[Treatment] ASV settings for treatment of complex sleep apnea

[Geer1]

If you look closely you can see how the ASV works to blow the flow limitations apart. Specifically look at your 00:05 example. One flow limited breath then PS of 6-7 brings next breath back in line, then a few breaths later one smaller breath so it bumps PS up to 4 ish, next breath still smaller so PS up to 6ish and back to normal breathing again. You can see similar work being done in your other examples.

With APAP or bilevel the machine doesn't react so you often have numerous repeated bad breaths and my understanding is that it is the buildup/extended time of flow limitations that is the main issue that ends up causing arousal (by increasing CO2 levels). The ASV seems more than competent to make the corrections early enough that this likely is not a problem (or at least a less severe problem then with APAP or bilevel). 

Pretty darn cool technology, I didn't realize that these machines were that fast to react.

[JoeyWallaby]

Yea, it’s good but a lot of the breathes have a flat inspiratory curve, I think the machine sees the tidal volume is good so it doesn’t care.

[Sleeprider]

It is common to see a flat inspiratory curve on all machines that backup a patient's breathing. While pressure support can cause the minute vent or tidal volume target to be met, the lack of inspiratory effort flattens out the curve. This is what a ventilation supported breath looks like, and without the support it might be apnea or hypopnea. I have said on a number of occasions, we can generally ignore some flow limitation with ASV and ST type machines because it doesn't always arise from airway restriction, rather lack of spontaneous effort.

[JoeyWallaby]

Ok last night, first part of night is Min EPAP 7.2, Min PS 4.2. Second part is Min EPAP 7.2, PS 5.4. Woke up from first part because people were playing music (new years), humidification was too high and mask was leaking. Turned down humidification for second part.

Overview
First part - event

First part - waveforms


First part - end of night

[JoeyWallaby]

Second part - waveforms

---

Second part - end of night

[JoeyWallaby]

It's interesting that this night, the PS increased so much, with the best waveforms being when PS was approx 9/10.

Aerophagia is gradually improving.

[SarcasticDave94]

I don't know if you're a side or back sleeper, but for me, when new to the ASV I began left side sleeping. It helped me with aerophagia and GERD. Best wishes to your success.

[JoeyWallaby]

Thanks Dave, I've always fell asleep on my side but roll onto back when asleep sometimes. I'm hoping the aerophagia will gradually go away by itself.

I've tried to set the Min EPAP to the point where my airway, consciously fully relaxing it, feels supported on exhale (and vice versa, Min PS so that airway feels supported on inhale). I found this quote from B. Tucker Woodson in the book "Sleep Apnea and Snoring" related to this...

Airway collapse during sleep is both dynamic and passive. Dynamic collapse occurs during inspiration. Passive collapse occurs during expiration. Both are the result of a combination of applied forces that collapse and dilate the airway. In a structurally small airway during sleep, when dilating forces that stabilize the airway are greater than the collapsing forces, the airway is obstructed.

Obstruction during sleep is the result of a complex cascade. During inspiration, upper (pharynx) and lower (chest wall and diaphragm) airway muscles are activated. The lower airway muscles create a negative intraluminal force balanced by upper airway muscles that stiffen and dilate the airway. Increases in negative airway pressure or loss of muscle dilation will obstruct the airway. In sleep-disordered breathing both occur. Increased upper airway resistance leads to more negative intraluminal pressure and activation of upper airway dilator muscles is delayed or decreased. During expiration, positive pressure forces dilate the airway, and upper airway muscle tone is reduced. If the balance is unfavorable and the effects of tissue mass are not compensated, collapse and obstruction occur.

The tipping point for apnea is poorly understood, but is likely initiated by passive expiratory collapse. It is this collapse that triggers the dynamic events during inspiration. Without passive airway collapse, the cascade of progressive inspiratory flow limitation, increased negative luminal pressure and increased upper airway resistance may be aborted. If adequate airway size is maintained during expiration, inspiratory obstruction is prevented.

Since during expiration the largest decreases in airway size occur in the hypopharynx, treatment of this segment may be critical for most if not all individuals with sleep-disordered breathing. The tongue suspension procedure was conceived as a means of providing an extraluminal dilating force to the lower pharyngeal airway in contrast to nasal Continuous Positive Airway Pressure (CPAP) which is an intraluminal dilating force. This is accomplished by passing a submucosal suture into the posterior midline tongue. The suture prevents passive collapse while not interfering with anterior and superior tongue movements which are involved with swallowing and speech. Placement is directed towards the level of the foramen cecum.

Also, this is apparently how ResMed ASVs determine respiratory cycle phase
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4629962/

And more info



If passive airway collapse on exhale is causing some of the inspiratory flow limitation, but not enough to cause apneas/hypopneas, the machine isn't going to increase EPAP but instead the PS (since it can't tell of course). Maybe I should try a higher Min EPAP and see if the required PS to achieve a good waveform is decreased?

[JoeyWallaby]

More on inspiratory vs expiratory collapse/narrowing

Upper airway obstruction during sleep is characteristically attributed to inspiratory narrowing owing to a collapsing subatmospheric pressure against a hypotonic pharyngeal airway. However, several lines of evidence implicate expiratory narrowing as a possible mechanism of the initial narrowing. First, ventilatory motor output is an important determinant of upper airway patency. Oscillation of ventilatory motor output, during the characteristic periodic breathing of OSA, is associated with pharyngeal narrowing or obstruction at the nadir of the motor output, especially in individuals with a highly collapsible airway. Second, an obstructive apnea is often preceded by expiratory narrowing of the upper airway as evidenced by increased expiratory resistance or progressive expiratory narrowing, detected by fiberoptic imaging. Finally, although upper airway narrowing or occlusion occurs during a spontaneous or induced hypocapnic central apnea or induced hypocapnic hypopnea, pharyngeal narrowing during central hypopnea occurs during the expiratory phase only and is associated with increased expiratory upper airway compliance. Therefore upper airway obstruction may occur in either inspiration or expiration. Individuals with a high surrounding tissue pressure may be particularly susceptible to expiratory pharyngeal narrowing during such low ventilatory motor output and driving pressure.

From chapter "Anatomy and Physiology of Upper Airway Obstruction", in "Principles and Practice of Sleep Medicine 4th edition".

[jaswilliams]

Joey, no comment only your data for no but now your using an ASV can you replace the pressure graph with the mask pressure graph this will give us a better understanding on what the ASV is doing on a breath by breath basis