Link between OSA and the "beer gut"

[Ergin]

As a result everybody can predict his/her pressure by measuring the thickness of the fat tissue on the abs.
For example I have about 5cm (2") fat on my abs.
If the fat below the abs about 2cm, my total pressure is about 7cm H2O.
My APAP pressure range is 10.5-12cm.

So the medical people should explain why I need the extra 5cm H2O pressure during REM.

Are you trying to say that APAP pressure should be the same as abdominal pressure? Did you get this 5cmH20 number by subtracting 12 (APAP pressure) minus 7 (abdominal pressure)?

I am trying to say that, by laws of physics, abdominal pressure is predictable by simply measuring the thickness of the abdominal fat.

You are right, during REM my APAP goes to 12cm H2O that's still 5cm H2O higher than my abdominal pressure.

Every patient is different, in my case, I conclude that my abdominal fat is not the sole reason for my OSA.

By simple logic, the static pressure can not be the sole reason for OSA, because the above calculation only holds for the case of a lying down patient. OSA persists even if one sleeps on side, where the abdominal pressure is zero. In this case the abdominal muscles are still in trouble due to excess fat tissue, which they have to swing together.

Well, there is good experiment one can do to study the dynamical effect of the fat tissue on OSA. If one strengthens his abdominal muscles by regular excersize, then he should observe an improvement in OSA. For the next 30 days I will train my abs and check my average APAP pressure and SI. Others are welcome to join the experiment and share the feedback.

[split_city]

As a result everybody can predict his/her pressure by measuring the thickness of the fat tissue on the abs.
For example I have about 5cm (2") fat on my abs.
If the fat below the abs about 2cm, my total pressure is about 7cm H2O.
My APAP pressure range is 10.5-12cm.

So the medical people should explain why I need the extra 5cm H2O pressure during REM.

Are you trying to say that APAP pressure should be the same as abdominal pressure? Did you get this 5cmH20 number by subtracting 12 (APAP pressure) minus 7 (abdominal pressure)?

I am trying to say that, by laws of physics, abdominal pressure is predictable by simply measuring the thickness of the abdominal fat.

You are right, during REM my APAP goes to 12cm H2O that's still 5cm H2O higher than my abdominal pressure.

Every patient is different, in my case, I conclude that my abdominal fat is not the sole reason for my OSA.

By simple logic, the static pressure can not be the sole reason for OSA, because the above calculation only holds for the case of a lying down patient. OSA persists even if one sleeps on side, where the abdominal pressure is zero. In this case the abdominal muscles are still in trouble due to excess fat tissue, which they have to swing together.

Well, there is good experiment one can do to study the dynamical effect of the fat tissue on OSA. If one strengthens his abdominal muscles by regular excersize, then he should observe an improvement in OSA. For the next 30 days I will train my abs and check my average APAP pressure and SI. Others are welcome to join the experiment and share the feedback.

[GeneS]

I think that we can figure out more things about sleep apnea by studying the physics of breathing and sleep apnea. That seems to be where these posts are heading. PV=nrt, bernules sp? energy laws. Free body diagrams of the lungs, airway inside and out, mouth, nose etc. Look at the various forces with and without cpap and what will affect them. Air Flow, friction losses etc. That is how I figured what the pressures had to be when breathing but I think we could figure out a lot more. I would imagine that someone is doing this.

GeneS

[split_city]

[quote="GeneS"]I think that we can figure out more things about sleep apnea by studying the physics of breathing and sleep apnea. That seems to be where these posts are heading. PV=nrt, bernules sp? energy laws. Free body diagrams of the lungs, airway inside and out, mouth, nose etc. Look at the various forces with and without cpap and what will affect them. Air Flow, friction losses etc. That is how I figured what the pressures had to be when breathing but I think we could figure out a lot more. I would imagine that someone is doing this.

GeneS

[GeneS]

_________________



One hot area of interest relates to ventilatory instability. If there are any engineers in the room, I'm sure you have heard about loop gain. There are now groups looking at the effect of a disturbance on the respiratory system and then looking at the response. For example, what would the response be to a few breaths of air with increased CO2? People with a high loop gain overcompensate while people with a low high gain hardly respond to the disturbance. High loop gain can lead to a cyclical breathing pattern (Cheyne Stokes breathing is an example). I'm not going to go into any great detail, but OSA patients tend to have a high loop gain. This high loop gain may perpetuate OSA.

I understand this somewhat but I am a civil engineer not an electrical engineer. My daughter is an electrical engineer and does signal processing so I will ask her about it. I guess there is more than one way to model this. I was thinking of statics, dynamics, and fluid flow. You could think of differential movements of the diaphram. Forces on the diaphram and outside of the lungs. (pv=nrt) lung pressure would drop below atmospheric so a pressure gradiant would develop from the mouth or nose to the lungs. Air would flow from high (atmosphere)to low pressure(lungs). while flowing Energy in lungs + head loss from flow = energy in atmosphere. head loss from flow could be friction, expansion, contraction etc. etc. You could analyize inhaling and exhaling using small increaments and adding up the effect or integrating until you accounted for the volume of a breath ? There will be venturi effects, forces pushing on the outside of the airway when pressure drops while inhaling etc. When or can these forces cause the airway to collapse? I think a model like this could be developed and refined both inhaling and exhaling with a cpap machine and without. It could be calibrated by actually checking reqd cpap pressure and airway dimensions, restrictions or whatever to see what actually affects the reqd pressure.

I know that what I just wrote is a simplistic, not complete or all technically correct. It would take a lot of work but I am trying to explain the type of calculations I was talking about. There probably have been many new methods developed since I went to school. Now I sometimes do calculations for water systems, pumps etc. Not air or gasses. I do not know if compressible flow would have to be considered. Someone who works with airflow could do these calculations with less effort.

I assume that people have done this type of calculation before and tried to model breathing with and without a cpap.

GeneS
_________________

[Guest]

So the daytime cramps I used to get throughout my ribcage - front side and back - could have resulted from overusing the muscles at night trying to breathe? ie exerting my muscle pressure against those other pressures you're talking about?

[split_city]

So the daytime cramps I used to get throughout my ribcage - front side and back - could have resulted from overusing the muscles at night trying to breathe? ie exerting my muscle pressure against those other pressures you're talking about?

hhmm...don't know. A lot of factors could have contributed to those cramps.

[Guest]

If you can only study so much in three years you might learn how to spell apnea. There are many factors that contribute to OSA, only one of which can be weight issues. I am 5'11" and weigh 170, so I really don't think a weight issue would be present. As a matter of fact, mine is caused more by my jaw and tounge. I just don't think there is a "one size fits all" diagnosis for OSA, as there can be many factors that cause it. It's only a suspicion on my part, but the "beer gut" you refer to could be because of the sleep apnea causing lack of energy. Or the explanation could be simpler still: Drinking too much beer.

[split_city]

If you can only study so much in three years you might learn how to spell apnea.

It's spelt APNOEA here in Australia

[Bamalady]

split_city-

Thanks for telling us about David White. I have been trying to make my way through some of his work. The following quote is very interesting to me. I truly hope that the research people are doing will lead to greater understanding of this disorder. I need to read more about loop gain.

On the other hand, obstructive sleep apnea can develop as the result of a variety of physiologic characteristics. The combinations of these may vary considerably between patients. Most obstructive apnea patients have an anatomically small upper airway with augmented pharyngeal dilator muscle activation maintaining airway patency awake, but not asleep. However, individual variability in several phenotypic characteristics may ultimately determine who develops apnea and how severe the apnea will be. These include: (1) upper airway anatomy, (2) the ability of upper airway dilator muscles to respond to rising intrapharyngeal negative pressure and increasing Co2 during sleep, (3) arousal threshold in response to respiratory stimulation, and (4) loop gain (ventilatory control instability). As a result, patients may respond to different therapeutic approaches based on the predominant abnormality leading to the sleep-disordered breathing.

[split_city]

split_city-

Thanks for telling us about David White. I have been trying to make my way through some of his work. The following quote is very interesting to me. I truly hope that the research people are doing will lead to greater understanding of this disorder. I need to read more about loop gain.

On the other hand, obstructive sleep apnea can develop as the result of a variety of physiologic characteristics. The combinations of these may vary considerably between patients. Most obstructive apnea patients have an anatomically small upper airway with augmented pharyngeal dilator muscle activation maintaining airway patency awake, but not asleep. However, individual variability in several phenotypic characteristics may ultimately determine who develops apnea and how severe the apnea will be. These include: (1) upper airway anatomy, (2) the ability of upper airway dilator muscles to respond to rising intrapharyngeal negative pressure and increasing Co2 during sleep, (3) arousal threshold in response to respiratory stimulation, and (4) loop gain (ventilatory control instability). As a result, patients may respond to different therapeutic approaches based on the predominant abnormality leading to the sleep-disordered breathing.

[blarg]

Oh Snoredog, where are you?

His sig explains it all. He's right, just that science hasn't caught up with him yet. He's THAT smart.

[split_city]

I think his science has been "lost in translation"

[Snoredog]

split_city-

Thanks for telling us about David White. I have been trying to make my way through some of his work. The following quote is very interesting to me. I truly hope that the research people are doing will lead to greater understanding of this disorder. I need to read more about loop gain.

On the other hand, obstructive sleep apnea can develop as the result of a variety of physiologic characteristics. The combinations of these may vary considerably between patients. Most obstructive apnea patients have an anatomically small upper airway with augmented pharyngeal dilator muscle activation maintaining airway patency awake, but not asleep. However, individual variability in several phenotypic characteristics may ultimately determine who develops apnea and how severe the apnea will be. These include: (1) upper airway anatomy, (2) the ability of upper airway dilator muscles to respond to rising intrapharyngeal negative pressure and increasing Co2 during sleep, (3) arousal threshold in response to respiratory stimulation, and (4) loop gain (ventilatory control instability). As a result, patients may respond to different therapeutic approaches based on the predominant abnormality leading to the sleep-disordered breathing.

[split_city]

That's the best you could come up with? I've only been here for a week and even I know that's a poor attempt by you