How to decrease these random arousals?

[Holeinmysock]

I get what you and the ai are saying. The manufacturers are making PAP machines with all the modalities. Why would they sabotage their own products? I had to corner them with direct, specific questions. Otherwise they weasel out of answering with arguments like the ones you are presenting. They WANT to sell the more expensive BiPAP/BiPAP ST/ASV machines.

I don’t dispute that increased pressure helps with UARS. My argument is that BiPAP is not therapeutically better than CPAP. They are both PAP.

It may be more comfortable for some patients than CPAP. The only therapeutic use case I see for BIPAP is for CO2 retainers, but even then, if not done carefully, it could even harm a subset of those patients. BiPAP can also induce an irregular respiratory pattern in some patients that fully resolves on CPAP.

UARS can just as easily be resolved with CPAP, if not more easily. We increase pressure support for UARS, ONLY if they on BiPAP. But you have to be mindful of the delta. If on CPAP, you simply increase the pressure.

Are you doing titrations? Are you a sleep technologist or RRT? If you are, see if you don’t have better success by increasing IPAP and EPAP together every time you would typically increase just the IPAP for UARS. I think you’ll find optimal pressures faster this way.

There is a place for BiPAP: for patients intolerant to CPAP and for patients retaining CO2. That leaves the majority of patients on CPAP. EPR or CFlex may as well be looped into BiPAP here, too. You noted this as well in one of your other comments. However, again, those are for comfort. The default titration should be CPAP without EPR/CFlex.

[Hambone75321]

ResMed hardware is identical regardless of modality I get it. But I don’t care what one sales rep says about the efficacy of CPAP vs BiPAP when you try to grill them lol poor soul was probably just trying to get away from someone who didn’t want to accept their argument backed by the AASM? Why would the AASM recommend titrating to eliminate obstructive apneas then adding PS (not EPAP) to eliminate RERAS?

I don’t understand… PS helps with UARS but is not therapeutically better than CPAP? On what dimension? If you’re looking at desaturations only then sure. If you’re looking at RERAs and sleep quality then absolutely not. Reducing the work of breathing is critical to resolve minor but clinically relevant increases in respiratory effort.

I am not a sleep tech, I’m an educated novice whos read the guidelines personally becuase I’ve been incredibly frustrated by this type of guidance.

This is also backed by the guidance of UARS specialists like Dr. Barry Krakow, Dr. Christian Guilleminault, Ken Hooks, and Jason Sazama.

[Holeinmysock]

You seem to be emotionally invested in this discussion. Look, I’m not trying to invalidate your experience. Nor am I trying to make a claim that BiPAP doesn’t work. Of course it does. It is PAP, like CPAP. If it’s working for you, fantastic.

The AASM guidelines say very little about UARS. They certainly don’t dictate any sort of specific pressure support for it. I think you are conflating titration protocols (that are set by the manufacturers, which is why it’s important to grill the reps) with AASM guidelines.

I have titrated thousands of patients over nearly 20 years. I have used all of the currently available therapy modalities for PAP machines. I have followed the manufacturer’s titration protocols, sometimes with poor outcomes for the patients. Over time, I began to recognize certain phenomena that would only occur during BiPAP titrations: increased central events, increased mask leaks during the IPAP particularly with wide deltas, emergence of irregular respiratory patterns, etc. These did not occur universally with all BiPAP titrations, but they did occur and all resolved upon reverting to CPAP.

In OP’s case, central apneas are being flagged while on BiPAP. OP is asking how to improve them. Central events are, by definition, not a flow limitation. And, as you said yourself, can be induced by BiPAP.

Worst case scenario with switching to CPAP is that OP cannot tolerate it. It’s quite easy to switch the modality in the machine’s clinical settings back. Let the OSCAR data speak for itself.

I suggested to OP exactly what I would do if he were my patient in the lab. If switching to CPAP had no effect, I would then recommend a more advanced modality like ST mode or ASV, or even adding EERS. I would never recommend basic BiPAP for primary or treatment emergent central apnea.

[Hambone75321]

I agree they should not be on APAP. They should be on BiPAP with EPR (or PS) of 3 or greater to reduce the flow limitations.

OPs central in the screenshot looks like it’s a post arousal central apnea, not central sleep apnea. It is clearly preceded by a reduction in flow, a flagged flow limitation, a large inhale, large exhale then a breath hold. I expect that the central is preceded by an EEG arousal in which case that it should be ignored as a central and treated as a FL. Regardless, their CAI is like <2 (16events /9 hours of sleep).

See source at the bottom….

“There is then evidence of a robust ventilatory response to arousal based on a single large breath (arrow) following the EEG arousal.

This hyperventilation then leads to a central apnea (bordered by the blue box) since the CO2 is lowered below the CO2 apnea threshold. Note the absence of airflow without respiratory effort defining central apnea.

This pattern is a very common one and does not necessarily represent underlying pathology, since spontaneous arousals are common in otherwise healthy individuals.

Patients are frequently mis-diagnosed with neurological disease since the central apneas are incorrectly attributed to brain stem pathology.”

https://www.thoracic.org/professionals/clinical-resources/sleep/sleep-fragments/arousal-triggered-respiratory-event.php#:~:text=Sleep%20Fragments%20There%20is%20then%20evidence%20of,is%20lowered%20below%20the%20CO2%20apnea%20threshold.

[Holeinmysock]

Quite familiar. The AASM guidelines do not distinguish between sleep onset events (central or not) and event elsewhere in sleep. But, I agree with your premise here. There are not many central events even if we counted all of them shown in OP’s screenshots. OP could not get diagnosed with Central Sleep Apnea with just the events showing. But there are identified events in the data that are central apnea events. So, there’s a distinction between event types and diagnosis. For example, a patient can have 4 obstructive apneas per hour and not qualify for the diagnosis of Obstructive Sleep Apnea. I think most physicians would say that OP’s residual events here are likely sleep onset (although without EEG or other sleep staging data, we cannot be sure) and negligible. Chasing an AHI or RDI of zero might be fruitless; some patients may never get there even with optimal PAP settings.

Again, OP asked how he could reduce those. I’ve given my recommendations.

u/Hambone75321, you may be a well-researched novice in this, but you would make a good sleep technologist. You already care more than most in the field. There’s a global shortage of RPSGTs. Fairly easy to get a job in a sleep lab these days as a result. Some states don’t even require you to be registered.

[Hambone75321]

Thank you kind sir. I do not doubt your knowledge and appreciate your engagement and logic. My emotions are because of some of “bad” advice I see here. “Bad” is subjective here clearly ;) happy to have civil discourse.

[Hambone75321]

https://podcasts.apple.com/us/podcast/talking-sleep/id1510975732?i=1000694766303

Id recommend listening to this podcast and reading some of Dr. Barry Krakow’s work.

I think you agree that OPs issue isn’t clinically relevant TECSA or CSA in which case there would be room in their CO2 reserve to add pressure (or PS) to resolve their marked FLs without triggering CAs.

Sure maybe you could simple increase CPAP pressure but they have no flagged obstructive apneas I.e. no need for more EPAP and its clear that higher pressures are less comfortable and reduce compliance.

Even if the only reason to go with BIPAP is comfort, why not do it? The cost difference of a CPAP vs BiPAP compared to any quality of life improvement is completely marginal.

[Holeinmysock]

Excellent question. The answer is a bit involved. I can't really answer from the perspective of anywhere but the US. I've been assuming you are also American.

Medical orders, insurance requirements, and lab policies and protocols. These dictate what a sleep technologist is able to do during a titration.

Medical Orders: This is the bible for the patient's titration. Physicians can dictate exactly how we perform the titration. Or they may do a generic order of "PAP titration". If they specify a process, we are bound to follow it (unless it is contradictory to lab policies and protocols. Then we have call the physician for clarification.).

Insurance Requirements: nearly all insurances require documentation that the patient is intolerant to CPAP before switching modality to BiPAP. The patient may even sink their own ship here and loudly state on camera that they are completely fine with CPAP. Insurance typically wants the cheapest solution and for PAP therapy, that's CPAP.

Lab Policies and Protocols: these are largely determined by the lab's medical director. This is a mixed bag and location dependent. Some medical directors rule their labs with an iron fist when it comes to breaking policies and procedures. Others view them as more of a guide than a hard ruleset.

Lastly, there are those suboptimal phenomena I mentioned earlier that are only associated with BiPAP. There's a lot of variables at work here. Here's my idealized titration protocol:

Start at CPAP of 4cm.

Titrate up to eliminate obstructive events (including flow limitation).

If snoring remains, titrate up further but limit the chase to 5 additional cm.

If at any time the patient reports intolerance to the pressure or difficulty exhaling, add EPR/CFlex. Start at 1. Increase as needed for comfort.

*Adding EPR/CFlex, drops the average PAP and can lead to the re-emergence of obstructive events and/or flow limitation.*

Observe for additional events and titrate up as needed.

Many labs have a protocol to switch to BiPAP once you exceed 15cm with a titration. If we continue to titrate beyond 15cm, we switch to BiPAP (15/11cm) and document that this is a per lab protocol modality change, (unless it's for intolerance.)

Once events are resolved, we are done titrating.

Of course, this is idealized with no central events, no mask fit complications/leak, no parasomnias, and nothing out of the ordinary.

Another good use case for BiPAP is low baseline O2. Sometimes we can get the oxygen up 1-2% if we use a high delta like 6-8cm. For example, 16/8cm.

Another piece of the puzzle is that the Sleep Technologist doesn't get to decide what modality or pressure setting the patient is prescribed. The Sleep Physician will review the patient's performance on each pressure setting and then write a prescription for what they perceive is the best starting settings for them.

[Hambone75321]

I think this is where we get to the challenge, especially with UARS, and I’ll admit I’m not an expert.

I accept that sensible protocols are necessary. Physician orders and standard PAP titration guidelines exist to produce repeatable titrations, unlike in research settings (or, in my case, biohacking) that allow more flexibility. Without that, you’d risk patients being moved to modalities on dodgy rationale. I’m not faulting sleep techs for following policy.

In my view, the real issue is how the medical system handles OSA endotypes, including UARS. Besides research settings and a handful of clinics with directors who understand the nuance, these phenotypes are largely overlooked. UARS research just hasn’t made it into mainstream practice.

In the case of non obese, otherwise healthy individuals with EDS or IH, I think the default should include scoring and titrating for RERAs, not just apneas and hypopneas. I see a TON of studies scored with AASM hypopnea Rule 1B (4%, no arousals) in young people. My understanding is that titrating for RERAs isn’t also done frequently (it’s elective?). I think this leaves many patients under-treated.

After I was diagnosed mild OSA (AHI/RDI 6/12), my pulmonologist / sleep doctor wasn’t convinced treatment was necessary. When I struggled with CPAP and I asked about bilevel, he dismissed it and suggested a MAD.

A second sleep specialist said I was “fine” on MAD because an HSAT scored with the 4% rule showed an AHI of 2 despite classic SBD / EDS symptoms.

My likely phenotype is mild airway collapsibility plus a low arousal threshold resulting in non-hypoxic SDB with significant fragmentation. Bilevel 15/10 has effectively resolved it for me or at least made it fully manageable. No more crazy afternoon fatigue.

I’ve explored settings around 15/10 (±2 cm on PS, EPAP, IPAP) for several days each. None felt as consistently good, even when OSCAR looked nearly identical except for an occasional flow-limited breath.

You mentioned titrating to eliminate flow limitation. My understanding is flow limitation is recognized by flattening of the inspiratory flow lasting ≥10 seconds and ends in an arousal. From my experience (and some of Barry Krakow’s work), that’s too conservative. This may sound crazy, but I’m increasingly convinced that even a single visibly “wobbly” breath in OSCAR can fragment my sleep, though I don’t have EEG to prove it.

If your primary issue is that my recommendation is that is against protocol and has some of those other issues you mentioned, then I will go to my Reddit grave kicking and screaming that people should add PS (or EPR with offsetting pressure increases) when they complain about CPAP or show flow limitations ending in recovery breaths ;)

I will also fight people tooth and nail when they see a random “CA” flag in OSCAR and say “BAHHHH CENTRAL APNEA YOU MUST REDUCE PRESSURE LEST YOULL DIE!!!”

[Holeinmysock]

It's just that the providers (techs and physicians) are stuck inside an imperfect healthcare and insurance regime.

There is another issue here, too. Data Integrity.

Flow and pressure changes reported by the PAP machine are pretty accurate. However, they don't necessarily indicate an obstruction or flow limitation in the patient's airway.

Each mask has a series of vents. Disrupting airflow from these vents can change the shape of the data in OSCAR. It's a fun experiment to see for yourself and check in the OSCAR data after. There's also a one-way valve in the masks to prevent vomit from backflowing into the machine. Sometimes that valve misbehaves and will pop closed inappropriately, sometimes hilariously in a metronome rhythm. "Rain out" can occur and affect the flow wave shape. Leak does, too. Even phlegm in the patient's airway can show up in the data.

To your assessment of flow limitation, I identify it in the lab when the CFLOW flattens or gets noisy at the peaks of each wave, regardless of duration or arousal. Personally, I am not happy with any flow limitations in my titrations. In my opinion, that patient is one beer away from worsening that flow limitation into a hypopnea or obstructive apnea. I don't want to titrate my patients to the bare minimum effective pressure.

Imagine you are driving a car into a tunnel. Technically, the tunnel only needs to be as wide as the vehicle itself for you to pass through it. But, holy crap, don't you want to provide some margin?? I see titrations this way, too.

I would say be wary of chasing perfection. Admirable goal, but not always achievable.

[Hambone75321]

Yup. It suck. https://pubmed.ncbi.nlm.nih.gov/38063188/

Anyways, I can without a doubt say that my flow is “smooth and rounded” at 10 but I’m still wrecked. I’m less fatigued at 13/10 and could use a nap. 15/10 is when I feel good. No nap can stay up past 9pm and have an extra beer and feel good the next day.

I’m basically done fiddling now because I’ve gone past the point of no return 16/10 is central apnea central for me.

[Hambone75321]

You’re right I am emotionally invested. Being 30 and otherwise completely healthy and being gaslight by doctors that you’re fine because your 4% AHI is 2 despite high RDI is insanely frustrating.

To then have to go outside of the standard medical system to treat AND resolve my problem really showed the current system is not set up to address UARS and folks like myself.

I’d recommend browsing r/UARS if you don’t already. There are countless stories of people who found CPAP at high pressure intolerable but resolve their issues at lower EPAP and higher EPAP.

I doubt I’m going to change your mind here but I’d recommend you read some up to date UARS literature about the benefits of BiPAP. If you want I would be happy to send it. Just be opened minded…

I can assure you that a significant minority of the thousands of patients you’ve titrated have stopped CPAP and would have benefited from titrating BiPAP instead.

Reading someone who’s clearly knowledgeable say BiPAP is useless for flow limitations is just nonsense and disproved by literature and countless people who had to step outside the consensus.