Flow limitation: when are they considered significant?

[tan]

I have seen recently people complain that they don't sleep well even if their AHIs are below 1. There may be other factors like meds, sleep hygiene, mask leaks, GERD, etc. But rarely do their FLs charts come into picture.

In reviewing some of my old SleepyHead charts, I frequently encountered that relatively low flow limitations could drive pressure up:

[Sleeprider]

Flow limitations and snores are the drivers of pressure increases. I include Flow Limitations in the Events graph so they are marked. File/Preferences/Events, and check the box next to Flow Limitations.

[tan]

Flow limitations and snores are the drivers of pressure increases. I include Flow Limitations in the Events graph so they are marked. File/Preferences/Events, and check the box next to Flow Limitations.

It doesn't look like those settings have any effect for my type of machine. The only thing I can rely upon is the Flow Limitation chart.

Anyway, my point was that machine consider even low flow limitation significant enough to drive pressures up, a fact which may often go overlooked, if only AHI is in the picture.

[palerider]

I have seen recently people complain that they don't sleep well even if their AHIs are below 1. There may be other factors like meds, sleep hygiene, mask leaks, GERD, etc. But rarely do their FLs charts come into picture.

if you read posts in the forum, you'll see that this is extensively discussed.

four things cause pressure to increase, apneas and hypopneas, after the fact, and snores and flow limitations. the machines can't "power through" apneas so they don't raise pressure until after.

snores and flow limits, because they indicate a failing airway, will raise pressure faster in an attempt to avoid collapse resulting in an apnea or hypopnea.

[tan]

I have seen recently people complain that they don't sleep well even if their AHIs are below 1. There may be other factors like meds, sleep hygiene, mask leaks, GERD, etc. But rarely do their FLs charts come into picture.

if you read posts in the forum, you'll see that this is extensively discussed.

four things cause pressure to increase, apneas and hypopneas, after the fact, and snores and flow limitations. the machines can't "power through" apneas so they don't raise pressure until after.

Right, and people usually pay attention to the first two out of the four and still occasionally and erroneously cite that anything less than 0.4 on FL stats (95%) is not a concern.

snores and flow limits, because they indicate a failing airway, will raise pressure faster in an attempt to avoid collapse resulting in an apnea or hypopnea.

Does it mean that pressure increase should be limited or that the minimum pressure should be increased?

[Pugsy]

Does it mean that pressure increase should be limited or that the minimum pressure should be increased?

Usually it's the minimum pressure (if using auto adjusting mode) or EPAP if using bilevel is what needs to be increased to better help hold the airway open in the first place and thus prevent the partial collapse of the airway that a FL is a warning sign to maybe be happening. Flow limitations don't always grow up to be full grown OAs or hyponeas but they can grow up and that's why the machines will try to respond to their warning signs with more pressure.

[tan]

Does it mean that pressure increase should be limited or that the minimum pressure should be increased?

Usually it's the minimum pressure (if using auto adjusting mode) or EPAP if using bilevel is what needs to be increased to better help hold the airway open in the first place and thus prevent the partial collapse of the airway that a FL is a warning sign to maybe be happening. Flow limitations don't always grow up to be full grown OAs or hyponeas but they can grow up and that's why the machines will try to respond to their warning signs with more pressure.

and if FLs don't grow into apnea or hypopneas, they can be on their own harmful, can't they?

[Pugsy]

and if FLs don't grow into apnea or hypopneas, they can be on their own harmful, can't they?

Possibly.
I think that is where we begin to suspect UARS when we see FLs and low AHIs and people still complaining of feeling like crap or poor sleep quality or truckloads of arousals.
Can FLs be a problem or harmful?..sure but just like everything else with CPAP therapy there aren't any absolutes and it shouldn't be assumed that everyone has a huge problem with FLs because sometimes near total annihilation creates problems also and not every FL causes harm.

Clinical correlation plays a big factor.

[Morbius]

...erroneously cite that anything less than 0.4 on FL stats (95%) is not a concern.

Who said that?

[tan]

...erroneously cite that anything less than 0.4 on FL stats (95%) is not a concern.

Who said that?

You didn't. But some people thought you did and cited accordingly

[Wulfman...]

Doing some Google searching will produce LOTS of stuff to read.

Here are some of the excerpts from documents I've saved over the years include the following:

Den
.

Flow Limitation - the partial closure of the upper airway impeding the flow of air into the lungs.


However, quantifying the magnitude of flow limitation is difficult, because the conventional concept of airflow resistance (or its reciprocal conductance) is not directly applicable during flow limitation.


During the flow limitation event, only a slight decrease in flow occurs during each inspiration.


The contour of inspiratory flow tracing from a PAP system can be used to infer the presence of elevated upper airway resistance and flow limitation, and this contour appears to be the simplest vari­able that best correlates with the lowest esophageal pressure during PAP titration.


Reduction of this resistance has been demonstrated by increasing pressure until esophageal pressure swings (if measured) or the shape of the inspiratory flow limita­tion curve are normalized, or by increasing pressure by 2 cm H2O but no higher than by 5 cm H2O.


Flow limitation as a noninvasive assessment of residual upper-airway resistance during continuous positive airway pressure therapy of obstructive sleep apnea. Condos R, Norman RG, Krishnasamy I, Peduzzi N, Goldring RM, Rapoport DM.


Patients may experience periods of flow limitation that do not generate neuro-cortical arousal. This is particularly common during slow-wave sleep when the arousal threshold is depressed. In the absence of arousal, these periods probably do not represent clinical disturbance.


QUESTION 8: What is flow limitation and what does it look like?2
During inspiration, the collapsibility of the upper airway causes a Starling resistor-like behavior and results in a maximum flow, regardless of increases in effort. The normal “sinusoidal” inspiratory airflow becomes flattened (develops a plateau). The incomplete airway obstruction also causes inspiratory time to increase. Overall, this appears as a flattening of the waveform and is typically seen in breaths of decreased amplitude (Figure 8.2). These events are usually associated with increased respiratory effort and may represent either hypopneas or RERAs. To correctly see this flattening, a time constant setting of 3 – 6 seconds (low frequency filter 0.01 - 0.03Hz) should be established.


From Respironics' Auto w/C-Flex Algorithm Reference Guide

FOUR PARAMETERS USED IN DETERMINING FLOW LIMITATION

1. Roundness, deviation from sinusoid with same rate and peak
2. Flatness, deviation from middle mean flow Middle is from 20% to 80% of inspiration
3. Peak Flow, peak inspiratory flow
4. Shape patterns
These parameters are monitored simultaneously
Long term trending (minutes) and short term trending (last 4 breaths) calculations are performed and compared

KEY POINTS

•This flow limitation analysis will cycle continuously throughout the night
•Utilizes “statistically significant” changes approaching 10% change from the baseline flow signal
•Basic premise of Pcrit & Popt searches is to evaluate the profile of the patient flow waveform for improvement or degradation

.

[tan]

Doing some Google searching will produce LOTS of stuff to read.

Here are some of the excerpts from documents I've saved over the years include the following:

Den
.

Thanks, but how to apply this at home for regular people without sophisticated equipment? How much should pressure be increased? Should one keep increasing, if tolerated, until the machine stops doing the same?

[Morbius]

Here are some of the excerpts from documents I've saved over the years include the following:

What?

You did not save this classic post from April 2005?

Mountainwoman, early PB 420e marketing literature touted IFL1 and IFL2 as being special functional parameters aimed at UARS. Yet IFL1 and IFL2 are merely on/off switches for the two algorithmic triggers dealing with: 1) flow limitation runs, and 2) hypopneas that are concomitant with flow limitation runs (respectively). Interestingly, the other “modern” AutoPAP models also trigger on flow limitations, they also aggresively trigger on concomitant hypopneas, and they tend to very cautiously treat (via proactive techniques) non-concomitant hypopneas for fear of pressure-inducing central apneas.

So what’s the difference with the 420e design relative to UARS, then? My hunch is that the difference lies in how very aggressively the 420e will trigger on and elevate pressures when flow limitations are detected (via the IFL1 trigger). So aggressively, that more than a few 420e users have had to turn IFL1 off. There are actually two ways to turn IFL1 off: 1) within the environs of the Silver Lining 3 software, or 2) directly from the 420e’s LCD control panel (by setting “FL” to 0 versus 1). There is no way to turn IFL2 off from the 420e’s LCD control panel, however. In my way of thinking that probably implies that IFL1 must be turned off more often than IFL2. The 420e can be very pressure-aggressive relative to attempting to eliminate flow limitations which are believed to be associated with UARS.

Yet flow limitations can occur for an entire variety of reasons, many of which are not associated with UARS. Some UARS patients receive adequate elimination of their upper airway restrictions via air pressure, and yet others do not. When a UARS patient does happen to receive efficacious treatment from air pressure therapy, that implies the UARS patient’s upper airway resistance was successfully eliminated via PAP’s inflation of the elastic portions of the upper airway. Yet it is entirely possible that upper airway impedance can be high for rigid structural reasons entirely unrelated to soft tissue. In this latter UARS case, PAP inflation of the upper airway will not completely (if at all) alleviate UARS symptoms—assuming the UARS diagnosis adheres to the most common etiology attributed to UARS.

That most commonly accepted etiology of UARS entails exactly that which the acronym implies: Upper Airway Resistance Syndrome. Specifically this most commonly accepted UARS etiology entails extreme flow limitations that result from extremely high impedance in the upper airway—most often nasal impedance. The etiological distinction doesn’t stop there, however. Because the upper airway is so severely flow-restricted, the diaphragm must create extreme negative pressure on inhalation in order to draw in an adequate volume of air necessary for normal respiration. When the diaphragm creates this excessive negative pressure, it can not only be measured all the way into the esophagus, but the UARS patient is typically pestered with negative-pressure-based cortical arousals throughout the night. The UARS specific etiology of sleep disordered breathing actually stops there for some patients. However, if the UARS sourced negative diaphragm pressures are of an extreme magnitude, then the airway itself can start to laterally collapse during inspiration, much as a paper straw collapses when you try to draw a very thick milk shake through it. If that lateral airway collapse is only partial, then a UARS-specific hypopnea tends to result. If that lateral airway collapse is a total collapse for adequate duration, then a UARS-specific apnea results. These UARS-specific hypopneas and apneas are quite different than the classic etiology of hypopneas and apneas that entail simple sagging of the soft palate.

In summary it is the extreme negative diaphragm pressures that are required in order to overcome the extreme upper airway impedances that cause both cortical arousals and obstructive airway events. A UARS patient might have: 1) UARS events only, 2) UARS events coupled with UARS-based lateral-airway-collapsing apneas and/or hypopneas, 3) UARS events coupled with classic soft palate apneas and/or hypopneas, 4) UARS events coupled with both types of apneas/hypopneas, 5) UARS events coupled with any sleep disordered breathing and/or other concomitant sleep disorder known to modern medicine. In addition we said that the UARS-based upper airway restrictions may be soft-tissue related and thus air pressure responsive, or perhaps related to hard or dense structure airway characteristics, and thus likely nowhere near as air pressure responsive as the soft-tissue case.

Add to that the fact that many MDs simply diagnose UARS if the patient’s sleep events are exclusively/predominately flow limitations and/or hypopneas, and you likely have several failing airway etiologies attributed to UARS. When you put all the above UARS-related “ifs”, “ands”, as well as “buts” together, my very strong hunch is that the ability to achieve a total of four therapeutic combinations relative to IFL1 and IFL2 just may lend those diagnosed with UARS an edge in finding suitable/comfortable therapy. If a UARS patient happens to have air-pressure-unresponsive UARS events coupled with classic soft-palate-related apneas and/or hypopneas (which are generally very air pressure responsive) then that patient may fare better with IFL1 turned off and IFL2 turned on—-or quite possibly with both IFL1 and IFL2 turned off. The conjecture being that there are very likely quite a few combinational sleep disordered breathing etiologies related to UARS, and the ability to experiment with IFL1 and IFL2 combinations is in and of itself an experimental advantage for UARS patients in general.

Back then, this machine PB420E had this option called IFL1 which would attack FLs. Rarely/occasionally/frequently the pressure would max out (even if it was like 20.0 cmH2O) in the quest to beat the FLs into submission (it didn't).

[Morbius]

PB420E measured pressure proximally:





which certainly begs the questions:

• Is measuring pressure from within the machine even (relatively) accurate?
• If not, then will an aggressive FL attack, at least in some cases, be inappropriate?
• Does waveform filtering further compound the issue (what the machine sees and what you see are 2 different things)?

[Morbius]

Wow.

Coming up on the 10 year anniversary of the mountainwoman post.

I think we need to have a party!