Little Larissa - please read

-SWS wrote: I'm still trying to figure out exactly what functionality that model offers Laryssa that her current BiPAP model running as a BiLevel S/T does not already offer. The specifications and marketing literature from Respironics don't show any crucial differences that I can tell. And that's not to say there aren't crucial differences functionally embedded in the machines.

I don't think it will be very long before Laryssa can make good use of assured 200 ml volumes (the minimum assured setting). In the meantime if AVAPS is turned off I think we have all the machine capabilities as the BiPAP S/T you linked to (but could be wrong). And does that, then, translate to pretty much the same S/T capabilities the doctors can achieve with her current BiPAP autoSV model when configured that way (with the only exceptions of straight timed mode and AVAPS pressure control)?

The SV and PC (AVAPS Pressure Control) would be categorical derivatives of the BiPAP ST Grey Model. The unique SV and PC algorithms are the only thing that separate each from the BiPAP ST Grey Model. Both SV and PC can be switched off, returning each machine to BiPAP ST Grey Model mode, as you suggest. Interesting concept, if you ask me.

-SWS wrote:I'm also under the impression that the AVAPS model is everything the above linked BiPAP S/T model happens to be, with optional AVAPS that can be turned off or on (so $800 additional list price to have AVAPS capability):
https://www.cpap.com/cpap-machine/respi ... chine.html

So perhaps it makes more sense to wait until she can use 200 ml assured volumes, and let that be her next machine---if the doctors even think she needs it.

Price may become a factor. The BiPAP ST Grey Model is 1/2 the price of an SV. I'm assuming the BiPAP ST Grey Model is also 1/2 the price of an AVAPS.

-SWS wrote: In the mean time it would be nice to get a hold of the BiPAP S/T and AVAPS clinician's manuals to better compare capabilities.

Agreed. Or at least see how to set them up.

Banned

Before you guys send another machine down there, you might wanna consider a few points.

1. Why don't you ask Vergara et al what they think she needs, because
2. The degree of intervention far exceeds what everyone thinks they're trying to treat. Is it moderate OSA? Not the sole component with that degree of intervention for that duration of time. Central apnea as Vergara suggests? I don't see any evidence of that. Out of the blue ALTE's? You don't need NIPPV for that. Ventilatory failure? Due to what? Pulmonary disease? Maybe. Neuromuscular disease? Probably.
3. While AVAPS sounds appealing, since it is not known what's being treated, it is similarly not known if this would be appropriate either (we are assuming that Laryssa will grow to at least 25 kg.). Does whatever process she has include failure to thrive/grow? 200 ml as a target volume may not necessarily be the case if she doesn't grow into it, and/or if permissive hypercapnia is utilized (which is what could very well be happening now, whether you want it or not).
4. Another assumption is overall prognosis. Right, prognosis of what. The assumptions to date only consider her getting better, or at least remaining stable (the disease process has ceased, is in remission, or is reversible). If it is a progressive disease, then the eventual possibility of invasive ventilation appears, and then you're looking at a different machine entirely (LP 10, or LTV 950 if you're flashy). BTW, even though VPAP ST-A offers a far more appropiate range of parameters, it has a minimum age/weight requirement (40 lbs/7 years old)(OK, outside of mechanical ventilators and that thing, nobody really has an "accepted" pediatric NIPPV machine).

SAG

Thanks for weighing in with your opinions, SAG! Very much appreciated in my own opinion.

I think we're all in agreement that there's absolutely no point in blindly sending a different machine down unless there's sound technical rationale. SAG, I see you haven't ruled out obstructive apnea. That was the original diagnosis after the PSG. And I see where she has a tendency to sleep on her stomach---common sleeping behavior in response to obstructions. It is possible that Laryssa just may have a mixed etiology.

SAG wrote:The assumptions to date only consider her getting better, or at least remaining stable (the disease process has ceased, is in remission, or is reversible)

Not to confuse this thread's main focus of conversation with assumptions about prognosis:

As early as page ten I wrote:...a toddler with a potentially serious pulmonary and/or neurological disorder.

Two pages ago I wrote:However, oximetry monitoring without alarms may not be wise if the exact etiology and disease progression is still unknown.

Six posts above this one I wrote:My hunch is there's nowhere near enough to buy an AVAPS or volume ventilator should that scenario some day play out.

While I agree that the focus of our conversations have been largely optimistic, our assumptions have been rather quietly realistic all along. Regardless, thank you for reminding us that the prognosis is still unknown here. That realistic information needs to be shared in this thread. That information is much better coming from a health professional IMO. So thanks once again for sharing those realistic points of view.

Okay, I don't mean to sound fixated on the chewed mask issue....

But Nelson observed only a slight cushion crack on Laryssa's birthday and now significant deterioration from chewing. At that fairly rapid rate of cushion deterioration I'm thinking we're going to have to send down more than just one replacement cushion.

Banned, Nelson, et al--- how many cushion replacements are needed to get Laryssa by until the next supply interval (whenever that may be)?

AFAICT the Bipap S/T Grey Model is the basis for both the BipapSV and the AVAPS.

I have taken both the Bipap Grey model & Bipap SV apart & can't see any difference other than the software functionality.

Thus, a BipapSV can be run just like a Bipap Grey as the literature implies.

The third level PS (SV) support is an interesting extra that appears to have many benefits that go beyond those specifically claimed by Respironics (who I am sure are mindful of FDA approvals and what they can and can't claim in regard to an approved model).

So if Laryssa does well on the machine in Bipap S/T mode that is great. There may come a day when she is a bigger girl (perhaps just a year) where that SV facility may offer added benefits.

I sure can't see any good reason to take the BipapSV away & provide anything else at this time.

DSM

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CPAPopedia Keywords Contained In This Post (Click For Definition): respironics, bipap

-sws wrote:SAG, I see you haven't ruled out obstructive apnea. That was the original diagnosis after the PSG.

Right. But an obstructive index of 4.0 - 5.6 doesn't land you in a PICU for months on Pressure Support.

-sws wrote:

SAG wrote:The assumptions to date only consider her getting better, or at least remaining stable (the disease process has ceased, is in remission, or is reversible)

Not to confuse this thread's main focus of conversation with assumptions about prognosis:

As early as page ten I wrote:...a toddler with a potentially serious pulmonary and/or neurological disorder.

Two pages ago I wrote:However, oximetry monitoring without alarms may not be wise if the exact etiology and disease progression is still unknown.

Six posts above this one I wrote:My hunch is there's nowhere near enough to buy an AVAPS or volume ventilator should that scenario some day play out.

Your analysis has been quite accurate and appropriate, -sws.

However, in regard to $$, you could do the invasive option relatively cheaply:

http://www.dotmed.com/listing/6554?utm_ ... paign=Base

Also, if pCO2 management is the goal here, a rough idea on overall treatment effectiveness might be had by looking at venous CO2 (Total CO2 Content, -HCO3, or whatever they have down there) vs ETCO2 or TcpCO2. I would imagine that she is getting periodic venous boodwork, so just toss in some electrolytes.

SAG

-SWS wrote:And does that, then, translate to pretty much the same S/T capabilities the doctors can achieve with her current BiPAP autoSV model when configured that way (with the only current exceptions of missing straight timed mode and missing AVAPS pressure control mode)?

Question:) What does 'Timed Backup Rate' mean? Are all Backup Rates timed? When would you want to use a Timed Backup Rate and what machines have it?

Banned

Banned wrote:

-SWS wrote:And does that, then, translate to pretty much the same S/T capabilities the doctors can achieve with her current BiPAP autoSV model when configured that way (with the only current exceptions of missing straight timed mode and missing AVAPS pressure control mode)?

Question:) What does 'Timed Backup Rate' mean? Are all Backup Rates timed? When would you want to use a Timed Backup Rate and what machines have it?

Banned, all back up rates are times. Here are the modes:

Spontaneous or "S" Mode-- the BiLevel machine cycles from EPAP to IPAP purely as a result of patient breath detection.

Spontaneous/Timed or "S/T" Mode-- the BiLevel machine cycles from EPAP to IPAP based largely on patient breath detection. However if the patient misses a breath or is late initiating a breath, then timed mode will initiate the breath. This is also called backup mode and is always a function of time.

Timed or "T" Mode- the BiLevel machine cycles from EPAP to IPAP at a machine-timed rate every single breath. The patient's own spontaneous respiratory drive never causes the BiLevel to cycle by design. That might be because the patient's spontaneous respiratory drive is too dysfunctional or unstable to safely trigger the machine.

Only that last mode is missing from the BiPAP autoSV. We don't see any information or evidence yet to think that straight timed mode is key for Laryssa's therapy.

SAG wrote:However, in regard to $$, you could do the invasive option relatively cheaply:

http://www.dotmed.com/listing/6554?utm_ ... paign=Base

Much thanks. We can swing a cost like that if the scenario should become a reality. However, that scenario tends to be one of progressive neuromuscular disorder. I can see why Dr. Vergara wants to observe Laryssa's progress for six months.

Now let's touch on one other scenario not discussed. One with a much better prognosis: that Laryssa is the world's first documented case of pediatric complex sleep apnea (compSA/CSDB). We know she's one very special angel to say the least. And she already has us performing differential analysis in the realm of improbability as it is.

-SWS wrote:Spontaneous or "S" Mode-- the BiLevel machine cycles from EPAP to IPAP purely as a result of patient breath detection.

Spontaneous/Timed or "S/T" Mode-- the BiLevel machine cycles from EPAP to IPAP based largely on patient breath detection. However if the patient misses a breath or is late initiating a breath, then timed mode will initiate the breath. This is also called backup mode and is always a function of time.

Timed or "T" Mode- the BiLevel machine cycles from EPAP to IPAP at a machine-timed rate every single breath. The patient's own spontaneous respiratory drive never causes the BiLevel to cycle by design. That might be because the patient's spontaneous respiratory drive is too dysfunctional or unstable to safely trigger the machine.

Only that last mode is missing from the BiPAP autoSV. We don't see any information or evidence yet to think that straight timed mode is key for Laryssa's therapy.

Thanks SWS,

Based on the limited info for the AVAPS, would the AVAPS in PC (Pressure Control) mode function similarly to an SV in SV mode, only slower? Since The AVAPS literature says the AVAPS is good for CSA because it adjusts IPAP to the patients breathing.. isn't that exactly what the SV does?

Banned

Banned wrote: Based on the limited info for the AVAPS, would the AVAPS in PC (Pressure Control) mode function similarly to an SV in SV mode, only slower?

Slower or more gradual for sure, Banned. There are more functional differences.

Banned wrote:Since The AVAPS literature says the AVAPS is good for CSA because it adjusts IPAP to the patients breathing.. isn't that exactly what the SV does?

They both adjust IPAP, but there are crucial differences in each IPAP adjustment method. I'll oversimplify to demonstrate the "nutshell" of those two methods:

Let's pretend that SV has recent averaged a target of .5 liters (or "500 ml")

Now with the above target in mind let's pretend a patient is getting ready to breath the following untreated volumes during the next five breaths: .3, .3, .5, .7, .7

What will SV do to each of the above breaths? It will try to turn the above somewhat random appearing sequence into this corrected sequence: .5, .5, .5, .5, .5 Note that SV aims to fix each breath according to a recent-average derived target.

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By contrast AVAPS will have an "assured average target" entered by the clinician. So let's pretend the clinician entered a target of .5 liters. Let's also pretend that same untreated sequence is once again getting ready to occur: .3, .3, .5, .7, .7

So what does AVAPS with a clinician-entered target of .5 do for the above sequence? Absolutely nothing, by design, because it all averages out nicely to that clinician-entered target of .5 liters. So already we can see that SV is going to fix periodic breathing irregularities more handily than AVAPS, by virtue of addressing each irregular breath on the fly.

So what good is AVAPS, then? Well let's say that the patient's target shouldn't be .5 liters. Rather it should be .9 liters. So now let's pretend an unusually persistent hypoventilation patient that should breath .9 liter volumes gets ready to breathe the following sequence of untreated breaths into the SV: .5, .5, .5, .5, .5 . In fact, our patient with sustained hypoventilation has been breathing that sequence into the machine long enough that the target has been recent-averaged all the way down to .5 (an admittedly extreme hypothetical case).

So here's what SV will do on the system output: .5, .5, .5, .5, .5 (in other words SV does nothing in this extreme and numerically improbable scenario). Darn! That was supposed to be a patient breathing .9 liters on average. SV didn't fare well in that scenario. But what would AVAPS do?

AVAPS will gradually raise the IPAP so that the following system output is achieved (from the above string of .5 untreated breaths): .9, .9, .9, .9, .9

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So you can see each method of control and targeting is different. Each has its pros and cons. And most importantly each has its targeted disorders. A CSA patient could use either one. A periodic breathing patient should use the SV. A COPD or obese hypoventilation patient should use the AVAPS. Unfortunately neither algorithm or targeting method is well suited for a three-year-old girl.

Again, those were grotesque simplifications to demonstrate the "nutshell" differences between SV and AVAPS. More algorithmic details are offered in the corresponding Respironics patent descriptions (6951217, 6920875).

SWS,

Your example is a good simplified one & helps explain the point you make. But the SV machine sets its target peak flow based on a 4 min moving window (The VpapSV does it to a 3 min window ).

At the nominal 15 breaths per minute, that is something like 60 breaths.

So using 5 breaths as an example simplifies the example away from what the machine actually does.

Also one other point worth getting clarification is that all the docs I read tell me the BipapSV *will* do timed only mode. The manual I am looking at says "Auto, Off & Fixed" I haven't seen how it does it but the manual seems to say it can. I know that in Off, the INSP value appears in the clinicians menu.

I just assumed that setting the BPM=<a number> would then allow setting of INSP & the machine would somehow run at a timed only rate. I guess what I am saying here is, I can't yet see how it does it (haven't tried it on mine yet) but I believe the manuals say it can run timed only mode, but the manuals can appear ambiguous.

I'll take a look tonight on my machine if I can get the time.


DSM

dsm wrote:Your example is a good simplified one & helps explain the point you make. But the SV machine sets its target peak flow based on a 4 min moving (The VpapSV does it to a 3 min window - at 15 breaths per minute, that is something like 60 breaths.

So using 5 breaths as an example simplifies the example away from what the machine actually does.

Doug, the 5 breath simplification is, indeed, grotesque.

But the point is that SV sometimes does not fare well for the same two-fold reasons: 1) downward skewing of targets happens in the real world (sustained well in excess of four minutes), and 2) no assured average volume exists in the SV implementation as a secondary control variable to compensate.

Does that happen in five breaths? Of course not. But the explanation is much simpler to understand compared to more realistic examples of say thirty or sixty breaths. However, as a real world example, what happens when a patient with obesity hypoventilation rolls over on his or her stomach for those three/four targeting minutes (not to mention sixty solid minutes)?

He/She gets three or four solid minutes of downward-skewed targeting, as I had hoped to demonstrate in the oversimplified five-breath "nutshell" explanation above. The SV will then under-deliver for lack of an assured average volume as a secondary control variable.

dsm wrote:Also one other point worth getting clarification is that all the docs I read tell me the BipapSV *will* do timed only mode. The manual I am looking at says "Auto, Off & Fixed" I haven't seen how it does it but the manual seems to say it can.

That is interesting documentation. Auto gets us "S/T", off gets us "S", and fixed gets us "S/T".

And yet there's absolutely no input setting either in the menu or documentation to yield a "T". Is there? I'm thinking the technical writers lifted some text from a grandfathered machine/document, and forgot to drop the mentioning of "T" which appears nonexistent in the SV platform---at least as far as I can tell.

.

-SWS wrote:By contrast AVAPS will have an "assured average target" entered by the clinician. So let's pretend the clinician entered a target of .5 liters. Let's also pretend that same untreated sequence is once again getting ready to occur: .3, .3, .5, .7, .7

So what does AVAPS with a clinician-entered target of .5 do for the above sequence? Absolutely nothing, by design, because it all averages out nicely to that clinician-entered target of .5 liters.

That describes AVV (Average Volume Ventilation). AVAPS would adjust that sequence to .5, .5, .5, .7, .7.

-SWS wrote:AVAPS will gradually raise the IPAP so that the following system output is achieved (from the above string of .5 untreated breaths): .9, .9, .9, .9, .9

The AVAPS response is instantaneous.

-SWS wrote:Now let's touch on one other scenario not discussed. One with a much better prognosis: that Laryssa is the world's first documented case of pediatric complex sleep apnea (compSA/CSDB).

I'm guessing you're basing that scenario on the apneas scored in Encore reports, -sws. At this point, I think it would safer to throw out a lot of that info, especially events (which largely reflect machine activity, not patient activity), peak flow (reported out in multiples of 5 LPM), anything that looks like effective event management (which seems to be more closely correlated to 100% machine-controlled breaths and the analysis window becomes more stable)(and I think there are scenarios where even the % of machine breaths reporting becomes suspect) and for that matter, the whole SV Mode (since the thing now just buries itself at MaxIPAP).

Anyway since CompSAS is a phenomenon of hyperventilation and increased chemoresponsiveness, her baseline pCO2 in the 50s makes her a very unlikely candidate.

-SWS wrote:

SAG wrote:However, in regard to $$, you could do the invasive option relatively cheaply:

http://www.dotmed.com/listing/6554?utm_ ... paign=Base

Much thanks. We can swing a cost like that if the scenario should become a reality. However, that scenario tends to be one of progressive neuromuscular disorder. I can see why Dr. Vergara wants to observe Laryssa's progress for six months.

LP10 also offers a 100 ml tidal volume. And with those ALTEs and the requirement of continuous nocturnal pressure support, we're already at critical mass.

BTW, it also has a great battery back-up.

-SWS wrote:Auto gets us "S/T", off gets us "S", and fixed gets us "S/T".

That's correct. Although the Auto Mode starts out with a rate of about 7. Which if they "experiment" with that Mode down there, they're courting tragedy.

I think you should have sent the Synchrony.

SAG

StillAnotherGuest wrote:

-SWS wrote:By contrast AVAPS will have an "assured average target" entered by the clinician. So let's pretend the clinician entered a target of .5 liters. Let's also pretend that same untreated sequence is once again getting ready to occur: .3, .3, .5, .7, .7

So what does AVAPS with a clinician-entered target of .5 do for the above sequence? Absolutely nothing, by design, because it all averages out nicely to that clinician-entered target of .5 liters.

That describes AVV (Average Volume Ventilation). AVAPS would adjust that sequence to .5, .5, .5, .7, .7.

-SWS wrote:AVAPS will gradually raise the IPAP so that the following system output is achieved (from the above string of .5 untreated breaths): .9, .9, .9, .9, .9

The AVAPS response is instantaneous.

Thanks again, SAG. What you describe above, especially the instantaneous part, sounds to me like a prior VAPS implementation (prior to AVAPS) and without the graduality Respironics marketing literature ascribes to AVAPS.

According to Respironics prior VAPS is instantaneous and does quickly addresses each inspiratory cycle as you suggest:

In describing VAPS (not AVAPS) Respironics Patent Literature wrote:It is also known to operate a ventilator in a volume assured pressure support ("VAPS") mode in which the pressure is controlled by the ventilator in a manner so as to ensure that a set minimum volume is always delivered to the patient during each breath.

In this mode of volume ventilation, if, during an inspiratory phase, the patient's inspiratory flow is not sufficient to provide the set volume for that breath, the ventilator transitions to a volume controlled mode of operation and increases the pressure of the fluid flow to the patient to meet this set volume. This typically occurs at the middle or near the end of the inspiratory phase when the ventilator determines that the patient's inspiratory rate will not be sufficient to achieve the set volume for that breath. Because this increase in pressure typically occurs near the end of the breath, when the patient is most likely to want to exhale, this mode of ventilation can be uncomfortable to the spontaneously breathing patient.

However, AVAPS can't instantly hit each breath's volume target as described above when it does this:

Respironics AVAPS Literature wrote: Inspiratory pressure smoothly changes (< 1cmH2O/min) not to deteriorate patient comfort and prevent patient-ventilator disynchronization

http://www.schoolofventilation.com/docs ... /avaps.pdf

SAG wrote:The AVAPS response is instantaneous.

So the prior VAPS response is instantaneous. But AVAPS will very slowly migrate to average volume targets. And for typical BPM rates .3, .3, .5, .7, .7 coupled with a .5 average assured volume target can yield no change whatsoever (really depends on temporal variable values with respect to those moving windows).


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SAG wrote:I'm guessing you're basing that scenario on the apneas scored in Encore reports, -sws...

Anyway since CompSAS is a phenomenon of hyperventilation and increased chemoresponsiveness, her baseline pCO2 in the 50s makes her a very unlikely candidate.

It's a theory that's far less considered than when I proposed that very initial CSDB diagnostic criteria had yet to factor in lesser CSDB pathological severity gradients with commensurate diagnostic criteria.

So what I have in mind here is admittedly very under-baked. I'm thinking that CompSA/CSDB pathogenesis is entirely unknown. We don't even know if it can occur in pediatric cases. However, if it does occur in pediatric cases, infantile or early-stage pathogenesis may manifest as machine-induced defensive hypoventilation rather than pathogenically progressed adult-like periodic breathing with subsequent hyperventilatory or overshooting tendencies. That overly heightened chemoreceptor responsivenesses may very well be pathogenically progressed into adulthood---albeit principle to an intervening and maladaptive stimulus/response catalyst in pathophysiology (rather than root cause regarding initial pathophysiologic and especially pathogenic sequence).

This theory of pathogenesis would be based on the progression of the physiologically-defensive mechanism present during gestation and infancy that protects the airway from fluid aspiration associated with infantile acid reflux and common regurgitation. That physiologically defensive mechanism will conceivably regress in functionality and prominence from gestation to infancy and especially into childhood/adulthood.

If that physiologically defensive mechanism plays an overly heightened airway defensiveness role in the pathogenesis of CompSA/CSDB, then we might expect that symptom manifestations can be drastically different when comparing machine-related compSA in a child or infant with that of an adult.

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So Gracie's just as cute as can be and doesn't seem to have any sleep disorders that I can tell. But if she ever does... man is she in good hands.

-SWS wrote: So what I have in mind here is admittedly very under-baked. I'm thinking that CompSA/CSDB pathogenesis is entirely unknown. We don't even know if it can occur in pediatric cases. However, if it does occur in pediatric cases, infantile or early-stage pathogenesis may manifest as machine-induced defensive hypoventilation rather than pathogenically progressed adult-like periodic breathing with subsequent hyperventilatory or overshooting tendencies. That overly heightened chemoreceptor responsivenesses may very well be pathogenically progressed into adulthood---albeit principle to an intervening and maladaptive stimulus/response catalyst in pathophysiology (rather than root cause regarding initial pathophysiologic and especially pathogenic sequence).

This theory of pathogenesis would be based on the progression of the physiologically-defensive mechanism present during gestation and infancy that protects the airway from fluid aspiration associated with infantile acid reflux and common regurgitation. That physiologically defensive mechanism will conceivably regress in functionality and prominence from gestation to infancy and especially into childhood/adulthood.

If that physiologically defensive mechanism plays an overly heightened airway defensiveness role in the pathogenesis of CompSA/CSDB, then we might expect that symptom manifestations can be drastically different when comparing machine-related compSA in a child or infant with that of an adult.

I'll let RG comment on this,
but I have another AVAPS question:)

Why wouldn't AVAPS with an assured volume be a better alternative for Cheyenne-Stokes respiration than an SV? And why wouldn't they make an SV with an assured volume (PC)?

Banned