Did Your Titration Produce Normal Sleep and Breathing?

[rested gal]

I'm sorry to post in this thread as it will bump it up.

Maybe it's just me, but it seems as if the doctor jumped onto this forum primarily to push his new book, and advertise his sleep center.

Using the poll feature is guaranteed to make a topic stand out and get noticed. Looks like an infomercial to me.

Edited on Dec 12 - to add a link to my apology to Dr. Krakow for my rude reception:
viewtopic.php?t=26622&start=30

I'm glad to see him posting on this message board.

[krousseau]

Waiting to see the reply to EM about air flow measurement.

[DreamStalker]

I'm sorry to post in this thread as it will bump it up.

Maybe it's just me, but it seems as if the doctor jumped onto this forum primarily to push his new book, and advertise his sleep center.

Using the poll feature is guaranteed to make a topic stand out and get noticed. Looks like an infomercial to me.

I too got a similar feeling ... especially from the web site. However I thought I would on this rare occasion allow for the benefit of doubt to see if he joined to sell his idea about addressing flow limitations or to sell a book and business. I'm still awaiting worthwhile contributions to the forum's knowledge base.

[Snoredog]

Looking at the 4 PSG's I had Dr. Krakow, I see NO Flow Limitations "scored" on that report.

My understanding is they don't generally score those FL's because they are (or have not) been associated with any kind of drop in SAO2 levels.

But it seems for the Remstar & 420e Autopaps, they rely on those FL's with their response.

We have all viewed enough 420e reports here to know that an increase in FL "Runs" results in poor sleep.

Question: Which part of the human anatomy is the main culprit in FL's?

[BarryKrakowMD]

Responses to New Questions from Bottom to Top

1. Flow Limitation[/b]. Remember that a cardinal principle of SDB (sleep-disordered breathing) is that both sleep fragmentation and oxygen desaturations cause your daytime symptoms. Thus, while flow limitation is not linked to obvious oxygen desaturations, it is most assuredly linked to sleep fragmentation in most patients who suffer from it. Some of the APAPs do monitor FL in the form of "runs," and in our experience, the higher the runs, then the more they are suffering from UARS, which is why we started switching APAP patients to bilevel about 3 years ago. Last, I do not think there is a particular anatomical link to FLs, although certainly all of Dr. Christian Guilleminault's work on UARS points to a variety of factors in the nose and palate as influencing the condition.

2. Airflow measurement. Hope to post some graphics for you on my blog http://www.sleepdynamictherapy.com next week. For now, keep in mind that regardless of pressure or pressure gaps, most SDB patients will show either expiratory intolerance (pressure too high), expiratory flow limitation (pressure too low) or normal expiration (pressure just right). The key then is to find the right pressures to produce normal expiration, and to repeat, we find that wider bilevel boost produces normal expiration. However, there are exceptions, a patient with 8/6 could show normal, or a patient with 16/8 could still show expiratory intolerance and need a larger gap or expiratory flow limitation and need a smaller gap.

3. RERAs. Just to be clear RERAs (respiratory effort-related arousals) are essentially the same as FLEs (flow limitation events).

4. "Not provided enough info..." This was the main reason for my writing of my book, Sound Sleep, Sound Mind. I was disappointed to see how little information is given to sleep patients in both psychological and physiological realms. I trained at Stanford with Dr. Guilleminault and learned about UARS in 1993, 2 years after the discovery in adults. (He discovered it in children 10 years earlier). Yet, I still find myself in debates with other sleep professionals on the importance of UARS (aka FLEs, RERAs). The great news is that the American Academy of Sleep Medicine within the past year or so has finally recognized the importance of measuring this component of SDB.

5. Lack of Followup. This is a major area of discussion in the sleep medicine field, and everyone is scrambling to find new and better ways to connect with their patients on a more regular basis, which is why there is something of a push to move more sleep labs in the direction of becoming sleep centers.

6. Airflow Sensors. The key is get tested at a lab that regularly uses either nasal cannula pressure transducers or esophageal manometry or some other technique that offers a precise way to measure UARS. If the lab only uses "thermistor" technology, then it cannot accurately measure UARS. However, the good news is that pressure transducers are built into PAP therapy units, so during titrations, there is not excuse not to aggressively titrate out all the flow limitation, as it is readily observable on the tracing.

7. APAP vs CPAP in Heart Patients. Practice parameters clearly state that APAP devices are usually or never used in heart patients, particularly if they are known to suffer central apneas. The more recent technology for heart patients with both OSA and central apneas is the ASV (adapto-servo-ventilation) devices.

[mindy]

Responses to New Questions from Bottom to Top


7. APAP vs CPAP in Heart Patients. Practice parameters clearly state that APAP devices are usually or never used in heart patients, particularly if they are known to suffer central apneas. The more recent technology for heart patients with both OSA and central apneas is the ASV (adapto-servo-ventilation) devices.

Thanks, Dr Krakow! And also for the info on flow limitation.

Mindy

[DreamStalker]

Thanks for taking the time to respond. We are a grumpy and skeptical bunch here and I hope you understand why

I look forward to reading more about your perspective in treating our SDB condition(s).

[mindy]

We are a grumpy and skeptical bunch here and I hope you understand why

Hello DreamStalker!

I don't think it's too surprising that we're skeptical ... we have certainly had our share of posts by people trying to sell us on another web site, etc. etc. And we've also had people come along and try to bait us (sometimes successfully).

But, I think we're also a helluva good bunch and if people mean well, hopefully they realize where we're coming from

Mindy

[entremeler]

Thanks for the response, Dr. Krakow.
I don't know which airflow measuring device was used on my diagnostic, but since I was later titrated (twice), what you say suggests I got the result I needed. That's good to know. At least I'm dreaming again.

On another note, the thing that amazed me the most is that I no longer get up to go to the bathroom at night. Has anyone else had that result?
EM

[mindy]

On another note, the thing that amazed me the most is that I no longer get up to go to the bathroom at night. Has anyone else had that result?
EM

Oh yes! I've had same result 0 used to get up every night like clockwork. No longer. And I've read posts from others with the same result. Apparently it's some kind of brain chemical????

enjoy

Mindy

[RosemaryB]

Dr. Krakow, I have found your posts to be valuable. Ever since I had my sleep study, I've been trying to better understand the spontaneous arousals that were not treated by the titration pressures. I had about 24 S.A.s per hour during my initial study and about 21 S.A.s per hour during the titration study. But some of this may be because I was mistitrated.

Since I was mistitrated (at 5.0 cm H2O), I worked with my family doctor to find a better pressure. At 5.0, my AHI was 7-10/hour. If truth be told, I knew more about it than he did, mainly from reading voraciously on this forum. He's a great doc, and willing to explore areas he doesn't know a lot about.

I was able to get rid of most of my apneas and hypopneas by gradually raising my pressure to 9.0 H20 cm. My AHI is generally under 1.0 at this pressure. At a pressure of 10.0, I got a few centrals, so backed down to 9.0. Although I have an auto, my results seem to be better with straight cpap, because I seemed to be getting runaway pressures with the auto function turned on. These would wake me up. I don't use C-flex since it seemed to cause aerophagia for me.

Question: Are you saying that a straight cpap or auto with cflex won't reduce flow limitations/RERAS, even if a person only needs a lower pressure, like 9.0, that one needs a bipap for this? Or are you saying that this is true only for those with higher pressures? I was hoping that, having raised my pressures from 5.0 to 9.0, that might be taking care of what I called "UARS-like phenomena" seen in my sleep study (AKA spontaneous arousals on the sleep study).

I say UARS-like because UARS is only diagnosed in the absence of sleep apnea. I think that, since these diasnoses are mutually exclusive, this obscures that a person could have problems with both.

_________________

CPAPopedia Keywords Contained In This Post (Click For Definition): bipap, C-FLEX, cflex, Titration, CPAP, AHI, auto, aerophagia

[BarryKrakowMD]

New Responses

1. Dreaming. Increased dreaming is often, but not always a sign of increased REM consolidation. And, it is usually a reliable sign of a good PAP response in a patient who previously indicated no dreams or few dreams.

2. Nocturia. The biomolecule is atrial natriuretic peptide, which is released from the right atrium in the heart and which acts as a diuretic on the kidneys. For more details, you can visit yet another of our websites for a more detailed explanation: http://www.nocturiacures.com.

3. UARS titration. The issue of what is the best pressure delivery system (CPAP or APAP or CFLEX or bilevel) is moot. In other words, there is no reason why any of the systems won't work to titrate out UARS (aka flow limitations, RERAs). However, that's only the short answer. The long answer is coming up in another post, where I will discuss the relationships between UARS, anxiety, and erratic responses to PAP therapy.

[StillAnotherGuest]

The long answer is coming up in another post, where I will discuss the relationships between UARS, anxiety, and erratic responses to PAP therapy.

OK, looking forward to that, meanwhile, people might do some homework with some of your previously published material:

Prevalence of Insomnia Symptoms in Patients With Sleep-Disordered Breathing
Barry Krakow, MD; Dominic Melendrez, PSG-T; Emily Ferreira; James Clark; Teddy D. Warner, PhD; Brandy Sisley and David Sklar, MD

Relationships Between Insomnia and Sleep-Disordered Breathing
Ka-Fai Chung, MBBS, MRCPsych

Breathe-Right Strips, huh?

Hey RG, why not give those a shot to see if they help your FL Runs?

By-the-by, Dr. Krakow, I think your poll would more (fair, accurate, whatever) if you asked "Flow Limitations or RERAs or RDI", since this concept may be presented in a number of different approaches.

Course, if the responses still came back zero, that would be a little disheartening.
SAG

[BarryKrakowMD]

OK, the next post is so long, I assumed it would be more accessible to add it as a new one, so it's coming up next. Thank you for all your previous comments and questions.

Special thanks to SAG. Those references you posted were critical pieces to the puzzle that helped us make the connections between insomnia and sleep-disordered breathing. And, I want to mention that I got considerable help in working on that research from Dominic Melendrez, RPSGT, at Quality Sleep Solutions http://www.qualitysleepsolutions.com

[Catnapper]

BarryKrakowMD,

Would you care to tell us the machine, mask and any other devices you prefer for your own or your patients' treatments?

Just curious.