[Treatment] ASV settings for treatment of complex sleep apnea

[mper6794]

Good!.....are you taking any medication for sleep aid (back to sleep quickly after arousals....lowering arousal thresholds)?

all the best

[mper6794]

oops!....increasing arousal thresholds?

[Geer1]

So they are arousals then. Try and comb through them in detail to see if you think they are all spontaneous or if some of them may be related to breathing.

If primarily spontaneous then you need to start looking at other aspects of sleep, sleep hygiene, sleep aids, trying to reduce stress etc.

[JoeyWallaby]

Recent data. 16th to 18th are using EERS, first half of night on 19th is using EERS, second half is not. Didn't seem to improve things so I've stopped using it.

Looking at old data, events are clearly and obviously way lower than CPAP or BiLevel. Waveforms are better than CPAP and equivalent to BiLevel. I feel better than on CPAP or BiLevel, with the reduced leak rate, significantly reduced events and improved comfort, I say ASV is a success. One problem is sometimes waking up and not being able to fall back asleep with the CPAP on, I thought it could be due to PS spiking up high but looking at the data, there doesn't seem to be any relationship. Breathing is also unstable/inconsistent on a lot of nights, maybe with CAs about to occur, the PS spikes up which successfully prevents the CA but that disturbs sleep/causes arousal?

---

---

[Geer1]

Good to hear things seem to be improving.

The one thing I still wonder about is those periods of high pressure, low respiration rate and falling minute volume. If I was going to focus on anything it would be trying to figure out what those periods represent. They seem to occur post arousal semi frequently.

[JoeyWallaby]

Here's a big pile of information...

This study shows improvement in ventilatory stability with acetazolamide.
https://academic.oup.com/sleep/article/36/2/281/2596026

This is the source for all the following images.
https://academic.oup.com/sleep/article/4...33/4868556


zzz

zzz
zzz
zzzzzz

[JoeyWallaby]

This is the source for all the following images.
Principles and Practice of Sleep Medicine: Sixth Edition, Chapter 110 "Central Sleep Apnea: Diagnosis and Management" by Andrey V. Zinchuk and Robert Joseph Thomas
zzzzzzzzzzzzzzzzzz

This is the source for all the following images.
Nocturnal Non-Invasive Ventilation, Chapter "Nocturnal Noninvasive Ventilation and Adjuncts in Disorders of Breathing Control" by Robert Joseph Thomas
zzzzzzzzzzzz

[JoeyWallaby]

It's hard to see the pressure cycling with the images I posted above, with these images below you can see it clearly.

With the studies above, you see there are cases where EERS alone didn't help (like me) but did work combined with acetazolamide, I think I should try acetazolamide.

foxfire has used acetazolamide with EERS
http://www.apneaboard.com/forums/Thread-...any-better
http://www.apneaboard.com/forums/Thread-...some-sleep

[jaswilliams]

But pressure cycling is what an ASV does... the graph that shows a good patient with stable ASV pressures looks more like a patient without central apnoea

[JoeyWallaby]

It's basically loop gain but made more complicated since it's loop gain combined with the complexity of ASV


https://www.acponline.org/system/files/d...binson.pdf

Loop gain is an engineering method used to measure the stability of the negative feedback chemoreflex control system. The overall loop gain of the ventilatory system reflects the ratio of the ventilatory response to the disturbance that elicited the response (LG = ventilatory response/ventilatory disturbance). Therefore, when breathing deviates from eupnea (the point where ventilation matches metabolic demand), such as during a hypopnea, if the ventilatory response that is elicited is equal to the disturbance (LG = 1), ventilation will correct blood gases to re-establish eupneic levels. If the ventilatory response is disproportionately larger than the disturbance (LG > 1), ventilation will not only correct the disturbance to blood gases, but will overshoot such that PaCO2 will be reduced below eupnic levels. The resulting hypocapnia will then induce hypoventilation, upper airway muscle hypotonia and a secondary airway obstruction (apnea or hypopnea depending on prevailing upper airway mechanics), such that respiratory events become self-perpetuating. Thus higher loop gain reflects less stable ventilatory chemoreflex control.

Figure 1. Schematic of ventilatory loop gain. 1, A disturbance to breathing causes a reduction in ventilation below eupnea. 2, Reduced ventilation increases arterial CO2 (PaCO2) and reduces arterial O2 (PaO2). 3, Controller gain (CG) reflects the sensitivity of the peripheral and central chemoreceptors to blood gases and dictates the magnitude of neural drive to ventilatory muscles (ΔVE/ΔPaCO2). 4, Plant gain (PG) represents the effectiveness of the lungs to change blood gases (ΔPaCO2/ΔVE). 5, The product of controller and plant gain determines overall loop gain (LG). If loop gain is less than 1 (LG < 1), the fluctuations in ventilation will dampen out and breathing will stabilize. If loop gain is greater than 1 (LG > 1), the fluctuations in ventilation will increase in amplitude and instability will be self-perpetuating.