Sleep Apnea and COPD: What Patients Should Know

July 25th, 2011 | Author: Katelyn Turner

This blog post was written by Xavier Soler, MD, PhD, Assistant Professor of Medicine, Pulmonary and Critical Care Division, University of California San Diego

Chronic Obstructive Pulmonary Disease (COPD) is very common leading to frequent physician visits and hospitalizations and become the 3rd leading cause of death in the U.S. COPD is the only major disease among the top 10 that continues to increase. Because of the long pre-clinical period, signs and symptoms of COPD develop predominantly in older adults.

Sleep-related disorders are most prevalent in adults and are associated with increased mortality and morbidity from obesity, cardiovascular diseases, diabetes, and depression, resulting in reduced quality of life (QOL) and increased health care costs. Patients with severe COPD commonly exhibit abnormal sleep like insomnia contributing to chronic fatigue, daytime sleepiness. Additionally, medications used to treat COPD, such albuterol or prednisone may affect sleep quality. A nocturnal reduction of nocturnal oxygen levels commonly seen in patients with COPD can have profound effects and contribute to long-term sequelae, producing arrhythmias, myocardial stress, and, possibly, lower survival.

Photo by mystopsnoringcure.com

Sleep apnea (OSA) is a chronic medical condition where the affected person repeatedly stops or nearly stops breathing during sleep. These episodes last 10 seconds or more and cause oxygen levels in the blood to drop leading to important health consequences. Usually it is caused by obstruction of the upper airway, resulting in obstructive sleep apnea. However, it may be caused also by a failure of the brain to initiate a breath, called central sleep apnea. OSA is very common, especially in older adults, occurring in up to 70% of men and 56% of women. Patients with untreated OSA have more automobile accidents and suffer from more family and social discord. Other important risk factors associated with OSA include smoking and alcohol. The symptoms of obstructive sleep apnea include loud snoring and/or abnormal pattern of snoring with pauses and gasps. Other symptoms include excessive daytime sleepiness, memory changes, depression, erectile dysfunction and irritability. OSA occurs in about 10 to 15% of patients with COPD, a condition referred to as the “overlap syndrome”. Although the prevalence of OSA is similar in patients with COPD as in the general population, individuals with both conditions without CPAP treatment have an increased risk of death and more hospitalizations from acute exacerbations.

Effective available treatments for OSA include continuous nasal airway pressure devices (e.g., CPAP); a mask is worn over the nose during sleep while compressed air is gently forced through the nose to keep the airway open. Different patients need different mask sizes and different pressure levels for optimal treatment results.

Oxygen therapy is used for low nocturnal oxygen levels and, medications such as non-benzodiazepines and behavioral therapy are current treatments for insomnia. Another type of treatment for obstructive sleep apnea is surgery to correct obstructions in the airways. The most common surgery is called UPPP, for uvulopalatopharngyoplasty. This surgery removes tissue from the rear of the mouth and top of the throat. The tissues removed include parts of the uvula (the flap of tissue that hangs down at the back of the mouth), the soft palate, and the pharynx. Tonsils and adenoids are usually removed in this operation. Surgical interventions are sometimes considered but are rarely successful. Another approach to treating OSA involves the use of oral appliances intended to improve breathing either by holding the tongue in place or by pushing the lower jaw forward during sleep to increase the air volume in the upper airway. In treating insomnia in COPD, benzodiazepines such diazepam should be avoided. However, newer compounds, such as zolpidem, may be safer in less severe COPD. Melatonin agonists can also be used. Cognitive behavior therapy is still considered the primary first-line treatment for insomnia, but has not yet been studied in COPD.

Exercise has been demonstrated to improve sleep in epidemiological studies. In a prospective study of 86 patients with chronic lung diseases referred to the UCSD pulmonary rehabilitation program (PR), we demonstrated a significant improvement in sleep quality after pulmonary rehabilitation measured with the Pittsburgh Sleep Quality Index (PSQI), a well-validated measure of overall sleep quality. Further studies to better characterize sleep-related disorders among COPD are under way.

In conclusion, sleep is poor in COPD patients and sleep disorders such OSA have profound effects on this population. Prediction of the patients diagnosed of COPD who are at risk for sleep difficult but crucial because their clinical implications. Therefore, increase public awareness about this serious condition is of paramount importance. Clinicians should include sleep evaluation in patients diagnosed of COPD asking about daytime sleepiness, snoring, pauses while sleeping and insomnia symptoms, referring to the specialist when necessary to address treatment options of comorbid sleep disturbances, which may provide significant long-term benefit for such patients.

10 comments

  1. Lorenzo says:

    Hi there are using WordPress for your blog platform?
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  2. Patrice says:

    My mom has severe emphysema which is of idiopathic origin. She never smoked, was not exposed to hazardous air pollutants, and does not have a genetic cause for her disease. Her emphysema may have been caused by scarring due to pneumonia when shecwas ten tears old.

    She eats a healthy diet consisting of fruits, vegetables, protien, and fats. Although she always maintained a healthy weight, she is now very thin. Of recent months, she is no longer able to exercise andvcan only walk very short distances.

    Now, to make things moe difficult, she has recently developed insomnia possibly due to the side effects from medications. Does anyone have a
    suggestion for treating insomnia or improving sleep in a person with severe emphysema?

  3. robert says:

    i feel like i’m being suffocating using sleep apnea machine since i do have copd. should i use the apnea machine?

  4. Although Radon is the second leading cause of lung cancer and beryllium causes chronic beryllium disease, the EPA has never enforced the Safe Drinking Water Act for water supplies near Superfund Sites like the Broohhaven National Laboratory and hundreds of other EEOICPA sites. Women with a history of breast cancer should not drink New York tap water because it may be a blend of untreated well water containing gamma sources that cause mutations far more serious than the BRCA 1 gene. In response to numerous complaints to the EPA & NYS Health Commissioner Shah, Roger C. Sokol, Ph.D., Director, Bureau of Water Supply Protection wrote in a December 23, 2011 letter: “Please be advised that both federal and NY State drinking water regulations do not prohibit the practice of source blending to achieve drinking water MCL compliance. In fact, guidance developed by EPA suggests that water systems first explore non-treatment options, such as blending, to achieve compliance with the Radionuclide Rule.” Dr. Sokal ignored my original complaint that no NY-approved water quality report contains proof of compliance with Radionuclide Rule, which limits gross gamma+beta doses from 168 radionuclides to 4 mrem/yr because gamma rays are leading causes of DNA mutations & cancer. To no avail, in 2000, EPA revised the radionuclides regulation, which had been in effect since 1977. The revisions required new monitoring provisions to ensure that all customers of community water systems will receive water that meets the Maximum Contaminant Levels for radionuclides in drinking water. EPA also issued a standard for uranium, as required by the 1986 amendments to the Safe Drinking Water Act. The current standards are: combined radium 226/228 of 5 pCi/L; a gross alpha standard for all alphas of 15 pCi/L (not including radon and uranium); a combined standard of 4 mrem/year for beta/gamma emitters. The new MCL for uranium is 30 µg/L.

  5. Mike Roth says:

    This is a great informational piece. Well written.

  6. Patricia Anding says:

    I have been told I have COPD, however, my breathing problems began after I coded and was put on Sotalol. I have congestive heart failure and have been shocked out of afib 8 or 9 times. 3 weeks ago it only lasted a week, then back in afib. Then was put on Cartia 180 a day and increased sotalol to 160 a day. Had been on Cardizen 120 since May. When I had been up several nites trying to breathe (also on oxygen) I cut Sotalol in half and went back on Cardizem 120. I also do breathing treatments with a Nebulizer (2 a day). I have sleep Apnea, and am waiting until I can breathe well enough to do the CPAP study and breathing test again. My pulmonary doctor said I’m breathing at 66% of someone my age.

    I am just wondering if I really have COPD. My pulmonary doctor has not said so, just my internist and cardio doc, and they did no tests to prove it. Have appt. with pulmonary next week, and going to ask him if it is REALLY the 2 meds, because they cause breathing problems.

    In February they put me on Multaq, and the pharmacy mailed me a warning that it causes severe breathing problems and could be fatal. I finally convinced them in May to change the med.

    What do you think?

    Thanks.

    • Dear Patricia: Did your internist or “cardio doc” refer you to an Electrophysiologist for an ablation? If not, like me and my late son & mother-in-law, you are a victim of BDD (bad doctor disease) — for which there may be no cure. Unlike you I was diagnosed with COPD by a pulmonary doctor; contradicting a government workers’ comp EEOICPA/NSSP-doctor hired by NIOSH in February 2010 — 7 years after I was misdiagnosed. Yet I was not tested for Sleep Apnea until last month.
      Unlike you, my 1st of 5 cardiologists never tested me for COPD or sleep apnea. #2 prescribed amiodarone & multaq knowing I had COPD, beryllium disease, diabetes, thyroid disease, toxic neuropathy, afib, aflutter & pvc’s. ## 4 &5 took me off these medicines after I had bypass surgery with a MAZE procedure in September of 2011; the first of 3 ablations, The MAZE ablation cured my afib and those had in February & June of 2012 eliminated pvc’s & aflutter, respectively. Today, I take no heart medicines, but suffer their side effects: Hasimoto’s disease, toxic neuropathy, sleep apnea, etc.
      Finally, pending your CPAP study, didn’t your doctor recommend Oximetry? According to many studies it’s an easier alternative to formal sleep study (polysomnography). In one study, normal overnight oximetry was very sensitive and so if normal, sleep apnea was unlikely.[13] In addition, home oximetry may be qually effective in guiding prescription for automatically selfadjusting continuous positive airway pressure.[14] Last Friday, I bought an (See en.wikipedia.org/wiki/Sleep_apnea)
      Oximeter for $45 and use it to check my oxygen levels whenever I awake or my wife shakes me if I begin to snore. If I’s low, I watch TV until the oxygen level gose back to 97-98%. Since being diagnosed with central sleep apnea (CSA) on April 5, 2013 I began taking COPD medicine (Spireva) at bedtime instead of in the morning.

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