flow limitations expressed as an index?

[cathyf]

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!

[2SleepBetta]

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.

   

[2SleepBetta]

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)

[2SleepBetta]

This post has both an image and a data analysis demonstrating similarities and differences between Resmed flow limitation flags and measured actual breathing volume reductions from flow limitations (the latter as distinct from the FL symbol which can signify up to 3 other matters that may or may not involve a tidal volume drop).

My position is that what we do here and all sleep medicine does, or purports to do, is work to help people use all their PAP devices and good sense to achieve the  healthful and restful ventilation their bodies need to live and thrive: in 9 words, get their regular  tidal volume needs met in sleep. 

This post was motivated: 

1. Mostly to check whether simple addition of the Resmed FL unit severity-seconds, 0.01,  would produce, as I expected (and it does), the summary values for FL as are shown at left of our OSCAR curves. 

One graphic, with an OSCAR view, shows exactly that using some real sleep data of mine from years back. The green encircled items are on point.

2. Partly by some skepticism about conclusions in posts 39 and 40 of this thread (others too, as I recall). The tenor of those posts is that the FL flags are a dubious scaling of mixed values and cannot be made into anything intelligible, so a better summary of them, as was requested in the OP, would be worthless or worth little. 

I think the OP had a good suggestion and what I have done here shows the meaning or basis of what is already displayed in our OSCAR summary. But the OP and all subsequent posts do not answer what breathing deficit arises from the duration of flow limitations and FL indicators of all severity levels. About all that newly comes to mind for me is to borrow the drop count technique as is presently used to indicate heart rate and and SpO2 drops BUT the amount of either programming work or spreadsheet work such would require is prohibitive.

The other graphic portrays another member's flow rate (FR), real measured tidal volumes (TV) and  real measured tidal volume losses (TVd) to flow limitations. Further, the concurrent Resmed flow limitation flag values, FL, overlie the measured TVd losses for direct comparison.

Ideally, at least a  mask pressure curve and a showing of respiratory rate (RR) or duty cycle (dC) curve would also accompany these graphs. The corresponding dC curve and Inspiration time curves, as I recall, were recently posted in one of the below referenced Main Forum or Software threads. Those would help assess the three periods of largest disparities between FL and TVd. (A chore for another day and post.) 

Those interested and looking for more help with these matters may find it worthwhile to read the later, related, previous posts in my threads "Call for Excel help...." in the Software Forum and "Low AHI<1 . . " in the Main Forum. Posts with suggestions, criticism and questions, of course, are welcome.

         

[selfcoacher]

You have to produce a more controlled environment for your data experiments. Leaks distort your data, so you have to either fix all your leaks or ignore data with leaks present. If using nasal pillow, you have to mouth tape in order to avoid mouth breaths or expirations. Then you have the issue with EPR at incorrect times. Then you have the resmed corrections of flow rate curve which are a blackbox.

There are several factors that you should optimize therapy for. Apneas/hypopneas which involve desaturations for the most part. Desaturations are easy to measure. I use viatom/wellu O2ring and contec RS01 has oximeter as well. The contec has more sensitive data at 1s. Viatom claims to record at 1s, but presents at 4s, so a lot of Reras and hypopneas might be missed. O2ring imports in Oscar which is great as it provides O2, heart rate and movement data. Most therapies resolve any major desaturations.

Second stage of therapy optimizations which most of you seem to be tackling is the RERAs or Hypopneas without desaturation. These result in altered flow rate curve along with arousal. You can measure arousal via EEG or you can assume arousal via chin EMG (maybe you can try accelerometer attached to chin). You can assume arousal via movement as you cannot have movement without EEG arousal. For the more minor arousals you can approximate them via heart rate data as you will have 10%+ heart rate swings, so 5-6bpm increase. O2ring helps with both movement and heart rate data.

For O2 data I prefer the contec RS01, but it does not import in Oscar, which is a major drawback. Also, it provides 0 pressure flow rate curve that does not seem to be too altered in terms of filtering, so closer to raw nasal pressure data. It is just nasal pressure canula, so you still need to mouth tape in order to control for mouth breathing/leaks. You also get heart rate and PPG graphs.

For EEG, I use the Dreem 2, which is no longer sold to consumers. You get a decent hypnogram which imports into Oscar, but it is useless for heart rate, O2 and breathing data. It provides sleeping position data, but does not import in Oscar. It is useless for micro arousals/ RERAs. The hypnogram is decent in terms of accuracy, so it is a good metric in terms of optimizing for DEEP and REM sleep total time. Not very useful for fragmentation metrics. They do not sell to consumers, but they have a research version that provides raw data that you can analyze yourself. Alternatively, you have MUSE S with which I believe there is a way to get the raw data via third party apps and then if it is decent quality you can process it and score it in a separate software. I am not sure going the EEG route would be worth it for you as I pointed out you have many other proxies for arousals. MUSE S and DREEM 2 hypnograms blackbox auto scored hypnograms might be decent if you want to optimize for deep and REM sleep total time that can be affected by actual flow limits.

Bedside threshold sound recordings via phone apps or video recordings are also decent for digging deeper and are very cheap methods that can be employed.
Which devices currently import sound metrics into Oscar? I have seen Snore labeled Oscar charts here.

To simplify, most of your arousals will have either movement or heart rate spike. Once you mark those, you can zoom in on your flow rate and other data in order to try to determine if they were respiratory related or not. Try to minimize them and if you still have actual flow limits and feel bad than you can go the EEG route and see if the flow limits prevent you from entering or severely fragment your deep and REM.