APNEA -v- HYPOPNEA

Good discussion continues....

1. My sleep doc said that with pressure induced centrals everyone who has "it" is different and as he was explaining it to another doc next to him sitting in: when someone is hooked up in the lab they can be pumping along at 8 cm fine then they bump it up to 9 and all of the sudden the centrals start appearing and when they go back to 8 it is fine again.....and each person's threshold is different. And it is interesting he used the pressure of "8" as an example.
2. I think it is more of a problem than we think if the auto's are being designed to avoid them. I don't think the manufacturers are worried about 1% of the APAP users (If that was the % that had this problem), but if it is 10% that has the problem then that becomes something they have to worry about. Just my thinking.
3. So far I feel much better at fixed CPAP, so SWS your theory that a pressure induced central may make you feel worse than an obstructive one may be true even if just a theory.

Kurt

Tom, those 12 second apneas could be purely incidental central apneas having nothing to do with xPAP (ordinary people experience central apneas at low incidental rates, btw). They could be 12 second obstructive apneas that do not resolve at specific pressures (neuromuscular upper airway dyscontrol comes to mind). They could be 12 second central apneas that are pressure induced. One thing I can say with absolute certainty: neither Encore Pro nor your doctor can say for certain. Encore Pro will register all the above 12 second apneas in the same exact way: as if they were 12 second obstructive apneas. That much I can say with certainty.

Regarding your counterintuitive response to both APAP and prophylactic pressures, those are both characteristic of CSDB. I hope you had a chance to closely follow the physiologic etiologies at play with CSDB. Regarding the typical CSDB patient response to APAP, I will quote this from the CSDB medical research we have been analyzing:

"Minimizing Hypocapnia
The most critical component of any therapy for complex disease associated with CO2 dyscontrol is to minimize hypocapnia. Strategies include using the lowest pressure that allows reasonable control, avoiding modalities that destabilize (continuous and bilevel pressure may be less or more effective in individual patients; automatic continuous pressure machines should be avoided), the use of a nonvented mask, the use of enhanced expiratory rebreathing space, and controlled increases of CO2 concentrations in the inhaled air." (bold emphasis mine)

If you're saying you respond better to CPAP than APAP, and if your saying you have highly anomalous pressure-related data that may indicate concurrent pressure-opposed etiologies, then you just may be a slight-to-moderate case of CSDB. I personally think you should run methodical and somewhat prolonged titration experiments at various fixed pressures to determine which fixed pressure is best for you. If APAP's varying pressures are suspected of even marginally destabilizing your respiratory drive and thus impacting your AHI scores, then don't titrate with APAP's varying pressures. Rather titrate with several-night runs (each) of single pressures.

I would definitely recommend that you and your doctor review the highly atypical and even counterintuitive response that patients with CSDB manifest on PAP therapy. Perhaps you are marginally CSDB. Alternately you can just run fixed pressure titration experiments until you are pleased with your own clinical response.

kurtr wrote: So far I feel much better at fixed CPAP, so SWS your theory that a pressure induced central may make you feel worse than an obstructive one may be true even if just a theory.

Thanks for that observation, Kurt. I'm getting closer and closer to being convinced that overly symptomatic manifestations are all too often the case for CSDB patients. Even the Harvard researchers commented how "biologically uncomfortable" CSDB can be based on their own patient observations. If this is true, it's not at all a bad idea to titrate down as long as efficacious results can still be achieved at lower pressures.

Regarding the 8 cm threshold mentioned in the Respironics patent description (and perhaps even implicitly by your doctor's statement): I should point out that those 8 cm conclusions derived years ago presumably dealt primarily with the rate of occurence regarding pressure-induced frank central apneas. These extremely overt pressure related central manifestations have been very easily observed for many years now.

However, CSDB researchers are now additionally considering central hypopneas and other still unknown CSDB-associated debilitating effects. It was virtually impossible for manufacturers and other researchers to have factored all the unknown debilitating effects of CSDB when they reached their 8 cm and 10 cm conclusions years ago. Yet more food for thought regarding past conclusions related to xPAP pressure. CSDB has only been very recently discovered and is still largely unexplored. Only the most overt CSDB cases are now documented. Marginal and moderate CSDB cases are not even on the books yet despite being hooked up to PAP machines throughout the world.

SWS wrote:

"Minimizing Hypocapnia
The most critical component of any therapy for complex disease associated with CO2 dyscontrol is to minimize hypocapnia. Strategies include using the lowest pressure that allows reasonable control, avoiding modalities that destabilize (continuous and bilevel pressure may be less or more effective in individual patients; automatic continuous pressure machines should be avoided), the use of a nonvented mask, the use of enhanced expiratory rebreathing space, and controlled increases of CO2 concentrations in the inhaled air." (bold emphasis mine)

I see why you don't want Hypocapnia:
Hypocapnia, also sometimes known as acapnia, is a state in which the level of carbon dioxide in the blood is lower than normal. This can result from deep or rapid breathing, known as hyperventilation. Even when severe, hypocapnia is normally well tolerated.

However, hypocapnia causes cerebral vasoconstriction, leading to cerebral hypoxia and this can cause transient dizziness, visual disturbances, and anxiety. A low partial pressure of carbon dioxide in the blood also causes alkalosis (because CO2 is acidic in solution), leading to lowered plasma calcium ions and nerve and muscle excitability. This explains the other common symptoms—pins and needles, stiff muscles and tetany in the extremities, especially hands and feet.

Hypocapnia is sometimes induced in the treatment of certain medical emergencies, such as intracranial hypertension.

Because the body relies on the level of blood CO2 to trigger the urge to breathe, hypocapnia can suppress breathing to the point of blackout (cerebral hypoxia). Self-induced hypocapnia through hyperventilation is the basis for the deadly schoolyard choking game. It is also commonly used by underwater breath-hold divers to extend dive time but at the risk of shallow water blackout, which is a significant cause of drowning.

I wonder if there is any link or coralation between Hypocapnia and the brain disorder known as Small Vessel Disease. Small Vessel Disease can be seen and identified on a high-res MRI. Basically the blood vessels of the brain appear smaller than normal putting one at greater risk of small strokes due to vasoconstriction.

I also wonder about that "great refreshing full of energy feeling" we got the first few weeks when we first started cpap.

You know, that feeling everyone strives to get back to from then on. I sometimes wonder if that feeling is not from going on cpap and it changing the CO2 levels in the blood. Interesting.

Snoredog wrote:I wonder if there is any link or coralation between Hypocapnia and the brain disorder known as Small Vessel Disease. Small Vessel Disease can be seen and identified on a high-res MRI. Basically the blood vessels of the brain appear smaller than normal putting one at greater risk of small strokes due to vasoconstriction.

I also wonder about that "great refreshing full of energy feeling" we got the first few weeks when we first started cpap.

You know, that feeling everyone strives to get back to from then on. I sometimes wonder if that feeling is not from going on cpap and it changing the CO2 levels in the blood. Interesting.

Those are extremely interesting points, Snoredog. Really gets one to wondering about the importance of CO2 management in PAP therapy. Speaking of the influence of CO2, Rested Gal pointed me to one of Sleepy Dave's great posts on one of the other apnea forums:

http://www.apneasupport.org/about5054.html

In that thread Dave points out that frank pressure induced central apneas have in the past been attributed to hypercapnia, or too much CO2. Those hypercapnic-driven central apneas are specifically caused by fixed pressure's magnitude or amplitude (and physiology's resulting CO2 retention) as opposed to APAP's varying pressures (and physiology's resulting CO2 depletion). Both etiologies are pressure influenced and both etiologies destabilize the respiratory drive relative to each patient's diametrically unique CO2 trigger thresholds. Those past-case CO2 retention-driven central apneas are likely the physiologic mechanism that drove manufacturers to their past fixed 8 cm and fixed 10 cm conclusions regarding rates of frank central apnea occurrence. Those are frank hypercapnic central apneas that are likely the pressure induced etiology that Kurt's doctor had in mind when he cited his own 8 cm example. Interestingly, hypocapnic CSDB etiology is clearly pressure induced as well, but had never been considered in the old paradigm of pressure induction.

Now CSDB and it's CO2 related etiology enters the picture. Unlike the above hypercapnic central apnea etiology, CSDB is a hypocapnic central apnea etiology. Where the above central apneas were largely driven by the build up of too much CO2 because of fixed pressure's sheer magnitude (and thus physiologic retention), CSDB's central apneas are largely driven by the fleeting transitions of CO2 depletion. As inadequate transient amounts of CO2 are encountered in this CSDB case, central apneas become a bit more driven by the pressures' transient influences on CO2. That is why CSDB patients tend not to fare as well on APAP, which delivers such transient pressures. Ironically, patients in that first hypercapnic case just might fare better on APAP's lower mean pressures, while patients in that second hypocapnic case (CSDB) tend to fare more poorly with the pressure and CO2 related transients imposed by APAP. Unfortunately CSDB can be problematic for some patients on CPAP or BiLevel as well.

So here we have two CO2 based etiologies that are on opposite ends of the spectrum regarding levels of CO2 required to induce respiratory dysregulation (one is hypocapnic and the other is hypercapnic). Both CO2 driven etiologies entail frank central apneas. Both are largely influenced by XPAP pressure's effects on CO2. Yes, it is conceivable that CO2 management (CO2 considerations at the very least) will have to play a much more prominent role in future xPAP therapies.

Thanks to Rested Gal for pointing me to that thread and thanks to Dave for all his threads.

APAP/Activa

AHI=1.5;AI=0.0;HI=1.5;Pressure (95%)=10.2

This is my fifth straight day using APAP with a 95% pressure averaging 10.15, and my numbers, especially HYPOPNEAS have NOT demonstrated a degradation over my CPAP trial at 8cmH2O. I haven't calculated non-parametric statistics to see whether this is significant, and of course, the sample size is too small for parametrics.

And, I'm feeling better.

C

_________________

CPAPopedia Keywords Contained In This Post (Click For Definition): CPAP, AHI, APAP

Chuck, you sure are proving to be a mystery. I too now suspect APAP's changing pressures just may not have accounted for your own increased HI. It is so intriguing that you seemed to have stabilized only after that trial at 8 cm fixed pressure, however.

Aside from analyzing statistical AI, HI, and mean pressure data, it might also be interesting if you had a look at just how much pressure delivery variation you experienced on the bad nights versus the good.

My other observation is that destabilization in unstable systems (in general) can occur rather episodically with respect to multifactorial inputs, particularly multifactorial triggers. Perhaps a marginally unstable respiratory drive can behave in much the same way: highly episodic trigger-induced destabilization in at least some cases. I thus still wonder if yours may be a highly marginal case of concomitant CSDB (manifesting in a highly episodic manner with respect to your own relevant multifactorial inputs, including but not necessarily limited to CO2 triggers).

Very challenging.

Hope this is not off topic but can hyponeas be caused by plugged sinus? not serverly plugged but more of a stuffy nose?

A question that I've been meaning to ask for some time...now's as good as any.

A person is using the ResMed S8 Vantage or an S7 Spirit in auto mode. The next morning, when the person holds down the right and left buttons to get into the patient's menu and looks at the efficacy data from the night before, they get to see: Press (pressure), AHI, AI, HI and Leak.

The pressure number they see in the efficacy data...is that:

A. the 95th percentile pressure?

B. the mean (average) pressure?

C. the highest pressure the machine had to use during the night?

or... something else?

I've always assumed it was the 95th percentile pressure, but have never been absolutely sure.

Have used both those machines but didn't have either manual for them.

Its the 95% pressure.

C

ok, adding to rested gals' question, I have my s8 vantage set on 8.8 for straight cpap - and when I look at my 'pressure' from the previous night, it says 8.4, sometims 8.6 ????? my leaks are under control - is that bizarre? I am feeling fine - just wondering why I set it at 8.8 and it is not showing pressure at that? no leaks like I said - wonder if the difference is so slight not a big deal?

Mine does the same thing in CPAP mode. Just goes to show you that the manometer in the thing is more accurate (presumably) than the pressure servo control.

That is a great clarifying question, Rested Gal. So, Chuck, you are really giving us the 95th percentile pressure from your data set? What other pressure and sleep event statistics can you easily mine from the S8 data set? Thanks.

Can sinus problems cause hypopneas? If sinus blockages can cause enough reduction in air flow, then I suspect they just might result in what a PAP machine scores as a hypopnea (amplitude reduction of the breath flow itself). If the flow blockage and thus amplitude reduction are constant, then the PAP will have baselined against that constant amplitude and presumably not score a hypopnea. If the nasal related flow blockage is highly variable and of adequate intermittent amplitude reduction (perhaps even more so in the case of highly variable rhinitis than in the case of sinus blockage), then I would expect hypopneas to be scored.

I know sinus problems can make PAP therapy very difficult in general.

rested gal wrote:A question that I've been meaning to ask for some time...now's as good as any.

A person is using the ResMed S8 Vantage or an S7 Spirit in auto mode. The next morning, when the person holds down the right and left buttons to get into the patient's menu and looks at the efficacy data from the night before, they get to see: Press (pressure), AHI, AI, HI and Leak.

The pressure number they see in the efficacy data...is that:

A. the 95th percentile pressure?

B. the mean (average) pressure?

C. the highest pressure the machine had to use during the night?

or... something else?

I've always assumed it was the 95th percentile pressure, but have never been absolutely sure.

Have used both those machines but didn't have either manual for them.

From the Resmed Clinical Manual:

The pressure transducer located in the unit measures treatment pressure; the average pressure is calculated and recorded each minute. The pressure reported in the Efficacy Data submenu (see Figure 9, The Clinical Menu Results series, on page 40) for a single session is the 95th centile pressure for mask-on time, excluding periods when the leak as exceeded hte 0.4L/s (24 L/min). For selected time intervals (lask week, last month, last 6 months or last year), the median of the daily 95th centril values is reported. Non-usage days are not included in calculations.

I guess the key word is "calculated", because the pressure shown is not the pressure used for 95 percent of the time,

it is more likely the pressure found that eliminates 95 percent of the events seen.

The Remstars seem to have the same vague meaning, when you look at the reports it finds the lowest pressure resulting in the fewest number of events, that becomes your 90%.

Then when you look on the very last page of the report it shows the avg. pressure used for 90% of time?? So you go back to each daily report and SUM up all the minutes and calculate the percentages for each pressure from that, they don't even come close to being 90%. So I assume they also mean pressure that eliminates 90% of the events seen, which makes more sense than the percentage of time spent.

You want to know the pressure that addresses the most if not the worst events, just like a cpap titration.

Yes, a pressure that has been calculated from historical data to show which fixed pressure would have eliminated 95% of Chuck's apneas and hypopneas. Thus "95th percentile" pressure.

Unfortunately not such a useful "standalone" metric in analyzing either hypocapnic pressure induction of central events (transient pressure-influenced physiologic CO2 depletion) or hypercapnic pressure induction of centrasl events (sustained pressure's influence relating to physiologic CO2 build up).