AHI - Useful or Useless?

rested gal wrote:I'm not a doctor

Me neither. And wouldn't want to be, especially these days.

rested gal wrote:nor have I ever met Dr. R.

I'd pay good money to be in the room when you do.

I like him. He makes me think.

rested gal wrote:. . . probably would not have written the magic Rx. . . .

When the research docs talk about meaning of AHI, they often mean, in my opinion, "AHI solely, without sleepiness or tiredness." So when a doc says "don't worry about AHI of 10," I believe he means "don't worry about that AHI in a patient that is not sleepy or tired."

Seems there is one line in the sand for AHI alone, and another line in the sand for the AHI of someone tired and sleepy. Context is supposed to clarify which line in the sand is being discussed whenever research docs go at each other. But that can get lost in translation between them even when speaking to one another. One is talking about useful as in "useful by itself" and the other is talking about useful in the sense of "useful in combination with other factors and indicators."

So, to me, the only actual "debate" is whether AHI alone can indicate pathological sleep below an AHI of 20 in the absence of symptoms. And, in practice, that is a meaningless debate, since people who aren't sleepy or tired aren't gonna have PSGs in the real world anyway. The theoretical debate has little practical value for enlightening the question of what to do with a particular patient, since the AASM already has useful guidelines that few question, as far as I know.

It will be decades before a PSG is routinely scheduled for everyone with hypertension or anxiety, for example. If ever. So the usefulness of AHI apart from symptoms of sleepy and tired people is mostly a moot point to me.

"pathological sleep" interesting concept JNK

Muse-Inc wrote:"pathological sleep" interesting concept JNK

I think that phrase may be a Dementism.

The paradox is that our society remains a vast reservoir of ignorance about sleep deprivation and sleep disorders. The benefits of the hard earned knowledge about normal and pathological sleep have not been passed on to the general public and practicing physicians. Millions of people are suffering and thousands are dying each year without ever knowing the true cause of their problems. -- http://www.stanford.edu/~dement/sleepless.html

Great quote, so true too! Untold thousands if not millions. I speak up (I've become a sleep study zealot ) whenever I hear someone talking about what sounds like apnea...so far no one's taken offense but then I'm pretty darned likeable since becoming a hosehead

jnk wrote:

rested gal wrote:nor have I ever met Dr. R.

I'd pay good money to be in the room when you do.

jnk wrote:I like him. He makes me think.

He's a charming speaker from what I've seen of his talks on videos. I like him, too.

jnk wrote:The theoretical debate has little practical value for enlightening the question of what to do with a particular patient, since the AASM already has useful guidelines that few question, as far as I know.

True, there are AASM guidelines. And Medicare guidelines.

However, what interested me about the "debate" between those two doctors was getting a glimpse at how the two of them think.

I was not impressed with Dr. R's saying this.... if the article in Respiratory Review was quoting him correctly:

SDB can probably be ruled out at an AHI of about 10 per hour.

Dr. Rapoport cautioned against over-interpreting the “gray zone” between AHIs of 10 and 20 per hour. “I do not quite know what that means,” he acknowledged."

He sounds pretty definite to me:
SDB can probably be ruled out at an AHI of about 10 per hour.

"gray zone" between AHIs of 10 and 20 per hour.

Even when I look at another of the statements attributed to him in the article... a statement which gives a bit more context (or waffling? ) to his remarks:

"Because the AHI is imperfect, Dr. Rapoport views it as a marker for the apnea-hypopnea syndrome and not as a definitive metric. He has found the AHI most useful for detecting severe apnea-hypopnea syndrome."

That's good. A marker, not a definitive metric.

But even with that statement in his favor ( ) I still can't get this out of my mind: "SDB can probably be ruled out at an AHI of about 10 per hour."

I think anyone with a diagnostic AHI of 10 (in a well done, competently scored full PSG sleep study) HAS sleep disordered breathing worth treating, even if the person reports NO sleepiness symptoms at all and doesn't have a high BP problem (yet.)

I'll echo just about everything that RG just posted. As someone with a strong background in statistics, I'm often frustrated when people are confused about what the term "correlation" means, which has been tossed around in this thread a few times. Let me mention a couple things about it, and then loop back to how it relates to this thread.

First, when a statistician uses the term correlation, it does not necessarily entail causality. (The methodological requirements to determine cause and effect are quite a bit more stringent.) There is a statistical measure known as the correlation coefficient that can describe how strong the correlation is. For example, a correlation coefficient of, say, 0.6 is often considered quite strong. It is not deterministic -- i.e., it does not mean that if A then B -- but it does mean that A and B are found together quite often.

To relate that back to this thread's subject, calling AHI "useless" is rather silly. Clearly, even those experts and those people on our forums who are dismissing the relevance of AHI cannot argue that it is useless or irrelevant. It's a tool in the toolbox. The relationship may be non-linear (which is what we're talking about when we mention certain cut points of AHI being more or less important than others). But I think it's abundantly clear that there is a relationship.

The risk of downplaying the relevance of AHI is, in my humble opinion, far greater than the risk of over-interpreting its significance or relevance. As such, I think a couple of the comments and quotations in this thread can be a little dangerous.

This is a statistician's version, really, of what RG and others have said in this thread. I just felt inspired to add my two cents.

I think the discussion here may have largely gone in the wrong direction. Not surprising, as In the cited article, Drs. Sullivan and Rappaport were each heading in somewhat different directions (at least in my understanding) while essentially agreeing that the AHI is often not a reliable measure of severity for particular subjects.

Common sense tells us that a high AHI usuallyy does correlate to the severity of the subject's apnea. But, what about a low AHI? Dr. Sullivan appears largely concerned with the situation in which the AHI either is or appears to be low but masks a severe case of sleep apnea. He refers to the limitations of thermister-based and other systems for measuring air flow, which could result in underreporting the AHI. He also refers to situations in which the AHI really is low, but the patient's nonetheless has severe sleep apnea in terms of its affects on the body:

"The AHI can mislead physicians about the severity of SDB, Dr. Sullivan added. At certain points in the menstrual cycle, for example, women with SDB may respond to apnea with a large rise in blood pressure (BP) rather than in the AHI. Catastrophic BP elevations with no change in the AHI were even observed during sleep apnea in a woman with preeclampsia.

In infants and children, apnea usually manifests as partial upper airway obstruction; breathing is loaded even though the AHI is very low. In these groups, the AHI is “unequivocally the wrong metric” of SDB, Dr. Sullivan stated."

Dr. Sullivan's comments are probably on the mark. While progress has been made, systems for measuring breath flow are imperfect, and the methods for scoring and calculating AHI are flawed, largely failing to take into account even the length of events. Many of us have noted that we can feel significantly worse after a night with a low AHI than with a much higher AHI on another night (and have developed our own theories why that might be so). I don't know anything about apnea in children, but Dr. Sullivan may well be right that there the AHI in its current form is even less reliable than with adults. That is troubling, as lately therehas been increased emphasis on treatment of apnea in children--using adult standards, so far as I know.

The AHI Index comprise of Apnea Index plus Hypopnea Index, but here are the reasons for most Sleep MDs to discard MOST Hypopneas,
at least for those who are using Resmed's APAPs:

From an interview with Dr Michael Berthon-Jones, in 2002.
Dr Berthon- Jones was the chief designer of the A8 and A9 Autosets.

Link to the interview: http://www.resmed.pl/fi/assets/document ... 0906r1.pdf

Question: Why doesn’t ResMed's AutoSet respond to
hypopnoea?

Answer: When you are lying quietly awake, or when you
first go to sleep, or when you are dreaming, you
can have hypopneas (reductions in the depth of
breathing) which are nothing to do with the state of
the airway. For example if you sigh, which you do
every few minutes, you usually have a hypopnea
immediately afterwards. This can also happen if
you have just rolled over and are getting settled, or
if you are dreaming. And the annoying thing is that
when you are on CPAP, this tendency to have what
are called central hypopneas - hypopneas that are
nothing to do with the state of the airway - is
increased. If you make an automatic CPAP device
that responds to hypopneas, you will put the
pressure up to the maximum while the patient is
awake.

Q-Do you think there is a misconception clinically
that all hypopneas should be treated ?

A- For simple obstructive sleep apnea, central
hypopneas should not be treated. They are not a
disease. Everyone has them. And they don’t go
away with CPAP.

There is a rare and important exception: central
hypopneas due to heart disease. This is called
Cheyne-Stokes breathing. CPAP does help with
that.

Q- Why doesn’t ResMed's AutoSet respond to
apnea above 10 cmH2O in pressure?

A-I mentioned before that the higher the pressure,
the more central hypopneas you will have. At a
pressure somewhere around 10 cmH2O, the central
hypopneas become central apneas. On the other
hand, the vast majority of obstructive apneas are
already well controlled by 10 cmH2O, and we are
only fine tuning using snoring and flattening. So it
is a pretty good bet that if the pressure is already
above 10 cmH2O, any apneas are most likely
central, and you should leave them alone (except
in patients with central apneas due to heart failure).
But if the pressure is below 10 cmH2O, most
apneas will be obstructive and you should put the
pressure up. There’s nothing magical about 10
cmH2O, it’s just a good place to put the line in the
sand.

Q-Can you over-treat apnea?

A-You can’t over-treat obstructive apnea. You
really don’t want the patient having unresolved
obstructive apneas. And we want not just to prevent
apnea - we also want to keep the airway sufficiently
open for the subject to breathe easily and regularly
and stay asleep.

But you can use too much pressure. The higher
the pressure, the greater the side effects. Although
this has never been proven, it is rather obvious - no
pressure, no side effects! So you want to use the
lowest pressure possible while keeping the airway
nicely open.

Q-Likewise can a device that responds to
hypopnea over-treat it ?

A-The funny thing is that it can both over-treat and
under-treat. It will put the pressure up through the
roof in some subjects, who have lots of central
hypopneas. And it can completely miss repetitive
severe silent inspiratory flow limitation that is totally
disturbing the patient’s sleep without there being
any hypopneas. If this occurs without CPAP, it is
called upper airway resistance syndrome. It is just
as bad for you as obstructive sleep apnea. But a
CPAP machine that responds only to hypopneas
will treat your obstructive sleep apnea, and give
you upper airway resistance syndrome instead.

Q-How can Automatic CPAP devices help
optimise treatment ?

A-CPAP devices, whether automatic or not, can
tell us - the clinician, the technician - about what is
going on when we are not there. Is the patient using
the device? Is there a leak, and if so, when and how
much? If it is an automatic device, what is the
pressure doing? How well is the patient breathing?
How steadily, how much? This might be particularly
important if the patient also has heart disease or
lung disease, or has had a stroke, and has other
reasons, apart from sleep apnea, for having
abnormal breathing during sleep.



Here are examples of cases when my sleep MD would disregard clusters of Central Apneas events,
because they occured during REM sleep:



Those CA events that occured after 4 a.m. would NOT be counted.

and



Yes, I slept without CPAP for 2 hours. Those CA events that occured at around 6 a.m. would be disregarded.

But you need to know what you're doing!

****************************

avi123 wrote: From an interview with Dr Michael Berthon-Jones, in 2002.
Dr Berthon- Jones was the chief designer of the A8 and A9 Autosets.

Emphasis added. That pretty important detail changes and, in a couple cases, invalidates much of what followed. There have been a lot of advances in the last nine years. Especially like, oh, I don't know, ASVs. And more widespread recognition of complex sleep apnea as a real and treatable condition. And...well, I'll just stop there.

BrianinTN wrote:

avi123 wrote: From an interview with Dr Michael Berthon-Jones, in 2002.
Dr Berthon- Jones was the chief designer of the A8 and A9 Autosets.

Emphasis added. That pretty important detail changes and, in a couple cases, invalidates much of what followed. There have been a lot of advances in the last nine years. Especially like, oh, I don't know, ASVs. And more widespread recognition of complex sleep apnea as a real and treatable condition. And...well, I'll just stop there.

I found and read the complete article, and, even if it was 2002, Dr. Berthon-Jones seemed quite "current" in his understanding of most of the science. Other articles show that he knew all about ASV at that time. ASV has actually been around a long time--we just haven't had access to it. See a 2001 paper co-authored by Dr. Berthon-Jones: Adaptive pressure support servo-ventilation:
a novel treatment for Cheyne-Stokes respiration in heart failure, Am J Respir Crit Care Med 2001;164(4):614-619, found at http://www.resmed.com/assets/documents/ ... ow_eng.pdf.

Since 2002, there has been better general understanding of sleep disordered breathing, but I'm afraid the basic science at the top hasn't advanced all that much, just the technology that is available "off the shelf" to patients and the understanding of their local sleep techs and doctors. Pioneers including Sullivan and Berthon-Jones identified most/all? of the current OSA issues long ago; it has just taken a disgustingly long time for some of the ideas to be brought into the marketplace.

While you are correct about access (2006 is when it started to be available in the US), the application of ASVs to treat complex sleep apnea is a relatively recent phenomenon. You'll find plenty of debate even just a few years ago about whether it's even "real" as a condition, or represents a transient and unimportant problem.

BrianinTN wrote:While you are correct about access (2006 is when it started to be available in the US), the application of ASVs to treat complex sleep apnea is a relatively recent phenomenon. You'll find plenty of debate even just a few years ago about whether it's even "real" as a condition, or represents a transient and unimportant problem.

Mostly, I agree. I recall a sleep doctor, probably in 2004, telling me that centrals and such things would disappear when obstructive apneas were properly treated, and completely discounting the idea that increased pressure could cause centrals. But, that was the general medical attitude. The researchers at Resmed and a few other places that focussed on the problem knew better long before the general medical community. Resmed's present definition of complex sleep apnea is: "CompSA consists of all or predominantly obstructive apneas which convert to all or predominantly central apneas when treated with a CPAP or bilevel devices." In the 2002 interview cited by Avi123, Dr. Berthon-Jones (who is Chief Science Officer at Resmed) said: "I mentioned before that the higher the pressure, the more central hypopneas you will have. At a pressure somewhere around 10 cmH2O, the central hypopneas become central apneas." So, Dr. Berthon-Jones seemed to know it was not a transient problem, and that if the pressure needed to suppress obstructive events was too high (and this would depend on the individual), you were essentially going to trade obstructive events for central events, the present definition of CompSA.

I can't recall the regulatory history of the ASV machines; but I believe it took years for Resmed to obtain the required approvals for them to be marketed for the treatment of CompSA, long after the technology was developed.

rested gal wrote: . . . I was not impressed with Dr. R's saying this.... if the article in Respiratory Review was quoting him correctly:

SDB can probably be ruled out at an AHI of about 10 per hour.

Dr. Rapoport cautioned against over-interpreting the “gray zone” between AHIs of 10 and 20 per hour. “I do not quite know what that means,” he acknowledged.". . .

If he said that with a sleepy/tired patient in front of him about that patient, I would be unimpressed too, since that would be using a test to deny a patient the opportunity to try PAP. As I see it, the real purpose of AHI is to prove to insurance that something objective changed with the application of PAP. Using AHI as a basis to deny a patient the right to try PAP is wrong under any circumstance, regardless of the PSG results, in my book.

Yet, I manage in my mind to excuse Dr. R's statement on the grounds that, strictly speaking, he is right from the perspective of a researcher as far as what has been proved in studies, depending on one's definition of SDB.

Put another way, if Dr. R is gonna run a study to prove that SDB leads to serious medical complications, he might do well to exclude those with an AHI below 10 from his study, since statistically speaking there are people walking around with an AHI that high who have no symptoms to speak of. (Some people just pause and sigh a lot in their sleep and their bodies show no obvious adverse effects from it.)

It is easy for researchers to say things that can be misused by others to deny patients care, but the researcher still has to say out loud what the research numbers seem to be showing at present. And I am aware of no studies that demonstrate that people with AHI below 10 have serious adverse health problems from it if it doesn't make them sleepy or tired. Those who are tired and sleepy and benefit from PAP and have better lives should be allowed to use PAP on that basis alone, regardless of the lack of studies indicating that an AHI of 10 or below is likely to ruin their health.

Nobody breathes perfectly when asleep. Measuring AHI may help to indicate who would benefit from PAP. BUT, someone sleepy and tired should be allowed to try PAP no matter what his or her AHI is. After all, even some UARS patients benefit from it when they have little AHI at all to speak of.

So I cut research docs a lot of slack when they talk about what tests do and do not seem to tell us and what studies can and cannot tell us. I just hope no one ever misuses Dr. R's words to deny any patient the opportunity to try PAP.