Complex sleep apnea and EPR

igdoc wrote:...I would ask you not to underestimate the potential effect of exhalation relief on excess central events. For example I have complex sleep apnea and, with a pressure of 8 and an EPR of 1, had an AHI averaging 29, all due to central events. Switching off the EPR dropped my AHI to between 5 and 6 and, more importantly, enabled me to start sleeping again. I have avoided needing an ASV machine.

CPAP devices produce steady pressure that does not change during the respiratory cycle. It is the first-line noninvasive treatment for OSAS, and can almost completely suppress obstructive respiratory events. But CPAP typically does not acutely resolve central apnea activity. Patients with CompSAS may have a poor initial experience with CPAP and thus may be nonadherent with therapy. Using retrospective data and OSAS patients as a comparison group, Pusalavidyasagar et al39 documented that although patients in both groups had a similar diagnostic AHI, CompSAS patients had a significantly higher AHI during the CPAP titration (CompSAS AHI on CPAP 24.6 ± 21.6 vs OSAS AHI on CPAP 2.1 ± 2.7), and most of the residual respiratory disturbance was from central apneas that emerged on CPAP. Mean time to the first follow-up was shorter in CompSAS patients (46.2 ± 47.3 days vs 53.8 ± 36.8 days), and interface problems were more common in CompSAS patients, especially air hunger/dyspnea (8.8% vs 0.8%) and inadvertent mask removal (17.7% vs 2.6%). Some researchers suggest that most CSA events can disappear after continued CPAP use. It is still not clear what proportion of patients with CompSAS may improve over time with continued CPAP treatment. Dernaika et al,30 in their prospective case-control study, documented the disappearance of central apnea activity with CPAP in 12 (86%) of 14 patients with CompSAS over 2–3 months. The investigators stated that CSA events occurring during CPAP titration were transient and self-limited, whereas only one patient with diastolic dysfunction on baseline transthoracic echocardiography showed continued CSA events. Unfortunately, the applicability of their data is limited because they excluded patients with any significant comorbidities, including CHF by history or previous echocardiography, chronic obstructive pulmonary disease or other significant lung disease, daytime hypercapnia or hypoxemia, cerebrovascular disease, seizure disorder, or a history of use of benzodiazepines, narcotics, or illicit drugs. In a retrospective case series, Kuzniar et al34 evaluated 13 patients who had CompSAS during the first overnight CPAP titration. Repeat therapeutic PSGs were performed after 195 (49–562) days. On the follow-up study, seven of 13 patients reached AHI < 10. The low number of patients and retrospective character of data collection are the main limitations of this study. Cassel et al37 investigated 675 patients with OSA receiving CPAP treatment. During the baseline CPAP night, 82 patients had CompSAS. The follow-up evaluations took place after a median of 14 weeks, and 30 patients fulfilled the criteria for CompSAS. The prevalence of CompSAS was significantly reduced from 12.2% to 6.9%. In a large retrospective study of 1286 patients with a diagnosis of OSA who underwent titration with CPAP, CompSAS occurred in 84 patients (6.5%). However, after 8 weeks of CPAP therapy, they estimate that 1.5% of the patients with OSA continued to have CompSAS with long-term use of CPAP.35 From these very limited data, it seems likely that most CompSAS patients will improve completely with long-term use of CPAP. This variability in CPAP response is probably due to heterogeneity in the CompSAS group or to variable factors governing adaptation that are not yet well understood. However, how to distinguish patients who might stabilize over time from those who will suffer ongoing complex apnea activity is unknown, and the time required for adaptation of ventilation is also unknown. Patients who have a bad initial experience with CPAP have a worse adherence to therapy, and those who fail with CPAP compliance over longer periods will not enjoy benefits of treatment while awaiting adaptation.

Pugsy wrote:...But I just don't see the need to go shout it from the rooftops and scare the hell out of every newbie who had a handful of centrals last night.
They get all worked up over the numbers (and usually better numbers than I get) when there's no need.

I think the post I comment about what you said..that thread was started by someone with an AHI of 1.0....and all centrals.
That's one per hour average and it doesn't need anything to be done about it. and it doesn't need to cause extra concern and worry.

People accept obstructive apneas but get all freaked out about Centrals and worry too much about stuff they should set on the back burner for a little while. ....

Delta4 wrote:I assume you're referring to my recent post where I said:
I have 4-5 bad nights each week (50-80 central events with a AHI of 4.5 - 8.) On my better nights, my AHI is less than 1. That leaves me with a monthly AHI of around 3.

Pugsy wrote:... People already panic when they see a central or two...I am not going to tell them to turn off EPR because EPR might be causing them. OMG I got Complex Sleep Apnea because of my exhale relief...I had 5 centrals last night....You have no idea how many panic message I get about centrals.

Not every central is caused by the unstable breathing....sleep onset centrals are normal and not related to pressure one way or the other. ...

Pugsy wrote:... Ian...you are the only person that I have ever known have documented evidence that turning off EPR was important in reducing centrals...only person in 5 years of helping people here on the forum. ...

Pugsy wrote:... But I just don't see the need to go shout it from the rooftops and scare the hell out of every newbie ...

Pugsy wrote:... When I do work with people who do have a number of centrals that I can't poo poo off....we look at all aspects and try all different combinations of settings to see if we can get any relief in an effort to avoid the ASV machine. ...

Delta4 wrote:... Pugsy, I'd really appreciate your thoughts on my situation. Please understand that I'm not trying to be combative. ...

Delta4 wrote:... I assume you're referring to my recent post where I said:
I have 4-5 bad nights each week (50-80 central events with a AHI of 4.5 - 8.) On my better nights, my AHI is less than 1. That leaves me with a monthly AHI of around 3.

On a later post in that thread, I gave more details:
On my bad nights, I have clusters of centrals 1-5 hours after I go to bed. By clusters, I mean I might have 20 events in a 30 minute period. Or 45 events in an hour. Unfortunately my averages get diluted because I sleep so long. I also wake up gasping for air during many of my bad nights. I have a headache after waking up most of the time which was rare before. All this screams to me that we need to try a different machine!

Here's some other information that isn't in that thread:

I'm not ignoring obstructive events because I rarely have them. Over 90% of my events in a month are central and only 3% are obstructive. ButI think that only looking at the monthly AHI doesn't make sense in my case because I have such wide swings in my nightly AHI. In other words, how can my doctor expect me to ever feel rested when I have 50-80 central events a night (usually in clusters) for 4-5 nights every week? I don't see how I can ever pay down my sleep debt continuing like this.

Sometimes I get up to use the bathroom after sleeping 10 hours and notice my AHI is around 11-12. I go back to sleep for 4 more hours and my AHI for the night ends up around 8 just because I had zero or only a few events in the last 4 hours of sleeping 14 hours. This situation happens frequently.

I waited until I had 3 months of these consistent results before posting about it here so I wouldn't appear to be overreacting to a few bad nights of data.

My family and friends tell me to quit using the cpap. I'm not doing that because it has my OSA under control. And I have other conditions which make me more likely to have a stroke. But I'm positive something needs to change with my cpap therapy because I started feeling significantly worse right after starting on cpap 3 months ago. I'm talking about debilitating fatigue, daytime sleepiness, and brain fog. I'm desperate for some relief. ...

igdoc wrote:The AHI dropped on the night I switched off the EPR and only returned to over 20 when I tried switching it back on one month later.

igdoc wrote:Switching off the EPR dropped my AHI to between 5 and 6 and, more importantly, enabled me to start sleeping again.

igdoc wrote:Just ask that reducing EPR/CFLEX/AFLEX be considered if large numbers of centrals appear.

igdoc wrote:Not going to enter into a contest.

...different effects of EPR and CFLEX/AFLEX.

Here's the waveform I generated at 20 cmH2O:



The first two arrows represent the termination of EPR (the first tiny waveform), and you can see how close they are to inspiration. This suggests that the trigger might be inspiratory flow, which could create a problem if you're trying to inspire from a sub-therapeutic pressure level. Or, it could be a very low expiratory flow rate. Try as I might, I could not verify this either way, so we'll have to wait for the manufacturer's response. But you really need to be at therapeutic CPAP level prior to inspiration, so we'll have to look at this carefully.
The second two arrows show where the EPR did not terminate, and inspiration occurred at well under therapeutic levels. I was able to generate this situation at all pressure levels. The obvious problem here would be if the EPR level was below the apnea threshold, therapy would not be effective. Again, I don't know why this occurred, and passed this information along to the rep.
This situation might be overcome by raising the baseline CPAP slightly, but the point is that using this EPR might change your CPAP requirements slightly.
I should also point out that there is a time function for EPR, if no breath is detected after a period of time, EPR is immediately suspended, so it seems that only a single breath would miss detection.

sleepydave wrote:When the coming of Expiratory Pressure Relief (EPR) was first announced, I had some questions as to whether this modality would offer relief on active expiration only during the CPAP mode, and perhaps address the issues that other expiratory adjuncts were having, or if the drop in expiratory pressure were carried out all the way to the next inspiration, relying on inspiration as the trigger to terminate EPR, and thus essentially operate in a BiPAP mode.

The following waveform analyses were performed on the EPR mode at 10 cmH2O with an EPR setting of 3 cmH2O. The breath rate is approximately 12.

The first graph shows the breathing waveform on top, inspiration being an upward deflection and expiration downward, while the bottom graph is measuring pressure. The pressure settings are seen as faint numbers at the left of the pressure waveform. You can see that the EPR, reflected as a drop in the therapeutic pressure on the pressure waveform down to about 7 cmH2O, is carried out all the way to the point of inspiration, and the inspiratory effort therefore takes place at a sub-therapeutic pressure. The baseline pressure returns to 10 cmH2O, but not until after inspiration has begun. In other words, inspiration is the trigger to terminate EPR, and instead of a CPAP pressure of 10 cmH2O with an expiratory adjunct, we are effectively left with BiPAP of 10/7:



This might not make a clinical difference if the patient ends up with the same results on BiPAP 10/7 that he would have on CPAP 10 cmH2O (which could be the case if there were only flow limitations, snores, or hypopneas). But if the new EPR-defined EPAP is below the apnea threshold, then there could be a problem.

In the second graph, the waveforms are superimposed to show more clearly that inspiration is occurring at a sub-therapeutic level:



There is a time limitation associated with the termination of EPR. In the next graph, you can see how the EPR eventually terminates and returns to baseline. In this instance, the breath rate was approximately 6, so the time to EPR termination was appoximately 5 seconds. The first arrow represents EPR termination, while the second signifies patient breath:



And here again, the graphs are superimposed to show the return to baseline relative to inspiration:



This means that eventually, there will be a return to baseline CPAP if in fact, an apnea occurs, and at the most, only one breath would be missed. Is the net result clinically relevant? I'm not sure either way. But if you're generating negative intrathoracic pressure or creating arousals, then there could be an issue.

In re: putting EPR in the AutoSet mode, that could be an effective way to overcome this supposed shortcoming of EPR. If events were to start occurring at, in this case, "10 cmH2O of CPAP". then baseline pressure could be raised, theoretically, to "13 cmH2O of CPAP", or effectively BiPAP 13/10. Course now we're right back where we started. The only outstanding question would be if the 13/10 format was better tolerated than the straight 10.

But how would the algorithm work? If the apnea identification in AutoCPAP is 10 seconds, and the EPR terminates at (in this case) 6 seconds, how would it know to increase the CPAP (really the "EPAP" segment of EPR) to address apneas? I would assume that flow limitations would be properly addressed with CPAP increase (because you're really raising the "IPAP" segment of EPR).

As an aside, therein lies the problem once you start talking about Auto-BiPAP. Do you increase the IPAP, and keep EPAP fixed, or do you vary the EPAP as well, looking to address apneas. You're gonna need two totally separate algorithms, and they can't interfere with each other.

There are a couple of options available with EPR. It can be used during the ramp period only, which would offer significant patient comfort during a time where the perhaps the greatest period of patient difficulty occurs. After the ramp period is over, it returns to the set pressure.

Before you select full-time EPR, though, and carry EPR throughout the night, you should consider how your particular situation might respond to this modality. And I think the key to EPR, AutoCPAP with EPR (should that ever come about) and AutoBiPAP will be how apneas are addressed. You might be OK dealing with hypopneas, snores and RERAs if you're of the belief that BiPAP can properly address these issues.

Pugsy wrote:

Delta4 wrote:I assume you're referring to my recent post where I said:
I have 4-5 bad nights each week (50-80 central events with a AHI of 4.5 - 8.) On my better nights, my AHI is less than 1. That leaves me with a monthly AHI of around 3.

No, I actually wasn't thinking of you or anyone recently in particular. I was thinking of past newbies that I have had to reassure that a few to several centrals don't mean that they have complex sleep apnea. I have had people PM me and want to know about getting an ASV machine because they developed 3 centrals and didn't have any during the sleep study.
Way too much "OMG, I have centrals" panic.

I only recently read your thread and have had other irons on the fire and really didn't have much to offer that would have been different from what was already offered.

When we have more bad nights than good nights and we feel worse than without CPAP therapy...something is changing or not right. Gotta try to figure out what before trying to fix it though..and that's sometimes really difficult.

Rather than muck up this thread...I will go back an read your thread again to see if maybe I missed a question to ask.