Preliminary Data - Current project (exciting!)

General Discussion on any topic relating to CPAP and/or Sleep Apnea.
split_city
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Preliminary Data - Current project (exciting!)

Post by split_city » Wed Oct 17, 2007 10:30 pm

I have been a busy bee running my current project. This project pretty much involves hooking up male OSA patients with lots of (important) equipment and then record what happens at sleep onset and during obstructive events.

Factors I have been measuring include:

1) Tongue (GG) muscle activity
2) Diaphragm muscle activity
3) Diaphragm position
4) Changes in thoracic and abdominal compartmental volumes
5) when does the airway collapse? i.e. at the end of expiration (passive collapse) or during inspiration (active collapse).

Here is a snap shot of some of the data in a patient I had in the other night.

Here's what everything stands for:

EMGgg = electrical activity of the genioglossus (tongue)
EMGdi = electrical activity of the diaphragm (measured by an oesophageal catheter)
Pmask = mask pressure
Pepi = epiglottic pressure
Poes = oesophageal pressure
Pga = gastric pressure
Sats = oxygen saturations

Image

So, as you can see, there is a pretty obvious decrease in GG activity just prior to an apnea and particularly during the apnea. Oesophageal and epiglottic pressure becomes more negative during respiratory attempts, indicating increased respiratory "drive." However, this drive does not seem to occur in respect to the GG. At the same time, baseline gastric pressure increases, likely indicating contraction of the abdominal muscles. These contractions are thought to help with diaphragmatic contractions, but perhaps to try and increase pressure inside the airway to "pop" open the airway.

You can see the subsequent hyperventilation period at the end of termination, again indicating the increased drive. While I did not show it, end tidal CO2 levels decrease during this hyperventilation. The patient may blow off so much CO2 that the begin to hypovenilate because their CO2 dips below their "breathing threshold." This period of low CO2 results in the dilator muscles being switched off. Obviously this leaves the airway vulnerable to collapse during the next inspiratory effort.

Now, at the same time, I have been measuring changes in anterior-posterior (front-back) dimensions of the chest and abdomen to evaluate alterations in thoracic and abdominal compartmental volumes. Here's a very rough diagragm showing these changes.

Image

Now, the respiratory flow is not shown as the lung volume stuff was recorded on another computer. We will try to incorporate this data later.

The first trace = anterio-posterior distance of the chest
Second trace = lateral dimensions of the chest
Third trace = anterio-posterior distance of the abdomen
Fouth trace = lateral dimensions of the abdomen

It's just easier to focus on the anterio-posterior traces. Sorry, I don't have any numbers on the picture.

Now, I don't know where the apneas are at this stage but I would bet there would be about six in there. You can clearly see the decrease in A-P dimensions of both the chest and abdomen (~2-4mm). Now, that might not sound a lot but these kind of numbers might represent a fall in lung volume of about ~200-400mL.

Just looking at abdomen changes in A-P. The abdomen is basically an incompressible structure (unlike the chest). In other words, you cannot change the overall "total" dimensions of the abdomen (for a given volume) i.e. a decrease in A-P distance would likely result in an increase in the lateral dimensions. Alternatively, the diaphragm may ascend, allowing the abdominal contents to enter the chest --> further reducing lung volume.

Therefore, as you can see in the picture, A-P dimensions of the abdomen decrease (there are changes in lateral distances). Depending on our analysis, this may suggest that the diaphragm is moving up into the chest.

Interesting times ahead...
Last edited by split_city on Thu Oct 18, 2007 10:26 pm, edited 1 time in total.

Guest

Post by Guest » Wed Oct 17, 2007 10:45 pm

Hey split. interesting. How are you measuring EMG of the tongue?

split_city
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Post by split_city » Wed Oct 17, 2007 10:46 pm

Intramuscular wires

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Snoredog
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Post by Snoredog » Wed Oct 17, 2007 10:56 pm

split_city wrote: In other words, you cannot change the overall "total" dimensions of the abdomen...
sure you can!! you drink a whole bunch a beers!

have any plans to test a saline injection via the catheter to look for associated arousal?

someday science will catch up to what I'm saying...

Guest

Post by Guest » Wed Oct 17, 2007 11:03 pm

Snoredog wrote:
split_city wrote: In other words, you cannot change the overall "total" dimensions of the abdomen...
sure you can!! you drink a whole bunch a beers!
Yep, and the subsequent beer belly contributes to the sleep apnea
Snoredog wrote:[have any plans to test a saline injection via the catheter to look for associated arousal?
No room for saline injections via the catheter. All lumens are in use.


mckooi
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Post by mckooi » Thu Oct 18, 2007 10:10 pm

Hi Split_City,

Another possible solution to Sleep Apnea....use the liquid oxigen...no more snoring, no more apnea or event hypapnea.

Mckooi

split_city
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Post by split_city » Tue Oct 23, 2007 2:14 am

Another teaser from another subject. It's known that there are generally less sleep apnea events during SWS. The reasons for this are as yet, not completely understood. Here's a snapshot of some data from a subject in SWS.

Image

First of all, you can see the patient is quite flow limited, with snoring and increased drive (greater suction pressures in the epiglottic and oesophageal regions). The activity of the tongue (GG) is also increased, but not enough to completely open the airway. Now about a 1/3 of the way in, flow gets very limited. At the same time GG activity also decreases. Eventually, GG activity cranks up which helps to (partially) open the airway. A desaturation occurs. There were no arousals during this time, nor were there during the entire time the patient was in SWS. This was despite hypopneas and desaturations. Neverthess, the events were less frequent and less severe than what they were during stage I/II sleep.

One train of thought is that the arousal threshold is higher in SWS compared to light sleep i.e. it takes much more drive (suction) to wake you up. Susequently, there might be enough time for your dilator muscles to become active to reopen the airway (if an event occurs) before you arouse.


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StillAnotherGuest
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Flow Limitation?

Post by StillAnotherGuest » Tue Oct 23, 2007 4:22 am

split_city wrote:There were no arousals during this time, nor were there during the entire time the patient was in SWS. This was despite hypopneas and desaturations. Neverthess, the events were less frequent and less severe than what they were during stage I/II sleep.
Yes, that is interesting.

Can you post the rest of the montage (EEG, whatever other EMG, ECG, etc.) during those events? In 30-second and 2-minute epochs?

And maybe the effort belts (abdomen and thoracic) for laughs. Hey, bandwidth is cheap. Thanks.

SAG
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Aromatherapy may help CPAP compliance. Lavender, Mandarin, Chamomile, and Sweet Marjoram aid in relaxation and sleep. Nature's Gift has these and a blend of all four called SleepEase.

split_city
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Re: Flow Limitation?

Post by split_city » Tue Oct 23, 2007 4:35 am

StillAnotherGuest wrote:
split_city wrote:There were no arousals during this time, nor were there during the entire time the patient was in SWS. This was despite hypopneas and desaturations. Neverthess, the events were less frequent and less severe than what they were during stage I/II sleep.
Yes, that is interesting.

Can you post the rest of the montage (EEG, whatever other EMG, ECG, etc.) during those events? In 30-second and 2-minute epochs?

And maybe the effort belts (abdomen and thoracic) for laughs. Hey, bandwidth is cheap. Thanks.

SAG
Unfortunately, I am recording all the sleep related variables (EEG, EMGsubmental, EOG, effort etc) on another computer. We don't have enough channels and computing power on the computer where I have recorded the above signals. Recording twenty three signals uses a lot of the CPU and RAM capacity!

I still need to get these studies scored and then time match the data (between the two computers) so that we can identify each stage, obstructive events, arousals etc.

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StillAnotherGuest
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Commodore64?

Post by StillAnotherGuest » Tue Oct 23, 2007 5:05 am

split_city wrote:Recording twenty three signals uses a lot of the CPU and RAM capacity!
Lemme tuneup your system for you. I can run 20 channels, simultaneous videophotography (which is over 10 times the the size of the montage signals) and still play "Hearts".

That oximetry signal looks pretty coarse. What are you using, a rock?

SAG
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Aromatherapy may help CPAP compliance. Lavender, Mandarin, Chamomile, and Sweet Marjoram aid in relaxation and sleep. Nature's Gift has these and a blend of all four called SleepEase.

split_city
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Re: Commodore64?

Post by split_city » Tue Oct 23, 2007 7:03 am

StillAnotherGuest wrote:
split_city wrote:Recording twenty three signals uses a lot of the CPU and RAM capacity!
Lemme tuneup your system for you. I can run 20 channels, simultaneous videophotography (which is over 10 times the the size of the montage signals) and still play "Hearts".

That oximetry signal looks pretty coarse. What are you using, a rock?

SAG
lol at the commodore64 comment...

I probably overexaggerated the lack of computing power. Despite pretty high sampling rates (1kHz for all muscle EMG activity), we have plenty of RAM and CPU power to spare. The data above is recorded using a program called Windaq. We have the capacity to record 32 signals simultaneously. Of those 32, we have 12 channels dedicated to amplifiers. While sleep related data can be recorded via these channels, all the amplifiers are in use - Diaphragm EMG signals (8 amplifiers), GG (1 amplifier) and other surface respiratory muscle recordings (scalence, abdominal, and intercostal; 3 amplifiers). Subsequently, I am recording all sleep related data through compumedics on a separate computer.

In regards to the sats, the range on the screen is from 90-100%. That's why it might look a bit rough?

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StillAnotherGuest
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Still Need the Rest of the Story

Post by StillAnotherGuest » Wed Oct 24, 2007 5:01 am

split_city wrote:In regards to the sats, the range on the screen is from 90-100%. That's why it might look a bit rough?
Can you put the % grid up? How much are those individual saturation decreases?

By any criteria, the "flow limitation" that you have identified would be an apnea by waveform reduction rule. It would seem to meet duration criteria as well (I'm assuming that with a RR of 18, that's a 60 second epoch, the first event slides right in there at 11 to 12 seconds, and the second event is going to be well beyond that).

My interest in the other effort belts concerns the Pes activity. If that respiratory event you have noted were it fact obstrucitve in nature, the Pes reversal would have gone from more negative (progressively deeper drop) during the event to a higher level during baseline (could you post the pressure grid to that too?).

Image

That the Pes reversal is "reversed" would imply that this is, at least initially, a central event.
split_city wrote:I still need to get these studies scored...
Oh, go ahead and post the raw data, we've been working on our SWS scoring skills:

To SWS, or Not To SWS

SAG
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Aromatherapy may help CPAP compliance. Lavender, Mandarin, Chamomile, and Sweet Marjoram aid in relaxation and sleep. Nature's Gift has these and a blend of all four called SleepEase.

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StillAnotherGuest
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Whadz He Mean?

Post by StillAnotherGuest » Wed Oct 24, 2007 6:33 am

SAG wrote:That the Pes reversal is "reversed" would imply that this is, at least initially, a central event.
For reference, s_c had a good example of a more traditional Pes reversal up on top there:

Image

Here you can see how Pes activity increases during the obstructive event, then decreases when normal breathing resumes.

SAG
Image

Aromatherapy may help CPAP compliance. Lavender, Mandarin, Chamomile, and Sweet Marjoram aid in relaxation and sleep. Nature's Gift has these and a blend of all four called SleepEase.

split_city
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Post by split_city » Wed Oct 24, 2007 9:22 am

Here you go SAG

Image

You're right. There is less drive/suction during the really flow limited breaths (in this example anyway).

Here's another snapshot later in the recording (still SWS) showing the reverse i.e. increased drive during the hypopnea/apnea breaths.

Image

The patient tended to only have hypopneas when in SWS whereas he was having apneas during stage I/II sleep. However, there was probably one apnea in the above example.
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mckooi
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Post by mckooi » Wed Oct 24, 2007 4:01 pm

HI Split_city and SAG,

From the diagrams, what would be the main trigger of the sleep apnea? In sequence, random or cluster?

Mckooi