Can EPR use cause Central Apnea Events?

[pholynyk]

I am one of those people who needs EPR = 3 to reduce my hypoapnea index. I have verified this by looking at my Statistics Changes to Prescription section. I tried EPR = 2 several times, and my AHI went up, and once after a visit to my DME to check the calibration (they set the EPR off during the check) my AHI went way up, I didn't sleep well, and reset the EPR to 3. Problem solved. If I could get a bi-level, I would, but my AHI is typically below 2 now, so it probably won't happen.

[Sleeprider]

Ron, thanks for the link to the comparison of expiratory relief implementations. As it says, the Resmed EPR is much more like bilevel, where the patient respiratory effort triggers and cycles the pressure change. The Respironics pressure changes are predictive, and that gets a lot of people in trouble with poor sync. Most bilevels without backup trigger and cycle on spontaneous effort rather than timing or predictive algorithms.

I have not observed this to be true: "Interestingly, the EPR in ResMed’s machines will reduce automatically if any flow limitation is detected through the night. This means that the full treatment pressure is given in these periods, so as to reduce the likelihood of a respiratory event."

If anyone can find confirmation of that by looking at the mask pressure or pressure wave-forms, it would be interesting to see.

[Ron AKA]

What I find confusing in this issue is that you often see BiPAP machines recommended for treatment of CA events. It strikes me that a BiPAP machine is like an APAP using EPR but on steroids. The both reduce pressure during expiry compared to inhalation, but the BiPAP can do more than 3 cm. So why would there be any advantage in using a BiPAP for CA treatment, if there is any validity to the theory that pressure differentials between inhale and exhale CAUSE CA in the first place. This is confusing! I know there are even more sophisticated machines beyond BiPAP that actually force inhale and exhale, and I can see how that could help.

[OpalRose]

What I find confusing in this issue is that you often see BiPAP machines recommended for treatment of CA events. It strikes me that a BiPAP machine is like an APAP using EPR but on steroids. The both reduce pressure during expiry compared to inhalation, but the BiPAP can do more than 3 cm. So why would there be any advantage in using a BiPAP for CA treatment, if there is any validity to the theory that pressure differentials between inhale and exhale CAUSE CA in the first place. This is confusing! I know there are even more sophisticated machines beyond BiPAP that actually force inhale and exhale, and I can see how that could help.

There is no advantage to using bipap/Bilevel for CA treatment.

Not sure how this works in Canada, but here in the US, when a person shows high CA events, the first step is to prescribe a Cpap/Apap.  Then the patient has to prove failure at Cpap (which is likely to happen.)  The next step is that the insurance industry here will want you to try BiPap, which will likely be another failure.  After that, and usually many months later, the patient may be prescribed an ASV which will treat Cental Apnea by forcing a breath.  

This is our crazy medical/insurance system at work.  It amazes me that folk just don’t give up on therapy after all that.

[Sleeprider]

A BiPAP with a backup rate is a different animal from the fixed bilevel or auto bilevel without backup. There are a few "flavors". The spontaneous/timed (ST) machines wait for a patient to take a spontaneous breath, and on a timed interval will supply the fixed (usually 8 to 15 cm higher than EPAP) inhale pressure to attempt to cause a breath. The Adaptive Servo Ventilator (ASV) supplies IPAP pressure between 0 and 15 to cause a breath. These machines are specialized and have different intended uses. How deep do you want to go?

[Ron AKA]

These machines are specialized and have different intended uses.  How deep do you want to go?

My interest is in the issue of whether or not a lower EPAP compared to IPAP actually affects the incidence of CA events. It is not so obvious that it does. The point I am getting to with my research is that one's autonomous nervous system potentially becomes adapted to regulating with higher CO2 levels, and when presented with a sudden improvement in O2 and reduction in CO2, as a result of CPAP therapy, it does not respond well, and actually causes CA events. And, there seems to be some evidence that this is a temporary situation and over time the CA events may reduce as the nervous system adapts to the lower CO2. I guess my point is that having a EPAP/IPAP differential is not necessarily a bad thing in my opinion, but there does not seem to be a lot of hard evidence to support that thought.

[Sleeprider]

higher EPAP or positive end expiatory pressure (PEEP) improves oxygenation. Individuals that have a tendency towards central apnea, need steady fixed pressure with out pressure support or EPR. There is a lot of research on invasive ventilation and non-invasive ventilation that discusses these relationships. It is applicable to CPAP/BPAP, but the research mainly comes from the ventilation studies.

[SarcasticDave94]

Quote:
"For most people EPR is probably harmless, it's just that there are risks, and the number of people for whom it is a problem, albeit the minority, is still pretty significant."

Hmm, a significant minority or a minority with significant numbers? OK.

I do agree with others posting here, EPR can be useful and effective. I would think most possibly benefit from it, excepting those that it actually does cause an issue. IMO it doesn't seem that "blanket" or "cookie cutter" methods are effective or respectful of the individual patient. BTW EPR seems to effectively make your CPAP mimic a BPAP.

My answer to the scare tactic Duck or DME/RT: I'll be arranging to get your replacement later today.

[Ron AKA]

My interest in this subject was instigated by the observations that with CPAP treatment my sleep apnea which was diagnosed at an AHI of 37, has been significantly reduced to about 3, but now the ratio of apnea incidents have become central sleep apnea (CSA) dominated. This raises the question of how one optimizes CPAP settings to minimize AHI and in this case CSA events. 

The advice on how to do this is kind of all over the map, but the most frequent advice is to keep the maximum treatment pressure as low as possible. And after that it is often suggested to limit or eliminate the use of Expiratory Pressure Relief (EPR). Why would this be? Well there is a fairly common theory as to why CSA event frequencies are revealed or even elevated when CPAP therapy is introduced. Greatly simplified, your body adapts to higher levels of CO2 in your blood due to untreated general sleep apnea. When CPAP is introduced the efficiency of breathing is suddenly improved, and CO2 levels go down during sleep and treatment. Your body responds to the lower CO2 by suppressing respiration, and that can cause CSA events. 

Basic physics tells us that when we put higher pressure air in our lungs it will contain more oxygen, and as we know breathing is much easier at sea level than it is on top of Everest. If we limit the maximum pressure in the lungs, then breathing efficiency is reduced and CO2 is relatively elevated. With the EPR pressure is even further reduced in the exhale cycle. This improves the total air mass transferred during each inhale and exhale cycle. If EPR is limited or eliminated then breathing efficiency is again reduced and CO2 increased. Again a good thing in trying to avoid CSA events. 

The dilemma of course is that this may be the opposite strategy to what we want to use to minimize obstuctive sleep apnea (OSA). So what does one do? If one is in this situation there is some good news. Studies have found that in the majority of cases this is only a temporary condition. This quote from an emedicine article is a good summary of the study knowledge:

"Central sleep apnea may emerge during titration of CPAP in patients previously diagnosed with obstructive sleep apnea. This syndrome, termed complex sleep apnea, has become a controversial topic in the sleep literature [9] and has been raised as a possible type of difficult-to-treat obstructive sleep apnea. As many as 6.5% of patients with obstructive sleep apnea may develop emergent or persistent central sleep apnea with CPAP treatment. CPAP emergent central sleep apnea is generally transitory and is eliminated after eight weeks of CPAP therapy. Persistent CPAP-related central sleep apnea has been observed in approximately 1.5% of treated patients. 

In other words in about 75% of cases the incidence of CSA will be reduced over the first 8 weeks of treatment. As a result of this I have come up with a personal strategy on how to deal with my situation. I will ignore CSA events and optimize my CPAP setup based on OSA and hypopnea events only. Then after 8 weeks I will review the situation again, and only if necessary then will I reduce maximum treatment pressure and EPR use. But of course, I will hope that this is not necessary.

Here is a good article from Fisher & Paykel that does a good summary of the issue.

The True Prevalence of Central Apneas in CPAP Patients

And if you want to do a deeper dive there is the emedicine article that the quote above was taken from.

Central Sleep Apnea Syndromes

[Walla Walla]

I wouldn't make a hard and fast rule about changing settings for CA. If you start waking up and feeling like someone beat you over the head with a baseball bat you might want to make a change. I don't think I'd wait 8 weeks to feel better.