Squishing the belly increases AHI

[split_city]

A closer look at respiratory events reveals that many hypopneas are central in nature:



With a lack of increased activity in the Poes channel during this event (an increased downward deflection would indicate attempting to inhale against obstruction), and rather, an actual decrease in the downward deflection, this event is central in nature.

This was taken from the same person. Cuff condition was max (40cmH2O). I have ignored scales as I simply wanted to show that swings in Pepi and Pes do in fact increase in some of these events. Agreed?

[NotMuffy]

There is missing data in the example you put up (SWS stuff). Patient's were asked to buzz us if they wished to switch positions. We unplugged the pneumotach when they moved and we didn't analyze this data.

However, there's also a lot of stable Duece in there as well.



This is pretty close to duece:



Here is some nice solid Duece with pneumotach in place:



A pile of stable sleep during the period when the pneumotach was off (admittedly with a lot of delta activity):



so when you have stable sleep, you have stable breathing.

Yes we used magnetometers to measure changes in FRC with compression. We measured A-P and lateral dimensions of the chest and abdomen. I haven't analyzed this data yet and it's going to take a bit of work. In a perfect world, we would have liked to measure absolute FRC. This is in the "too hard basket" as this stage unless we get patients to sleep in a body box.

I meant doing it while awake.

[NotMuffy]

A closer look at respiratory events reveals that many hypopneas are central in nature:



With a lack of increased activity in the Poes channel during this event (an increased downward deflection would indicate attempting to inhale against obstruction), and rather, an actual decrease in the downward deflection, this event is central in nature.

This was taken from the same person. Cuff condition was max (40cmH2O). I have ignored scales as I simply wanted to show that swings in Pepi and Pes do in fact increase in some of these events. Agreed?

Yes, I did see that, but I think you gotta get your babe to incorporate that Pes in scoring and cull out those central hypopneas, cause there were a lot.

[NotMuffy]

Also, can you get this guy's drug list (if any, legal or not)(assuming you guys got laws over there). He seems to be putting up a lot of spindles.

[split_city]

However, there's also a lot of stable Duece in there as well......

so when you have stable sleep, you have stable breathing.

Yeah, and? No smoke and mirrors with that statement. Not sure what you're getting at......

Are you basically saying the increase in AHI is simply due to post-arousal hypopventilation, due to increased arousability as a result of compressing the abdomen and has nothing to do with changing the mechanics of the upper airway? How can I prove that the increased arousals weren't simply due to respiratory events OR due to making it harder for them to sleep? What's causing what?

Yes we used magnetometers to measure changes in FRC with compression. We measured A-P and lateral dimensions of the chest and abdomen. I haven't analyzed this data yet and it's going to take a bit of work. In a perfect world, we would have liked to measure absolute FRC. This is in the "too hard basket" as this stage unless we get patients to sleep in a body box.

I meant doing it while awake.

No we didn't measure changes during wakefulness. We were more concerned with what happened during sleep.

Yes, I did see that, but I think you gotta get your babe to incorporate that Pes in scoring and cull out those central hypopneas, cause there were a lot.

If that's the case, why shouldn't we measure Pes in all PSGs?

I think that's being a bit harsh to exclude them all. Now without looking at any PSGs, I would predict a number of hypopneas, that directly follow arousals, would start as one of these central hypopneas i.e. period of hypoventilation and decrease in Pes swing as drive dissipates after the initial period of post-arousal hyperventilation. As the hypopnea continues, drive would likely increase (greater swings in Pes) due to mechano- and chemo- stimuli. Do I exclude these events as well? Do I exclude any events which don't show at least 1 breath of increased drive? Or do I exclude any events which occur directly after an arousal? At the end of the day, these are still respiratory events.

Also, can you get this guy's drug list (if any, legal or not)(assuming you guys got laws over there). He seems to be putting up a lot of spindles.

Will need to check when I get to work. Can't recall him being on any drugs though.

[NotMuffy]

There is missing data in the example you put up (SWS stuff). Patient's were asked to buzz us if they wished to switch positions. We unplugged the pneumotach when they moved and we didn't analyze this data.

I wasn't going to mention that, however, since you brought it up...

What was the criteria to put it back?

[split_city]

There is missing data in the example you put up (SWS stuff). Patient's were asked to buzz us if they wished to switch positions. We unplugged the pneumotach when they moved and we didn't analyze this data.

I wasn't going to mention that, however, since you brought it up...

What was the criteria to put it back?

Allowed them to have about 30 mins in a different posture and then went in and moved them back to their study position.

[NotMuffy]

How can I prove that the increased arousals weren't simply due to respiratory events OR due to making it harder for them to sleep?

Do a baseline NPSG without all that stuff hangin' off 'em.

If that's the case, why shouldn't we measure Pes in all PSGs?

I think RIP is fine, but my point is, now that you have information, don't ignore it in order to make your data fit your hypothesis.

[NotMuffy]

There is missing data in the example you put up (SWS stuff). Patient's were asked to buzz us if they wished to switch positions. We unplugged the pneumotach when they moved and we didn't analyze this data.

I wasn't going to mention that, however, since you brought it up...

What was the criteria to put it back?

Allowed them to have about 30 mins in a different posture and then went in and moved them back to their study position.

However, in this case, important information is now excluded.

[split_city]

How can I prove that the increased arousals weren't simply due to respiratory events OR due to making it harder for them to sleep?

Do a baseline NPSG without all that stuff hangin' off 'em.

Actually I might have a better idea. What about my first abdominal compression study, the one where I showed abdominal loading increased upper airway collapsibility. Patients were on CPAP during that study so there weren't any respiratory events. Abdominal compression was similar to that achieved in the present study. I also have arousal data. If I show there was no difference in arousal frequency (during stage 2 sleep) between cuff conditions, would this suggest that cuff inflation has no apparent effect on arousability? Obviously CPAP is a confounding factor but still, if abdominal compression makes it harder to sleep, then there should be increased numbers of arousals with abdominal loading.

If that's the case, why shouldn't we measure Pes in all PSGs?

I think RIP is fine, but my point is, now that you have information, don't ignore it in order to make your data fit your hypothesis.

I haven't massaged any of the data. At the end of the day, AHI (based on standard) PSG measurements is the primary outcome. What type of event and if you want to dig dipper, what type of "hypopnea" it is, is a secondary outcome. If we are going down this line, then the results by Heinzer (Effect of increased lung volume on sleep disordered breathing in patients with sleep apnoea) and any other looking at the effect of lung volume on AHI, need to be questioned as well.

What would your inclusion/exclusion criteria be for the hypopneas?

[split_city]

There is missing data in the example you put up (SWS stuff). Patient's were asked to buzz us if they wished to switch positions. We unplugged the pneumotach when they moved and we didn't analyze this data.

I wasn't going to mention that, however, since you brought it up...

What was the criteria to put it back?

Allowed them to have about 30 mins in a different posture and then went in and moved them back to their study position.

However, in this case, important information is now excluded.

Such as?

[NotMuffy]

There is missing data in the example you put up (SWS stuff). Patient's were asked to buzz us if they wished to switch positions. We unplugged the pneumotach when they moved and we didn't analyze this data.

I wasn't going to mention that, however, since you brought it up...

What was the criteria to put it back?

Allowed them to have about 30 mins in a different posture and then went in and moved them back to their study position.

However, in this case, important information is now excluded.

Such as?

There's a lot of stable Duece in there.

I would also submit that since the guy slept like a rock once you removed some stuff, that aggravated sleep continues to be the major cause of this particular patient's problem .

[NotMuffy]

What would your inclusion/exclusion criteria be for the hypopneas?

I would back all the way out and do full NPSG, baseline and then each pressure, so now you have like 4 nights total. Sleep efficiency <85% excludes the study.

[split_city]

What would your inclusion/exclusion criteria be for the hypopneas?

I would back all the way out and do full NPSG, baseline and then each pressure, so now you have like 4 nights total.

Sure. Got any free time? Or got a student lined up to undertake it? That would be a PhD in itself.

Sleep efficiency <85% excludes the study.

Rrrriiiigggghhtttt. So having four nights isn't enough for you? You also want to exclude studies based on sleep efficiency as well? And also exclude "central" hypopneas (you still haven't actually clearly defined the inclusion/exclusion criteria for these events). I take back saying this would be a PhD in itself. It would take longer than one PhD to complete.

In reality, a sleep efficiency >85% is rarely achieved in these types of studies, even without respiratory events.

[split_city]

Ok, I have done a very quick calculation of sleep efficiency within each cuff condition. Correct my calculations if they are wrong. I calculated sleep efficiency as: sleep (in epochs)/total epochs under each cuff condition. This is what I got:

Deflated: 69.1+/-5.1%
Mid: 65.2+/-4.4%
Max: 59.3+/-4.6%

There was no significant difference in sleep efficiency (p=0.132)