Interpreting PSGs: Hypopneas, Central & Mixed Apneas

[BrianinTN]

Many of you have been helping me the past few months as I've transitioned from CPAP to BiPAP S/T to ASV. I've now obtained the full sleep reports for all four of my PSGs, and even though I have two docs in the loop, I would appreciate any fresh thoughts you all might have. I've previously linked my ASV PSG results, so I'll include just the other three at the bottom. There are 14 pages, so apologies in advance -- hope I shrunk 'em enough so they're still legible but don't blow up everyone's monitors!

To summarize the past 13 months into a single paragraph: The diagnostic study was conducted in May of last year. Over 306 minutes, it revealed 148 hypopneas, 23 obstructive apneas, 5 central apneas, and 9 mixed apneas. The diagnosis was "moderate obstructive sleep apnea" and "moderate PLMD." CPAP titration a month later yielded a prescribed pressure of 13 cm/H2O. At home, the CPAP led to periodic breathing, many central apneas, and exhaustion, so I had a BiPAP S/T titration in February. The home experience here was even worse (extreme daytime sleepiness plus AHI in the mid 30s, comprised mostly of hypopneas), which led to my ASV titration in May. In contrast to what the CPAP and BiPAP titrations suggested, a very low EPAP on my ASV seems to address almost all obstructive apneas. However, I still don't feel great and I have residual hypopneas (nightly HI average is 8, but nights range from 4 to 18) which so far occur regardless of IPAP.

Generally speaking, I'm interested in what you all make of the two reports below. What stands out to you? Are there any areas of concern I should ask my docs about specifically? Most important, are there insights for what might make my ASV work better for me?

I also have some specific questions.
• I've read that mixed apneas are usually assumed to be predominantly obstructive in nature. Is this correct? If the answer is "it depends," what can we infer about my case?
• While I had significant treatment-emergent central apneas on the CPAP and at lower pressures on the BiPAP S/T, which I believe would be classified as traditional complex sleep apnea, does that have any bearing on the relatively few central apneas that appeared in my diagnostic? Or can we still generally write those off as mostly insignificant?
• As you can see from the diagnostic PSG results, hypopneas were dominant. Over at the binarysleep boards, the technicians have discussed how some of their labs attempt to classify hypopneas as obstructive or central, whereas others do not. Can we shed any light on the source of my hypopneas and the proper course of action to address them? Does it even matter? I know the general rule of thumb is that increasing IPAP addresses hypopneas and flow limitations, but so far my hyopneas exist even when IPAP approaches 20.
• What about the Brady-tachycardia that was observed? From what I've read it seems to be somewhat common in OSA patients, but I'm way out of my league here.
• In the CPAP titration, at least to my untrained eye, it looks like I never stabilized. What am I missing that led them to settle on a pressure of 13 and send me on my merry way with that?
• I've gathered that chasing apnea and PLMD can be a little bit of a chicken-and-egg exercise. Does seeing this data make anything stick out to you?

Thanks in advance.

DIAGNOSTIC PSG





CPAP TITRATION PSG






BIPAP ST TITRATION PSG

[HoseCrusher]

It is my understanding that classic obstructions to the airway involve the heart rate slowing down at first (the brady part), then your body releases a shot of adrenalin to wake you up and this is accompanied by a rapid increase in heart rate (the tachy part). When you wake up and take a breath, everything goes back to normal, until the next event.

I don't think there is much concern until your heart rate drops below 30 beats per minute for an extended period of time, or rises above 100 beats per minute for an extended period of time while resting.

From an obstructive perspective, oxygen desaturation below 90% is a concern.

[BrianinTN]

Bumping this for more replies. I know it's a lot of pages, which probably deters responses, but I wanted to be thorough. Really summarizing it in a nutshell, the diagnostic PSG showed mostly hypopneas, and low pressures on CPAP/BiPAP made those go away but replaced them with centrals. Higher pressures on BiPAP S/T had me back to dealing with hypopneas, and that's the case now on my ASV -- but I can't figure out any pressure settings on my ASV to get them to go away consistently.

[avi123]

It is my understanding that classic obstructions to the airway involve the heart rate slowing down at first (the brady part), then your body releases a shot of adrenalin to wake you up and this is accompanied by a rapid increase in heart rate (the tachy part). When you wake up and take a breath, everything goes back to normal, until the next event.

I don't think there is much concern until your heart rate drops below 30 beats per minute for an extended period of time, or rises above 100 beats per minute for an extended period of time while resting.

From an obstructive perspective, oxygen desaturation below 90% is a concern.

Crusher, from where did you dig those numbers and theories, and do you want to emply that heart rates are not as important as O2 desats?

As I understand it heart rates differ in persons:

The resting heart rate (HRrest) is a person's heart rate when they are at rest, that is lying down but awake, and not having recently exerted themselves. The typical healthy resting heart rate in adults is 60–80 bpm,[2] with rates below 60 bpm referred to as bradycardia, and rates above 100 bpm referred to as tachycardia. Note however that conditioned athletes often have resting heart rates far below 60 bpm. Cyclist Lance Armstrong had a resting heart rate around 32 bpm. Cyclist Miguel Indurain had a resting heart rate of 28 bpm.[3] It is also not unusual for people doing regular exercise to have resting heart rates below 50 bpm.

But in this forum we are dealing also with sick people whose heart rate could be problematic. This is also the reason that pacemakers mfg have lots of business.

[HoseCrusher]

From my cardiologist.

Keep in mind that we are looking at a report while people are sleeping. Your numbers are good while you are awake, but when you fall asleep the heart rate can slow down.

[JohnBFisher]

BraininTN, my apologies for my delay in posting this. Wading through data is harder for me these days that it used to be. A four hour nap this afternoon helped restore my ability to wade through the data.

I am not certain I can add any significant thoughts, but let's see if you have noted these:

• Most of your central apneas occur a lower pressures! This is a surprise. In your shoes, I might argue about ComplexSAS, since the central apneas seem to decrease as the pressure increases. It at least may be something to discuss with your doctor.
• The sleep stage summary data shows abnormal sleep architecture. The BiLevel sleep study shows a sleep stage summary that is closer to normal. This can mean you have fewer arousals during the sleep study than you did with other sleep studies.
• Under the BiLevel study the hypopneas seem to increase as the pressure increases.
• You also struggle with a lot of Periodic Limb Movements (PLM). Those numbers are high enough to significantly interfere with your normal sleep architecture.

I do not remember if your doctor is addressing the PLM. It could be he is making one change at a time. Sometimes PLM results from sleep issues. So breathing first makes good practical sense. However, it's all too easy to overlook it. If you have (as your studies indicate) significant problems with PLM, then you may need medication to help reduce the PLM related arousals.

Remember, I am just trying to answer "What would I do in your shoes?". From what I can see, PLM may be a significant factor in how poorly you feel every morning. You are in fact not sleeping as well as you would like. All three tests seem to show that.

Anyway, I hope that helps.

[BrianinTN]

A four hour nap this afternoon helped restore my ability to wade through the data.

I hope you didn't have to nap on my account! Just reading through what I posted makes me want to take a nap though. Seriously, thank you for taking the time to weigh in.

Most of your central apneas occur a lower pressures! This is a surprise. In your shoes, I might argue about ComplexSAS, since the central apneas seem to decrease as the pressure increases.

(emphasis added)
When you say "I might argue about," do you mean that you question whether it's true ComplexSAS? If yes, any ideas on what the heck might be going on? It certainly strikes me as weird that my progression was: hypopneas in the diagnostic --> centrals at low pressures on CPAP and BiPAP --> hypopneas at high pressures of BiPAP and on all pressures of ASV.

Under the BiLevel study the hypopneas seem to increase as the pressure increases.

Yes. And even though they stabilized me at 20/16 in the lab, my home experience at those pressures was absolutely awful, both subjectively and objectively (lots of hypopneas). Of note, tinkering at home led me to discover that 20/13 kept my AHI consistently below 3, but (a) left me feeling horrible still and (b) suppressed my own respiratory drive, demonstrated by my PTB plummeting. The relevant part of my BiPAP S/T saga thread is here: viewtopic.php?f=1&t=61719&st=0&sk=t&sd= ... 30#p583820

I do not remember if your doctor is addressing the PLM.

Prior to my ASV study, he gave me samples of Mirapex ER to try. Because I wanted that analysis to be a pure look at my breathing without any contaminating variables, I didn't take it that night. I did take clonazepam that night, which I know can also be prescribed to treat PLMD, but only to help me get to sleep. As you can see from the numbers, it didn't appear to help.

A few weeks into my ASV treatment at home, I started taking the Mirapex. So far, it has not seemed to improve my sleep, and it might even be making things a little worse. I feel like my sleep is more fragmented while on the Mirapex -- although I have so much variation from night to night that it's difficult to tell. At my last doc's visit about 10 days ago, he gave me a prescription for Requip, which I'll begin after I see the neurologist this coming Friday.

[JohnBFisher]

...

Most of your central apneas occur a lower pressures! This is a surprise. In your shoes, I might argue about ComplexSAS, since the central apneas seem to decrease as the pressure increases.

(emphasis added)
When you say "I might argue about," do you mean that you question whether it's true ComplexSAS? If yes, any ideas on what the heck might be going on? It certainly strikes me as weird that my progression was: hypopneas in the diagnostic --> centrals at low pressures on CPAP and BiPAP --> hypopneas at high pressures of BiPAP and on all pressures of ASV. ...

I am not sure what it is. There is no doubt that you are reacting to the pressure. However, this does not appear to be a classic case of ComplexSAS. But, this is one of those cases where I freely and quickly admit I am just a layman in this. As I noted, i would ask my doctor if that pattern makes sense. But do not be surprised if your doctor is just as puzzled.

...

I do not remember if your doctor is addressing the PLM.

Prior to my ASV study, he gave me samples of Mirapex ER to try. Because I wanted that analysis to be a pure look at my breathing without any contaminating variables, I didn't take it that night. I did take clonazepam that night, which I know can also be prescribed to treat PLMD, but only to help me get to sleep. As you can see from the numbers, it didn't appear to help.

A few weeks into my ASV treatment at home, I started taking the Mirapex. So far, it has not seemed to improve my sleep, and it might even be making things a little worse. I feel like my sleep is more fragmented while on the Mirapex -- although I have so much variation from night to night that it's difficult to tell. At my last doc's visit about 10 days ago, he gave me a prescription for Requip, which I'll begin after I see the neurologist this coming Friday. ...

I wish you luck in finding the right medication that work for you. I use Requip to help with Restless Legs Syndrom (RLS). Without it, I can not stand how my legs feel as I try to go to sleep. Fortunately, it does not take a lot of medication to help me address the symptoms. As you probably know, what works for one person may be useless or worse for another person. So, here's hoping it will help you.

[avi123]

[quote="BrianinTN"]

The home experience here was even worse (extreme daytime sleepiness plus AHI in the mid 30s, comprised mostly of hypopneas), which led to my ASV titration in May. In contrast to what the CPAP and BiPAP titrations suggested, a very low EPAP on my ASV seems to address almost all obstructive apneas. However, I still don't feel great and I have residual hypopneas (nightly HI average is 8, but nights range from 4 to 18) which so far occur regardless of IPAP.

Generally speaking, I'm interested in what you all make of the two reports below.

Reply:

I would disregard the past tests and experiences with the CPAP and BIPAP and focus only on the ASV. Tests with the ASV started here:

viewtopic/t65239/viewtopic.php?t=63954

TOPIC: ASV: Hypopnea Index Remains High


I would give the ASV more time to show results. Something like 9 months. I say it after reading this report (actually a story):

Treating the "Untreatable"

Excrept

The patient's initial subjective response to ASV was good. After more than 9 months of quite regular ASV use (both self-reported and from the compliance monitoring built into the device), he said he was now often swimming 3,000 yards, something he had been unable to do previously, and was sufficiently pleased with his outcome to give written consent to have his case presented.

Link:

http://www.sleepreviewmag.com/issues/ar ... -06_03.asp

[JohnBFisher]

avi123, you make a good point and one that does need to be emphasized.

The following comment is based on my own personal experience - and not a scientific study. So, take it with a grain of salt.

Part of what happens with ASV therapy is that is many cases it seems to help train the nervous system to embrace a healthier style of breathing. This leads to better sleep and better health. It is not immediate and it does take time (and constant reminding). I find my breathing when I awaken is much more regular now than it was when I started. Without my ASV my breathing does deteriorate. But it takes more than one nap without the ASV for it to get really bad.

In essence, my breathing improved over time. It's still not great. But it's MUCH better than when I stated ASV therapy.

So, it does take time (months in some cases) for the therapy to have full impact.

[BrianinTN]

So, it does take time (months in some cases) for the therapy to have full impact.

The tactical challenge this poses for me (as you've seen from my other threads) is figuring out what settings are optimal. If progress measured quantitatively (i.e., AHI) improves slowly over time, it's difficult to ascertain what the appropriate min EPAP and PS values "should" be.

Warning: I'm about to take this thread on a little tangent that has absolutely nothing to do with my PSGs. Then again, I seem to not be not be alone in this boat. Paper_Nanny, JIMCHI, Bons...we're all recent ASVers who, despite differences in our diagnoses, all seem to be suffering from residual hypopneas early in our treatment. At least three of those four have tinkered with increasing min PS (min IPAP), and so far it hasn't yielded any clear impact on those hypopneas. And we're all on the Respironics ASV. n=4 is a very small sample size, but I'm still wondering whether there's something systematic that's contributing to our hypopneas -- or the machine thinking we're having hypopneas.

Back to my regularly scheduled program...

I am not sure what it is.

Well, that makes two of us! The whole series of results seems puzzling and not exactly run-of-the-mill OSA. Which leads me to my next question, for JBF or anyone else with ideas. As I mentioned earlier, I'm seeing a local neurologist who also heads up their sleep department this week. Between the 20 pages of PSG results above and the literally hundreds of pages of reports from my CPAP, BiPAP S/T, and ASV, I have an awful lot of paperwork. I'd be living in fantasyland if I thought the doctor would carefully look through all of this during my appointment. What ideas might there be to consolidate, collapse, or summarize the data so as to maximize the likelihood that I get helpful answers out of my appointment about what the heck is going on with me?

[máirtín]

Here's my 2¢ worth (WARNING: this is pure speculation and conjecture on my part):

The hypopneas are not hypopneas but part of the cycle of Cheyne-Stokes Respiration. CSR always ends with a central apnea event.
The machine is monitoring this pattern and delivers a burst of pressure to prevent the apnea. The part that the machine is monitoring is registered as hypopnea and no apnea is registered because the machine has headed it off.

The machine monitors breathing over time. It needs several breaths to establish the pattern and decide how to respond. It responds very effectively in preventing the pattern ending in an apnea. But this pattern is continuing all night so sleep quality is compromised and I still feel tired in the morning even though there have been few or no actual apneas.

I am not discounting leaks as a serious source of sleep disruption but this explanation of what I think is happening accords better with what the machine is specifically designed to do for people who have documented and diagnosed CSA and CSR. CSA and CSR have neurological origins rather than pulmonary origins. The machine is only designed to deal with the pulmonary effects of the neurological process.

[JohnBFisher]

BrianinTN, I would recommend using representative data from several nights. As you note, don't drown your doctor in data or try to summarize it.

I do understand how someone might have a LOT of data in their files. My neurologist has information from the past fifteen years or so. My files are huge. What I've learned on how to present meaningful information that cuts through that cloud of data comes from my own experience.

From my own experience, I know that representative nights seem to cut through the information as well as anything. However, when you present the data, be clear that you realize this is effectively just "windsock" data. You know it is not a full sleep study. However, it does seem to show various patterns, which have you wondering....

That just my own thoughts from a similar set of experiences. I suspect the underlying cause of our poor sleep is different, but the circumstances we face (at the doctors office) feel very similar. So, consider what you paid of this advice (Zilch!) and take action accordingly.

[BrianinTN]

So, consider what you paid of this advice (Zilch!) and take action accordingly.

So far, I feel like I've received an excellent value.