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flow limitations expressed as an index?
#61
RE: flow limitations expressed as an index?
(10-01-2021, 06:58 AM)pholynyk Wrote: It's important to remember that the sensors in the machine only measure pressure and total flow - in fact the total flow is calculated from the pressure differential across a known obstruction. Every thing else is calculated. I like to think of the breathing as ripple riding on the steady state venting of the mask. The venting of course varies with the pressure, and ResMed must assume some standard vent curve; also EPR complicates things. And transient leaks change things even more.
So suspecting the flow rate curve gets mangled by transient leaks is not unreasonable.

As an FFM wearer who often manages zero leaks, I'm also suspicious of what's going on inside the reasonably closed system where mouth leaks end up contained in the air flow. We have this picture of this "alternating current" of air being sucked into the lungs and then pushed back out. But we are measuring the pressures at the machine, and the mouth/nose/throat are between the lungs and the machine, and are between the lungs and the mask, for that matter. If my cheeks are inflating and deflating in some totally random pattern, that superimposes a large amount of noise. If I have a partially obstructed upper airway then the air is bouncing off the obstruction, too, and probably from both sides.

I can certainly see that what's happening is totally confusing the machine's calculation of respiration rate, because the noise is crossing over zero rapidly -- the phrase "doesn't know whether it's coming or going!" seems particularly appropriate!
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#62
RE: flow limitations expressed as an index?
If you read or scan nothing else below, just take a look at the two linked papers and attachment. If interested after that, there is (should be) some context below.

Two beginning "Givens" for this straying post in this thread about FL summarization:

1.     I could not agree more with pholynyk's point that pressure change detection--whether sensed from  motor speed or pneumatic changes - is ALL the firmest information we get from our devices (airway tools). All our talk here strives to optimize our TV realization across our sleep time. We work to serve that goal by attaining our best-personal pressure supply--recognizing that differences in PAP devices do better or poorer jobs than others for the various breathing irregularities.

2.     Our airways and  normal airflow control are horrendously complex for laminar airflow, let alone for our frequently turbulent airflows at persistent or episodic constrictions. This is because humans have a mix of firm airway and variably elastic or compliant airway segments that are themselves surrounded by similar tissue. For whatever reasons ( genetic and health endowments are two)  many of us have seemingly unique additional problems, chronic or temporary.  Moreover, most of the differing airways' lengths have a natural mucus covering that can contribute to constriction.  Excessive vacuum levels in collapsible walled tubes tend to cut down or off airflow--become actual elemental flow limitations not just a number,  idea, or couple words we use loosely.

Other air wave makers and responders: 

World class violinists, for example,  seek (inherit or buy?) a Stradivarius instrument, though to my layman's eye it will not look much different than a new public school device and make only noise in my hands. The maker's combination of  shaping, glues, assembly, and use of resonance of choice woods set it apart musically. Its varying sound wave, all alone, conveys a spectrum of signals and emotion: joy, order, chaos, anger, etc.. One kind of wave with lots of meaningful differences and it is perceived differently in and between persons.
 
Wind together with excessive elasticity and resonance explain failure of the Tacoma Narrows bridge (Galloping Gertie). Our airway and its surrounds have a rich variety of those properties to thank or regret, depending on varied conditions. https://dot.wa.gov/TNBhistory/bridges-failure.htm#6 . A quote there about complexity of natural phenomena, "The fact that engineers still argue about the precise cause of the Galloping Gertie's collapse is testimony to the extraordinary complexity of natural phenomena. Today, the 1940 Tacoma Narrows Bridge's failure continues to advance the "scientific method.""

Normal airways are far more variably resilient and complex than what is in my two examples, and they are also vulnerable to derangement. Few will read  this research paper which is mainly about mechanical properties of our upper airway  where most flow limitations and UARS arise. It's wealth of information explains where, when, how and what are most factors underlying SDB  here  https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3770742/ . The Abstract is short.

3.     I'm another out of pocket buyer of the VAuto (for its PS 4), after years of Autoset use (EPR 3) that virtually eliminated OA, but not FL. I maintain that the disparaged Autoset has a huge place in OA therapy as it did for me, though it is unused now. It was not designed for the most exotic OA case and it may have even the VAuto's capabilities that are locked out, inactivated functions (like much equipment and software have long had), as "jailbreak" tinkers claim. But there is little basis for continually faulting the device for its failure to handle pathologically extreme breathing cases of my own (down to almost nothing now thanks to VAuto) or among Kings or Queens of Autoset FL or other SDB land.

4.     Further, it has long been my position (after my dim light bulb lit up) that the Autoset and VAuto write "trouble" signatures in the tips of the inspiratory wave for all to read  a 1,000 ft up, not 30,000 ft. And yes, imperfect teasing out of pronounced cardioballistic (CB) effects make wave tip reading difficult and our findings uncertain. Long uncertain, l can't be sure that the central drop in the M-tip of the I-wave is or is not CB effect and neither are the Autoset or VAuto sure in many cases; the dip gets flagged part of the time when occurring once in isolation from other FL, many times not at all.

5.     Re the graphics cathyf posted just above. My take is a "shot not in complete darkness" being better informed  now than before and commenting sensibly, I hope, to the extent I've understood Geer 1 and SleepRider in this and other cases:  Those  graphics show  luxurious CB not just in low-flow endings of E-waves, but  in some or all the M-tips, and in the curved butt rests of outdoor canvas chairs, and  all "Chairs", and in the bottoms of more "Scooped" (concave topped)  I-waves.  IMO, the  butt fitting chair seats and, especially the bottoms of scoopings  of negative effort dependence (NED) are impressionable attractors of yet more algorithm confusing CB and all derived signals of APAP go awry leaving only the pressure variation evident  in a chaotic FR. Yes, this is according to my understanding (misunderstanding?) of  our best analysts' dissections of FR, but if wrong it's all my error. 

6.  From the paper linked above the graphic below is an illustration of NED scooping between waves and as it develops in one wave. Real NED is when an increase in muscular efforts to draw an inspiration will not increase airflow into lungs. But near NED, I assume, can be incipient or intermittent just as is true of troubling flow limitations, fL, below Resmeds' FL flagging threshold; such fL are often only indirectly felt in poor sleep and its arousals. My guess is that the lower illustration in the attachment depicts wave stage progression with a stage not all that different from what cathyf shows if CB effect were superimposed. There is in those graphs the initial high flow rate and peak with irregularity from CB or other airway disturbances as flow slows nearing the axis. As cathyf and others observed, the waves episodically become wildly chaotic and the device loses track trying to execute normal responses and apparently makes chaos worse. The sharp FR peak is a critical time where airway passages constrict and there is high turbulence at the narrows. After the peak we see flow restrictors (and CB?) respond to the turbulence and to  the higher breathing vacuum at peak flow.

Assessment of cathyf's possible suffering of near or actual NED,  is a driver of my continued (requested) work on her example case. The goal is to see what her inspiratory efforts were breath by breath; how high was her breathing "duty cycle", dC , (the fraction of her total single breath time that was inspiratory time). That information can be compared to her coincident, parallel FR, FL, TV and estimated fractional losses of TV for the same sleep period, which has recently been presented in this and another thread  at AB. Further, there are indications in sleep literature of typical dC to use as our guideline (I've seen nothing about use of the more erratic I/E times ratio) . For a guideline example, one indication was that sleepers' dC is about 0.3, the wakeful's are about 0.4. Accordingly, if we see a sleeper at continually 0.4 or more, we know they are doing a lot of unrestful work--if not in NED--much as if they were awake or physically working.

   
I have no particular qualifications or expertise with respect to the apnea/cpap/sleep related content of my posts beyond my own user experiences and what I've learned from others on this site. Each of us bears the burden of evaluating the validity and applicability of what we read here before acting on it.  (Disclaimer use permitted by sheepless)

 
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#63
RE: flow limitations expressed as an index?
I have long intended to correct my statement above, "Real NED is when an increase in muscular efforts to draw an inspiration will not increase airflow into lungs." But I delayed thinking I'd have more than this correction to post. 

The statement failed to state that increased inspiratory effort to draw in air would reduce rather than increase airflow when one is in the technical NED breathing state. 

NED and "negative effort dependence" matters are easily found online.

Here is one example: "Negative effort dependence (NED), decreased airflow despite increased driving pressure, has been proposed as a specific obstructive sleep apnea (OSA) phenotypic characteristic."

The source:  Feedback modulation of surrounding pressure determines the onset of negative effort dependence in a collapsible tube bench model of the pharyngeal airway - PubMed (nih.gov)
I have no particular qualifications or expertise with respect to the apnea/cpap/sleep related content of my posts beyond my own user experiences and what I've learned from others on this site. Each of us bears the burden of evaluating the validity and applicability of what we read here before acting on it.  (Disclaimer use permitted by sheepless)

 
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