ASV progress: born again and resurrected

jamiswolf wrote:Good Morning Ameriken,

Whoah, a minimum of 10 is way different then 10. Your breath rate has been running in the mid teens...like 16 so the auto rate was probably running 12 at least.

Good morning Jamis....I'm posting last nights report below...I took the backup off 12 and put it on 'auto'.

You can see my PTB's are not much better than when backup = 12. On auto, the BPM bottoms at 10. Also, for the first time since the last time I had it on auto, my AHI is higher. 3 is still good, but I ran 1 and 2 on backup rate = 12. Plus, my minute vent is lower, and my avg BPM is lower when set to 'auto'.

jamiswolf wrote:Basically I was responding to DDs suggestion that you were using the machine as a ventilator and suggesting a way to explore and possibly back off on that. But if you're feeling better, perhaps it's not such a bad thing.
Jamis

What I understand about the ASV, is it is not a ventilator...unless your own breathing has dropped. The backup rate is just that...a backup. It is not the primary. The patient is primary and when their breathing quits, the backup starts functioning to keep the patient breathing.


Anyhow, here is last night on 'auto'. Higher AHI, lower minute vent, lower avg BPM. I think tonite I'll go back to backup= 12

jamiswolf wrote:Basically I was responding to DDs suggestion that you were using the machine as a ventilator and suggesting a way to explore and possibly back off on that. But if you're feeling better, perhaps it's not such a bad thing.
Jamis

No problem, your posts are quite helpful.

Being a non-medical layperson, I can't argue with DD on the algorithms and other specifics of the Respironics ASV. I'm simply trying to determine the best settings for my breathing.

Ameriken,
Thanks, I try..

I see that you mean. During those low/absent PTB periods, your BPM drops to 10. Setting the BPM rate to 10 (manual) would probably yield very similar results as auto.

Why aren't there any CAs scored prior to the machine taking over? I suppose it could just be that your own respiratory rate dropped below 10 bpm...yet no actual CAs.

Your tidal volume is within normal limits...even during the periods of good PTB. That would tend to minimize excess CO2 retention...as I see it. So I disagree with DD on that issue.

What is your respiratory rate while awake? Not in bed on BiPap, but while at rest...say watching TV. Just curious as a comparison to the rate during treatment.
Take care,
Jamis

jamiswolf wrote:Your tidal volume is within normal limits...even during the periods of good PTB. That would tend to minimize excess CO2 retention...as I see it. So I disagree with DD on that issue.

If the Average VE is 10.1 L and the Average RR is 11.7, then the Average Tidal Volume is 863 ml.

Do we think that to be normal?

Is he 10 feet tall (sorry, inside joke)?

Further, is the goal to get rid of CO2 (if he does, in fact, have CO2 retention) or preserve CO2 (if the underlying issue is CompSAS)?

DeltaDave wrote: If the Average VE is 10.1 L and the Average RR is 11.7, then the Average Tidal Volume is 863 ml.
Do we think that to be normal?

I actually meant to write minute ventilation. His tidal volume isn't even graphed. So my mistake. His RR is generally above average which demonstrates (along with Min. Vent.)that he's compensating adequately for his situation.

DeltaDave wrote: Is he 10 feet tall (sorry, inside joke)?

I actually get that one...reference to comments made in WEKs thread.

DeltaDave wrote: Further, is the goal to get rid of CO2 (if he does, in fact, have CO2 retention) or preserve CO2 (if the underlying issue is CompSAS)?

No, of course not...but it's very important. When I go back in the thread to see this...

DeltaDave wrote: If this boy's got CO2 retention (there is hx of chronic narcotic use (methadone), restrictive lung dz (scoliosis), and obstructive lung dz (emphysema)), this is the ONE time you could've suggested AVAPS and at least be on topic.

I realize you were just making comments to JustanotherGuess and not really suggesting that Ameriken needs an AVAPS. There was an "IF" in there.

so Ameriken, like so many threads, this one went off track from it's original intent...but all with good intent.
Jamis

jamiswolf wrote:I actually meant to write minute ventilation. His tidal volume isn't even graphed. So my mistake. His RR is generally above average which demonstrates (along with Min. Vent.)that he's compensating adequately for his situation.

How ya figure?

deltadave wrote: If this boy's got CO2 retention (there is hx of chronic narcotic use (methadone), restrictive lung dz (scoliosis), and obstructive lung dz (emphysema)), this is the ONE time you could've suggested AVAPS and at least be on topic.

Now leeme alone, I gotta get ready for FB. I need the Ducks to pull this one out in order for the Master Plan to work.

Let me clear up some assumptions on my medical history because you are mostly right on, however there are some significant differences that I should clarify.

1) Narcotic use: yes, methadone for low back and right leg pain (sciatic)
2) No restrictive lung disease. Yes, I do have scoliosis, and while it is the cause of back pain, it's a 30 degree curve and is not acute enough to affect my lung or lung funtion (thankfully).
3) Emphysema: I have not been diagnosed with full blown emphysema or COPD. When I got my lung xray 14 months ago, the reading doctor wrote 'emphysematic changes'. I took a pulmonary function test (the blowhard test) and scored well above all their minimums. The tech who did the test stated quite emphatically "theres no way you could have emphysema". Thus, no oxygen was recommended since my lung capacity appeared ok.

All the above was prior to my discovery of sleep apnea. I had 2 sleep studies. The first I failed titration as the CPAP did nothing. That is when they saw my O2's drop into the 80's both with and without CPAP. I went back for a second study to be titrated on the ASV. The below is the report from the second study. What caught my attention is recommendation #2 and that is what has prompted me to go with a different back-up than 'auto'. (Getting in to see this VA doctor is next to impossible, so I've relegated myself to going at it alone).

jamiswolf wrote: so Ameriken, like so many threads, this one went off track from it's original intent...but all with good intent.
Jamis

No worries. I'm always open to suggestions, if they're clear. I'm not a doc so I won't get into arguing about the specifics about the machine.

deltadave wrote:

jamiswolf wrote:I actually meant to write minute ventilation. His tidal volume isn't even graphed. So my mistake. His RR is generally above average which demonstrates (along with Min. Vent.)that he's compensating adequately for his situation.

How ya figure?

Because if one variable in a 3-component equation is way off the mark (forget what's happening clinically, and just think mathematically), then another variable must also be abnormal.

Since VT x f = VE and VT is abnormally high, VE is also abnormally high. Further, since VE is simply the product of VT and f, changes in it's value cannot be referred to as "compensation" for anything. The compensatory mechanism for high VT would be low f.

ameriken wrote:3) Emphysema: I have not been diagnosed with full blown emphysema or COPD. When I got my lung xray 14 months ago, the reading doctor wrote 'emphysematic changes'. I took a pulmonary function test (the blowhard test) and scored well above all their minimums. The tech who did the test stated quite emphatically "theres no way you could have emphysema". Thus, no oxygen was recommended since my lung capacity appeared ok.

Thanks for clarifying that. It would be easy to conclude by the statements:

ameriken wrote:I don't have an oximeter at home, but my sleep study states my O2's during my sleep studies while on the machine were still in the 80's. I believe this is because I was also diagnosed last year with 'emphysematic changes' in my lungs due to my prior smoking history.

that there was "emphysema" present.

However, are we to take the word of a "high priest" tech, whose expertise is limited as to whether the generic brands of Eye of Newt and Wing of Bat have the same potency as the National Brands?

BTW, I could never understand why emphysema is classified as an "obstructive" dz, because it's largely diffusional in nature.

BTW2, I wouldn't classify TCU beating Boise as an "upset". TCU is no slouch.

The Master Plan continues on target...

Getting back on track (or merrily continuing on in glorious derailment, depending on how one looks at it), the above segment of NPSG Report gives great support to the original point that

One cannot determine conclusively if their sleep is better without actually measuring sleep (OK, we can debate using something like the ESS, and I will be happy to make some concessions).

However, since the subject of surrogates has been brought up, as previously noted, Minute Ventilation does not suggest improvement in sleep quality.

and the "dial wingin' does/did little (if anything) to improve sleep quality.

In other words, treating numbers will not change "how one feels" unless sleep quality is improved. While it may be easy in many cases that the syllogism will be true ("My AHI was 80 and now it's 2 and I feel great so that's why"), "IMHO", that is not what has happened here because

• The improvement is AHI due to "tweaks" is small;
• It was non-toxic to begin with;
• Real improvement may not have occurred, and that the way the machine measures events has simple changed;
• The role that ASV has anything to do with this (as implied in the thread title) may be false since this machine now is essentially operating in S/T Mode; and most important
• The list of reasons other that SDB why the subject could have been "foggy" is absolutely staggering, and it may be that improvement in those conditions is the cause for feeling better.

Specifically, these reasons include:

• Rhinitis that could affect compliance
• Reflux that could affect sleep continuity
• Underlying pain
• A spontaneous arousal index of at least 16
• Auditory hallucinations (consider narcolepsy, a notorious sleep continuity destroyer)
• Consider Restless Leg Syndrome
• Way too much caffeine way too late in the day
• Horrible sleep efficiency. If one is only sleeping 60% of the night, an improvement in AHI from 6.0 to 2.0 would be Yossarian in nature.

Lastly, the "good" sleep and SDB response noted in NPSG (the 47-minute block) would need to be analyzed in context. For instance, if it (or most of it) occurred during SWS (a sleep stage renown for it's ability to stabilize SDB, where just about any settings are "good" settings), then the conclusion that those settings solve all SDB issues would not be valid.

deltadave wrote:The role that ASV has anything to do with this (as implied in the thread title) may be false since this machine now is essentially operating in S/T Mode.

However, without determining baseline pCO2, discussion cannot occur in re: is this good, bad or indifferent (if f is set > fresting, this would appear to be hybrid: namely, a rapid-response AutoBiPAP).

deltadave wrote:

deltadave wrote:The role that ASV has anything to do with this (as implied in the thread title) may be false since this machine now is essentially operating in S/T Mode.

However, without determining baseline pCO2, discussion cannot occur in re: is this good, bad or indifferent (if f is set > fresting, this would appear to be hybrid: namely, a rapid-response AutoBiPAP).

The importance of determining pCO2 was pointed out in this editorial comment by Zwillich and Welsh from Denver. While this article is largely concerned with bariatric patients, their main points are still quite relevant here:

Unfortunately, clinicians may underestimate the severity of illness of these patients and often miss an opportunity to intervene. Presenting symptoms are nonspecific and include fatigue, sleepiness, subtle changes in mental status, and headaches. Since there is often no increase in respiratory rate or use of accessory muscles to breathe, their tenuous status is not fully appreciated. Even the underlying obstructive sleep apnea (OSA) as well as the hypoventilation in these patients is often missed. When oxyhemoglobin desaturation and right-heart failure are detected, supplemental oxygen is often provided without the knowledge of arterial blood gas abnormalities. Therefore, these hypercapnic patients often go unrecognized and undertreated with high risk for recurrent hospitalization and even early death.

http://chestjournal.chestpubs.org/conte ... /1729.full

deltadave wrote:hypercapnic patients often go unrecognized and undertreated with high risk for recurrent hospitalization and even early death.

Is there a description for 'daytime hypercapnea' in the literature? if I had it, how would I know?