CPAPtalk.com

Liam1965 wrote:Oh, I had two more thoughts.

Second, there's central apneas. Straight pressure not only does nothing to solve them, it can actually INDUCE them. I found myself suddenly gasping for air when I was on the straight pressure (before some kind soul told me how to give my doc the metaphorical finger by turning on my own CFLEX), and I'd realize that I'd suddenly forgotten to breathe. After adding CFLEX to the mix, that happened much less frequently, but it still happened.

Liam, who never got to try it to find out.

It takes allot of pressure I mean allot to cause the barrow receptors to give you a central because of the Pressure You would have to be above 20 or more unless you’re a very little person with small lungs like a Child. More then likely you got a few Sleep onset centrals which is normal Blowing off Co2. But lowering the CPAP would do nothing for a true Central. Now if you were having problems with the pressure you may have held your breath while you were sleeping because you were not used to the back pressure. Then Cflex would have fix that but not centrals. A true Central is not fixed by pressure. It has everything to do with blowing off to much Co2 or a brain injury. If you blow off to much Co2 your body will cause a central to rebalance itself. Stop breathing build up C02 to much you yawn or take a sigh breath. Its all Acid and base body stuff.

CPAPs are the "gold standard". They have been proven to work for some of the people some of the time. Yet, with an abysmal compliance rate of less than 50% you would think compliance would be a major issue the sleep med administators would be working hard to address?

"Several small studies31-34 have shown encouraging results with APAP systems. A study with 20 patients by Teschler and Barthon-Jones24 revealed a reduction of the main airway pressure of up to 37% with no decreased effectiveness when compared with conventional CPAP. Two larger studies, one with 50 patients35 and the other with 60 patients,36 confirmed findings from previous studies. The mean mask pressure was significantly lower (8.1±2.5 cm H2O vs 6.7±1.7 cm H2O37 and 10.6±0.4 cm H2O vs 6.4±0.4 cm H2O38) and the compliance rate was higher in both APAP groups. On the basis of these studies, it seems that APAP would be beneficial in many OSAS patients except those who require low pressure to treat their obstructive events."

Why APAPs are not embraced enthusiatically by the powers that be mystifies me. The more comfortable the treatment is, the better the compliance. If your pressure needs vary from 8 to 14 in a night then why have CPAP blasting 14 all night long when you could have an APAP accommodating your needs? Higher pressure can lead to more problems with mask leaks, aerophagia, etc. Add C-Flex for even more comfort and therefore, even better compliance.
Is the technology just too new? Are doctors just more willing to prescribe a tested, yet problematic older machine out of fear of the new?

I agree with yea coffee yea just have to keep the pressure close to each other is all. The big reason is the insurance companies. They are the one's who control what you get. The DME companies for the most part are not the problem. There needs to be a different class of reimbursement for the APAP machines from the major insurance companies. Like anything some doctors have embraced APAP and others don’t. If you want it find a doctor who likes it and see if you can get the DME Company to do the doctor a favor and make less profit off of it. What you have to understand is there is a very small profit margin on CPAP. After the delivery to your house with a respiratory therapist (which depends on the state you live in some states have no law so anyone can set you up on CPAP this would included the guy flipping burgers last week.) The profit margin is down to $240 dollars reimbursed over 6 months sometimes with a 90 wait before you see the first penny role in. Now add one mask refit or pressure change and you’re down to about 125 dollars in profit over 6 months. This is due to Respiratory Therapist time not being reimbursed like a nurse's time is and the cost of the mask. Oh this is for a normal mask give them a full face and the profit just went down some more.
Also any mask change is FREEEE before the 3- 6 month period. This is due to insurance companies that will not pay for a different one until you wait from 3-6 months depending on the policy. We all know it takes a night or two of sleep on a mask . So how do you make a choose when the therapist is there with yea for 30 mininutes. Now let’s add in the extra cost of a APAP to a CPAP lets say its $110 bucks well you just made $15 dollars over the next 6 months YEAA. Best case which never happens you made $130 over the next 6 months. Now that is based on the average reimbursement some may be higher but allot are even lower so you would defiantly make nothing. The DME companies are in a business to make money there not non profit.

Now convince the insurance companies that better compliance = less sick people in the long wrong which = more money in there pockets. Then you will get your APAP paid for or you hope the DME Company is kind enough to do it for you for not less profit but close to Free. $15 = free in my mind LOL

Study showing that APAP is as effective as CPAP

Here is the real problem in finding accurate data proving that Auto's raise compliance is that the studies as of yet have not been properly designed to determine it

...Future studies need to consider the effects of treatment in participants who are poorly compliant. The studies assembled were characterised by high machine usage in the control groups, and low withdrawal rates making it less likely that any benefit could be demonstrated.

Link

Now if you are overweight, and plan on having bariatric surgery, there is a study that suggests that Auto CPAP is the preferred therapy.

Auto-titrating PAP devices have promise for facilitating the management of CPAP therapy during this time

Anonymous wrote:
It takes allot of pressure I mean allot to cause the barrow receptors to give you a central because of the Pressure You would have to be above 20 or more unless you’re a very little person with small lungs like a Child. More then likely you got a few Sleep onset centrals which is normal Blowing off Co2. But lowering the CPAP would do nothing for a true Central. Now if you were having problems with the pressure you may have held your breath while you were sleeping because you were not used to the back pressure. Then Cflex would have fix that but not centrals. A true Central is not fixed by pressure. It has everything to do with blowing off to much Co2 or a brain injury. If you blow off to much Co2 your body will cause a central to rebalance itself. Stop breathing build up C02 to much you yawn or take a sigh breath. Its all Acid and base body stuff.

Guest,

When I had my titration study I was gradually increased in pressure from 5 to 14. I had apneas until 9 and hyponeas until 12. I had nothing at 13 but a central at 14. My setting for a CPAP was 13. I was later changed to a BiPap (without another titration) and pressures were set at 13/9. I was told they "stopped raising the test pressures at because "they created a central at a pressure of 14."

From your quote above, whatever it was that I had at a pressure of 14 was not a true central. Is that correct?

You sound as though you have a medical background, but on these boards no one may be certain.

With all courtesy and respect, do you have a medical degree? And/or how certain are you that pressures must be at least 20 before they cause central apneas?

Thank you for your help,
Andy

CPAP induced Central Apnea is Rare. The reason that AutoCPAPs only go to 18 or 20, is that it is above those pressures that people start having pressure induced central problems that’s true 99% of the time.

Everyone is different so yea always have to say most of the time. There will always be the exception to the rule.

I find it hard to understand how your therapeutic level could be 1 cmH2o below were the cpap was so high for you it started causing the central apnea. So who knows maybe you are the exception to the rule. Maybe you had a central for another reason and they backed off I was not there.

You keep posting these assertions with little to back them up, and when asked for your credentials, ignored the question.

Simply because you assert something in an authoritative manner does not make it true, I'd really like to see some kind of backup to your assertions, both in the way of who it's coming from and also in the way of independent studies which confirm what you say.

Because frankly, what you (guest) say is in conflict with a lot of what I've read on the subject. Now, if you're in fact a medical doctor, perhaps you have access to information I don't have. On the other hand, if you're just a blow-hard doctor wannabe, that's also important information to have.

This is why I really don't tend to trust information from guest posters and/or newly registered posters: They have not had time to differentiate for us whether they are knowledgable or just want to be seen as such.

Liam, for better or worse, you have a history to compare my writings against.

I agree with liam. We need to know how Guest came to his conclusions. I was on cpap for a year with a pressure of 11. This was determined from ONE nites study. Things in the human body change day to day. Having a fixed pressure makes no sense. I finally bought a auto at my own expense. I m waiting for a refund from insurance company. Just for a test, I set the machine on cpap, at 11. My AHI was 25. With the auto at 8-16, its between 6 and 11. Many nites my pressure stays around 8 or 9. It makes no sense to have it at 11. And the c-flex is great. I only learned this because of the software.

I wish there was as much information about BiPaps on this forum as there is auto. My RX is for Bi, and I really don't understand much about it other than I will have a pressure set at 11, and probably the low around 4.
I also have a little central apnea every so often, and wonder how bipap will handle it.
I do understand, though, that most of you are on auto, so that's what you know and share.
I really enjoy reading about your thoughts, as you people have it DOWN.
Betty

Whilst I feel I have grasped the concept of raising the lower APAP level, to reduce the onset of events I would appreciate some further comment regarding our anonymous guest's assertion, that certainly sounds credible, that the higher pressure should be reduced to a range that sounds like 4-6 cm H20 above the lower level to prevent aberrant high pressures.

Sorry about that I am an RRT with many years in Home care and Sleep.

I will try to find you studies on CPAP induced Centrals but I am finding that kind of hard so here is a few references on central apnea. I will ask around for hard evidence on the pressure stuff. I am thinking though since there are probably 15000 or more Auto CPAP out there . Most of them set to go to a max of 18-20 cmH20 and the manufactures have not be sued out of business yet . That pressure induced Central apnea below a pressure of 18-20 is very Rare.


http://www.e-breathing.com/

Baro receptors or
Stretch receptors in the lungs also act to modify respiration. The Hering-Breuer reflex is stimulated when the lungs are stretched. Stretch receptors in the bronchi and bronchioles transmit inhibitory signals to the inspiratory center. This is a protective measure to prevent the lungs from being overinflated. Stretch receptors also send information about lung deflation to the brainstem. Respiration is affected by emotional cues and input from the position sensors (proprioceptors) in joints and muscle.

Chemoreceptors in the carotid and aortic bodies provide additional information to the integrating centers in the brainstem regarding peripheral levels of oxygen and carbon dioxide. Such regulation maintains alveolar PCO2 at normal levels, holds H+ in check and elevates PO2 as necessary. Alveolar PO2 is higher than needed to saturate hemoglobin. Therefore, changes in alveolar PCO2 have a greater effect on respiration. The carotid bodies are located at the branch point of the carotid arteries and the aortic bodies are found within the aortic arch. Carotid chemosensors sense a decrease in arterial PO2, especially below 50 mmHg, and increased PCO2 and H+. The aortic bodies sense increased PCO2 and H+. Chemoreceptors in the brain monitor the concentration of H+ in cerebrospinal fluid which closely parallels the PCO2 in blood.






http://www.highwire.org/cgi/searchresul ... disp_type=




Journal of Applied Physiology
Vol. 82, No. 3, pp. 918-926, March 1997
CONTROL OF BREATHING, CIRCULATION, AND TEMPERATURE

Effects of inhaled CO2 and added dead space on idiopathic central sleep apnea
Ailiang Xie, Fiona Rankin, Ruth Rutherford, and T. Douglas Bradley

Sleep Research Laboratory, Queen Elizabeth Hospital, and Department of Medicine, Toronto Hospital, University of Toronto, Toronto, Ontario, Canada M5G 2C4


Received 21 February 1996; accepted in final form 3 November 1996.

Xie, Ailiang, Fiona Rankin, Ruth Rutherford, and T. Douglas Bradley. Effects of inhaled CO2 and added dead space on idiopathic central sleep apnea. J. Appl. Physiol. 82(3): 918-926, 1997.We hypothesized that reductions in arterial PCO2 (PaCO2) below the apnea threshold play a key role in the pathogenesis of idiopathic central sleep apnea syndrome (ICSAS). If so, we reasoned that raising PaCO2 would abolish apneas in these patients. Accordingly, patients with ICSAS were studied overnight on four occasions during which the fraction of end-tidal CO2 and transcutaneous PCO2 were measured: during room air breathing (N1), alternating room air and CO2 breathing (N2), CO2 breathing all night (N3), and addition of dead space via a face mask all night (N4). Central apneas were invariably preceded by reductions in fraction of end-tidal CO2. Both administration of a CO2-enriched gas mixture and addition of dead space induced 1- to 3-Torr increases in transcutaneous PCO2, which virtually eliminated apneas and hypopneas; they decreased from 43.7 ± 7.3 apneas and hypopneas/h on N1 to 5.8 ± 0.9 apneas and hypopneas/h during N3 (P < 0.005), from 43.8 ± 6.9 apneas and hypopneas/h during room air breathing to 5.9 ± 2.5 apneas and hypopneas/h of sleep during CO2 inhalation during N2 (P < 0.01), and to 11.6% of the room air level while the patients were breathing through added dead space during N4 (P < 0.005). Because raising PaCO2 through two different means virtually eliminated central sleep apneas, we conclude that central apneas during sleep in ICSA are due to reductions in PaCO2 below the apnea threshold.



Oh and I can find you studies where they are treating Certain Central apnea with CPAP pressure and 02



This is the most common cause of Central apnea which is heart failure which causes Cheyne-Stokes breathing. Very tricky to titrate well.

hypocapnia = not enough Co2 so you hold your breath to build up enough in your system causeing a Central Apnea .

Am. J. Respir. Crit. Care Med., Vol 150, No. 6, Dec 1994, 1598-1604.


Effect of continuous positive airway pressure on central sleep apnea and nocturnal PCO2 in heart failure
MT Naughton, DC Benard, R Rutherford and TD Bradley
Sleep Research Laboratory, Queen Elizabeth Hospital, Toronto, Ontario, Canada.

We have previously shown that hypocapnia triggers Cheyne-Stokes respiration with central sleep apnea (CSR-CSA) in patients with congestive heart failure (CHF). Nasal continuous positive airway pressure (NCPAP) may attenuate CSR-CSA in patients with CHF and CSR- CSA. Accordingly, we hypothesized that attenuation of CSR-CSA by NCPAP would be related to an increase in PCO2. Therefore, we examined the effect of NCPAP on the frequency of apneas and hypopneas, transcutaneous PCO2 (PtcCO2), and minute volume of ventilation (VI) in 12 consecutive patients with CHF and CSR-CSA during stage 2 sleep. A control group of six patients, who did not receive NCPAP, was also studied. In the control group, there were no changes from baseline to 1 mo in the frequency of central apneas and hypopneas, mean PtcCO2, mean VI, or mean SaO2 during stage 2 sleep. In contrast, from baseline to 1 mo the NCPAP group experienced a decrease in the frequency of apneas and hypopneas (58.7 +/- 5.2 to 23.2 +/- 6.0/h of sleep, p < 0.001), an increase in mean PtcCO2 (34.6 +/- 1.4 to 40.8 +/- 1.1 mm Hg, p < 0.001), a reduction in mean VI (8.1 +/- 1.0 to 5.2 +/- 0.5 L/min, p < 0.01) and an increase in mean SaO2 (91.6 +/- 1.1 to 95.0 +/- 0.5%, p < 0.025) during stage 2 sleep while on 10.2 +/- 0.5 cm H2O nasal CPAP. We conclude that likely mechanisms through which NCPAP reduces CSR-CSA are by increasing SaO2 and raising PaCO2 during sleep toward or above the apneic threshold.

Gee Whiz,plain English please.

Thanks for posting the study.But,I will readily admit,I don't understand any of it.

I have been on cpap for 7 months,and am doing great.Should I consider another titration study to see if I need an apap?How often does one need to be titrated? Only when there are problems?
Most seem to really go the apap route.When I was first diagnosed,I didn't even know there were different machines,no one told me anything,even different masks,have learned all of this from this forum.


Marie

Central Apneas are common below 20 cmH20. This is why the A10 algorythm used by ResMed's Autoset technology does not raise the pressure when apneas above 10 cmH20 are detected. This is also why PB's 420E does not raise pressure on apneas when an open airway is detected (by cardiac oscillations).

In one of the links provided by guest, a study from the Division of Pulmonary and Critical Care Medicine, New York University Medical Center, New York, NY. Supported by National Institutes of Health-National Heart, Lung, and Blood Institute grants HL53931 and RR00096, and by grants from Mallinckrodt Nellcor Puritan Bennett and the Foundation for Research in Sleep Disorders states:

"The presence of cardiogenic oscillations on the CPAP flow signal is a specific indicator of central apnea and may have a role in self-titrating CPAP algorithms. We speculate that transmission of these cardiac-induced oscillations may relate to the relaxation of thoracic muscles during central apnea and is impeded by high muscle tone during obstructive apnea."

In this 1999 study by Ayappa et al, the prescribed CPAP level was 10 +/- 3 cmH2O. The name of the study is, "Cardiogenic Oscillations on the Airflow Signal During Continuous Positive Airway Pressure as a Marker of Central Apnea."

Here's the address of the direct link:

http://www.chestjournal.org/cgi/content ... urcetype=1


Regards,
-John

P.S. My titrated pressure was 7 cmH2O. My physician originally did not want to prescribe an APAP because he was afraid that the machine "would induce runaway centrals" due to higher pressures. I finally convinced him otherwise and got him to write a script for a 420E. And yes, it has detected quite a few central apneas using the method described in the study above.

Defintion of Cardiogenic Oscillations (CGO)Cardiogenic Oscillations (CGO) are respiratory oscillations of cardiac origin, i.e., originating from the heart, which are usually apparent on respiratory recordings made by a spirometer (a device which records the movement of air into and out of the lungs. It means that on the read out you may see the breathing pattern going up and down with the cardiac output. the study is implying that by watching the CGO you can predict a central Apnea.

Here is an eample of what it would look like on a sleep study Air flow read out . http://utopia.knoware.nl/users/zden/page06.html

Ok but that’s not pressure induced Central Apnea. That’s what we were talking about right ? No one said you can not have a central on low pressure. There are allot of reason to have a central. Here are at least 6 reasons a central happens. Five of them you can have on any pressure. One is Cardiac ( Example chain Stokes Breathing) . Another one is when you change sleep stages such as sleep onset Centrals. Another is in REM you may have a central but that’s normal since anything goes in REM. Yet another is called Idiopathic central Sleep apnea that means they don't know were it came from LOL. Then there are the brain stem injuries. So you see Centrals are not always related to pressure.

I may have missed some so please add to the reason for a central Apnea.

True Liam, my APAP is an older model ResMed Autoset T. But the sleep labs I've spoken with recently still aren't satisfied with APAPs. Just a little clarification, the reflex to breath is actually not a decrease in O2 sat., but a rise in CO2. A moot point since none of the autoPAPs measure either, but other responses like vibration, etc. Therefore, an apneic event has to be started for an APAP to recognize the need for increased pressure.

Vicki