S9 VPAP Adapt two modes of attack for centrals

[summer]

Hi,

I have been researching the way a normal bilevel pap machine could possibly address central apneas and the different approach that the Resmed S9 VPAP Adapt would take. Am I right in thinking that because the Adapt is also a bilevel, that the two pressures alone could also address centrals before it needs to use it pressure pulsing algorithms. That is, if a normal bilevel machine was successful in addressing centrals, but you were then given an S9 VPAP Adapt, its possible that the bilevel part of the machine may do the job first or is that too simplistic?

[JohnBFisher]

Hi,

I have been researching the way a normal bilevel pap machine could possibly address central apneas and the different approach that the Resmed S9 VPAP Adapt would take. Am I right in thinking that because the Adapt is also a bilevel, that the two pressures alone could also address centrals before it needs to use it pressure pulsing algorithms. That is, if a normal bilevel machine was successful in addressing centrals, but you were then given an S9 VPAP Adapt, its possible that the bilevel part of the machine may do the job first or is that too simplistic?

A true BiLevel only machine will not address central apneas. That is, if you fail to breathe then since the machine is only a "spontaneous" machine .. that is it only changes to inhalation pressure when you inhale .. then it will NOT address a central sleep apnea.

The ASV machines include a timed response to the a decreased volume of air. When you fail to breathe, after a certain period of time it switches to inhalation pressure, which is often enough to restart respiration.That is how a BiPAP S/T unit behaves.

However, an ASV unit goes one step further. If it detects that you still will not meet your target volume it will quickly increase the inhalation pressure to help ascertain your respiration and thus break the undershoot/overshoot cycle.

Hope that makes sense.

[summer]

Hi John,

Thanks for your reply, I'm more thinking that there are individuals out there that have problems with arousals that trigger sleep onset centrals rather than primary central apnea. These individuals some times are treated successfully due to the +4cm drop in expiration enabling better 'blow off' of CO2. I note that there have been a number of posts citing this.

[-SWS]

That is, if a normal bilevel machine was successful in addressing centrals, but you were then given an S9 VPAP Adapt, its possible that the bilevel part of the machine may do the job first or is that too simplistic?

That's my take as well. If you remove Adapt SV's ability to adaptively fluctuate IPAP, then you are left with BiLevel S/T functionality. And we know that BiLevel S/T functionality does, indeed, succesfully treat many central apnea cases. I think we can thus assume S9 VPAP Adapt's core functionality (BiLevel S/T without adaptive IPAP) treats at least some of the central apneas presented to that machine.

These individuals some times are treated successfully due to the +4cm drop in expiration enabling better 'blow off' of CO2.

I suspect the CO2 blow-off/exchange dynamics across the ASV patient population might entail more than one scenario. I think we can assume ordinary elastic recoil in many/most ASV patients suffice to exchange CO2, based on lack of iatrogenic symptoms. In yet other cases accessory chest-wall muscles seem to compensate, based on some patients reporting sore chest muscles. In yet other cases PAP might actually interfere with proper CO2 exchange, based on insufficient elastic recoil versus PAP's inflationary effect at Rx. In other words, I think the CO2 exchange dynamics might be somewhat individualized across the patient population.

However, Adapt SV is intended to treat patients with transient hypocapnia issues (transient CO2 insufficiency) rather that hypercapnia problems (CO2 retention). So I'm not certain that faciliatting CO2 blow-off is the mitigating factor for these patients who primarily have issues with depleting CO2 too rapidly in the first place.

[JohnBFisher]

... I'm more thinking that there are individuals out there that have problems with arousals that trigger sleep onset centrals rather than primary central apnea. These individuals some times are treated successfully due to the +4cm drop in expiration enabling better 'blow off' of CO2. I note that there have been a number of posts citing this. ...

Ah! You are correct. In fact, I'm an example of someone who had issues with that early on. During one of my early sleep studies the sleep technician noted that I had arousals all over the place. He switched me to BiLevel and the arousals went away. I slept better than I had in months.

Of course, I then (a few years later) had another sleep doctor (who I fired after this incident), who scolded me for moving to BiLevel so quickly .. it was not needed .. I needed a new sleep study .. that showed clearly that I needed a BiLevel machine. He was one who told me that I could not have central sleep apnea because it is so rare. I asked what the numbers show. He told me that regardless of the numbers, I could not have it because it is so rare. Idiot!

Anyway, you are definitely correct that the BiLevel pressure allows greater exchange of gas during respiration, thus helps promote better sleep. Thanks for clarifying your thought. I definitely agree. In that case the ASV units help in three ways. First, the BiLevel therapy helps promote better respiration. Second it has a timed response to help kick start respiration. And third, it will increase pressure to help sustain respiration when needed.

Here's an example of periodic breathing (from me) that shows all three:



The unit uses the pressure pulse to see if the airway is open. The red line below shows the pressure during inspiration and expiration that shows the increase as needed to address a low volume from my breathing. Of course, it shows the normal change from inhale to exhale and back again. And it also shows the timed responses when it felt I had not breathed frequently enough.

Hope that helps.

[JohnBFisher]

... However, Adapt SV is intended to treat patients with transient hypocapnia issues (transient CO2 insufficiency) rather that hypercapnia problems (CO2 retention). So I'm not certain that faciliatting CO2 blow-off is the mitigating factor for these patients who primarily have issues with depleting CO2 too rapidly in the first place. ...

Oh, I suspect the BiLevel therapy does make a huge difference in the arousal level. But as you point out, the primary difference it has over the BiPAP S/T type system is that it attempts to break the overshoot (hypocapnia) / undershoot (hypercapnia) cycle. Breaking the cycle decreases the number of central apneas and thus improves sleep.

Upon seeing my waveform data, I've been amazed at how frequently my ASV unit steps into the situation to help regulate my breathing. The numbers it reports shows very little of that. I get hundreds of "Timed" responses per night. I get hundreds of times it increases the pressure to address a volume insufficiency. Wow! It's amazing how much it jumps into the situation and helps regulate my breathing.

[-SWS]

... However, Adapt SV is intended to treat patients with transient hypocapnia issues (transient CO2 insufficiency) rather that hypercapnia problems (CO2 retention). So I'm not certain that faciliatting CO2 blow-off is the mitigating factor for these patients who primarily have issues with depleting CO2 too rapidly in the first place. ...

Oh, I suspect the BiLevel therapy does make a huge difference in the arousal level. But as you point out, the primary difference it has over the BiPAP S/T type system is that it attempts to break the overshoot (hypocapnia) / undershoot (hypercapnia) cycle.

We may have to agree to disagree on this, John. Sequencing and initial trigger-event are key. The core or initial issue in pathophysiology for ASV patients is transient hypocapnia. The white papers and literature descibe ASV as mitigating a hypocapnia-triggered pathophysiology by encouraging CO2 retention---not encouraging the depletion of CO2 with a minimum PS. Resmed initially described their minimum PS as facilitating the work of breathing (WOB).

That physiology problem is documented to typically commence with hyperpnea. Hyperpnea is frequently the intial ventilatory overshoot and central disturbance triggering havoc: the ventilatory overshoot commencing loop-gain based oscillations in central control of respiratory pump muscles. The term overshoot and undershoot primarily characterize ventilation's overshoot and undershoot in these hypocapnia-triggered patients. Transient blood-gas exchange oscillations result as secondary, until that hypocapnia-triggered ventilatory overshoot/undershoot cycle finally subsides. But the problem is triggered in a hypocapnic threshold having been initially crossed combined with problematic loop-gain that approaches one.

But since the entire sequence of overshoot and undershoot is triggered with hyperpnea and hypocapnia, ASV endeavors to ecourage CO2 retention by avoiding ventilatory overshoot as much as possible. I would also point out that Respironics ASV defaults and prefers PS=0. But I do not agree that setting a constant PS mitigates hypocapnia-triggered patients by continually encouraging the depletion of CO2.

John, thank you for all you do here!

[JohnBFisher]

... The white papers and literature descibe ASV as mitigating a hypocapnia-triggered pathophysiology by encouraging CO2 retention---not encouraging the depletion of CO2 with a minimum PS. ...

Interesting. In this instance - as the patient - I beg to differ with the experts, who while they might understand the physiology they don't LIVE the condition. My problem is that *INITIALLY* I fail to breathe enough. THAT sets up the repetitive cycle. I do NOT initially blow off too much CO2.

But then there is likely something I do not understand about the process. Again, the difference appears to be that of perspective. What I experience differs from the academic viewpoint.

... John, thank you for all you do here!

Thank you. I try to help others learn to live with their situation and not settle for second best when dealing with central sleep apnea. But I am the FIRST to admit that I have a lot to learn. I constantly learn from your posts. Thank you for all you do.

[avi123]

Hi,

I have been researching the way a normal bilevel pap machine could possibly address central apneas and the different approach that the Resmed S9 VPAP Adapt would take. Am I right in thinking that because the Adapt is also a bilevel, that the two pressures alone could also address centrals before it needs to use it pressure pulsing algorithms. That is, if a normal bilevel machine was successful in addressing centrals, but you were then given an S9 VPAP Adapt, its possible that the bilevel part of the machine may do the job first or is that too simplistic?

Question,

Do the rest of the Bilevel machines treat centrals and not the Adapt only. Resmed has six types of BiLevel S9 VPAPs (including the Adapt):

http://www.resmed.com/us/products/s9_vp ... nc=dealers

If I see on my graphs centrals from my S9 Autoset, would a BiLevel machine suppress them, or is it applicable only to those with CSAS?

Example of my data:

[-SWS]

... The white papers and literature descibe ASV as mitigating a hypocapnia-triggered pathophysiology by encouraging CO2 retention---not encouraging the depletion of CO2 with a minimum PS. ...

Interesting. In this instance - as the patient - I beg to differ with the experts, who while they might understand the physiology they don't LIVE the condition. My problem is that *INITIALLY* I fail to breathe enough. THAT sets up the repetitive cycle. I do NOT initially blow off too much CO2.

Central-apnea academics, PAP manufacturers, and practitioners recognize that some central-apnea disorders are based in hypercapnic pathophysiology---while other central-apnea disorders are based in hypocapnic pathophysiology. John, your pathophysiology is neither treatment emergent (typical CompSAS) nor is it based in heart failure.

Those two central-disorder types are based in hypocania and thus targeted by ASV, which encourages CO2 retention. BiLevel S/T, AVAPS, and ventilators (not Rx'ed in the sleep labs) are typically selected to treat hypercapnic central-apnea disorders:


That said, ASV actively treats ventilatory undershoot with IPAP increases, while passively dealing with ventilatory overshoot by abstaining from IPAP increases. It's plausible that ASV treats your sequence. Recall that ASV was initially contraindicated for hypoventilation disorders (hypercapnic). The fear was ASV's less-than-100% flow targeting might allow a gradual "downward force" on the inhibited respiratory drive. However, despite that initial fear, some hypoventilation patients actually fared okay on ASV. I think hypoventilation is now removed as an ASV contraindicaton. Regardless, AVAPS is considered a better choice for hypoventlation.

[-SWS]

Question,

Do the rest of the Bilevel machines treat centrals and not the Adapt only.

Avi, I'll take a crack at that question. The BiLevel machines that have no backup rates are usually targeted for obstructive patients. The different flavors of BiLevel machines having backup rates are usually targeted for various types of central breathing disorders.

[JohnBFisher]

... Central-apnea academics, PAP manufacturers, and practitioners recognize that some central-apnea disorders are based in hypercapnic pathophysiology---while other central-apnea disorders are based in hypocapnic pathophysiology. John, your pathophysiology is neither treatment emergent (typical CompSAS) nor is it based in heart failure. ...

Doh! Yes, of course you are correct. Your explanation is wonderful - as usual.

... That said, ASV actively treats ventilatory undershoot with IPAP increases, while passively dealing with ventilatory overshoot by abstaining from IPAP increases. It's plausible that ASV treats your sequence. Recall that ASV was initially contraindicated for hypoventilation disorders (hypercapnic). The fear was ASV's less-than-100% flow targeting might allow a gradual "downward force" on the inhibited respiratory drive. However, despite that initial fear, some hypoventilation patients actually fared okay on ASV. I think hypoventilation is now removed as an ASV contraindicaton. Regardless, AVAPS is considered a better choice for hypoventlation. ...

As you can see from the following waveform diagram, it tackles my breathing issues through timed response and increased pressure as needed.



I am guessing that my doctor felt that the flexibility of the unit (to address both timed response and insufficient volume) would make a better choice to tackle my problems than just AVAPS and/or BiPAP S/T. However, I had wondered about my options if I had a continued decrease in muscular control (I sometimes feel quite weak when my environment gets very busy). This helps highlight a very viable direction.

Again, thank you for taking the time to help me better understand.