So, every patient that needs CPAP treatment is getting BiPap?
Never said they did. But Bilevel and ASV had better be in the toolbox if you're going to titrate central apnea.
RAM_Sleep wrote:
Also, Stellate has new software that is a bit more updated than the software released in 1996.
Can it calculate Pulse Transit Time? If not, I could also use Rembrandt or Alice.
RAM_Sleep wrote:
In any event, if you honestly think that all sleep labs have top of the line equipment, then you are fooling yourself. In fact, I bet if you did enough reading, you will see that the majority of labs do not offer what you THINK you need to properly conduct studies.
At this point, a lab without ASV isn't a lab. If you're doing children (my question from before) then you absolutely need ETCO2. If you don't have that capability, then you shouldn't be doing kids.
If you're not doing children, then I'll let ETCO2 slide.
Regardless, I am acutely aware of what a lot of labs don't have.
RAM_Sleep wrote:
Heck, look at the studies that are posted on here. Some of them are as basic as you can possibly get. I wish that they all measured Pes, ETCO2, Etc, but they dont and they arent likely to do so anytime soon.
Routine studies may not need enhanced parameters and modalities. But some or all of these parameters and modes are critical for adequate diagnosis and treatment of the various forms of CSA.
BTW...
RAM_Sleep wrote:
There is even a syndrome called Complex OSA, but, in my opinion, the verdict is still out on it. We'll see what comes out of it as more research pours in.
I know CompSAS. It has clearly already been accepted since the hallmark paper by Drs. Gilmartin, Daly and Thomas back in 2005.
And with the estimate of CompSAS put at about 15%, a clear understanding of the Recognition and Management of Complex Sleep-Disordered Breathing had also better be in the toolbox.
I understand, but in those scenarios we, and maybe only our lab, but im positive other labs do this too, would not use BiLevel because they wouldnt be titrated for the centrals.
I agree that a lab without BiLevel isnt fit to be called a lab.
Enough is enough though.
We'll let someone else jump in when they feel the need.
We'll let someone else jump in when they feel the need.
What a drag! After all the time I just spent building this pitcher of the waxing and waning of TcpCO2 during central apnea (classic CSR), on its way to successful treatment with ASV!
Cheyne Stokes breathing is something all together different and doesnt just show up because of pressure.
Oh, really? Other than cycle length (long vs short) and consequently ASV approach, once pressure-induced CSA/CompSAS begins, I don't see any difference whatsover.
BTW, TcpCO2 clearly identified the apnea threshold at about a pCO2 of 42 mmHg. Once ASV allowed the pCO2 to stabilize at about 45 mmHg, the CSA cycle was broken and normal breathing ensued.
Clearly, this information can also be employed to guide other modalities such as EERS to treat the other forms of hyperventilatory central apnea.
Ed
Cheyne Stokes breathing is something all together different and doesnt just show up because of pressure.
Oh, really? Other than cycle length (long vs short) and consequently ASV approach, once pressure-induced CSA/CompSAS begins, I don't see any difference whatsover.
Ed
We may be talking about two different things. I do know that the patients that we use the wait and see approach get acclimated and their centrals, which were a result of the pressure, cease. Stage 1 centrals CAN be benign, although there are cases that are not benign. Its on a case by case basis. You can use a text book or a rule book to treat every patient. It doesnt work. You can find research article after article, yet find someone who will break the mold. As a technician, you have to adapt the treatment. Maybe the wait and see method doesnt work, then we begin adjusting pressure. What is the harm is giving the patient 10 minutes to acclimate to the newly introduce pressure? Nothing. In fact, if it works, then the patient may be better off.
We usually have hours to work with a patient, although split night studies are different. This is the exact reason why we do not split Central Apnea patients. It can take a long time to get things just right.
When a get a patient who exhibits Cheyne Stokes breathing, then treatment is needed. End of story.
In any event, you use your rule book and I will use mine.
Finally, breathing has become completely stable, as is the TcpCO2.:
Now, the PSG of short-cycle pressure-aggravated CompSAS gets a little busier, but I think if you can understand this concept in a nice clean CSR, then it's easier to understand CompSAS. The underlying approach is still the same, break the cycle.
As to whether or not the onset events impact the body, well sure. However, most patients "grow" out of them once they get comfortable with their equipment, so they are USUALLY temporary.
Are those patients brought back into the lab for short-term follow-up titrations to make sure they outgrew the onset events? Otherwise, it seems they would be incorrectly titrated if the onset and post arousal events are not factored in to the pressure settings.
Sorry for all the questions and thanks for the answers.
As to whether or not the onset events impact the body, well sure. However, most patients "grow" out of them once they get comfortable with their equipment, so they are USUALLY temporary.
Are those patients brought back into the lab for short-term follow-up titrations to make sure they outgrew the onset events? Otherwise, it seems they would be incorrectly titrated if the onset and post arousal events are not factored in to the pressure settings.
Sorry for all the questions and thanks for the answers.
The company that we refer our patients to (although no binding agreement is established) only sells data capable machines. Therefore, the AHIs are calculated and reported monthly. If the AHI is not reduced after a months time, then we inquire about what the situation is.
Plus, patients fill out sleepiness scales monthly also. If the onset events are causing problems (IE fragmenting sleep all night long), then those same patients will be fatigued.
This is where it gets fuzzy with what you typed. The onset events that I am speaking of do not last. They may last 5-10 minutes, but most cases the patient enters stage II and the events cease. They are not an ongoing problem or else we would diagnose that as CSA.
The company that we refer our patients to (although no binding agreement is established) only sells data capable machines. Therefore, the AHIs are calculated and reported monthly. If the AHI is not reduced after a months time, then we inquire about what the situation is.
Which machines do they use? Are they set up in APAP Mode? This is quite pertinent in that different machines report out centrals differently (and some not at all).
This is where it gets fuzzy with what you typed. The onset events that I am speaking of do not last. They may last 5-10 minutes, but most cases the patient enters stage II and the events cease. They are not an ongoing problem or else we would diagnose that as CSA.
Sorry. Guess we are talking about different scenarios. I was thinking more of the people who spend the night having arousals/awakenings and bouncing back into stage 1 and 2 without reaching SWS for any decent length of time, so it becomes a night of recurrent periods of sleep onset and post arousal centrals.
The recommended montage is now F4, C4, O2. Your montage may underestmate SWS in that you are not monitoring frontal leads.
Ed
I follow the guidelines that are set by the labs I work for. If you want a debate or feel like nitpicking, then go for the thousand of labs that do not follow your suggestions and do not have the top of the line equipment that you need. I really don't care anymore.
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