CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

Muffy wrote: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:

Thank you for the clarification, Muffy. I perfectly understood the first time that you felt the cited reference was irrelevant to CSDB. I agree that Gilmartin et al might have cited a better reference---or better yet cited no reference at all since their paper WAS the original and seminal description of CSDB. The pickings for prior CSDB citations were slim to nonexistent.

Regardless of the imperfect citation, the title of this paragraph is a dead giveaway that Gilmartin et al are describing what they observe in their own CSDB patients:

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.[8] Direct visualization of the upper airway shows collapse at the nadir of the respiratory cycle to be common even in polysomnographic 'central' disease. The therapeutic response to positive airway pressure is variable in these cases. A recent report has clarified some of the features of more subtle forms of mixed disease. These include periodic short cycles of obstruction, minimal disease in REM sleep, and incomplete responses to positive airway pressure. Qualitative scoring of this type of disease is limited by imprecision of terms such as 'mixed apnea,' and accurate scoring of central hypopneas is impractical in routine clinical practice. The term 'complex' is used to convey the high likelihood that both obstructive and control factors are involved in creating this pattern of disease (Fig. 1).

If you view the above paragraph as NOT describing what Gilmartin et al routinely observe in their own CSDB patients, then we shall have to politely agree to disagree. I don't plan on debating that point further.

blizzardboy wrote:CompSA, Hypoventilation, PLMs, Bradycardia and Hypotension?

Blizzardboy, in light of your bradycardia and hypotension, these would be my two main areas of investigation if I were you:

1) Complete Cardiac Diagnostics- Why the bradycardia, hypotension, and central apneas? Are there any undiagnosed heart problems?

2) Hypoventilation- Is that genuine and persistent hypoventilation? If so, that would be a key feature of your sleep-related breathing disorder and needs to be factored into your treatment plan (per underlying cardiopulmonary etiology).




Also, I think it's essential for your doctors to differentiate exactly WHICH type of complex sleep disordered breathing condition you might have:

-SWS wrote: 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.

So would it be fair to say that when centrals are unmasked in a titration, or are induced with application of pressure, sometimes everything straightens out on its own over time with regular CPAP but that for other patients it may turn out that an ASV is needed? Or does that simple statement miss the point completely?

http://ajrccm.atsjournals.org/cgi/conte ... /181/2/189

I also think this is a nice statement about CompSA:

"The efficacy of a particular modality of therapy should clearly be demonstrated in the sleep laboratory in an individual patient before its use." -- http://www.chestnet.org/accp/pccu/compl ... a?page=0,3

jnk wrote:So would it be fair to say that when centrals are unmasked in a titration, or are induced with application of pressure, sometimes everything straightens out on its own over time with regular CPAP

There are multiple recent studies supporting that. So I think that statement is true...

jnk wrote: ...but that for other patients it may turn out that an ASV is needed?

And since the entire CompSA/CSDB population will not adapt to CPAP, that statement is true also IMO.

Well, if CompSA/CSDB variability can occur in any one night, the recent adaptation studies prove that CompSA/CSDB longitudinal variability can be highly beneficial for some patients. However, there may be yet other facets of longitudinal variability that CompSA/CSDB researchers have not yet discovered. For instance, I strongly suspect that some of the supposedly "adapted" CompSA/CSDB patients are experiencing occasional flareups or nightly episodes of central dysregulation. And I suspect that marginally-adapted versus well-adapted CompSA/CSDB patients might still fare better with ASV treatment instead of CPAP.

The scant few CompSA/CSDB longitudinal studies that have been published to date managed to "PSG-sample" scant few nights of sleep. Their ongoing methodology is not at all conducive to discerning whether CompSA/CSDB might also present in some patients with highly episodic characteristics---as can occur with other neurologically-related disorders that might present either consistently or episodically in those respective patient-population subsets.

-SWS wrote:Thank you for the clarification, Muffy. I perfectly understood the first time that you felt the cited reference was irrelevant to CSDB.

Never thought that you didn't, -SWS, just responding to kathy and SU's comment that our explanations are confusing (actually mine are great, yours are confusing).

Regardless, if bb had a "bunch" of centrals on diagnostic, one would wonder about their origin, because as noted, CompSAS centrals should not appear until intervention.

Like an underlying "sleep" problem in addition to (or instead of?) a "sleep apnea" problem.

Fluoxetine..........

Muffy

...............probably ain't helping the PLMs a lot:

http://www.rls.org/Document.Doc?id=346



Or are helping them a lot, depending on how you look at it.

Muffy

Muffy wrote:Never doubted that you didn't, -SWS, just responding to kathy and SU's comment that our explanations are confusing (actually mine are great, yours are confusing).

When I have the attention/stamina to wade through it this AND I understand it, I'll know I'm "cured"! They should use this instead of the MWT!

Regardless, if bb had a "bunch" of centrals on diagnostic, one would wonder about their origin, because as noted, CompSAS centrals should not appear until intervention.

Complex Sleep Apnea does not appear until CPAP is initiated... Are you saying Central apneas aren't seen on a diagnostic PSG unless they are secondary to something like a medication (whose class we won't mention less we fuel another debate about their overuse/misuse, etc.)?

I gotta look this stuff up... I need a short, nontechnical tutorial on the types of apneas other than obstructive/hypopnea, and which can be seen on PSG vs. titration, and their implications for treatment.

BTW, hypotension requires titration in a clinical setting if one is going to use ASV, and 80 mmHg systolic BP is the point where one should consider discontinuing therapy. I hope that is/was a monitored titration.

Muffy

SleepingUgly wrote:They should use this instead of the MWT!

A complement never felt so good... NOT!

Muffy wrote:just responding to kathy and SU's comment that our explanations are confusing (actually mine are great, yours are confusing).

A complement never felt so good... NOT!

I did that in honor of Echo's return to our message board.

Muffy wrote:BTW, hypotension requires titration in a clinical setting if one is going to use ASV, and 80 mmHg systolic BP is the point where one should consider discontinuing therapy. I hope that is/was a monitored titration.

Point well taken. Here's a description of the physiologic mechanism whereby PAP can induce or exacerbate hypotension:

Shahrokh Javaheri, M.D wrote: Central Sleep Apnea in Congestive Heart Failure: Treatment of Central Sleep Apnea

Furthermore, caution should be exercised with use of nasal CPAP. Because of increased intrathoracic pressure, cardiac output may decrease resulting in hypotension, particularly in patients with atrial fibrillation[99] and those in whom right ventricular volume pressure characteristics are on the ascending limb of the Frank-Starling curve. In such patients, right ventricular stroke volume is preload dependent, and a decrease in venous return could result in hypotension. A similar mechanism may result in hypotension in patients in whom left ventricular stroke volume is preload dependent. Such reduction in cardiac output could result in reduction in coronary blood flow and ischemia, particularly in patients with established coronary artery disease.

Supposedly the effect can be even more extreme with ASV's higher IPAP pressures...

But in a nutshell PAP's applied intrathoracic pressure can decrease venous return in patients with the above ventricular characteristics---thereby inducing or aggravating hypotension. And accordingly, the following is listed as one of the VPAP AdaptSV contraindications:

Resmed VPAP Adapt SV User Guide wrote: Contraindication: Hypotension or significant intravascular volume depletion.

Muffy wrote:Fluoxetine..........

I knew if they put that stuff in our municipal water supply and tooth paste there were going to be problems in River City... with a capital...

-SWS wrote:

SleepingUgly wrote:They should use this instead of the MWT!

A complement never felt so good... NOT!

LOL! Sorry, I didn't mean it that way. I just meant that your thought process is on such a high level that one needs a high degree of alertness and good cognitive resources to follow along and understand it. If one could do that, that would be stronger evidence than a MWT that treatment was successful. I should be so lucky to lose my EDS and gain 20 IQ points by air up on nose!

Can I ask a question here (let me know if this is "hijacking" the thread)... I'm confused about the business of SDB masking PLMD and PLMD masking SDB... Can PLMS and SDB both be diagnosed accurately in one sleep study...that is, would it be clear whether PLMS are respiratory-induced vs. primary? Also, what are the implications of going into a sleep study on 1200mg of Neurontin? Would that allow for discovering SDB that might otherwise not surface due to PLMS disrupting sleep? But would it prevent knowing what role PLMS play? Is it accurate that Neurontin does not "fix" PLMS that are respiratory-induced?

I guess my fear is that the cause of my EDS is multifactorial, or at least that there many be several abnormal findings, and I won't know what proportion of the variance in my EDS is accounted for by SDB vs. PLMS. Trying to figure out how I will know what is driving the EDS.

Thanks - let me know if I should start a new thread!

-SWS wrote:

Shahrokh Javaheri, M.D wrote: Central Sleep Apnea in Congestive Heart Failure: Treatment of Central Sleep Apnea

Furthermore, caution should be exercised with use of nasal CPAP. Because of increased intrathoracic pressure, cardiac output may decrease resulting in hypotension, particularly in patients with atrial fibrillation[99] and those in whom right ventricular volume pressure characteristics are on the ascending limb of the Frank-Starling curve. In such patients, right ventricular stroke volume is preload dependent...

Well, in re: Starling just about everybody's SV is preload-dependent, and while Javaheri may imply that a fluid challenge may/will alleviate ascending-limb risks, an additional, greater concern would be those patients with depressed cardiac performance (the aforemention low EF, represented by the blue line):



Preload must be optimized from both directions-- too little fluid and their blood pressure crashes (need loading), too much fluid and they go into failure (need unloading).

You know the old expression-- "The only way a CPAP machine can hurt you is if it fell on your head!"

Obviously, whoever came up with that one was in sales and not clinical.

Muffy

SU- Muffy, Kathy, and others here are more knowledgeable about RLS, PLMs, and PLMD than I am. And, of course, Muffy runs a well-respected sleep center. I'll offer what few thoughts I have, hoping others can pipe up with better information. Blizzardboy has plenty of PLMs, so I am sure he doesn't mind more PLM discussion in this thread...

SleepingUgly wrote: Can I ask a question here (let me know if this is "hijacking" the thread)... I'm confused about the business of SDB masking PLMD and PLMD masking SDB... Can PLMS and SDB both be diagnosed accurately in one sleep study...that is, would it be clear whether PLMS are respiratory-induced vs. primary?

My understanding is that SDB and PLMD can mask and confound each other in multiple ways. Since the severity/presentation of either disorder can be sleep-stage dependent, those two conditions can sometimes mask severity by masking or preventing what would have been more severe sleep stages in some patients.

However, SDB and PLMs can also confound each other as being a matter being primary/secondary or stimulus/response. PLMD, obstructive SDB, and central SDB all have primary etiologies for which the respective physiologic control circuits fail to function properly. When any of these malfunction as a matter of primary failure in biology, my understanding is that PSG sequencing of the failures reflect these events as either unaccompanied by other etiological events, or as initial in the sequence of PSG events.

Those were cases of PLMD, obstructive SDB, and central SDB as primary etiological failures reflected in sequence. Since they are primary and initial, those failures in biology might also serve as stimuli for neurologically reflexive responses---that would be both secondary failures in etiology and reflect as secondary or non-leading in PSG sequencing. Limb kicks, upper airway closures, and central withdrawal of respiratory drive are ALL highly rudimentary defensive reflexes. As a matter of highly basic reflexology, any of those three might be primary etiologic failures, with any of those three also presenting in the time domain or PSG sequencing as stimulus/response based reflexive occurrences. At least that is the way I understand it as a layperson, SU...

SleepingUgly wrote:I guess my fear is that the cause of my EDS is multifactorial, or at least that there many be several abnormal findings, and I won't know what proportion of the variance in my EDS is accounted for by SDB vs. PLMS. Trying to figure out how I will know what is driving the EDS.

If you happen to score borderline or high on this non-scientific HSP screening questionnaire then I personally suspect that your stimulus/response equation to poor sleep and EDS is probably highly multifactorial as a matter of both hypersensitivity and hyper-responsiveness.

SleepingUgly wrote: Also, what are the implications of going into a sleep study on 1200mg of Neurontin? Would that allow for discovering SDB that might otherwise not surface due to PLMS disrupting sleep? But would it prevent knowing what role PLMS play? Is it accurate that Neurontin does not "fix" PLMS that are respiratory-induced?

Hoping Muffy or Kathy can comment on this one.

Muffy wrote:You know the old expression-- "The only way a CPAP machine can hurt you is if it fell on your head!"

Obviously, whoever came up with that one was in sales and not clinical.

<snicker> ...As if you didn't know which former CEO said that.

Not to muddy the waters (then again, why not, hey, yeah, let's ), but I sometimes wonder how many labs (or, "centers," nod to SAG) actually score PLM-related arousals "correctly," anyway. Sounds complicated to me:

M.4.

In our lab we score arousals associated with PLM's. Since you cannot score arousals unless there is 10 seconds of sleep preceding the arousal, can I score an arousal that is associated with a PLM when there can be as little as five seconds since the last PLM with arousal?

The short answer is no, you cannot score arousals with less than 10 seconds of intervening sleep. Members of the Movement Rules and Arousal Rule task forces were consulted on this question. The Movement Rules perspective was that conceptually it would be possible to have multiple limb-movement related arousals with the minimal interval between limb movements (five seconds from onset to onset). However, the Arousal Rule perspective is that the scoring of such arousals would be technically quite difficult. Since an arousal must last a minimum of three seconds, this would leave only two seconds to determine that sleep had resumed. The Steering Committee reviewed both perspectives and determined that the arousal rule should hold and that a minimum of 10 seconds is necessary to reliably determine that the patient has returned to sleep. When periodic limb movements occur with an interval of less than 10 seconds and each is associated with a three second arousal, only the first arousal should be scored though both limb movements may be scored. In this scenario, the arousal index and PLM index with arousal but not the Periodic Limb Movement Index would be influenced by not scoring the second "arousal".--http://www.aasmnet.org/SMFAQs.aspx

jeff (still limping from the blower that fell on his toes, but at least it missed his head )

-SWS wrote:My understanding is that SDB and PLMD can mask and confound each other in multiple ways. Since the severity/presentation of either disorder can be sleep-stage dependent, those two conditions can sometimes mask severity by masking or preventing what would have been more severe sleep stages in some patients.

However, SDB and PLMs can also confound each other as being a matter being primary/secondary or stimulus/response. PLMD, obstructive SDB, and central SDB all have primary etiologies for which the respective physiologic control circuits fail to function properly. When any of these malfunction as a matter of primary failure in biology, my understanding is that PSG sequencing of the failures reflect these events as either unaccompanied by other etiological events, or as initial in the sequence of PSG events.

Those were cases of PLMD, obstructive SDB, and central SDB as primary etiological failures reflected in sequence. Since they are primary and initial, those failures in biology might also serve as stimuli for neurologically reflexive responses---that would be both secondary failures in etiology and reflect as secondary or non-leading in PSG sequencing. Limb kicks, upper airway closures, and central withdrawal of respiratory drive are ALL highly rudimentary defensive reflexes. As a matter of highly basic reflexology, any of those three might be primary etiologic failures, with any of those three also presenting in the time domain or PSG sequencing as stimulus/response based reflexive occurrences. At least that is the way I understand it as a layperson, SU...

So, if I understand you (and that's a big IF), you're saying that they should be able to tell which event occurs first, and then those that immediately follow will be attributed to initial event. Therefore, they ought to be able to tell whether the respiratory events triggered the leg movements, or vice versa. HOWEVER, if I have both disorders, one may prevent the other from being detected or from presenting as severely because, for example, a leg movement might wake me, keeping me from spending a lot of time in REM, where my respiratory events will be most severe. Correct?

If you happen to score borderline or high on this non-scientific HSP screening questionnaire then I personally suspect that your stimulus/response equation to poor sleep and EDS is probably highly multifactorial as a matter of both hypersensitivity and hyper-responsiveness.

I've seen this questionnaire cited several times on this forum. I don't know what established construct it's trying to measure, or anything else about its validity or reliability. It almost seems to be some kind of measure of sensory issues, as in sensory integration disorder.

Dr. Park holds that those with UARS have a hyperarousable nervous system, and that Dr. Guilleminault thinks that's why they tolerate CPAP as well (although I have yet to see anything Dr. Guilleminault has written along those lines). There is lots of information about people with UARS having lots of functional somatic syndromes, such as Irritable Bowel, Fybromyalgia, etc. I was under the impression that much of this resolves when the underlying SDB is treated. So IF there is a hyperarousable NS in UARS patients, I wonder if it's the chicken or the egg. In any event, other than being a very light sleeper, and a few other mild symptoms such as startling when a bird crashed into my window 3 feet from my head just now, leaving the contents of his GI track all over it, I don't think I qualify for whatever it is this scale is measuring.

SleepingUgly wrote: Also, what are the implications of going into a sleep study on 1200mg of Neurontin? Would that allow for discovering SDB that might otherwise not surface due to PLMS disrupting sleep? But would it prevent knowing what role PLMS play? Is it accurate that Neurontin does not "fix" PLMS that are respiratory-induced?

Hoping Muffy or Kathy can comment on this one.

Muffy?

Muffy wrote:
You know the old expression-- "The only way a CPAP machine can hurt you is if it fell on your head!"

Why didn’t anyone warn me of this CPAP machine peril? Where is the warning in the owner's manual?
Now that I am forewarned, I must find ways to take precautions...

-SWS wrote:

Muffy wrote: Obviously, whoever came up with that one was in sales and not clinical.

<snicker> ...As if you didn't know which former CEO said that.

C'mon...tell us which one?

SleepingUgly wrote:
….. HOWEVER, if I have both disorders, one may prevent the other from being detected or from presenting as severely because, for example, a leg movement might wake me, keeping me from spending a lot of time in REM, where my respiratory events will be most severe. Correct?

PLMs can prevent manifestation, or perhaps detection, of respiratory events in NREM as well.

SleepingUgly wrote: Also, what are the implications of going into a sleep study on 1200mg of Neurontin? Would that allow for discovering SDB that might otherwise not surface due to PLMS disrupting sleep? But would it prevent knowing what role PLMS play? Is it accurate that Neurontin does not "fix" PLMS that are respiratory-induced?

I don’t know about neurontin, but I’ve had three PSGs subsequent to being prescribed Requip with 0 PLMs recorded. But then that may simply mean that I am not subject to respiratory induced PLMs.



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