[quote="Velbor"]As an invited, but not necessarily welcomed, guest at this cocktail party (per page 18 ), I will now exercise my boorish freedom to barge into your conversation, asking naive questions and making uneducated comments. You have been talking about OSA and CPAP models, and that has caused me to think (a rare and dangerous condition) and question the models in my own head.
The principal model in my head is that of the long limp balloon and the "pneumatic splint." Can't suck through a limp balloon (OSA?). But you can blow through it (CPAP?), and thereby it is "held open" (pneumatic splint?). I have a problem with this model, and I might even hope that responding to me ("If you can't explain it so a child will understand ....") might be helpful for others as well.
The balloon model works because the pressure of blowing is effectively directed radially outward. The internal pressure differential is operative against the external atmosphere "pushing" radially inward on the balloon. But is this applicable to our upper airway structures? Does the neck "expand" as we breathe (as the chest wall does) or in response to CPAP? If the neck is more like a rigid tube (as it seems to me) than like a limp balloon, what is "radial" pressure "pushing" against? (I know that the words do not do justice to the physics.) Against "soft tissue"? But where is the pressure differential? Gobs of grease inside a rigid tube are not "flattened" by increasing pressure in the tube. Is CPAP "squeezing" blood and fluids out of the tissues by its radial pressure? Possible, but I've never heard THAT as the proposed mechanism of CPAP efficacy.
Or put another way: does the upper airway "collapse" due to some "radial" pressure which is opposed by CPAP? The "collapse" of OSA is usually attributed to muscle relaxation and gravity. Tell me where there is a radial pressure differential, and perhaps I will be able to understand how CPAP can "push" soft tissues or a tongue muscle "out of the way". There is a difference, I think, between a rigid tube (from the perspective of radial pressure) with "movable" and possibly occlusive movable "goop" or "growths" along the inside wall, and a balloon.
Or put yet another way: does the negative pressure within the chest on attempted inspiration (with respect to the outside air) CAUSE a "radial" collapse of the upper airways? If so, where is the "outside" pressure acting radially on which "flexible" parts of the neck?
Being of limited imagination, I am having trouble visualizing OSA as a pressure-caused radial collapse of the upper airways, and therefore I am having trouble visualizing CPAP working as a radially-oriented "splint". If the airway "collapse" of OSA is due to the physical movement of "attachments" inside an otherwise relatively rigid tube (from the perspective of external pressure), i find it hard to see how CPAP, viewed as operative radially, can "expand" anything, whether immediately or preemptively.
So .... if not radially (assuming that anything I have expressed above makes any sense at all), does CPAP work by exerting its pressure "axially," along the length of the upper airway? Here, at least, I can find pressure differentials, with respect to the flexible-walled chest and the lungs. Does CPAP work, then, by its pressure differential (with respect to the negative pressure within the thorax on inspiration) "pushing axially downward" (i.e., toward the lungs)? Would loose floppy tissue, or tongue protuberances, be "bent" (rather than "lifted") out of the way, because their bases are "fixed" to the "rigid" upper airway wall? (The vectors of such movement would have a radial component! But not due to a radial "pressure" differential!) And once air is moving, would the dynamics of the "wind" play a role?
And here I stop, because my imagination and my knowledge of physiology and physics, perhaps already long exhausted and inadequate, comes to an end. Corks? Eggs? Pneumatic splints? Someone, please, take over.
Finally, to offer hopefully some socially-redeeming value to my presence at this cocktail party, I offer the following link which seems to me to be fairly current (2008), reasonably good, and hopefully new to you:
http://medind.nic.in/iae/t08/i1/iaet08i1p137.pdf
Overview and Implications of Obstructive Sleep Apnoea
Hanish Sharma and S.K. Sharma
Obstructive sleep apnoea (OSA) is a leading public health problem both in the developed and developing nations. However, awareness regarding diagnostic options, management and consequences of untreated OSA remains inadequate. In developing nations, the resources for adequate sleep medicine facilities are scarce. Therefore, there is a need for low cost, simple and accurate diagnostic and therapeutic modalities exists. Untreated OSA leads to excessive daytime sleepiness, diminished performance and an overall poor quality of life. The role of OSA in promoting insulin resistance, atherosclerosis, hypertension and a procoagulant state has now been established. Newer insights into the biochemical and genetic mediators of OSA have raised hopes regarding the development of a “cure”. However, as of now, continuous positive airway pressure (CPAP) therapy remains the first-line treatment. Though its use improves the quality of life as well as metabolic derangements observed in OSA, patients’ acceptance remains low. Its high cost and long-term use are also cumbersome. Newer modes of delivering CPAP, oral appliances and upper airway surgery are the other options available. It is hoped that their appropriate use to increase patients’ compliance may improve the quality of life as well as provide a survival benefit.
[Indian J Chest Dis Allied Sci 2008; 50: 137-150]
someday science will catch up to what I'm saying...
