American Academy of Sleep Medicine versus Minnesota Medical Cannabis Program

The American Academy of Sleep Medicine (AASM) came out with a position statement about the use of medical cannabis for obstructive sleep apnea (OSA).  In brief they think it is not a good idea.  The entire statement can be read at the link.  I think that it is important to keep in mind that they concerns about safety and efficacy are generally dependent on the fact that like most of the conditions on the Minnesota list,  there is minimal to no scientific data to back up the suggested uses.

The AASM is not the first professional society to take a position on medical cannabis.  One of the first purported applications of medical cannabis was for glaucoma.  The American Academy of Ophthalmology has a position statement on Cannabinoids for Glaucoma  that reviews the history of this application and concludes that although cannabinoids can lower intraocular pressure, the duration of this effect is too short and the side effect profile too problematic for cannabinoids to be used for this application.  The statement points out that long acting cannabinoids for this application were recommended by the Institute of Medicine in 1999, but as of 2018 statement - there has been not suitable cannabinoid derivative.

That brings me back to the familiar refrain on this blog and that is the fallacy that cannabinoids or any street drug for that matter represents some form of miracle drug. Humans have been aware of cannabis for many applications for about 5,000 years.  A reasonable question is why some miracle application or even one less than a miracle has not been found at this point in time.  Why for example, were opioids developed as effective pain medications from the natural compounds over the same period of time?  I have attended the lectures on physicians who advocate for medical cannabis.  Some of them invoke Chinese medicine and quasi-scientific explanations like the entourage effect  about why the whole plant needs to be smoked. I don't really see a need for physicians to certify people to access these largely unproven treatments, especially when medical colleagues are describing them as potentially unsafe and ineffective.

I have no problem with the state of Minnesota supplying medical cannabis to people with a condition that has no clear cut treatment. I have no concerns about the state supplying cannabis to people who are terminally ill.  I do have a problem when cannabis is listed as a treatment when in fact there is little to no evidence that it is effective and vastly superior treatments exist.  Glaucoma and obstructive sleep apnea are two of these conditions.  From a purely psychiatric standpoint post traumatic stress disorder, and autism have existing treatments and autism has a newly approved treatment.  In the case of Tourette's syndrome and other movement disorders - the data remains very preliminary.     

As a prescribing physician, I have serious doubts about the thinking that goes into prescribing cannabis as an actual medication.  I prescribe medications every day.  These medications are all approved for use by the FDA.  There are specific indications and off label uses. There are potentially serious side effects.  The medications have to be prescribed to take the patient's chronic illnesses into account.  For example, I would not prescribe a sedative to a patient who I thought might have obstructive sleep apnea.  Prescribing cannabis, even in a special program that eliminates smokable cannabis continues to not make any sense to me. 

The list at the top of this page is directly from the Minnesota Medical Cannabis program as of today.  It lists all of the current conditions that qualify a person to take it.  I see the list as a political compromise to delay and potentially thwart the recreational marijuana movement.  It should not be a surprise that medical cannabis has always been a mainstay of the strategy to legalize recreational marijuana.  While that drama plays out - I hope that people in Minnesota don't forgo effective medical treatment for medical cannabis.  Today that means CPAP for obstructive sleep apnea and glaucoma drugs and surgery for glaucoma.

There is no evidence that medical cannabis can come close to the medical effectiveness of those options. At the political level - this is also a great example of how politics negatively impacts quality medical care.


George Dawson, MD, DFAPA


References:

1:  Ramar K, Rosen IM, Kirsch DB, Chervin RD, Carden KA, Aurora RN, Kristo DA, Malhotra RK, Martin JL, Olson EJ, Rosen CL, Rowley JA; American Academy of Sleep Medicine Board of Directors. Medical cannabis and the treatment of obstructive sleep apnea: an American Academy of Sleep Medicine position statement. J Clin Sleep Med. 2018;14(4):679–681.

2:  Petitions to Add Qualifying Medical Conditions to the Medical Cannabis Program.  This document documents the review process for adding qualifying conditions to the list.  Link 



Graphic: 

The table at the top of this post is directly from the Minnesota Medical Cannabis web site and is used here as a public document.

Sedating Patients For Imaging Studies

An article in this week's JAMA hit me like I was still on my old inpatient job.  It was about the issue of sedating patients for imaging studies.  Quality brain imaging - whether it is an MRI or a CT scan depends on the patient being able to lie very still.  Any movement causes artifact that can obscure critical brain areas of interest.  The reasons for the agitation vary quite a bit based on the population but the agitation is not necessarily any easier to treat.  The setting is often different.

As an example, agitated patients on our neurology service when I was an intern were typically agitated due to brain disease.  One of the first patients I saw was elderly and extremely agitated.  Delirium or psychiatric illness was suspected because of examination limitations.  When I examined the patient in the emergency department (ED) - and did the otoscopic exam - there was a large amount of pus coming out of the left ear.  Subsequent lumbar puncture showed that the diagnosis was pneumococcal meningitis.  Like all agitated neurology patients, the chief resident came by and administered intravenous fentanyl.  The junior resident and I stood by next to the CT scanner in the event the patient became excessively sedated or apneic because of the fentanyl.  Without it the CT scan would have been impossible.  She was subsequently admitted to the ICU and had a very complicated course, but eventually survived and left the hospital.

On the psychiatric side. things are a little bit different.  The indications for brain imaging are all based on psychiatric diagnoses.  The medical status of the patient may be completely unknown, based on their ability to cooperative with a review of systems and physical examination.  In most inpatient psychiatry settings these days the patient has come through the emergency department but the complete diagnostic evaluation is deferred to the inpatient side.  Assessment by the inpatient staff the next day may indicate that brain imaging is needed.  The ability to cooperate may vary from an inability to sit still to overt aggression based on the illness.  It is a common occurrence to get a request from radiology to sedate the patient before they go for a brain imaging study.

The issue from an inpatient psychiatric unit is several fold.  Many of the patients are very vigorous and have no physical illnesses.  The medications used on psychiatric units are not anesthetic agents and they do not work immediately.  Psychiatric units are rarely staffed at a level that several physicians can accompany the patient and give them an agent that would work immediately.  Even if they could - the question would be qualifications to supervise that process. At the minimum, they would need to be qualified to administer that agent and manage a cardiopulmonary arrest.  Finally, there is the hospital wide issue of how much support can psychiatry count on.  Can psychiatry for example request an anesthesiology consult for the purpose of imaging study sedation?

In the case report, an elderly man with a BMI of 39 and an history of stable coronary artery disease presented to the ED with dizziness. He ahd associated hypertension, hyperlipidemia, history of carotid endarterectomy, and obstructive sleep apnea (OSA).  He was treated symptomatically with meclizine and ondansetron but a neurology consultant recommended an MRI scan of the brain. He was not able to tolerate the close confines of the MRI scan and was given 1 mg of lorazepam for anxiety reduction.  Over a period of about 15 minutes in the MRI scanner he became incoherent and eventually unresponsive and a cardiac arrest code was called.

The article reviews the errors made in this case beginning with the administration of lorazepam.  Lorazepam is commonly used on inpatient psychiatric units for detoxification, agitation, and insomnia.  The exact dose in this case is a dose that I have administered many times to patients who were going for imaging studies and it is frequently not enough for that purpose.  In this case the patient has OSA and risk factors such as increased age that place him at higher risk for complications.  In this case the authors suggest the minimal dose and if more is needed to monitor heart rate, pulse oximetry and blood pressure in high risk patients.  I would typically do that by requesting an anesthesiology consult for the purpose of sedating the patient for an MRI scan.

Associated measures of care in  this situation include equipment availability.  They recommend the availability of a fiberoptic bronchoscope in case the patient needs immediate intubation and the intubation is difficult.  They consider it to be a priority in the case of patients who have risk factors for airway loss after sedation.   

The American Association of Anesthesiologists has designated dexmedetomidine as a sedative that does not compromise the cardiorespiratory status of patients.  It is a alpha-2 adrenoreceptor agonist.  I did a search on psychiatric applications of dexmedetomidine and the results of that search can be found here.  The package insert discusses the limited applications of ICU intubation and sedation of non-intubated patients for procedures.   

Communicating the patient's OSA status was also viewed as a key error correction process.  OSA is a highly prevalent condition making it more likely that patients with this condition will be sedated for MRI scans.  The suggest including an OSA section in the MRI checklist.

When I think about how this procedure has been done over the course of my career - it was hardly standardized and apart from my neurology team monitoring critically ill neurology patients inside a CT scanner - little monitoring was done.  About 15 years ago that landscape started to change.  Suddenly anesthesiology consults were much easier to get and much more successful.  That was a great relief compared to a process when additional medications were being requested and nobody was there to monitor the patient.  In a few cases, I called off the scan until adequate monitoring could be established.         

The precautions noted in this case report should be studied by every psychiatrist who finds themselves ordering sedation for MRI scans or other procedures.  It is entirely possible that MRI technology may be available in some hospitals but not the appropriate monitoring staff.

In that case I would recommend forgoing the procedure if all of the recommended staff and equipment is not available. 




George Dawson, MD, DFAPA


Reference:

1:  Blay E Jr, Barnard C, Bilimoria KY. Oversedation of a Patient With Obstructive Sleep Apnea Prior to Imaging. JAMA. 2018 Feb 6;319(5):495-496. doi: 10.1001/jama.2017.22004. PubMed PMID: 29411034.  



Graphics Credit:

MRI Images are from Shutterstock per their standard licensing agreement,





         

CPAP Follow-up - Reinforcing Daily Use

I posted on obstructive sleep apnea (OSA) and continuous positive airway pressure (CPAP) last year and it was well received.  Since then I have given out a lot of advice on CPAP based on that post and in general to people I have consulted with.  I continue to encounter all of the problems that I mentioned in the original post.  The message that I am continuing to give people is that they cannot view CPAP as an option.  It may not seem like it but it is a critical intervention to prevent the cardiac and metabolic complications of obstructive sleep apnea.  There are several of them and they are severe and potentially life shortening.  Anyone with this diagnosis owes it to themselves and their family to make CPAP work to avoid the morbidity and mortality associated with OSA.

It is very common in my practice to do my standard sleep assessment and hear that a person was diagnosed in a sleep study and that CPAP was recommended but for various reasons they are not using the machine.  I frequently hear about how the patient just "throws it off in the middle of the night" and how they "can't stand to have anything on my face" even in the case where they were diagnosed with severe sleep apnea.  Comments like those seem to understate the seriousness of the problem.  In many cases, insurance companies have asked for the machine back because the record on the SD card in the machine shows that it is not being used.  A person sitting in front of me with untreated OSA is complicated because their physical health is compromised and the immediate complications of untreated apnea and hypertension also compromises their psychiatric care.  The OSA and daytime somnolence becomes insomnia and that person may expect medical treatment for insomnia.  The prescription of sedating drugs is actually not a good idea for people with sleep disordered breathing.  The same think is true for hypertension.  There are several medications that can make hypertension worse and that I would not prescribe to people with uncontrolled hypertension.  Despite those qualifiers - I see medication and doses that I would not prescribe being given to people with untreated OSA.  It is untreated largely because the person does not give CPAP a chance.

Here are a few tips that I give people that they have found to work.  I am not working in a sleep lab or clinic so I am seeing them after the study has been does and after they have seen a wide range to technicians who were supposed to help them with mask fit and instructions on how to use the machine.

1.  Try various masks and types of CPAP - 

A lot of people try the full face mask and throw it off repeatedly at night and decide that's it.  If feeling confined by a mask is a problem there are smaller modified masks and nasal CPAP.  Try several until you find the one that works the best.

2.  Use humidification - 

It is surprising how many people think that they will save time by not using the humidification system with the machine.  Not using the humidification is another sure way to not tolerate CPAP.  Maintain and adjust the humidification for maximum comfort as you are adjusting to CPAP.  

3.  Make sure there are no air leaks -

In order for CPAP to work there has to be air pressure transmitted into the upper airway to maintain a splinting effect and prevent obstruction.  Air leaks put that pressure at risk and can prevent the effective use of CPAP.  Trying to find air leaks can be frustrating because after the fitting occurs by the technician or respiratory therapist there are problems at home associated with sleep positions.  With the wide array of equipment available it is very unlikely that you will not be able to find a device that works, but in some cases it may take a while.  An APAP device with a readout each morning (see graphic) will tell you if there have been any significant air leaks (100% mask fit = no air leaks).


4.  Get a modern APAP machine with feed back -

APAP is an abbreviation for Automatic Positive Airway Pressure.  This machine is able to sense increasing obstruction and adjust the pressure.  One of the main advantages is that a lower baseline pressure can be used and then as any obstruction occurs the devices increases the pressure to overcome it.  Standard CPAP devices have the pressure set based on the original sleep study. In the case of significant obstruction that could mean a constant high pressure.  Constant high pressures can lead to some side effects such as ear pain from pressure effects.  The really strong point of APAP devices is that they are generally much more sophisticated pieces of equipment. They can make the data available over the Internet to a sleep medicine physician who can remotely adjust the settings based  on downloaded data.  They also allow the patient to download their data each morning via a smartphone app (see the above graphic) so they know the hours that they wore the device each night, what the pressure settings were, and how many apneic/hypopneic episodes occurred (AHI or  Apnea/Hypopnea Index) per hour.


5.  Optimize your sleeping position and preparation each night based on the APAP readout - 

The modern APAP allows the individual patient unprecedented control over the treatment of sleep apnea.  With the feedback every morning they can be assured the device is working.  In the previous example, I showed a patient with increasing upper airway obstruction who eventually had some episodes of atrial fibrillation.  He had no idea that his system had airleaks and his AHI was increasing until he developed the atrial fibrillation.  With a new APAP system he would have had immediate feedback on day 1.

Sleep positions can also lead to better APAP/CPAP performance.  With the APAP device, feedback will be there within a few days if side sleeping is better (lower AHI) than back sleeping.  Looking at the readout of an AHI of 1.3  from Monday in the above example, this patient determined that by sleeping on his side he had consistently fewer episodes that if he slept on his back where his AHIs were all in the 3-5 range.

The final advantage of knowing that there is an APAP device out there allows the patient to advocate form themselves.  I don't know if it is widely known but there are clearly some health plans who only provide CPAP devices to patients diagnosed with OSA.  APAP devices are more expensive and based on what I have written it is clear that they are superior devices.

6.  Oral appliances for OSA are inferior to CPAP on measured outcomes like AHI-

I updated this post to include a comment on oral appliances (OA) for CPAP based on a question that I received.  I commonly see people who dislike CPAP and use the OA instead.  They claim that is "works better" than CPAP but I doubt it.  It does improve snoring and can reduce the AHI based on that improvement.  The problem is the improvement in AHI is generally not nearly enough to be considered an adequate level of treatment (AHI < 5) (1).  For that reason, expert guidelines recommend the OA for snoring alone or OSA in the case that the patient is intolerant of CPAP(2). Advertisements for a dental approach to OSA are commonplace and usually cite the years of experience of the clinician as being the determining factor.  I would recommend considering a sleep study with the OA in place to see just how much the AHI had improved.  In the case of the APAP machine you can read the number off your smartphone app every morning.  Use those numbers to determine the best treatment for your condition.

If you have been newly diagnosed with OSA and prescribed CPAP - be sure that you get a complete discussion of CPAP versus APAP and why your doctor is recommending one over the other.  Ask your sleep medicine physician the ideal solution rather than what your insurance company covers.  If cost is the only limiting factor - used and resanitized equipment may be an option.

The treatment of OSA with CPAP/APAP has never been better.  Make sure that you get a machine and a system that you are comfortable with and that works.  APAP devices can give you consistent feedback that is easily accessible.  There are some ways that you can hack a CPAP device and read the information on the SD card, but it is much easier to pull up the data with an app.

The immediate daily feedback that you have a working device and the lowest possible AHI is strong reinforcement to keep using it.      



George Dawson, MD, DFAPA


References:

1: Van Haesendonck G, Dieltjens M, Hamans E, Braem MJ, Vanderveken OM. Treatmentefficacy of a titratable oral appliance in obstructive sleep apnea patients: a prospective clinical trial. B-ENT. 2016; 12 (1): 1-8. PubMed PMID: 27097387.

2:  Ramar K, Dort LC, Katz SG, Lettieri CJ, Harrod CG, Thomas SM, Chervin RD. Clinical Practice Guideline for the Treatment of Obstructive Sleep Apnea and Snoring with Oral Appliance Therapy: An Update for 2015. J Clin Sleep Med. 2015 Jul 15;11(7):773-827. doi: 10.5664/jcsm.4858. Review. PubMed PMID: 26094920

 "CPAP is superior to OAs in the measured outcomes and, therefore, should be the first-line option for treating OSA"

Supplementary:

I am not a sleep medicine physician and do not prescribe these devices.  The information posted here is based on my experience doing sleep assessments as part of the standard psychiatric evaluation, referring patients for polysomnography, and getting the results of those tests during the treatment of my patients.  In follow up, I have to assist people in the proper use of the equipment and the pitfalls they encounter trying to establish a routine to use CPAP.  I have no competing financial interests of any kind.


Attribution:

The graphic at the top of this post is from the smartphone app that is used to download (via Bluetooth) all of the data on the screen each morning.  It keeps a running bar graphic and rolling over that graphic gives the data for each day. The data is assembled by a remote server through a wireless connection each day and the patient's sleep medicine doctor can monitor this data and set the machine remotely without needing to visit that physicians office.

Please Use That CPAP Machine!

 
The best way to start out this post is by taking a look at the above graphic.  This is the graphic of a 60 year old man with diagnosed obstructive sleep apnea who is using a continuous positive airway pressure (CPAP) machine.  CPAP creates an airsplint in the airway to prevent airway collapse and snoring but more importantly hypoxemia due to obstruction.  The bottom graph is downloaded from his CPAP machine and it shows the number of apneic and hypopneic episodes. What is not shown on the graph is that around October 12 this patient got an upper respiratory infection.  As the nasal congestion worsened he changed his CPAP mask from nasal CPAP  to a full face mask.  He had a number of air leaks from this mask and as he found out later - he experienced nightly air leaks.  Some of the air leakage was enough to wake up his wife who was sleeping in the same bed.  As the hypopneic episodes worsened - he started to wake up with palpitations in the morning.   The orange timeline shows that this patient developed atrial fibrillation for about 2 minutes on 10/28/2016 and 90 minutes on 11/15/2016.  At that point he went in to see his pulmonologist the the AHI index was downloaded.

Sleep is a central part of any psychiatric evaluation.  Many of my colleagues and residents have gone on to do sleep medicine fellowships and I think it is a logical career path for any psychiatrist.  General psychiatrists need to know quite a lot about sleep and how to assess and treat sleep problems.  During my assessments, obstructive sleep apnea (OSA) is a very common problem and it is a standard series of questions in my evaluation.  I am consistently impressed with number of people who have already been diagnosed with OSA by polysomnography and prescribed continuous positive airway pressure (CPAP) devices who either do not use them or who just gave up trying to use them.  There are a number of misconceptions about OSA and CPAP that I thought I might address in this post.

1.  OSA is a benign condition:

The best way to start this discussion is to look at a complex graphic of the association of OSA and CPAP with atrial fibrillation - a known comorbidity of OSA.  In this case we have a 60 year old man with a known diagnosis of OSA.  He has been on CPAP for about 8 years.  Before the OSA diagnosis he had an episode of paroxysmal atrial fibrillation while exercising.  After starting the CPAP he was asymptomatic for 5 years before getting an upper respiratory infection and changing the mask he was using with his CPAP machine.  The first papers on OSA and cardiovascular risk began appearing in the 1990s.  Since then further research has demonstrated cardiovascular, endocrine, and cognitive comorbidity.   Recent research suggests that severe but not mild to moderate OSA increases risk for all cause mortality (1).  In the case of the above patient 40-50% of  patients with atrial fibrillation have obstructive sleep apnea (2).  In addition  to clear disease states OSA puts people at increased risk for motor vehicle accidents and occupational hazards from both cognitive symptoms and excessive daytime somnolence.

2.  CPAP is an elective intervention:

I am always shocked by the number of men who view a sleep study and the use of CPAP as elective procedures.  I doubt that a lack of adequate explanation of the problem and its implications is the issue, especially once the diagnosis is made in a sleep lab.  During my assessments I am often discussing chronic fatigue, insomnia, hypersomnolence, cognitive problems, depression, attentional problems and anxiety as prominent features of the disorder.  The wish on the part of the patient is that I can give them a pill that will solve some of all of these problems.  There was a time in the early days of OSA (about 1985) when a specific tricyclic antidepressant was thought to treat be useful in treating the disorder but that was disproven early on.  

They have often been treated with sedative hypnotic or anxiolytic drugs for this same purpose.  In some cases they are also taking opioid medications or muscle relaxants.  Opioids have demonstrated dose-dependent respiratory ataxia (3).  All of these medications decrease respiratory drive and either prolong apneic episodes or directly interfere with other respiratory mechanisms.  Alcohol use is another complicating factor either by itself or in combination with other medications that adversely affect OSA or normal respiration.

3.  If I lost some weight I probably don't need to use CPAP any more:

Although high body weight is a general feature of modern American society and some medications that are prescribed for psychiatric disorders can lead to significant weight gain and metabolic effects - many patients undergo profound weight changes in both directions.  It is common to see patients with OSA who have had a significant weight loss and decided to stop using CPAP on that basis.  They have not reconsulted with Sleep Medicine or had repeat polysomnography.  They are placing too much value on the correlation between BMI and sleep apnea.  Losing weight can result in resolution of OSA, but it is also possible to have OSA without obesity- suggesting that at a minimum Sleep Medicine should be reconsulted on the issue of discontinuing CPAP.  The complex relationship between obesity and OSA was highlighted in a recent review (4).  The authors point out that obesity, weight loss and sustained weight loss are difficult problems.  Of the three controlled trials of a weight loss intervention there were improvements in AHI with weight loss and worsening of AHI with weight regained.  They also looked at more extreme weight loss with with bariatric surgery and concluded that a drop of 1 BMI unit was associated with a 2.3 unit improvement in AHI,  The authors compile a table of earlier studies that look at weight losses of 22% to 65% with accompanying improvement in AHI of up to 88%, but unfortunately in only 3 of those studies was AHI measured at < 5 or about 4% of subjects.  In 18/19 studies the subjects had a post-op BMI of > 30.  They conclude that the majority of bariatric surgery candidates remain overweight after the surgery and the many will still have moderate OSA and the need for CPAP.  Their overall thesis is that OSA is a complex disorder and therefore no single intervention (like weight loss alone) can be used.      

4.  If I am not snoring as much - I don't need to use CPAP any more:  

Snoring is caused by vibration of the same upper airway tissues that are involved in the obstruction.  Snoring can be caused by number of acute and chronic conditions as well as being an artifact of normal genetically determined anatomy.  More men and women snore than have sleep apnea.  In many people snoring is positional and occurs much more often in the supine than side sleeping position.  Snoring also depends on detection.  Snoring and apneic spells directly observed by a sleep partner are more diagnostic than self report of waking up gasping or snoring - although those reports should also be investigated.  Snoring - like body weight is an approximate correlate of OSA and the decision to stop CPAP should be made with the assistance of a Sleep Medicine physician.  Modern CPAP equipment can provide a significant amount of in home data to assist with that decision.  

These are a few considerations about the diagnosis of OSA and  prescription of CPAP.  Any person seeing me is strongly encouraged to do whatever is necessary to use their CPAP machine and reduce risk factors including any unnecessary medication that may affect respiration.  I may be reluctant to consider some therapies that while not directly impacting on respiration may have some effect due to synergies with other compounds (like antidepressant and trazodone combinations for sleep).  You can also count on hearing about comorbid conditions (like the atrial fibrillation in this case) that are clearly affected by OSA.

So if you have that diagnosis and had a CPAP machine - please use it.  The modern autotitrating machines are much easier to use and allow for direct patient access to the data.  It is now possible to download a smartphone app and get your relevant sleep data directly from the SD card on your machine in the morning.  That gives you immediate detailed information on how you slept, what your AHI was, how the mask performed and what corrective action might be required.  In some cases it allows your Sleep Medicine physician to adjust your machine setting remotely to optimize therapy and reduce the need for office visits for that purpose.

Sleep better and live better.

George Dawson, MD, DFAPA

References:

1:  Pan L, Xie X, Liu D, Ren D, Guo Y. Obstructive sleep apnoea and risks of all-cause mortality: preliminary evidence from prospective cohort studies. Sleep Breath. 2016 Mar;20(1):345-53. doi: 10.1007/s11325-015-1295-7. Review. PubMed PMID: 26779904.

2: Hohl M, Linz B, Böhm M, Linz D. Obstructive sleep apnea and atrial arrhythmogenesis. Curr Cardiol Rev. 2014 Nov;10(4):362-8. Review. PubMed PMID: 25004989; PubMed Central PMCID: PMC4101201.

3: Walker JM, Farney RJ, Rhondeau SM, et al.  Chronic Opioid Use is a Risk Factor for the Development of Central Sleep Apnea and Ataxic Breathing. Journal of Clinical Sleep Medicine : JCSM : official publication of the American Academy of Sleep Medicine. 2007;3(5):455-461.

4: Romero-Corral A, Caples SM, Lopez-Jimenez F, Somers VK. Interactions between obesity and obstructive sleep apnea: implications for treatment. Chest. 2010 Mar;137(3):711-9. doi: 10.1378/chest.09-0360. Review. PubMed PMID: 20202954; PubMed Central PMCID: PMC3021364.

5:  Phillips B.  Kryger MH.  Management of obstructive sleep apnea hypopnea syndrome.  In:  Kryger MH, Roth T, Dement W, eds.  Principle and Practice of Sleep Medicine, Fifth Edition.  St. Louis, Missouri: Elsevier Saunders, 2011: 1278-1293.   

Supplementary:

Some sleep medicine definitions used in the above post.  For more technical definitions see reference 5 above:

Apnea:  Cessation of airflow for at least 10 seconds.  The technical definition depends on the sensors used for this measurement such as a drop in thermocouple excursion by 90% for 10 seconds.  The thermocouple in this case would be measuring the temperature of exhaled air.  Obstructive apneas are present when there is inspiratory effort during the apnea and central apneas are present when there is none.  There can also be mixed apneas. 

Hypopnea:  Shallow breathing or a low respiratory rate for 10 seconds.  The technical definition again depends on the equipment usually defined as a drop in nasal pressure excursion and a percentage of hemoglobin saturation.

AHI:  Apnea Hypopnea Index - an index of severity of OSA defined as the number of apneic and hypopneic episodes per hour.  The general goal of therapy is to have an AHI of less than 5.

BMI:  Body mass index or weight in kilograms divided by the square of height in meters.  Several sites like the CDC offer BMI calculators and brief instructions on how to interpret these numbers.  Higher BMI and neck circumference increases the risk of OSA.