CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

Hi there,

I am new poster to this forum but have been enjoying reading posts for a few months now. A most helpful forum.

Following two nights in a sleep lab, I was recently diagnosed with CompSA (AHI=28) and put on a VPAP Adapt SV. I was also found to have 450 PLMs every eight hrs when asleep. A recent report shows that my mean minute volume is 3.7L/min. I am 171cm, 76kg and 38yo. Using a CMS-50E I see that my heart rates dips into the high 40s when asleep. Futhermore, using a CMS-60C ABPM I find that my blood pressure drops to 80/43 during the night. My resting blood pressure when awake is around 110/75.

I am confused as to exactly what I am suffering from. I would be interested to hear from anyone with similar symptoms and/or comments on my condition or the best way to get to the root of my sleep issues.

As an aside, I found that when I used full faced masks the bridge of my nose would break out in sores and become inflamed. I am now using baby wipes (fragrance- and alcohol-free) to make a liner between the mask and my face and I am now free of bridge soreness. I just fold the wipe in half longways and then cut out with scissors. Each one lasts me 2-4 nights. I also use these wipes to clean my mask each night. Pretty cheap fix to a annoying problem. I now use the Resmed Quattro mask with these home-made liners. I was using the Mirage Liberty because of the bridge issue but have stopped for now.

Thank for your attention.

Hello,

I saw your post and I wil try and clarify somethings. Auto SV is used for patient's that have complex sleep apnea, central sleep apnea, periodic breathing, and mixed apena. I assume when you had your sleep studies, more of your evens where mixed events or central apneas. Complex sleep apnea can be caused by soo many things, CHF (congestive heart failure) certain types of medication (pain), or when you where placed on CPAP, central apneas started to emerge and you needed non insasive vent support. Hope this helps

Hi there LV Sleep Tech,

LV Sleep Tech wrote: I saw your post and I wil try and clarify somethings. Auto SV is used for patient's that have complex sleep apnea, central sleep apnea, periodic breathing, and mixed apena. I assume when you had your sleep studies, more of your evens where mixed events or central apneas. Complex sleep apnea can be caused by soo many things, CHF (congestive heart failure) certain types of medication (pain), or when you where placed on CPAP, central apneas started to emerge and you needed non insasive vent support. Hope this helps

Thanks for the info. Yes, during my diagnostic sleep study I had both OSA and CSA events. My centrals tend to be bunched towards the latter part of my night. I take 20mg of Fluoxetine (Prozac) for mild depression and anxiety. My BMI is around 26kg/m2.

Before the overnight sleep studies I had previously (Oct 09) undergone a take-home sleep study. The result of this was a diagnosis of moderate OSA with AHI=36. I was treated with an S8 Auto for 12 weeks without me or the sleep technician ever having seen the detailed sleep report. I functioned somewhat better after a few weeks on the S8 but never really felt fully treated. When I finally saw the sleep doctor (some 12 weeks after the sleep study) I discovered that I had actually had bunches of central events. I was somewhat surprised by this revelation and concerned that I was being treated appropriately.

So I dumped this sleep clinic and pursued an overnight PSG in a sleep clinic and a new doctor. I was asked to go off CPAP for the 4 weeks that it would take to schedule and complete the diagnostic and titration studies in order to get my body to its natural state. By the end of this 4 weeks period I was virtually non-functioning due to excessive daytime sleepiness. Following the titration study I immediately started on the Adapt SV. I still don't really understand the implications of 450 PLMs in a nights sleep. My SpO2 averages about 93% when sleeping with the Adapt SV.

In the meantime I have come to discover that my minute volume av. is 3.7l/min from the Adapt SV reports. Also, I have purchased an ABPM because I was suspicious of hypotension when asleep due to low daytime blood pressure readings over the years.

I am now waiting until the end of this month to see my new sleep doctor for the first time after the PSG diagnostic and sleep studies. My trial period with the Adapt SV ends this weekend and I am now faced with spending $4500 to get my own machine without having seen the doctor yet and with doubts in my mind that the Adapt SV is actually the best machine for me given my lowish tidal volume.

Am I worried about nothing or do I have some genuine reason for concern?

Strange asking strangers questions but I feel quite in need of direction. I am 38 yo and having to wrap my brain around a lifetime of CPAP and the appropriate form of CPAP.

I am a scientist by trade so it is natural for me to want to understand every detail of my treatment.

Cheers,

Thst's a lot of limb movements. Did many of them result in arousal? Just be mindful that they can keep your sleep disrupted so you may continue to feel bad even if your cpap treatment is working well.

blizzardboy wrote: I am confused as to exactly what I am suffering from.

Me too! But I'm impressed you can spell all of those.

I'll just bid you welcome, wish you luck and let the experts decipher the big words...

Greetings blizzardboy! Welcome to the ASV crowd. You will note there are several of us in the Forum who use ASV units (including others from Australia).

Background Material

You note:

blizzardboy wrote:... I am a scientist by trade so it is natural for me to want to understand every detail of my treatment. ...

As an engineer by trade, I share your interest. So, I will point you to some links that should provide good background reading. Over the years many posters provided some background information on Central Sleep Apnea (CSA) and Complex Sleep Apnea (ComplexSA) Syndrome. Rested Gal gathered these together into a post with various links of interest:

Links to Central Apnea discussions
viewtopic.php?p=22702

Since you've been diagnosed with ComplexSA, I think it is important you understand that central sleep apnea occurs as our repiratory systems oscillate between an overshoot and undershoot condition as they attempt to control CO2 levels in our blood. The following article is excellent background material:

Central Sleep Apnea: Pathophysiology and Treatment
http://chestjournal.chestpubs.org/conte ... l.pdf+html

Next, I highlight the following Complex Sleep Apnea articles:

Complex Sleep Apnea: It Really Is a Disease
http://www.ncbi.nlm.nih.gov/pmc/article ... .5.403.pdf

The Quest for Stability in an Unstable World: Adaptive Servoventilation in Opioid Induced Complex Sleep Apnea Syndrome
http://www.ncbi.nlm.nih.gov/pmc/article ... .4.321.pdf

Complex Sleep Apnea
http://www.chestnet.org/accp/pccu/compl ... a?page=0,3

I also highlight the following two articles about ASV and ComplexSA:

Efficacy of Adaptive Servoventilation in Treatment of Complex and Central Sleep Apnea Syndromes
http://chestjournal.chestpubs.org/conte ... l.pdf+html

Adaptive Servoventilation Versus Noninvasive Positive Pressure Ventilation For Central, Mixed, And Complex Sleep Apnea Syndromes
http://www.resmed.net/us/documents/Morg ... ilevel.pdf

That should keep you busy for a couple of minutes! ... Though I jest about that, you will find I think it is very important to fully understand the situation and research that goes into the therapy options presented to us.

Comments

I noted from your comments:

blizzardboy wrote:... Yes, during my diagnostic sleep study I had both OSA and CSA events. My centrals tend to be bunched towards the latter part of my night. ...

From my reading that pattern is a bit different. You will probably want to get a copy of your sleep study, if possible. Normally, the CSA events in ComplexSA tends to occur during NREM (non REM) sleep throughout the night. But it's possible that as you fall deeper into sleep your neural activity decreases and the normal control of your brain stem decreases, thus decreasing the control of your respiratory system. Thus during deeper sleep (later in the evening) the over/undershoot scenario emerges along with the resulting central apneas.

blizzardboy wrote:... When I finally saw the sleep doctor (some 12 weeks after the sleep study) I discovered that I had actually had bunches of central events. I was somewhat surprised by this revelation and concerned that I was being treated appropriately. ... So I dumped this sleep clinic and pursued an overnight PSG in a sleep clinic and a new doctor. ...

Wise choice. Some doctors (just as scientists and engineers) tend to ignore something if they don't understand it. Paradigm shifts can be difficult. And you don't want to go through the process of teaching your doctor. It is often best to find a doctor who understands such a condition and will properly treat it.

blizzardboy wrote:... I still don't really understand the implications of 450 PLMs in a nights sleep. ...

Well, essentially when your body suddenly moves it causes an arousal. That is, it tends to drag you form a deeper level of sleep to a lighter level of sleep. This disruption of the normal sleep cycle tends to result in increased sleepiness throughout the day.

However, most doctors will first try to address both OSA and CSA events, since PLMs often occur as an attempt by the brain stem to minimize OSA and CSA events. Research into neural networks often reveal that they can find truely unique and unexpected solutions to problems. It appears that rather unexpectedly our brains find that PLMs help reduce OSA/CSA events, thus improving sleep.

blizzardboy wrote:... I am now waiting until the end of this month to see my new sleep doctor for the first time after the PSG diagnostic and sleep studies. My trial period with the Adapt SV ends this weekend and I am now faced with spending $4500 to get my own machine without having seen the doctor yet and with doubts in my mind that the Adapt SV is actually the best machine for me given my lowish tidal volume. ...

Well, I'm definteily not the right person to ask if there are alternatives. I agree the low tidal volume may be an issue. And unfortunately, from what I am aware of the various machines, those that include control of the minute ventilation tend not to include the ASV feature.

However, while low minute ventilation might be an issue, the greatest concern is typically the oxygen saturation. You noted that you are above 90%, so I suspect most doctors will deem the therapy viable. Though it might not be optimal, as you know, tweaking systems to get that last 5 to 10 percent is often cost prohibitive.

blizzardboy wrote:... Am I worried about nothing or do I have some genuine reason for concern? ...

A scientist, who is not concerned about understanding abnormal values? I would be more worried if you were not concerned!

blizzardboy wrote:... Strange asking strangers questions but I feel quite in need of direction. ...

Well, all too often doctors are not good teachers. And the more complex the case, the more we need someone to help us learn. Why? So we can understand what we need to monitor to help maximize our therapy. A sleep problem is a chronic condition. It is very analogous to diabetes. It is a silent, slow killer. Left untreated the results of both are all too predictable. With diabetes you need to monitor your blood sugar to be certain you keep your blood glucose in check. The same should be the normal recommendation from doctors to their sleep patients. You should monitor your therapy. Did the system have excessive leaks? What is the AHI values? Is anything "out of normal range"? And if it does not return to normal values, then you should seek advice from your medical team.

Unfortuantely, many doctors do not understand that they need to explain this (for diabetes or sleep disorders). But patients who live with the condition day in and day out *KNOW* this is necessary. So, strangers may well be better able to tell you how to live with a chronic condition to a level of detail that a doctor simply does not know. There is a lot to be said for experience. Our doctors often carry the book knowledge and experience of helping patients. But they often lack the first hand experience of living with these conditions.

Strangers can often provide much greater insight into this life experience.

blizzardboy wrote:... I am 38 yo and having to wrap my brain around a lifetime of CPAP and the appropriate form of CPAP. ...

I was in my early 30s when diagnosed, so I do understand. Fortunately for you an ASV unit *IS* available. Just a few years ago, this unit was not an option for patients. And trust me, an ASV unit does so much better compared to CPAP and BiPAP units for CSA events.

So, while you are unfortunate to be in this situation, you are very fortunate to have a good option to help address it.

Hope that helps.

kteague wrote:Thst's a lot of limb movements. Did many of them result in arousal? Just be mindful that they can keep your sleep disrupted so you may continue to feel bad even if your cpap treatment is working well.

Hi kteague,

Alot, oh I see. I had no reference point. What would be the mean level of PLMs in those with PLMD?

5-7% of my PLMs cause arousal, which translates to around 3 per hr. So, for now, looks like I am scheduled to be woken every 20 minutes I am asleep, irrespective of the state of my airway. Hopefully with prolonged application of the VPAP Adapt SV my neural networks will exhibit their plasticity and work out that they can tone down on PLMs.

JohnBFisher wrote:Greetings blizzardboy! Welcome to the ASV crowd. You will note there are several of us in the Forum who use ASV units (including others from Australia).

You note:

blizzardboy wrote:... I am a scientist by trade so it is natural for me to want to understand every detail of my treatment. ...

As an engineer by trade, I share your interest. So, I will point you to some links that should provide good background reading. Over the years many posters provided some background information on Central Sleep Apnea (CSA) and Complex Sleep Apnea (ComplexSA) Syndrome. Rested Gal gathered these together into a post with various links of interest:

And trust me, an ASV unit does so much better compared to CPAP and BiPAP units for CSA events.

So, while you are unfortunate to be in this situation, you are very fortunate to have a good option to help address it.

Hope that helps.

Hi John,

Thank for your detailed and well thought out response. I truly appreciate your generosity and the way you problem solve. I will read all those links (some of which I am already well acquainted) with much interest. I suspect that I have some form of brain damage resulting from meningitis as a baby at the age of 7 months. I would love to find out the state of my brain but have no real clue as to how this could materialise at present. Be interesting to see where this journey takes me!

Today I purchased my Adapt SV and will take possession of it later next week. I am also getting Rescan v3.7 and the serial adapter. I decided to save myself over $1200 and buy from a discount supplier. The sleep shop that I approached to manage my ADAPT SV trial wasn't interested in selling at any less than RRP. Health care unfortunately collided with business. So now I am sort of out on a limb having walked away from my second sleep shop in 3 months. But I figure if I can manage complex physics experiments then I can probably sit in the drivers seat of my day-to-day sleep management.

It really bugs me here in Australia that the people who are supposed to manage machine settings and create data reports are also the people that you have to purchase equipment from. I feel this is a conflict of interest between health care and business. I did not enjoy trying to negotiate prices with the person who has been helping me trial the VPAP.

Writing in this forum certainly is a helpful way to debrief.

Cheers,

LinkC wrote: I'll just bid you welcome, wish you luck

Thanks LinkC, happy to be on board!

Welcome aboard, blizzardboy. A great summary by John, IMO.

blizzardboy wrote:... Yes, during my diagnostic sleep study I had both OSA and CSA events. My centrals tend to be bunched towards the latter part of my night. ...

That pattern is typical of Complex Sleep apnea:

Geoffrey S Gilmartin; Robert W Daly; Robert J Thomas wrote:Complex Sleep-Disordered Breathing: Introducing a New Practically Useful Category

Variably 'mixed' rather than pure obstructive or central ('control') patterns are common and easily recognized. Examples include mixed apneas, variable degrees of flow limitation intermixed with periodic breathing, position-dependent variability (central while not supine, obstructive when supine), stage-dependent variability (periodic breathing during non-REM (NREM) sleep and severe obstructions during REM sleep) and time of night variability. In the latter instance, what starts as clearly obstructive disease at the beginning of the night evolves into predominantly central disease by the end of the recording.

http://www.ncbi.nlm.nih.gov/pubmed/16217173

-SWS wrote:Welcome aboard, blizzardboy. A great summary by John, IMO.

blizzardboy wrote:... Yes, during my diagnostic sleep study I had both OSA and CSA events. My centrals tend to be bunched towards the latter part of my night. ...

That pattern is typical of Complex Sleep apnea:

Geoffrey S Gilmartin; Robert W Daly; Robert J Thomas wrote:Complex Sleep-Disordered Breathing: Introducing a New Practically Useful Category

Variably 'mixed' rather than pure obstructive or central ('control') patterns are common and easily recognized. Examples include mixed apneas, variable degrees of flow limitation intermixed with periodic breathing, position-dependent variability (central while not supine, obstructive when supine), stage-dependent variability (periodic breathing during non-REM (NREM) sleep and severe obstructions during REM sleep) and time of night variability. In the latter instance, what starts as clearly obstructive disease at the beginning of the night evolves into predominantly central disease by the end of the recording.

http://www.ncbi.nlm.nih.gov/pubmed/16217173

Well -SWS, I think that comment is taken out of context, because that reference

Overnight shift from obstructive to central apneas in patients with heart failure: role of PCO2 and circulatory delay

involved a bunch of guys (and one babe) with congestive heart failure, and ble-zard don't look the type.

Muffy

Well, I disagree with your disagreement, Muffy.

Regarding context: the original authors' entire purpose for the white-paper excerpt I have above is to comment on variability itself---in somewhat common hypocapnic complex disease. They clearly see a lot of patients with the hypocapnic complex disease they are focusing on in that paper, and dedicate that paragraph to common variability examples they have observed. They further comment that variability can include mid-session or late-session onset of the central component (what they term "time of night variability"). If Gilmartin, et al didn't observe those variability patterns in their own patients, I don't think they would have dedicated a section of their white paper to those variable facets of presentation. I think the cited reference serves to exemplify the clear pattern itself rather than limit etiology.

However, my understanding is that hypoventilation is NOT at all common for the typical hypocapnic complex sleep apnea Gilmartin et al go on to describe in great detail. Rather, hypoventilation is a feature of less common hypercapnic complex disease according to that same white paper I have cited above:

Geoffrey S Gilmartin; Robert W Daly; Robert J Thomas wrote:This review focuses primarily on hypocapnic complex disease. Examples of hypercapnic complex sleep-disordered breathing include central congenital hypoventilation, advanced chronic obstructive lung disease, and obesity hypoventilation, which are beyond the scope of this review.

So if hypoventilation really is a feature of blizzardboy's complex presentation, then I would encourage that he and his doctor consider COPD and other hypoventilatory associated disorders that can also present with respiratory central complexity during sleep.

In summary for blizzardboy:
1) Hypoventilation, if persistent, is likely a key hypercapnic complex-disease differentiating feature,
2) Central SDB emergence upon treatment with CPAP usually serves as a hypocapnic complex sleep-apnea differentiating factor, and
3) Arranging another PSG with CO2 monitoring would serve as further diagnostic means of differentiating hypercapnic complex disease from the more-common hypocapnic complex sleep apnea described in the seminal white paper by Gilmartin et al.

Diagnostic differentiation is crucial since optimal treatment methods differ significantly for those capnic polar-opposite categories of complex Sleep Disordered Breathing.

Layperson's disclaimer as usual...

Welcome Blizzardboy, I am already lost in this discussion (as per usual once -SWS and Muffy start getting technical). But that is a lot of PLMS... I wonder if any of them are respiratory-induced and your sleep lab didn't catch it.

I'm lost right out there with SleepingUgly so I'll leave the technical stuff to the scholars. Just want to say that you won't likely know the true significance of your limb movements until your breathing issues are effectively treated. When that time comes, if they are still a problem, it's likely your prior studies will not reflect their current status, whether for the better or the worse. Some docs prefer to just put a person on meds and see how they feel. My doc retested me while on cpap using my familiar mask at my proven effective pressure.

Right now I would think your other issues take priority, so I'll bow out so the deep stuff can resume.

In an attempt to clarify,

blizzardboy wrote:... Yes, during my diagnostic sleep study I had both OSA and CSA events. My centrals tend to be bunched towards the latter part of my night. ...

and then

-SWS wrote: That pattern is typical of Complex Sleep apnea:

noting that

Geoffrey S Gilmartin; Robert W Daly; Robert J Thomas wrote:...and time of night variability. In the latter instance, what starts as clearly obstructive disease at the beginning of the night evolves into predominantly central disease by the end of the recording.

but

Muffy wrote:I think that comment is taken out of context, because that reference

Overnight shift from obstructive to central apneas in patients with heart failure: role of PCO2 and circulatory delay

involved a bunch of guys (and one babe) with congestive heart failure, and ble-zard don't look the type.

because if you refer to that study referenced in the statement

what starts as clearly obstructive disease at the beginning of the night evolves into predominantly central disease by the end of the recording[8]

you get to

8.Tkacova R, Niroumand M, Lorenzi-Filho G, Bradley TD. Overnight shift from obstructive to central apneas in patients with heart failure: role of PCO2 and circulatory delay. Circulation 2001; 103:238-243.

which is

http://www.circ.ahajournals.org/cgi/con ... /103/2/238

where they note:

We have demonstrated in CHF patients having both OSAs and CSAs during the same night that OSA events predominate at the beginning and CSA events predominate at the end of the night. This overnight shift from OSA to CSA events was accompanied by reductions in PCO2 resulting from increases in VI and by lengthening of circulation time. The close relationship between the overnight lengthening of circulation time and reductions in PCO2 strongly suggests that the fall in PCO2 and shift in apnea type are linked to an overnight deterioration in cardiac function.

So this shift occurs without the addition of positive pressure which is absolutely a whole different "phenotype" from CompSAS, defined as

Patients with complex sleep apnea syndrome are mostly similar to those with OSAHS until one applies continuous positive airway pressure. They are left with very disrupted breathing and sleep on continuous positive airway pressure.

by Morgenthaler in

Complex Sleep Apnea Syndrome: Is It a Unique Clinical Syndrome?

The Tkacova patients, as presented, are NOT CompSAS patients, nor is there any documented evidence to say the CompSAS vulnerability occurs

blizzardboy wrote:towards the latter part of my night.

Rather, since the application of pressure therapy and the concomitant sleep-wake instability happens at the beginning of the night, CompSAS happens right out of the gate.

Now if blizzardboy's EF is <40%, we can certainly take this discussion in a whole new direction.

Muffy