Sleep Apnea CPAP Compliance Craziness

One of my biggest pet peeves is how doctors use the word compliance. If a patient doesn’t comply, it usually implies it was the patient’s fault. In sleep medicine, compliance is often used to measure how well patients use their CPAP machines. But compliance is not the same thing as success.

 

Various studies report CPAP compliance rates at 29% to 83%. The problem is that the definition of compliance changes from study to study. More recently, we’ve adopted the new Medicare requirement for CPAP compliance, which requires that the patients use CPAP at least 70% of the time over a 30 day period, for at least 4 hours every night. Otherwise, the machine has to be returned.

 

If you sleep 7 hours every night, it comes to 210 total number of hours per 30 days that you’re sleeping. Seventy percent of 210 hours is 147 hours. If you sleep only 4 hours every night, then this figure drops to 88 hours, which means that you have to use your CPAP machine only 40% of the total time that you’re sleeping to be considered "compliant." This doesn’t take into consideration if you’re actually feeling better or if the machine is being used effectively. 

 

Since CPAP works only if you’re using it, if only 40% of people are still using CPAP regularly 5 years after beginning treatment, then the CPAP success rate is at best 40%. But not all people who use CPAP will benefit, so this figure is likely to be much lower. Many more people are likely to stop using CPAP as the years go by. 

 

There are many patients that are 100% compliant with CPAP, using their machines 100% of the time they are sleeping, with no leaks and a low AHI, and still feel no better. Sometimes they can even feel worse than when they don’t use CPAP.

 

From what I’ve seen with CPAP compliance studies or even with sleep apnea surgery studies, they all manipulate the numbers to make their results look great. In very tightly controlled research studies with frequent follow-up and intensive intervention, results are likely to be good. But in the real world, with fragmentation of care, poor follow-up and lack of patient education, true success (the patient feels much better AND the numbers show it) is disappointingly low, no matter which option you choose. 

 

Despite all these obstacles, there are proven ways to improve CPAP success. With a systematic and formalized education program, along  with intense counseling, follow-up, and long-term support, many more people can benefit from CPAP. Ultimately, a major part of poor CPAP compliance is due to the health care system that’s dropping the ball.

 

Am I being realistic or too pessimistic? Let me know what you think of this issue in the comments box below.

Please note: I reserve the right to delete comments that are offensive or off-topic.

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124 thoughts on “Sleep Apnea CPAP Compliance Craziness

  1. I was diagnosed with severe sleep apnea 9 months ago. Having 80 episodes a night with my oxygen levels going down to 36%. I was given a cpap and with a pressure set to 15 with a 3 point variable on this setting.

    I have used it every night since getting it but felelt really ill with all the symptoms I had before starting the cpap, even with the pressure set to 15. My data card said my AHI was down to 3 and that all is well.
    The pressure suddenly went up to 17 for approx 1 month and I began to feel better which was great. Then it dropped again and all the symptoms came back including the neurological problems with memory and clear speech. The sleep clinic told me there is no way my symptoms have anything to do with the OSA. Im feeling confused because on a pressure of 17 I feel ok and anything lower I feel dreadful. Is it possible to have great clinical data and still suffer the symptoms of OSA if the setting is not suited to an individual therapuetic level?
    I think I’ve had this a long time and with the severity of my OSA, how can I find out about any potential brain damage that might have occured? My cognitive ability is definitely a lot less than it used to be. My left foot also drags at times now.
    The other thing that has started to happen is that when I wake up, I can be fully awake, have a conversation etc but cannot get my eyelids to open without physically pulling them open.

  2. Great paper, Dr. Park. I am a patient with Apnea and also am on disability for bipolar and anxiety disorder. Also, i must use the full mask due to mouth breathing. The insurance company, UPMC for Life/medicare, want to take the machine due to non-compliance. It’s bizarre. I am trying to convince them that my sleep patterns and lack of sleep are part of bipolar. When I do use the cpap it helps me tremendously, and a good nights sleep is a wonderful aid to the bpolar and anxiety! But I was not able to make the 4.0 hour per night average within 90 days. Why don’t these people allow me more time to get used to the machine? Seems insane to me. Lol

  3. Diagnosed in 2001 with moderate obstructive sleep apnea. During the overnight test, I had 19 events per hour. Was feeling like a zombie during the day and sleeping at my work desk with my office door closed. I used the CPAP with nasal pillows (and eventually humidifier) every night but usually took it off in my sleep after about 4 hours. It was a real struggle for the first couple of months to even use the darn machine. Sore nose, sore upper lip. Sore cheeks from straps. I called it my iron mask. But I used it … until about 4 months ago. After 15 years, three machines, and countless accessories, I decided that I always sleep on my side and wake up in the same position as I am when I go to sleep. I do not roll over on my back during the night. I use an oximeter to record my oxygen saturation levels and they are regularly 90 – 95 throughout the night with few exceptions. With the CPAP the saturations are 95 to 99. My wife tells me that I snore when I don’t use the CPAP but I don’t see any evidence that I stop breathing from the oximeter readings. I am a 2 phase sleeper – with or without the CPAP – because I have other medical conditions that cause me to sleep/stay in bed only 4 to 5-1/2 hours a night. I stay up as late as I can so that I am really tired then go to bed and fall asleep within a few minutes. I get up and go about my morning rituals then go back to bed after about 3 hours. I sleep another 2 to 3 hours (without my CPAP). I’m then good for the rest of the day, which lasts about 16 hours. The sleep doctors told me back in 2001 that I had excess tissue in my throat that caused the OSA. They said it was a risky procedure to remove it and in my case probably wouldn’t make much of a difference. I do have a fairly thick neck which is considered an indicator for OSA. I am going to use a digital record in a few days to record my sleeping to see if my breathing is regular or I appear to have any times when I am struggling to breath or actually stop breathing. If everything is good, then I’m content that I can continue to sleep without my CPAP. Maybe I’m kidding myself but enough is enough with the CPAP. I gave it my all, which in my case was about 4 hours per night. Now, I’m 71 years old and have less patience with the whole thing. Did I cut my life expectancy by going years before I was diagnosed with OSA? Perhaps. Did I add years to my life by using the CPAP? Perhaps. Am I undoing all the good by not using the CPAP now after 15 years? Perhaps. But I think I’ve found a happy median whereby I sleep without the CPAP and use other devices to measure my quality of sleep. Not scientific but I believe they work. Maybe someday someone will invent a better CPAP – we really need it. Hope these comments still get to someone since the site was first started in 2009.

  4. I lost my job trying to be complaint with cpap. Sleep walked out of semi while my wife was driving about 60 mph. Never sleep walked before cpap usage. On seizure meds now also from seizure on 10/1/12. From what I’ve read oxygen in lungs is not the same as in your finger tips. Your lungs are designed to send proper level to blood stream. The brain is in-volved through brain stem to trigger breathing. Why do people practice deep breathing? At sleep lab I went to none of that was addressed. In my teens I was a mouth breather because of hay fever/runny nose. Using several types of alt healing one which really surprised me was self hypnosis. I can post articles on fraud in sleep industry. The a villi in lungs need dead air space. I don’t know how a cpap does that with. The pause between breaths allows better air exchange in lungs. Breath in 10 seconds, hold 10 sec’s, exhale 10 seconds. From what I’ve read most of us don’t breath that way.. You will fail a sleep test with a 10 sec pause in breathing. So test is designed for people to fail.. For me I think the cpap supplied enough air the brain thought I was awake. Causing sleep walking. Also the sleep test not valid at higher elevation. I was at about 7,700 elv. when I sleepwalked. In under water diving you can find much info on oxygen effects and mix of gasses used. As best as I can tell cpap is based at sea level. I have pic on my fb page. Billions have been made from cpap. Some clinics in N. Eastern states have closed.

  5. I had the Deviated septum operation done and was told i may need a cpap last July 2015 i put off getting one as long as i could . SO May of this year i was given one i knew nothing about them , i don’t sleep good to start with some times I don’t sleep at all or maybe only 3 hours a day . I thought i was in compliance so on August 1st before i go to see the DR so he could let me keep it i get a phone call from the supplier told me i wasn’t in compliance return the machine then the lady hung up . to me she very rude and thu out the trial i thought i was doing good but every time she called she ruined my day . your not in compliance etc … sigh . on top of that they have billed me and medicare for supply’s i never got and some of the supply’s they sent me did not fit the machine I did complain about that they ignored it and insisted i was wrong ,the cpad did help me when i did sleep but that doesn’t seems to mater i did use it every time i went to sleep i just didn’t sleep enough to fit the bill .I’m returning it and all ready told my DR, I’m not going thu that again , so don’t even suggest it no matter how much it helped, i don’t need the hassle to keep it . and i know all to well just what those study do and mean, i do one for one of my DR’s and have for years he asks after each stundy to join new unless there is waiting period i have wait, in return I get paid, get to see if there might be a cure one day for me . i won’t lie i do it for money but not just the money . but trying to keep the Cpad when it was clear from the start there was no way I could by the way i felt i was treated while i was using it , like i said to my DR, I’m not wasting more money just to go thu it again when it was clear it did help me but because of other issue i don’t sleep well it’s taken away because i didn’t meet compliance. no lie . I’m sure there are other with similar issues. but with me I’m not going thu it again i don’t want any favors just a little more understanding and them caring and not how much it costs.

    Harry

  6. I have used my cpap device for two nights and I’m afraid that my nights sleep is not being saved to the device. When I look at the nights greater than 4, it still reads 0. Am I doing something wrong?

  7. Are you using it for less than 5 hours a night? When I first started using mine, it was a pain in the backside to get past hours of sleep a night. When I would look at my info, I would see that I used it 1 night but not previous nights. When I tried for 5 hours then it started recording and keeping track.

    I been doing this for almost 2 years. The first year was a battle trying to stay asleep longer than 3 hours. I talked to my primary care doctor and told him that I am not doing good on it and that I have grown agitated and hostile due to a lack of sleep. That is not good for a truck driver. He asked me when am I going to see the sleep study clinic. I told him the the wonderful group health sleep clinic forced me on the machine and never once checked on me in a year. 2 weeks later I went in to see an actual doctor and not a P.A. Told him about what is going on and the symptoms I told him, that in scuba diving I would be in a hyperbaric chamber. He did some research real quick. Came back too me and told me that the pressure was too much. My machine started at 6 and sometimes it would go to 9 and really bad night it would hit 12. So he lowered pressure to 4. I told him to think about it. He is lowering the pressure and the results from my sleep study is nowhere to be found. And you doctors have failed to listen to me about my medical history. I had sinus problems all my life. If I snore it is from the mucus that constantly runs down my throat at night. He wanted me to do an in clinic study. I told him to get bent as they screwed me out of $4000.00 for the last one that was wrong. If you pay I will do. But if you don’t pay, then go f**k yourself.

    Changed headset to a dream wear under nose and lowered pressure to 4. I am now sleeping 7 to 8 hours and back to screwed up dreams.

    The sleep doctors are just guessing. Their equipment can not tell them if you darted or snore. Their systems are extremely flawed and they know it. They hate when a scuba diver is a patient. We know all about pressure and what it will do to a human body. Oh and yes quite a few patients dealing with the cpap have been put in hyperbaric chambers from the bends brought on by a cpap machine.

  8. CPAP, just drop the P and insert an R and you get the experience most folks have. I was diagnosed with mild-moderate sleep apnea earlier this year. The worst nights of sleep I’ve ever had came while wearing the CRAP machine. There is no way I will ever be compliant at 70%; compliance is not worth the added time, energy and monetary cost. Using CPAP I experienced absolutely CRAP sleep, it cumbersome to deal with in daily life, and I was getting calls from suppliers trying to sell me more crap for my CRAP machine on a bi-weekly basis. When you add a playful puppy and a 4 year old to the mix, the machine becomes a hazard. However, I now prefer to use it as a very expensive door stop.

    I started looking into why my Dr. prescribed me a CRAP machine as opposed to physical therapy (weight loss) or to a nutrition expert… Also, why was I getting so many supplier sales calls when the machine came with a 90 day supply of filters and masks? I read through the CRAP machine’s parent company Q2 2016 earnings report. Turns out the sleep respiratory business is their fastest growing segment and where the majority of their marketing budget is going, training doctors how and why to prescribe, and making average people think a CRAP machine should be the first response. They don’t hide this, I’m sure you can google any number of companies who make these machines and read the thinly veiled comments by their CEO’s. They are in it for the earnings, not to make you sleep any better.

    This particular company holds conferences at golf resorts and other places that make sleep health professionals want to go. When at the conference, they are entertained, as well as wined and dined into their own “compliance” box. Makes me think Goldman Sachs must be long on the sleep industry.
    To get to the point, its my opinion CPAP should be an option of last resort for mild-moderate sleep apnea sufferers. Therapies people can more easily stick with, but may offer less financial reward for the growing sleep industry, should be methods of first resort. Lower-caloric intake, exercise, and sleep hygiene.

    In my case, the CRAP machine was a catalyst of positive change. I shrugged off the sleep specialist and went to my primary care physician (who agreed with my opinion that CRAP machines are not the net aggregate best solution for most people, thus the reason behind a low compliance rate) she prescribed the harder to achieve route of lifestyle changes with a mild stimulant to kick-start the changes, then I signed up for my first organized run in 5 years, shed about 10 lbs through exercise and lifestyle changes, and start using breathe right strips at night. I was off the stimulant as the diet and exercise replaced the extra energy after a month. I was opposed to the stimulant idea at first, as I was lacking sleep; I think taking a stimulant did help during the first couple weeks of lifestyle changes as lowering my caloric intake while simultaneously reintroducing resistance and cardio training regimes to my daily routine was really challenging.

    I feel so much better with the “old-school” sleep remedies that I’m dismissing CPAP as load of CRAP for folks with mild-moderate apnea, and who are willing to take the extra steps to truly get healthy. This is my opinion, based on my personal experience.

    I wish I had my Co-pay back, I could use it to sign up for more runs.
    CPAP would have a higher compliance and success rate if it were prescribed more sparingly, only when there is truly a lack of an alternative. For now, shareholders are the true beneficiaries of CRAP machines.

    Every nail is unique, but we seem to be predisposed to hitting them all with the same hammer.

    I wish I could have hit my CRAP machine with a hammer and posted it on youtube, I’d be a tosh.o celebrity for at least 5 minutes, perhaps a full 15.

  9. Not to mention fraud. Also a 10 second pause is a set point for not breathing. If you purposely slow your breathing to 2 breaths per minute to relax. You will fail sleep test. Try breathing in for a ten count, hold for 10, exhale for 10. During the time you’re not breathing it allows the avili in lungs to work better. You can read my other posts. Glad you’re not attached to cpap.

  10. I have discontinued use of my CPAP machine. I could not get a good nights sleep with it and would be half awake all the time I used it. I would be sleepy all the next day and would spend much of the day sleeping. I’m 88 years old a

  11. I started using a cpap with a very low setting of 4. I had no follow up, no counseling, no second sleep test to see if things were as they should be. I also had horrid restless legs during sleep. I’d say it was a nightmare but you really have to sleep to have one! I went years thinking this is the best its going to get, bought so many masks and head gear to try to get it right. I was better than before because i did try to comply 100%. BUT, I started throwing it off, frustrated that I wasnt getting air and started going downhill, headaches, exhausted, etc. My dentist told me he was working with a sleep doc in tandem with treating tmj with appliances that didnt interfere with cpap gear or something to that affect. So, We talked and I went to a sleep specialist, Dr Guillaume. She worked with me, I did another sleep study, found I needed to be at 14 not 4, got to test lots of different nasal pillows, did another sleep study follow-up to see if there were leaks and that I actually slept well with them, and left knowing that this Doctor cared enough to coach me, cheer me on when I was frustrated enough to cry, and promised that we’d keep at it til I was truly sleeping properly! It is not only the patient who can’t give up but a doctor-patient relationship that has to work towards a common goal. The people who call monthly to sell you more supplies dont know enough about this condition to truly help you. People with apnea of any form need a doctor who specializes in sleep disorders! Not many around. My advice? Dont give up, research, find a specialist. Sleep apnea is incidiously detrimental to your health! It’s a hard condition to treat, and hard for one to sleep with an “alien” clinging to your face, a bite guard in your mouth, maybe even wrist braces, knee braces and arthritic cream on (like I’m getting dressed to go into battle!). Well, don’t laugh! It is a battle every night trying to find that elusive nirvana other normal people find within 5 minutes of getting horizontal! Sometimes I wack my husband awake just to watch him drop back onto the pillow and fall asleep instantly! So, I put that little pillow on the end if my nose, cross my eyes and look at the wrinkles I’m sure it’s bound to make permanent, breathe that high pressure life giving air in and concentrate on not noticing everything attached to me. Mind over matter. Not easy but you can do it. The alternative is fatigue, headaches, low metabolism, tendency to gain weight, increased chance of stroke and heart disease, and really really bad moods! Well, I’ve rambled enough and given more than what I intended but unless you’ve battled this its hard to empathize. Got to get a doc, and YOU got to find the right mask, the correct pressure, and keep the damn thing clean and wear it!!! Nighty night!

  12. Subject: oxyge toxicity
    From: roy ijams
    AbstractOxygen (O2) is life essential but as a drug has a maximum positive biological benefit and accompanying toxicity effects. Oxygen is therapeutic for treatment of hypoxemia and hypoxia associated with many pathological processes. Pathophysiological processes are associated with increased levels of hyperoxia-induced reactive O2 species (ROS) which may readily react with surrounding biological tissues, damaging lipids, proteins, and nucleic acids. Protective antioxidant defenses can become overwhelmed with ROS leading to oxidative stress. Activated alveolar capillary endothelium is characterized by increased adhesiveness causing accumulation of cell populations such as neutrophils, which are a source of ROS. Increased levels of ROS cause hyperpermeability, coagulopathy, and collagen deposition as well as other irreversible changes occurring within the alveolar space. In hyperoxia, multiple signaling pathways determine the pulmonary cellular response: apoptosis, necrosis, or repair. Understanding the effects of O2 administration is important to prevent inadvertent alveolar damage caused by hyperoxia in patients requiring supplemental oxygenation.1. IntroductionWhen administering supplemental oxygen (O2) to treat hypoxemia associated with acute and chronic conditions, O2 toxicity by overexposure may be present. Annually, the need for supplemental O2 is projected to be around 800,000 individuals at a cost of 1.8 billion dollars [1]. Suboptimal use of O2 is reflected in prescription and treatment errors that exceed those related to antibiotics [2–4]. The alveolar epithelial and alveolar capillary endothelial cells are vulnerable targets for O2-free-radical-induced injury caused by hyperoxia. In acute lung injury (ALI) caused by hyperoxia, hyperpermeability of the pulmonary microvasculature causes flooding of the alveolus with plasma extravasations leading to pulmonary edema and abnormalities in the coagulation and fibrinolysis pathways promoting fibrin deposition [5, 6]. Type II alveolar epithelial cells are injured by O2 free radicals leading to impairment of surfactant production [7]. Thus, the maximum positive biological benefit for this life essential but toxic molecule exists along a dose-response, deficiency–toxicity continuum.2. Pathophysiology of Oxygen ToxicityHyperoxia is a state of excess supply of O2 in tissues and organs. Oxygen toxicity occurs when the partial pressure of alveolar O2 (PAO2) exceeds that which is breathed under normal conditions. With continuous exposure to supraphysiologic concentrations of O2, a state of hyperoxia develops. Under hyperoxic pathological conditions, a large influx of reactive O2 species (ROS) are produced. In intracellular and extracellular biological systems, the mass effect of ROS elevation, caused by O2 overexposure, disrupts the balance between oxidants and antioxidants, and this disruption of homeostasis can result in damage to cells and tissues [8–11]. Exposure time, atmospheric pressure, and fraction of inspired O2 (FIO2) determine the cumulative O2 dose leading to toxicity. Oxygen is toxic to the lungs when high FIO2 (>0.60) is administered over extended exposure time (≥24 hours) at normal barometric pressure (1 atmospheres absolute (ATA)). This type of exposure is referred to as low pressure O2 poisoning, pulmonary toxicity, or the Lorraine Smith effect. Oxygen exposure after approximately 12 hours leads to lung passageway congestion, pulmonary edema, and atelectasis caused by damage to the linings of the bronchi and alveoli. The formation of fluid in the lungs causes a feeling of shortness of breath combined with a burning of the throat and chest, and breathing becomes very painful [12]. The reason for this effect in the lungs but not in other tissues is that the air spaces of the lungs are directly exposed to the high O2 pressure. Oxygen is delivered to the other body tissues at almost normal partial pressure of O2 (PO2) because of the hemoglobin-O2 buffer system [13–15]. Toxicity also occurs when the ATA is high (1.6–4) and the high FIO2 exposure time is short. This type of exposure is referred to as high pressure O2 poisoning or the Paul Bert effect and is toxic to the central nervous system (CNS). Central nervous system toxicity results in seizures followed by coma in most people within 30 to 60 minutes. Seizures often occur without warning and are likely to be lethal. Other symptoms include nausea, muscle twitching, dizziness, disturbances of vision, irritability, and disorientation [13, 16–20]. Oceanic divers are more likely to experience CNS toxicity [17].Pulmonary capillary endothelial and alveolar epithelial cells are targets for ROS resulting in injury-induced lung edema, alveolar flooding, hemorrhage, and collagen, elastin, and hyaline membrane deposits [11, 21, 22]. Above a critical PAO2, the hemoglobin-O2 buffering mechanism fails and the tissue PO2 can rise to hundreds or thousands of mm Hg. At high levels of O2, protective endogenous antioxidant enzyme systems become consumed by ROS leading to cell death [16, 23]. Oxygen toxicity caused by ROS progresses in overlapping phases based on degree of severity and reversibility of injury. The phases are initiation, inflammation, proliferation, and fibrosis. Initially, there are increased ROS and depleted antioxidant levels, and the lung fails to clear itself of mucous. The inflammation phase or exudative phase is characterized by the destruction of the pulmonary lining and migration of leukocyte derived inflammatory mediators to the sites of injury. The proliferative phase is subacute and there are cellular hypertrophy, increased secretions from surfactant secreting alveolar type II cells, and increased monocytes. The final terminal phase is the fibrotic phase in which the changes to the lung are irreversible and permanent. There is collagen deposition and thickening of the pulmonary interstitial space and the lung becomes fibrotic [24–27].Clinically, progressive hypoxemia, or high O2 tension in the blood, requires increased FIO2 and assisted ventilation, which further aggravate the pathophysiological changes associated with O2 toxicity. Chest X-rays may show an alveolar interstitial pattern in an irregular distribution with evidence of a moderate loss of volume from atelectasis, however there is no clinical way of diagnosing O2 toxicity. Lung biopsy specimens may show changes consistent with O2 toxicity but the primary value of the biopsy is to exclude other causes of lung injury. Air pressure changes within the enclosed lung cavity and ventilator-induced injury may accompany and be indistinguishable from O2 toxicity. Oxygen toxicity can be minimized by keeping the PAO2 less than 80 mm Hg or the FIO2 below 0.40 to 0.50 [12]. The pulmonary cellular response to hyperoxic exposure and increased ROS is well described. Anatomically, the pulmonary epithelial surface is vulnerable to a destructive inflammatory response. This inflammation damages the alveolar capillary barrier leading to impaired gas exchange and pulmonary edema. Reactive O2 species induces pulmonary cell secretion of chemoattractants, and cytokines stimulate macrophage and monocyte mobilization and accumulation into the lungs, leading to additional ROS. The ROS leukocyte interaction further exacerbates injury. Research has shown that as these highly reduced cell layers become increasingly oxidized and levels of antioxidants fall, ROS-induced activation of multiple upstream signal transduction pathways regulates the cellular response: adaptation, repair, or cell death by apoptosis, oncosis, or necrosis [28, 29]. Mitogen-activated protein kinase (MAPK), toll-like receptor 4 (TLR4), signal transducers and activators of transcription (STAT), and nuclear factor kappa beta (NF kβ) are a few well-researched protein pathways that communicate the receptor signal to the deoxyribonucleic acid (DNA) of the cell thereby determining the cellular response. The MAPK pathway is a regulator of cell death genes, stress, and transformation and growth regulation. Mitogen-activated protein kinase activation precedes extracellular signal regulated kinase (ERK1/2), a promoter of cell proliferation. C-Jun-terminal protein kinase (JNK1/2) and p38 kinase both induce cell death and inflammation [30]. The TLR4, STAT, and nuclear regulatory factor 2 (Nrf2) pathways are associated with survival gene expression such as caspase-3 proteins and antioxidant response element (ARE) [31, 32]. The NF kβ pathway is an up-stream signal for inflammation and survival genes: anti-oxidant enzymes (AOE), Bcl-2, AKT, heme oxygenase (HO-1), and heat shock proteins (HSPs). The AKT1-4 family of signals plays an important role in glucose metabolism, cell proliferation, apoptosis, transcription, and cell migration. The Bcl-2 proteins are antiapoptotic while HO-1 and HSPs are ubiquitous stress-response proteins [33]. These signaling pathways are regulators of the pulmonary epithelial cell response to increases in ROS and hyperoxia [18, 34]. Cytokine and chemokine overexpression in response to hyperoxic stress can be protective. Tumor necrosis factor alpha (TNFα), interleukin 1 beta (IL-1β), interleukin 6 (IL-6), chemokine receptor 2 (CXCR2), interleukin 11 (IL-11), insulin and keratinocyte growth factor expression, and the beta subunit of Na, K-ATPase have been shown to attenuate death signals [35–37].3. The Formation of Free RadicalsOxygen is a requirement for cellular respiration in the metabolism of glucose and the majority of O2 consumed by the mitochondria is utilized for adenosine triphosphate (ATP) generation [38, 39]. The mitochondrial electron transport chain reduces the elemental molecular O2 to ionic O2 by the relay of electrons making O2 usable for ATP generation, during this process, oxidizing free radicals are generated [40, 41]. Toxic levels of O2 lead to the formation of additional ROS, which can impose damage to lipid membranes, proteins, and nucleic acids. Reactive O2 species mediate physiological and pathophysiological roles within the body [42]. Free radicals are a type of unstable, reactive, short-lived chemical species that have one or more unpaired electrons and may possess a net charge or be neutral. The species is termed free because the unpaired electron in the outer orbit is free to interact with surrounding molecules [42, 43]. Cells generate free radicals, or ROS, by the reduction of molecular O2 to water (H2O) (Figure 1) [44, 45]. 260482.fig.001Figure 1: Reduction of oxygen. A single-electron transfer which converts molecular oxygen to the superoxide anion, creating an unstable molecule. The decomposition of hydrogen peroxide can be a source of the hydroxyl radical; this reaction requires both superoxide and hydrogen peroxide as precursors. These steps reduce oxygen to water by the addition of four electrons, yielding three reactive oxygen species: superoxide anion, hydrogen peroxide, and hydroxyl radical.Chemically, three types of reactions lead to the formation of ROS. The one-electron reduction of molecular O2 to the superoxide anion (
    ) is catalyzed by transition metals including iron (Fe) and copper (Cu) such as

  13. The simultaneous oxidation reduction reaction of to hydrogen peroxide

    to hydrogen peroxide (H2O2) and the addition of an electron to produce the hydroxyl radical (HO●). The
    in biological membranes can act in four different modes: electron transfer, nucleophilic substitution, deprotonation, and a hydrogen atom abstraction as in

    initiated Fenton-type reaction and the decomposition of H2O2 requires
    and H2O2 as precursors and Fe and Cu presence for completion. The HO● is the most injury producing in biological systems, reacting with molecules in close proximity. These reactions are called Fenton-like reactions generating O2 and HO● when Fe II or Cu I reacts with

    The sum of reactions (3) and (4), or the Haber-Weiss reaction shown in (5) above demonstrates HO● formation by the metal-catalyzed decomposition of H2O2. The interaction between

    and H2O2 is the source of the majority of damage to biological systems due to the reactivity of continuously produced, highly toxic HO● [18, 46, 47]. These ROS-producing reactions occur endogenously involving enzymes, neutrophils, and organelles such as the mitochondria and exogenously induced by radiation, pollutants, xenobiotics, and toxins. Cellular survival and adaptation in an oxidative atmosphere are dependent upon sufficient antioxidant defenses to counteract the effects of ROS on cells and tissues [48].4. Functions and Classifications of AntioxidantsOxidant antioxidant homeostasis is highly regulated and essential for maintaining cellular and biochemical functions [49]. A change in the balance toward an increase in the oxidant over the capacity of the antioxidant defines oxidative stress and can lead to oxidative damage. Changing the balance toward an increase in the reducing power of the antioxidant can also cause damage and is defined as reductive stress [50–52]. Reduction, antioxidant and oxidation, or pro-oxidant reactions result from a gain or a loss of electrons and a loss or a gain in O2 [50, 53, 54].An antioxidant (a reductant or reducing agent) is anything that can prevent or inhibit oxidation [55–57]. Delay of oxidation can be achieved by preventing the generation or inactivating ROS [58]. Prevention, diversion, dismutation (decay), scavenging, and quenching are specialized antioxidant properties (Table 1). Antioxidant defenses may be classified as nonenzymatic and enzymatic or endogenous and dietary. Examples of nonenzymatic antioxidants are glutathione (GSH), ascorbic acid, vitamin E, beta-carotene, and uric acid. Major enzymatic antioxidants are superoxide dismutase (SOD), catalase, and GSH peroxidase which divert or dismutate ROS into harmless products. Endogenous or dietary antioxidants are based on the ability of the antioxidant to be synthesized by humans. Endogenous antioxidants are SOD, catalase, GSH peroxidase, uric acid, and bilirubin. Dietary antioxidants are ascorbic acid, vitamin E, and beta-carotene [59, 60]. Ascorbic acid, vitamin E, uric acid, bilirubin, and GSH scavenge ROS by expendable, replaceable, or recyclable substrates. Vitamin E and beta-carotene quench ROS by absorption of electrons and/or energy.tab1Table 1: Locations and properties of antioxidants.Antioxidants can be classified into four categories based on function. (1) Preventive antioxidants which suppress formation of ROS, (2) radical scavenging antioxidants which suppress chain initiation and/or break chain propagation reactions, (3) the repair and de novo antioxidants such as proteolytic enzymes and the repair enzymes of DNA, and (4) antioxidants which allow for adaptation that occurs when the signal for the production and reactions of ROS induces oxidant formation and transport [10, 61].Superoxide dismuta (I cut word off R. I.)

    to H2O2 and has three isoforms widely distributed in mammalian organisms. (1) Cytoplasmic SOD (SOD1 or Cu zinc (CuZn) SOD) is located in the cytoplasm, nucleus, and peroxisomes, (2) mitochondrial SOD (SOD2 or MnSOD) is located in the mitochondrial matrix near the electron transport chain, and (3) extracellular SOD (SOD3 or EcSOD) is found in the extracellular fluids and extracellular matrix of all human tissues especially the heart, placenta, pancreas, and lung [62–64]. The protective effects of EcSOD in the lungs are extremely important and well-established [65–68]. Catalase, one of the most potent catalysts found mostly in the peroxisome, functions to decompose H2O2 to H2O. Catalase defense from oxidant injury to lung epithelial cells exists in the cytosol or the mitochondria. Glutathione reductase is an important antioxidant enzyme for maintaining the intracellular reducing environment. This enzyme catalyzes the reduction of glutathione disulfide (GSSG) to GSH [69]. Glutathione disulfide is produced through the oxidation of GSH by ROS that arise during conditions of oxidative stress. Due to the high concentrations of GSH, GSH/GSSG is considered to be the principal redox buffer of the cell and the ratio of GSH/GSSG is viewed as a major indicator of the cellular redox status. The ratio of GSH/GSSG decreases under an oxidative stress condition [70, 71]. Tissue damage may develop when an oxidant/antioxidant imbalance occurs as a consequence of hyperoxia [72, 73]. The damaging effects of hyperoxia can lead to O2 toxicity, cell death, and can be a triggering factor in ALI [22].5. Clinical Presentation of Hyperoxic Acute Lung InjuryAcute lung injury and acute respiratory distress syndrome (ARDS) are secondarily occurring, inflammatory syndromes caused by triggers or risk factors described as direct or indirect, pulmonary or extrapulmonary. The pathological changes associated with HALI mimic the ALI triggered by other conditions such as hemorrhagic shock, reperfusion injury, pneumonia, sepsis, or paraquat inhalation [23, 33, 74, 75]. The risk of developing ALI or ARDS after inhalation injury is dependent on the toxicity and concentration of the inhaled substance [17]. For example, the cells and structure of the alveolar capillary membrane are highly susceptible to damage by toxic levels of O2 [76]. Both ALI and ARDS are the same clinical disorder, differing only in severity of hypoxemia. The ratio between arterial pressure of O2 (PaO2) and the FIO2 concentration delivered by ventilator support distinguishes the two syndromes. For ALI, the PaO2/FIO2 is ≤300 mm Hg and for ARDS, the PaO2/FIO2 is ≤200 mm Hg [74, 75, 77]. The injury to the alveolus is thought to develop when pulmonary or systemic inflammation leads to systemic release of cytokines and other proinflammatory molecules. Mast cells, which express mediators that exert effects on lung vasculature, are also increased after hyperoxic exposure [78]. Cytokine release activates alveolar macrophages and recruits neutrophils to the lungs. Subsequent activation of leukotrienes, oxidants, platelet activating factor, and protease occurs. These substances damage capillary endothelium and alveolar epithelium, disrupting the barriers between the capillaries and air spaces. Edema fluid, proteins, and cellular debris flood the air spaces and interstitium, causing disruption of surfactant, airspace collapse, ventilation-perfusion mismatch, shunting, and stiffening of the lungs with decreased compliance and pulmonary hypertension. There is no pattern to the injury; however, dependant lung areas are most frequently affected [74, 79]. Tissue examination reveals that surfactant disruption, epithelial injury, and sepsis initiate the increased expression of cytokines that sequester and activate inflammatory cells. Increased release of ROS alters normal endothelial function. Microarray analysis has revealed increased expression of genes related to oxidative stress, antiproteolytic function, and extracellular matrix repair as well as decreased surfactant proteins in ozone-induced ALI [80]. Diffuse alveolar damage results with intra-alveolar neutrophils indicating the presence of an inflammatory response in the alveoli. Red blood cells, cellular fragments, and eroded epithelial basement membranes are present with formation of hyaline membranes, indicating that serum proteins have entered and precipitated in the air spaces due to disruption of the alveolar capillary barrier. Formation of microthrombi indicates the presence of endothelial injury and activation of the coagulation cascade [81]. Acute lung injury syndrome presents within 24 to 48 hours after the direct or indirect trigger. Initially, the patient may experience dyspnea, cough, chest pain, tachypnea, tachycardia, accessory muscle use, cyanosis, mottled skin, and abnormal breath sounds (crackles, rhonchi, and wheezing). Blood gas analysis reveals progressive worsening of hypoxemia, leading to respiratory failure. Bilateral infiltrates are seen on a chest X-ray and are consistent with pulmonary edema but without the cardiac component of elevated left atrial pressure. Treatment includes mechanical ventilation, supportive care, and treatment of the underlying causes [16]. The mortality of ALI has improved over the past decade; however, it still ranges from 30% to 75% [75, 77, 82, 83] and occurs in about 86 of 100,000 individuals per year [84].6. ConclusionOxygen, often used to treat hypoxemia in the clinical setting, is itself a triggering factor in HALI given that the exposure is sufficiently concentrated and of adequate duration. The lung is a vulnerable target for oxidant-induced injury, initiating a cascade of protein signals that determine the cellular response. The alveolar epithelial and alveolar capillary endothelial surfaces are injured. Hyperpermeability, microthrombi (resulting from altered coagulation and fibrinolysis), collagen deposition, and fibrosis alter alveolar structure and function. Understanding precise mechanisms of injury and pulmonary cellular responses to hyperoxia is essential evidence for expert practice.AcknowledgmentThis project was sponsored by the TriService Nursing Research Program (TSNRP) (N08-012, HU0001-08-1-TS08). The information or content and conclusions do not necessarily represent the official position or policy of, nor should any official endorsement be inferred by, the TSNRP, the Department of Defense, or the US Government.References

    V. Kim, J. O. Benditt, R. A. Wise, and A. Sharafkhaneh, “Oxygen therapy in chronic obstructive pulmonary disease,” Proceedings of the American Thoracic Society, vol. 5, no. 4, pp. 513–518, 2008. View at Publisher · View at Google Scholar · View at PubMed · View at Scopus

    AbstractOxygen (O2) is life essential but as a drug has a maximum positive biological benefit and accompanying toxicity effects. Oxygen is therapeutic for treatment of hypoxemia and hypoxia associated with many pathological processes. Pathophysiological processes are associated with increased levels of hyperoxia-induced reactive O2 species (ROS) which may readily react with surrounding biological tissues, damaging lipids, proteins, and nucleic acids. Protective antioxidant defenses can become overwhelmed with ROS leading to oxidative stress. Activated alveolar capillary endothelium is characterized by increased adhesiveness causing accumulation of cell populations such as neutrophils, which are a source of ROS. Increased levels of ROS cause hyperpermeability, coagulopathy, and collagen deposition as well as other irreversible changes occurring within the alveolar space. In hyperoxia, multiple signaling pathways determine the pulmonary cellular response:
    apoptosis, necrosis, or repair. Understanding the effects of O2 administration is important to prevent inadvertent alveolar damage caused by hyperoxia in patients requiring supplemental oxygenation.1. IntroductionWhen administering supplemental oxygen (O2) to treat hypoxemia associated with acute and chronic conditions, O2 toxicity by overexposure may be present. Annually, the need for supplemental O2 is projected to be around 800,000 individuals at a cost of 1.8 billion dollars [1]. Suboptimal use of O2 is reflected in prescription and treatment errors that exceed those related to antibiotics [2–4]. The alveolar epithelial and alveolar capillary endothelial cells are vulnerable targets for O2-free-radical-induced injury caused by hyperoxia. In acute lung injury (ALI) caused by hyperoxia, hyperpermeability of the pulmonary microvasculature causes flooding of the alveolus with plasma extravasations leading to pulmonary edema and abnormalities
    in the coagulation and fibrinolysis pathways promoting fibrin deposition [5, 6]. Type II alveolar epithelial cells are injured by O2 free radicals leading to impairment of surfactant production [7]. Thus, the maximum positive biological benefit for this life essential but toxic molecule exists along a dose-response, deficiency–toxicity continuum.2. Pathophysiology of Oxygen ToxicityHyperoxia is a state of excess supply of O2 in tissues and organs. Oxygen toxicity occurs when the partial pressure of alveolar O2 (PAO2) exceeds that which is breathed under normal conditions. With continuous exposure to supraphysiologic concentrations of O2, a state of hyperoxia develops. Under hyperoxic pathological conditions, a large influx of reactive O2 species (ROS) are produced. In intracellular and extracellular biological systems, the mass effect of ROS elevation, caused by O2 overexposure, disrupts the balance between oxidants and antioxidants, and this
    disruption of homeostasis can result in damage to cells and tissues [8–11]. Exposure time, atmospheric pressure, and fraction of inspired O2 (FIO2) determine the cumulative O2 dose leading to toxicity. Oxygen is toxic to the lungs when high FIO2 (>0.60) is administered over extended exposure time (≥24 hours) at normal barometric pressure (1 atmospheres absolute (ATA)). This type of exposure is referred to as low pressure O2 poisoning, pulmonary toxicity, or the Lorraine Smith effect. Oxygen exposure after approximately 12 hours leads to lung passageway congestion, pulmonary edema, and atelectasis caused by damage to the linings of the bronchi and alveoli. The formation of fluid in the lungs causes a feeling of shortness of breath combined with a burning of the throat and chest, and breathing becomes very painful [12]. The reason for this effect in the lungs but not in other tissues is that the air spaces of the lungs are directly exposed to
    the high O2 pressure. Oxygen is delivered to the other body tissues at almost normal partial pressure of O2 (PO2) because of the hemoglobin-O2 buffer system [13–15]. Toxicity also occurs when the ATA is high (1.6–4) and the high FIO2 exposure time is short. This type of exposure is referred to as high pressure O2 poisoning or the Paul Bert effect and is toxic to the central nervous system (CNS). Central nervous system toxicity results in seizures followed by coma in most people within 30 to 60 minutes. Seizures often occur without warning and are likely to be lethal. Other symptoms include nausea, muscle twitching, dizziness, disturbances of vision, irritability, and disorientation [13, 16–20]. Oceanic divers are more likely to experience CNS toxicity [17].Pulmonary capillary endothelial and alveolar epithelial cells are targets for ROS resulting in injury-induced lung edema, alveolar flooding, hemorrhage, and collagen, elastin, and
    hyaline membrane deposits [11, 21, 22]. Above a critical PAO2, the hemoglobin-O2 buffering mechanism fails and the tissue PO2 can rise to hundreds or thousands of mm Hg. At high levels of O2, protective endogenous antioxidant enzyme systems become consumed by ROS leading to cell death [16, 23]. Oxygen toxicity caused by ROS progresses in overlapping phases based on degree of severity and reversibility of injury. The phases are initiation, inflammation, proliferation, and fibrosis. Initially, there are increased ROS and depleted antioxidant levels, and the lung fails to clear itself of mucous. The inflammation phase or exudative phase is characterized by the destruction of the pulmonary lining and migration of leukocyte derived inflammatory mediators to the sites of injury. The proliferative phase is subacute and there are cellular hypertrophy, increased secretions from surfactant secreting alveolar type II cells, and increased monocytes.
    The final terminal phase is the fibrotic phase in which the changes to the lung are irreversible and permanent. There is collagen deposition and thickening of the pulmonary interstitial space and the lung becomes fibrotic [24–27].Clinically, progressive hypoxemia, or high O2 tension in the blood, requires increased FIO2 and assisted ventilation, which further aggravate the pathophysiological changes associated with O2 toxicity. Chest X-rays may show an alveolar interstitial pattern in an irregular distribution with evidence of a moderate loss of volume from atelectasis, however there is no clinical way of diagnosing O2 toxicity. Lung biopsy specimens may show changes consistent with O2 toxicity but the primary value of the biopsy is to exclude other causes of lung injury. Air pressure changes within the enclosed lung cavity and ventilator-induced injury may accompany and be indistinguishable from O2 toxicity. Oxygen toxicity can be minimized by
    keeping the PAO2 less than 80 mm Hg or the FIO2 below 0.40 to 0.50 [12]. The pulmonary cellular response to hyperoxic exposure and increased ROS is well described. Anatomically, the pulmonary epithelial surface is vulnerable to a destructive inflammatory response. This inflammation damages the alveolar capillary barrier leading to impaired gas exchange and pulmonary edema. Reactive O2 species induces pulmonary cell secretion of chemoattractants, and cytokines stimulate macrophage and monocyte mobilization and accumulation into the lungs, leading to additional ROS. The ROS leukocyte interaction further exacerbates injury. Research has shown that as these highly reduced cell layers become increasingly oxidized and levels of antioxidants fall, ROS-induced activation of multiple upstream signal transduction pathways regulates the cellular response: adaptation, repair, or cell death by apoptosis, oncosis, or necrosis [28, 29]. Mitogen-activated
    protein kinase (MAPK), toll-like receptor 4 (TLR4), signal transducers and activators of transcription (STAT), and nuclear factor kappa beta (NF kβ) are a few well-researched protein pathways that communicate the receptor signal to the deoxyribonucleic acid (DNA) of the cell thereby determining the cellular response. The MAPK pathway is a regulator of cell death genes, stress, and transformation and growth regulation. Mitogen-activated protein kinase activation precedes extracellular signal regulated kinase (ERK1/2), a promoter of cell proliferation. C-Jun-terminal protein kinase (JNK1/2) and p38 kinase both induce cell death and inflammation [30]. The TLR4, STAT, and nuclear regulatory factor 2 (Nrf2) pathways are associated with survival gene expression such as caspase-3 proteins and antioxidant response element (ARE) [31, 32]. The NF kβ pathway is an up-stream signal for inflammation and survival genes: anti-oxidant enzymes (AOE),
    Bcl-2, AKT, heme oxygenase (HO-1), and heat shock proteins (HSPs). The AKT1-4 family of signals plays an important role in glucose metabolism, cell proliferation, apoptosis, transcription, and cell migration. The Bcl-2 proteins are antiapoptotic while HO-1 and HSPs are ubiquitous stress-response proteins [33]. These signaling pathways are regulators of the pulmonary epithelial cell response to increases in ROS and hyperoxia [18, 34]. Cytokine and chemokine overexpression in response to hyperoxic stress can be protective. Tumor necrosis factor alpha (TNFα), interleukin 1 beta (IL-1β), interleukin 6 (IL-6), chemokine receptor 2 (CXCR2), interleukin 11 (IL-11), insulin and keratinocyte growth factor expression, and the beta subunit of Na, K-ATPase have been shown to attenuate death signals [35–37].3. The Formation of Free RadicalsOxygen is a requirement for cellular respiration in the metabolism of glucose and the majority of O2
    consumed by the mitochondria is utilized for adenosine triphosphate (ATP) generation [38, 39]. The mitochondrial electron transport chain reduces the elemental molecular O2 to ionic O2 by the relay of electrons making O2 usable for ATP generation, during this process, oxidizing free radicals are generated [40, 41]. Toxic levels of O2 lead to the formation of additional ROS, which can impose damage to lipid membranes, proteins, and nucleic acids. Reactive O2 species mediate physiological and pathophysiological roles within the body [42]. Free radicals are a type of unstable, reactive, short-lived chemical species that have one or more unpaired electrons and may possess a net charge or be neutral. The species is termed free because the unpaired electron in the outer orbit is free to interact with surrounding molecules [42, 43]. Cells generate free radicals, or ROS, by the reduction of molecular O2 to water (H2O) (Figure 1)
    [44, 45]. 260482.fig.001Figure 1: Reduction of oxygen. A single-electron transfer which converts molecular oxygen to the superoxide anion, creating an unstable molecule. The decomposition of hydrogen peroxide can be a source of the hydroxyl radical; this reaction requires both superoxide and hydrogen peroxide as precursors. These steps reduce oxygen to water by the addition of four electrons, yielding three reactive oxygen species: superoxide anion, hydrogen peroxide, and hydroxyl radical.Chemically, three types of reactions lead to the formation of ROS. The one-electron reduction of molecular O2 to the superoxide anion (
    ) is catalyzed by transition metals including iron (Fe) and copper (Cu) such as .
    I have more info on breathing if you want. Millions made from fraud. My sleep is without cpap. I have used self hypnosis for healing and If you like to read think about the practice of medicine and self healing. It is illegal to say I can cure someone because the body heals it’s self. May God bless you and yours. FYI Ann Sutton turned me on to herbal care. And book Hands of Light by Barbra Ann Brennan. Through energy testing Ann helped me find an essential oil I have used on my feet for years relief of itch. Wish I had more time to be into healing. I also have experienced healing through faith in Christ. I had prayed for healing while driving. Then went for a walk while in Joplin MO and meet Ann.

  14. “Despite all these obstacles, there are proven ways to improve CPAP success. With a systematic and formalized education program, along with intense counseling, follow-up, and long-term support, many more people can benefit from CPAP. Ultimately, a major part of poor CPAP compliance is due to the health care system that’s dropping the ball”.
    Yes, Yes, Yes! Our healthcare system is dollar driven. I believe this is the main reason for our failing healthcare system. I am a masters prepared RN with a sleep apnea condition and have experienced the fractured system on both ends: as a provider and a patient. The “blame” for non compliance has always been patient related causing the patient anxiety and guilt. I have lost my confidence in the ability of the system to provide effective medical treatment and to adequately meet the needs of the patient.

  15. I think if that’s the level of compliance you accept, that’s what your patients will give you. Would you accept one of your patients taking their blood pressure medication 70% of the time?

  16. Perhaps some background info would be useful to you.

    How usable is CPAP? A recent study outlines the sorry reality[1]:

    …Epidemiological data show that on average 25% of OSA patients do not accept CPAP treatment and, of those who undertake the therapy, only 30-60% can be considered adherent [8]. An acceptable adherence to therapy is usually considered a minimum of 4 hours/night for at least 70% of the nights of therapy [9]…

    So bottom line, between 78% and 55% of people find CPAP unusable.

    Most people find CPAP unusable.

    After looking at many studies regarding what they call “compliance” or “adherence” the numbers above look to me to be what I have read elsewhere. Yes I really do believe that it could be as low as 22% of people being able to use CPAP long term!!

    So why on earth do so many find CPAP unusable?! I think some hints are seen in the business portion of a recent study[2]:

    …Measurements and Main Results: Pathophysiologic traits varied substantially among participants. A total of 36% of patients with OSA had minimal genioglossus muscle responsiveness during sleep, 37% had a low arousal threshold, and 36% had high loop gain. A total of 28% had multiple nonanatomic features. … A three-point scale for weighting the relative contribution of the traits is proposed. It suggests that nonanatomic features play an important role in 56% of patients with OSA…

    CPAP can help to lessen the effects of airway collapse from anatomic causes. But nonanatomic causes are involved some 56% of the time. Most of the time.

    The noise, vibration, and discomfort of CPAP use are not likely to help with “arousal threshold” issues. Indeed one would think they may well exacerbate them. I believe they do with me.

    High “loop gain” (ventilatory control loop gain) is exactly what leads to hypocapnic central apnea. Breath too much, loose too much carbon dioxide going below the “apneic threshold” and a central apnea you will have.

    As I first started reading about finding the hypocapnic apneic threshold (AT) they appeared to simply be raising CPAP pressures to invoke the central apnea. In today’s research dealing with determining the AT[3] they tend to use timed pulses of pressure to increase breathing volume.

    What I find is that very simply the higher my CPAP pressure is the more I have a tendency to experience unstable breathing and “clear airway apneas” (likely hypocapnic central apneas). CPAP pressure does indeed seem to be a “plus” factor regarding respiratory control loop gain.

    So CPAP pressure tends to exacerbate the “control loop gain” issues.

    Another thing is that control loop gain and likely arousal threshold are not stable parameters. When I experienced traumatic stress I actually found myself hyperventilating to the point of aura during the daytime. The anniversary of the traumatic event, getting used to a new outside temperature (hot or cold), and even too much exercise – all of these I have tracked to being associated with the development of unstable breathing (loop gain problems) in my nightly CPAP data.

    I track my CPAP data regularly and so can and do respond to problems as they crop up. But the normal procedure is to set things up and let them be.

    It is no wonder to me that most people find CPAP unusable.

    [1] Lo Bue et al. Usefulness of reinforcing interventions on continuous positive airway pressure compliance, BMC Pulmonary Medicine 2014, 14:78

    [2] Danny J. Eckert, David P. White, Amy S. Jordan, Atul Malhotra, and Andrew Wellman “Defining Phenotypic Causes of Obstructive Sleep Apnea. Identification of Novel Therapeutic Targets”, American Journal of Respiratory and Critical Care Medicine, Vol. 188, No. 8 (2013), pp. 996-1004. doi: 10.1164/rccm.201303-0448OC

    [3] X. S. Zhou , J. A. Rowley , F. Demirovic , M. P. Diamond , M. S. Badr, Effect of testosterone on the apneic threshold in women during NREM sleep, Journal of Applied Physiology Published 1 January 2003 Vol. 94 no. 1, 101-107 DOI: 10.1152/japplphysiol.00264.2002

    [8] Catcheside PG: Predictors of continuous positive airway pressure adherence. F1000 Med Rep 2010, 2:70. doi:10.3410/M2-70.

    [9] Weaver TE, Grunstein RR: Adherence to continuous positive airway pressure therapy the challenge to effective treatment. Proc Am Thorac Soc 2008, 5:173–178.

  17. Great Article, I have to totally agree. I have only been on Cpap a little over 2 months but I am already a living example of it. I am 100% compliant but I am still waking up 6-8 times a night. For the first month I literally sat in bed awake most nights using Cpap for 4 hours just to be “compliant” and I still could not sleep. After meeting the 4 hour min and still not falling asleep I would take it off and actually sleep. For the first month If I did manage to sleep I would wake up in a panic soon afterwards as I turned onto my side and the machine would get a leak. Now I am able to sleep after about 3 hours with it but I still wake up every time it gets a leak. I was sent to the sleep center when I started falling asleep during the day at work and on my commute to work. When I was diagnosed I was told CPAP would make me feel much better. I was very determined because the last thing I wanted to do was to have to give up my job. But sadly CPAP did not help and actually made things worse so I had to resign. Sadly the sleep doc only wanted to talk about sleep apnia, Not the fact that I was having serious difficulty falling asleep in the first place and have some type of movement issue. Insurance refusing to do an on sight sleep study did not help. To make a long story short 100% compliant does not mean 100% better, especially if you are looking at Apnia without looking at other issues that might effect the situation.

  18. I am a long-time CPAP/BiLevel user-got my first machine in 1988 and have used it faithfully ever since I first received my old Healthdyne CPAP. My original doctor at Washington University center spent a lot of time reviewing my diagnostic and titration results and he put the fear of the Lord into me that I must use my machine. It was approached as a VITAL health issue.I was not on Medicare then, and my private insurer did not follow any “compliance” routine.

    Like many other patients, I experienced a lot of mask problems, and masks were really not very good back then, however I was grimly determined to use the machine. I succeeded in spite of the mask issue, and I had quick improvement of my condition. Prior to using CPAP I woke with a headache every day. All that went away, and I am now 86+ years and in vigorous good health. And I am a fervent disciple of diagnosing and treating sleep apnesa.

  19. I hear your pain!!! It took me a good 6 months just to acclimate to the process. No help from the medical community except, “it takes time.” I decided to take back my control and educate myself on the condition and treatment through research. My best research came out of Israel. I have a graduate degree in biological sciences so I tend to question everything, not a good habit to have with medical personnel. I found establishing a routine sleep hygiene program worked for me. I have changed my controls, to auto and adjusted pressures and ramp. The CPAP has a software package that you can monitor parameters on a PC which helped me to tract my efforts. I and use nasal pillows which require less pressure and does not have problems with large leaks because of the minimal surface area.
    I could not believe the lack of support and narrow knowledge base from some of the medical community involved in sleep apnea. I am finally a success with AHI numbers from 2-6, a far cry from the 30 and 40 I was at for the first six months. Their concern with compliance is directly related to reimbursement. If a patient is not compliant, they don’t get their money.
    This is not a linear process but an ongoing changing treatment. I have good nights and some bad nights however the good nights have become the norm. Look up the sleep apnea board on line and you will find the majority of CPAP patients have had the same problem you are experiencing during the first months on therapy. Good luck

  20. Cpap insurance compliance is crap if you know you don’t sleep well with something like an elephant’s trunk attached to the front of your face. If you know you function better with a mouth guard, the insurance companies should get the heck out of your way and treat you like you have a brain, and let you have your preference. Having to go through the same garbage each time you need a new mouth guard is BS.