathe, with more complete respiratory compensation (pH was only 0.037 below control), and would thereby tend to stabilize breathing.

Other observations in humans are consistent with those of Nakayama and colleagues. High-altitude periodic breathing is caused by hypoxia and is reversed by acetazolamide. Similarly, acetazolamide attenuates idiopathic CSA. Theophylline and CO2, central respiratory stimulants, alleviate CSA in patients with congestive heart failure, as does oxygen. The general principle arising from these studies is that factors that narrow ΔPetCO2, or provide inconstant respiratory drive, interact with other factors such as augmented chemosensitivity, pulmonary congestion, and arousals from sleep to destabilize respiratory control and predispose to CSA. Conversely, factors that widen ΔPetCO2 and provide a more constant respiratory drive stabilize respiration.

https://www.myapnea.org/blog/complex-sleep-apnea
This article is really interesting.

The next part of the story involves meeting a patient with complex apnea, with whom I collaborated in designing a device to use CO2 to stabilize breathing rhythms, and a method to use mask-venting modifications to trap part of exhaled CO2 when using PAP, called Enhanced Expiratory Rebreathing Space (EERS). EERS is used routinely (not FDA-approved and unlikely as it is a simple reconfiguration of common components; its use is “off label”) at the Beth Israel Deaconess Medical Center’s (BIDMC) and some other sleep centers to treat complex apnea patients, while the CO2 device remains investigational.

We found we could stabilize this abnormal breathing rhythm with this method. To date, we have treated over 1,000 patients successfully. The original patient has built and used a CO2-regulating device of his own for over 10 years now with continued benefit.

Along with EERS and CPAP, more recently I have used low doses of acetazolamide, which is commonly used to prevent and treat high-altitude sickness and sleep apnea.

Also, I have found that some patients benefit from use of sedative drugs to reduce awakenings from sleep which tend to especially worsen complex apnea. Brief awakenings from sleep result in large breaths which lower CO2 and thereby prompt central apneas. Sedative use tends to reduce these awakenings. Some newer sedatives have been shown to be relatively safe in patients with sleep apnea, but need to be used very cautiously, by highly-experienced sleep physicians who closely monitor patient responses. In particular, sedatives can make sleep apnea more severe in REM sleep. It seems that to recover from an apnea in REM sleep, arousal is needed, while in NREM sleep, arousals increase the risk of apnea by lowering CO2. It is crucial that patients struggling with CPAP do not use over-the-counter sedatives without discussion first with their physicians.

The reported prevalence [of complex sleep apnea/treatment-emergent sleep apnea] varies widely depending upon the particular criteria used for lab test scoring and diagnosis. It has been reported that 5 to 15% of patients with sleep apnea have this subtype. At BIDMC, we estimated that at least 10% of all apnea patients have complex apnea. Research from several different centers has shown that about 25 to 30% of apnea patients have a very strong breathing rhythm that causes apnea. If those who try hard but fail to get benefit from CPAP, and those who in frustration abandon its use altogether are also considered, it is probably far more frequent.

The sleep study report may indicate features of abnormal breathing rhythm. The terms used are often central apnea, mixed apnea, periodic breathing, and ataxic breathing. The patients may feel they are fighting the air pressure, or rip the mask off frequently, or feel no benefit, or even feel worse, when using PAP. Despite AHI numbers that suggest “normal” sleep on CPAP, the patient may still feel they slept poorly, and function poorly during the day.

[JoeyWallaby]

I've moved events and arousals chart closer to the hypnogram on my sleep study. The (small amount of) central events only occur in N1 and N2 sleep. Hypopneas seem to occur in N3 as well as N1 and N2. Arousals (which include spontaneous arousals as well as respiratory) occur predominantly in N1 and N2.



I don't know how accurate this is but we'll roll with it
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4246141/

A sleep study report describes the percentages of various sleep stages. The normal percentage of each stage is reported with the number of total REM Stage sleep cycles recorded overnight. In adults, approximately 5% of the total sleep time is Stage N1; 50% Stage N2; and 20% is Stage N3 sleep. The remaining 25% is REM stage sleep

This is my sleep stage percentages from the study.

REM is absent (despite sleeping three and a half hours in total), I really have no idea why. Proportionally increasing the figures to make up for absent REM sleep results in 6.65% N1, 66.5% N2, 26.6% N3 as being "normal". Based off those figures, my N1 was slightly increased (which has some alpha waves), N2 was significantly decreased and N3 was significantly increased (delta wave sleep).

According to the same study last linked,

Sleep staging is described in a separate section of the report. Stage N1 sleep is associated with the transition from wakefulness to sleep and is considered a direct measure of daytime alertness and the subjective refreshing quality of sleep. The quantity and the percentage Stage N1 sleep is an estimate of the degree of sleep fragmentation. A high percentage of the Stage N1 sleep is generally a result of frequent arousals caused by sleep disorders, like sleep apnea, periodic movement of sleep, or snoring. Other causes of sleep disruption, including environmental disturbances, may also lead to increased amount of Stage N1 sleep.

Stage N2 sleep predominates the sleep stages with 50% of the total sleep time. It follows the Stage N1 sleep and continues to recur throughout the night. A low percentage of Stage N2 sleep may be a result of sleep fragmentation, increased REM, Stage N3 or a result of obstructive sleep apnea-related arousals. An increased amount of Stage N2 sleep may also be noted in age-related changes in sleeping pattern and may be a result of medication effect.

Stage N3 is considered as ‘deep sleep’. It is sometimes referred as slow wave sleep. The Stage N3 sleep generally cycles frequently in the first third of the night and begins to reduce towards the second half of the night. A high amount of Stage N3 sleep is noted during rebound sleep (such as recovery sleep after sleep deprivation, initiation of nocturnal CPAP treatment, or treatment of periodic limb movement syndrome). Less Stage N3 sleep is noted as a side effect of certain medications, including benzodiazepines, TCAs, and barbiturates. Episodes of night terror sleep walking, sleep talking, and confusion arousals also occur during Stage N3 sleep. Stage N3 is also known to suppress the occurrence of sleep-disordered breathing.

The exact function of the REM is uncertain. However, it occupies approximately 25% of the total sleep time. REM sleep cycles occur every 90 to 120 min throughout the night with progressively increasing periods of time. REM sleep is associated with more frequent and longer duration apneas, hypopneas, and severe hypoxemia. REM sleep suppresses periodic leg movements of sleep. Certain medications suppress the REM sleep including amphetamines, barbiturates, TCAs, MAOIs, anticholinergics, and alcohol. Certain sleep disorders, including sleep apnea, REM behavior sleep disorder, and nightmares occur in REM sleep. A higher amount of REM sleep is notable during recovery sleep after selective deprivation of REM sleep. REM sleep ‘rebound’ occurs after discontinuation of REM sleep suppressing medications, alcohol, and initiation of CPAP therapy.

Of note, are the claims that N3 suppresses sleep-disordered breathing and that a low percentage of N2 may be a result of sleep fragmentation. This seems to explain why I had a low amount of N2 and almost no events in N3. The significant increase in N3 sleep (delta wave) matches up with UARS.
https://www.atsjournals.org/doi/full/10....1.5.16158a

In UARS, the arousal threshold is lower. The recognition of the internal respiratory load is exquisitely sensitive, therefore allowing the patient to wake up in response to small increases in inspiratory effort. The sleep EEG in UARS shows an increase in alpha rhythm. There is a relative increase in delta sleep, which persists in the later cycles of sleep.

[JoeyWallaby]

Okay so here's my plan

1. Improve sleep hygiene and consistency of sleep cycle
   
2. Use Min Epap high enough to eliminate obstructive apneas
   
3. Use PS high enough to eliminate flow limitations and basically everything expect for CAs and OAs
   
4. Fine-tune ti min, max, trigger and cycle... not sure exactly what to do there
   
5. Supplement thiamine 100mg (I have some lying around actually), maybe drink chamomile tea (contains apigenin and luteolin) for mild carbonic anhydrase inhibitor effect. If CAs persist with that and using EERS, very low dose acetazolamide before bed could be considered
   
6. Continue with chin strap, mouth taping and positional device for side sleeping. Not sure about cervical collar, I'll check the video footage when I don't use it to see if I'm tucking my chin
   

Any thoughts on this plan or anything I've posted would be highly appreciated 

[JoeyWallaby]

Min 6.4, PS 4.4, trigger medium, cycle medium, ti min 0.1, ti max 4.0
Just mouth taped

Feel pretty decent despite poor data

[mper6794]

Hi, Joey,

Congrats !

It looks yor are doing well on control.

Yet not sure about your normal Respiratory Rate, your dataset has been suggesting you could eventually try increase P.S up to some 6.0, maybe under a stable EPAPmin of 7.0.

all the best

[JoeyWallaby]

really really really ****ing tired of this ****

[Gideon]

Did you have EERS on the 12/12 screenshot? if so how much?

[JoeyWallaby]

no eers