Do all machines recognize central apneas...

Excellent, Sandy. You got a good machine. Hope you get some good, restful sleep.

snoredog wrote:Now since my explanation wasn't good enough, please explain to everyone your version on how these machines avoid centrals since you are the resident expert?

Well, I think Christine would say that the way ASV works is to break the cascade of centrally-oriented events by by (1) successfully ventilating through the central apnea and (2) avoiding overshoot during the ensuing respiratory cycle. This is done chiefly through careful manipulation of the CO2 level. This is an Adapt SV chugging merrily along, doing it's thing, from Page 13 of MegaMOAT:


We're only talking a couple of mmHg pCO2 here (OK, 3) to create all this mess.

We're trying to ventilate through that apnea to ameliorate the ventilatory overshoot. In other words, by controlling the central apnea, you control the ventilatory response, or the ensuing event. It's the egg that's the important part. It takes a little bit of time for this thing to catch:


But eventually it does:


In these waveforms, you can see the undulation of the CO2 level (TcpCO2). When the CO2 dips, respirations cease. When they rise, the patient (hyper)ventilates. Now, the CO2 waveform lags a little because of circulatory time (to the ear, where this is measured) and perfusion time (this is a trancutaneous electrode). Also, this is probably not exactly what the chemoreceptors actually see, by the time the CO2 level is actually resulted, a number of dampening forces have occurred, but nonetheless, this really shows well what is happening.

Moving the CO2 waveform about 45 seconds earlier so that it might represent what the chemoreceptors see:



it now becomes more clear to note how the the low CO2 levels cause central apnea, and the higher CO2 levels generate the periods of hyperventilation.

Referring to a number of outstanding points.

As you can see, you can still have apneas with an ASV, at least until the thing catches. So I'm not saying you can't have an AHI with ASV, but I, too, am curious as to why AHI is not being reported out in the US version. It would be measured in the ASV Flow channel.

Looking simply at an AHI can be very deceiving. CSDB is essentially a Stage 2 phenomena. In looking at a whole night's sleep, you would have to absolutely subtract Wake. If you're sure you have CSDB, then you have to subtract SWS and REM. We may leave Stage 1 in there because of scoring rules. So if you only look at AHI, then you'll probably underestimate the severity of CSBD by about half, anyway. And to re-emphasize, if you've got a lot of Wake in there, the number becomes increasingly inaccurate.

I know I'm going to regret this, and this part is by no means scientific, but is offered to try to afford explanation of how one number (AHI) might be interpreted (assuming my adds and gazintas are right). CHF/CSR and CSBD, once the cascade starts, will occur at a localized index of about 40-60 (long cycle) or 90 or more (short cycle). From "The CSDB Article":

In heart failure, the cycle length may be long (60 or more seconds), or much shorter (25-40 seconds) in those with preserved cardiac output.

If 50% of the night is Stage 2, then the Relative Severity of the phenomenon is 20-30 or 60-72, respectively. Now. if CPAP/BiPAP is usually about 50% effective, which is what a lot of studies show, then your Residual AHI is now 10-15 or 30-36. If you have a bad night, like with 75% sleep efficiency, then the AHI is 7.5-11.25 or 22.5-27.0. And if you don't go into the cascade during Stage 2 with 100% efficiency, which is usually the case, then that number is reduced even more.

I hope this isn't looked at as "Hmmm, my Residual AHI is 7.5, so obviously I must have Cheyne-Stokes Respiration and Congestive Heart Failure."

BTW, the above case, which is an outstanding example of CHF/CSR, has an AHI of 30.

Blaming any of this stuff on "Vocal Cord Closure" is a stretch, but certainly might be an area of interesting discussion.
SAG