May (or may not) convince you in regards to my studies :)

[split_city]

Ok, it seems that some of you are sceptical about my work. I can accept that given that a lot of what I said might sound like mumbo jumbo. Therefore, I thought I might provide you with some data from other studies which are relevant to my work, which may help you understand. I won't flood you with data and I'll take it one step (and one study at a time).

So a lot of you would be aware about my abdominal compression study. It seems that a few of you can't quite grasp the link between how abdominal compression may impact upon the upper airway. I totally understand if this is confusing. Therefore, I'll try and provide some useful data.

Now, I'm not going to go into any great details about my abdominal study. The main point to consider is that the increased pressure inside the abdomen, brought upon by abdominal compression, perhaps pushes the diaphragm up towards the head. I have been talking about the loss of tension on the airway following diaphragm ascent. However, movement of the diaphragm in this direction perhaps also reduces lung volume. Lung volume is known to decrease during anesthesia, which is partially attributed to the diaphragm moving upwards towards the head (this is still debated, but it has been shown to be true in some studies). So, we understand so far? Abdominal compression --> pushes diaphragm up -> lung volume goes down. It is known that if you reduce lung volume, the airway becomes smaller and more collapsible. This has been shown many times. So this perhaps explains my finding in the abdominal compression study i.e. airway became more collapsible when I compressed the abdomen.

So where is this data I promised you?

There was this study my Raphael Heinzer who looked at the effect of lung volume on AHI. While this study didn't look at abdominal compression, it kinda looks at the same physiological concepts as my study. Here is the abstract:

Effect of increased lung volume on sleep disordered breathing in patients with sleep apnoea.Heinzer RC, Stanchina ML, Malhotra A, Jordan AS, Patel SR, Lo YL, Wellman A, Schory K, Dover L, White DP.
Sleep Medicine Division, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. rheinzer@post.harvard.edu

BACKGROUND: Previous studies have shown that changes in lung volume influence upper airway size and resistance, particularly in patients with obstructive sleep apnoea (OSA), and that continuous positive airway pressure (CPAP) requirements decrease when the lung volume is increased. We sought to determine the effect of a constant lung volume increase on sleep disordered breathing during non-REM sleep. METHODS: Twelve subjects with OSA were studied during non-REM sleep in a rigid head-out shell equipped with a positive/negative pressure attachment for manipulation of extrathoracic pressure. The increase in lung volume due to CPAP (at a therapeutic level) was determined with four magnetometer coils placed on the chest wall and abdomen. CPAP was then stopped and the subjects were studied for 1 hour in three conditions (in random order): (1) no treatment (baseline); (2) at "CPAP lung volume", with the increased lung volume being reproduced by negative extrathoracic pressure alone (lung volume 1, LV1); and (3) 500 ml above the CPAP lung volume(lung volume 2, LV2). RESULTS: The mean (SE) apnoea/hypopnoea index (AHI) for baseline, LV1, and LV2, respectively, was 62.3 (10.2), 37.2 (5.0), and 31.2 (6.7) events per hour (p = 0.009); the 3% oxygen desaturation index was 43.0 (10.1), 16.1 (5.4), and 12.3 (5.3) events per hour (p = 0.002); and the mean oxygen saturation was 95.4 (0.3)%, 96.0 (0.2)%, 96.3 (0.3)%, respectively (p = 0.001). CONCLUSION: An increase in lung volume causes a substantial decrease in sleep disordered breathing in patients with OSA during non-REM sleep.

So to sum this up --> AHI was shown to decrease with increasing lung volume

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CPAPopedia Keywords Contained In This Post (Click For Definition): CPAP, AHI

[ozij]

Twelve subjects with OSA were studied during non-REM sleep in a rigid head-out shell equipped with a positive/negative pressure attachment for manipulation of extrathoracic pressure.

I understand that negative pressure within the shell was created in order to increase lung volume.

If that is so, the shell was sucking out the subjects' ribs, and fuctioning as a reverse "cpap": instead of positive pressure apllied to the obstruction from inside the airway, negative pressure was applied from outside the thorax.

Did I understand that description correctly?

O.

[tomjax]

Sounds like you have an in depth knowledge of our malady.

I would like a brief overview of the latest mechanism of reflux and how it is related to apnea.

Many different mechanism are floating out there. Some overly simple, some rather involved.
And why does PAP seem to relieve reflux in many people?

Thanks tom

[KAZ]

This might explain what happened to me and lead to complete respiratory failure. Due to undiagnosed SA I put on extreme weight which caused abdominal compression. Part of my rehab has been to lose the excess weight. The more weight I lose the better I can breath. Regards

[split_city]

I understand that negative pressure within the shell was created in order to increase lung volume.

If that is so, the shell was sucking out the subjects' ribs, and fuctioning as a reverse "cpap": instead of positive pressure apllied to the obstruction from inside the airway, negative pressure was applied from outside the thorax.

Did I understand that description correctly?

O.

Yes you understand the procedure correctly.

The group put each patient at their therapeutic CPAP pressure to assess the change in lung volume caused by the CPAP. They then used negative extra-thoracic pressure to induce the same increase in lung volume as what the CPAP did. Another part of the study involved increasing lung volume by a further 500mL above this.

One interesting point is that while AHI did decrease (compared to baseline)when lung volume was increased to the same level that therapeutic CPAP produced, the AHI was still quite high ~37. The group didn't mention what the mean AHI was when patients were on their therapeutic CPAP. I would predict that the AHI would have been much lower than 37. Therefore, this is likely to indicate two ways which CPAP maintains airway patency 1) By increasing lung volume (as shown in this study) and 2) CPAP acts as a 'splint' to open the airway by positive pressure. Increasing lung volume does help but splinting is also required to improve airway patency.

Here's something the authors discussed which relates to my work:

"Because the subjects we studied were overweight or obese
(like most patients with OSA), we suspect that their
diaphragm was pushed upwards (cranially) when lying on
their back. The negative extrathoracic pressure applied in the
lung almost certainly pulled the diaphragm and trachea to a
more caudal position, thereby increasing the traction on the
upper airway and making it less collapsible."

The didn't measure diaphragm position but the speculated that it moved towards the feet with negative extrathoracic pressure.

[split_city]

Sounds like you have an in depth knowledge of our malady.

I would like a brief overview of the latest mechanism of reflux and how it is related to apnea.

Many different mechanism are floating out there. Some overly simple, some rather involved.
And why does PAP seem to relieve reflux in many people?

Thanks tom

This isn't my area but I'll give it ago. Based on what I have read, reflux might occur commonly in OSA patients during sleep due to large pressure swings during an apnea. During these apneas, large negative pressures are generated in the chest. If the lower esophageal sphincter isn't wrapped tightly enough around the esophagus during these apnea events, some stomach acid may pass through this barrier.

Another study: Arousal in patients with gastro-oesophageal reflux and sleep
apnoea Eur Respir J 1999; 14: 1266±1270

This showed that reflux was common during the day in OSA patients but many reflux events occurred following an arousal, but not generally following an apnea event. I think a combination of obesity (increased pressure pushing stomach contents into the esophagus) and the large negative pressure swings during events may explain the higher prevalence of reflux in overweight OSA patients. I'm unsure of the prevalence of reflux in healthy-weight OSA patients compared to overweight individuals and overweight individuals with OSA. Perhaps members of this forum could help?

Nevertheless, it seems CPAP does help: Here is a study from a goup in Australia which looked at the effect of CPAP on lower esophageal sphinter pressure

Am J Physiol Gastrointest Liver Physiol. 2007 May;292(5):G1200-5. Epub 2007 Jan 18. Links
The impact of continuous positive airway pressure on the lower esophageal sphincter.Shepherd KL, Holloway RH, Hillman DR, Eastwood PR.
West Australian Sleep Disorders Research Institute, Department of Pulmonary Physiology, Sir Charles Gairdner Hospital, Nedlands, Western Australia 6009, Australia.

The lower esophageal sphincter (LES) is the primary barrier to gastroesophageal reflux. Reflux is associated with periods of LES relaxation, as occurs during swallowing. Continuous positive airway pressure (CPAP) has been shown to reduce reflux in individuals with and without sleep apnea, by an unknown mechanism. The aim of this study was to determine the effect of CPAP on swallow-induced LES relaxation. Measurements were made in 10 healthy, awake, supine individuals. Esophageal (Pes), LES (Ples), gastric (Pg), and barrier pressure to reflux (Pb = Ples - Pg) were recorded using a sleeve catheter during five swallows of 5 ml of water. This was repeated at four levels of CPAP (0, 5, 10, and 15 cmH(2)O). Pressures were measured during quiet breathing and during the LES relaxation associated with a swallow. Duration of LES relaxation was also recorded. During quiet breathing, CPAP significantly increased end-expiratory Pes, Ples, Pg, and Pb (P < 0.05). The increase in Pb was due to a disproportionate increase in Ples compared with Pg (P < 0.05). During a swallow, CPAP increased nadir Ples, Pg, and Pb and decreased the duration of LES relaxation (4.1 s with 0-cmH(2)O CPAP to 1.6 s on 15-cmH(2)O CPAP, P < 0.001). Pb increased with CPAP by virtue of a disproportionate increase in Ples compared with Pg. This may be due to either reflex activation of LES smooth muscle, or nonspecific transmission of pressure to the LES. The findings suggest CPAP may make the LES less susceptible to reflux by increasing Pb and decreasing the duration of LES relaxation.

[Patrick A]

Now I really do need more Bushmills and Coffee !!!!!

[roster]

............. I'm unsure of the prevalence of reflux in healthy-weight OSA patients compared to overweight individuals and overweight individuals with OSA. Perhaps members of this forum could help?

...........

As of this moment there are 20 people responding to a post (viewtopic.php?t=22016&postdays=0&postorder=asc&start=0) indicating that they have BMI of 24 or less.

Count me with a BMI of 23 and GERD.

Maybe some others will chime in.

... and then there may be many "skinnies" with silent GERD who are undiagnosed. It took me a long time to get a diagnosis of asymptomatic GERD.

[split_city]

Now I really do need more Bushmills and Coffee !!!!!

Don't forget the popcorn!

[Patrick A]

I do not like popcorn unless it's carmel corn

[Patrick A]

I had Gerd or Acid Reflux, way before I was ever diagnosed with OSA and a long time before I weighed over 175 pounds.

Of course if you lived on jalapeños and every other spicy and or greasy food you could find you would have Acid Reflux too, if you weighed less than 175 pounds I did.

I know it's hard to beleive that at one time I weighed less than 175 pounds

[jennmary]

I have had problems with GERD or reflux since infancy. The doctor had me on codein for the pain and my mother took me off because she found out it was addictive. Back then they didnt have very good treatment for infants with this kind of problem. I grew up with my mother cooking special food most of the time...and learned to sleep sitting up if I was going to eat something bad. I was underweight most of my life and have only been overweight for the last 3 years (since I was pregnant with my daughter).

[kurtr]

Split,

I find your posts interesting.
Is this situation reversable?
Ie; if a person loses the weight that is causing the abdominal compression, does the diaphram function and airway return to "preweight" condition?

Thanks,
Kurt

[split_city]

Split,

I find your posts interesting.
Is this situation reversable?
Ie; if a person loses the weight that is causing the abdominal compression, does the diaphram function and airway return to "preweight" condition?

Thanks,
Kurt

Hi kurtr,

There's three parts to ths question:

1) General weight loss --> in many cases (definately not all), weight loss does improve OSA and even cure OSA. Weight loss is accompanied by a reduction in pressure inside the abdomen, a decrease in fat around the neck and an increase in resting lung volume back to normal values. All help to reduce OSA.

2) Weight loss around the abdomen --> no-one has specifically looked at the effect of this in regards to OSA severity. I'm sure that losing weight from around the abdomen may help, but not necessarily cure OSA unless weight around the body was also lost as well. Who knows though? Nevertheless, losing weight from around the abdomen would certainly relieve pressure acting on the diaphragm, therefore reducing the degree of upwards displacement of the diaphragm.

3) Simply reducing pressure inside the abdomen or reducing pressure acting on the diaphragm --> this is something that we have very, very briefly thought of as a 'treatment.' Simply sleeping in a tilted position (while on your back) does improve OSA. This is perhaps due to less 'flopping back' of the tongue OR maybe because there is less pressure acting upon the diaphragm in this position.
There have been a few studies which used a device to reduce pressure inside the abdomen to reduce the symptoms of another condition (forgot what that was but I think it had something to do with bloodflow to the head and headaches). This device was a fibreglass shell which was connected to the abdomen. A 'vacuum' was connected to it and negative pressure was created inside the shell. This bascially sucked the abdomen up, relieving pressure inside the abdomen. I think a few groups decreased pressure inside the abdomen by about 5cmH2O (might have been higher). The patients could tolerate this device pretty well. Maybe a treatment option for OSA patients? However, I definately wouldn't say throw away your CPAP machines yet!!