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How to sleep with copd: How to Sleep Better With COPD


How to Sleep Better With COPD

Sleep is important for everyone. But if you have chronic obstructive pulmonary disease (COPD), getting a good night’s rest is essential to be able to breathe well and function the next day.

Studies have linked poor sleep with a worsening of COPD symptoms, as well as an increased risk of developing complications from the disease, according to the American Thoracic Society.

Trouble is, it can be hard to fall asleep — and stay asleep — when you’re feeling short of breath, coughing, and in pain. Indeed, more than 75 percent of people with COPD report nighttime symptoms and difficulty sleeping, according to the Sleep Foundation.

Some medications used to treat the condition can also make sleeping problems worse. Inhaled medications like theophylline 4 (Theo-24, Theochron, Elixophyllin) improve chest symptoms but can also reduce sleep quality for some people with COPD, per the Sleep Foundation. Prednisone can also affect your ability to sleep.

Many people with COPD also have undiagnosed sleep apnea, a condition in which your airway closes off and you may stop or nearly stop breathing multiple times throughout the night, making it difficult to get a good night’s rest.

Anxiety and depression, which often occur in people who have chronic conditions, can also cause or worsen insomnia in people with COPD, says E. Neil Schachter, MD, a pulmonologist and sleep medicine specialist at Mount Sinai Hospital in New York City.

RELATED: 12 Ways to Breathe Better With COPD

Sleep Tips for People With COPD

The positive news is that there are a number of things you can do to improve your sleep when you have COPD. Here are some strategies to try:

1. Adjust Your Sleep Position

Sleeping in a slightly upright position will take some stress off your lungs, says MeiLan K. Han, MD, a professor of medicine in the division of pulmonary and critical care at the University of Michigan in Ann Arbor and a spokesperson for the American Lung Association.

Slightly elevating your head also helps prevent acid reflux (when stomach acid backs up into your esophagus) from waking you up at night.

Known as gastroesophageal reflux disease (or GERD), this condition is common in people with COPD. According to a review published in May 2018 in the journal Chest, simple behavioral changes including proper positioning (to take pressure off the esophagus and allow gravity to keep acid down) can improve nighttime GERD symptoms, as well as sleep quality.

2. Avoid Napping During the Day

If you absolutely need a nap, keep it short — no longer than 30 minutes — and avoid napping in the late afternoon.

A short nap can restore energy, but a long or late nap can keep you awake at night and worsen the cycle of poor sleep and excessive daytime sleepiness, notes the Sleep Foundation.

3. Unplug From Electronics

Build in a 30- to 60-minute device-free buffer before bed. Cell phones, tablets, and laptops cause mental stimulation that is hard to shut off, notes the Sleep Foundation.

In addition, the blue light from screens suppresses production of the sleep-inducing hormone melatonin, which can make it harder to drift off. If you must look at a screen within an hour of bedtime, set your device to “night mode” to minimize the impact of the light.

4. Be More Physically Active During the Day

“Exercise is something that improves COPD in general,” Dr. Schachter says. In fact, a moderate exercise routine can improve your body’s use of oxygen, reduce your shortness of breath, increase your energy and muscle strength, reduce anxiety and depression, and aid sleep, says the American Lung Association (ALA).

“[Being physically active] improves your endurance so that you can do more during the day, and if you do more during the day, you will sleep better at night,” adds Schachter.

5. Try Some Yoga

Yoga is a great form of exercise for people with COPD because it reduces stress and also helps you control your breathing, says Martha Cortés, DDS, a dental and sleep disorders specialist in New York City.

A study published in May 2021 in the journal Complementary Therapies in Clinical Practice found that yoga can reduce the severity of shortness of breath and fatigue and improve sleep in people with chronic respiratory diseases such as COPD.

6. Establish a Consistent Sleep Routine

Going to bed and waking up at about the same time every day — even on weekends — can get your brain and body accustomed to getting the full amount of sleep you need, says the Sleep Foundation.

Also, try to follow the same pre-bed ritual — such as washing up, putting on PJs, and doing something relaxing, like reading, stretching, or meditation, for 30 minutes. This helps reinforce in your mind that it’s bedtime, making it easier to fall asleep.

7. Talk to Your Doctor About Using Oxygen Therapy

People with lung diseases lose oxygen in their blood overnight, especially during REM sleep (when dreaming takes place). Using oxygen therapy at night allows your body to get more oxygen into the bloodstream and can help you get a better night’s sleep, says the ALA.

“If you need it, it’s important that you be prescribed nocturnal oxygen,” Schachter says. While some people with COPD need oxygen, for a small percentage it can be dangerous, so make sure you have a thorough discussion with your doctor about using oxygen therapy.

RELATED: What Are the Four Stages of COPD and the Gold System for Grading?

8. Make Your Bedroom a Haven for Sleep

Keeping the bedroom quiet, dark, and cool can help you nod off. Consider buying light-blocking shades or using an eye mask to keep any light (including streetlights and early morning light) from entering the room, Dr. Cortés advises.

“Also, make sure your bed is big and comfortable enough to promote rest, especially if there are two of you,” she adds.

You may also want to use ear plugs or a white noise machine to drown out any sounds, and keep the temperature on the cooler side — around 65 degrees Fahrenheit is ideal, the Sleep Foundation says.

9. Get Tested for Sleep Apnea

If you have any signs and symptoms of sleep apnea — say, for example, your partner notices that you’re snoring a lot or sometimes gasp for air — ask your doctor about scheduling a test for this sleep disorder.

Sleep apnea, which occurs in about 10 to 15 percent of people with COPD, causes oxygen levels in the blood to drop and interrupts the sleep cycle, says the COPD Foundation. It can also cause other serious problems if left untreated.

The condition can be effectively treated by wearing a nasal continuous airway pressure device (i.e., CPAP) while you sleep, which gently forces air through your nose to keep the airway open.

10. Review Your Medications

Talk to your doctor about all of the medications you take, and ask whether any of them are causing you to lose sleep. You may be able to adjust the time you take them to prevent them from keeping you awake at night, Schachter says.

Also, let your doctor know if pain from COPD keeps you awake. Pain is very disruptive to sleep, notes Dr. Han, so it’s important to talk to your doctor about ways to manage it at night.

Sleep Tips for People With COPD

Many people with chronic obstructive pulmonary disease (COPD) find it hard to get a good night’s sleep. Medications, coughing, and breathing problems get in the way. Daytime sleepiness can make your COPD symptoms worse.

Consider these tips to improve your quality of sleep and manage your COPD better.

Lifestyle Changes

Make these healthy habits a part of your life:

If you smoke, get help to quit. Keep your entire house free of secondhand smoke, dust, and pollutants. When you inhale smoke, your air passages get smaller, which makes it harder to breathe.

Start an exercise program. Ask your doctor what you can do. People with COPD often experience drops in oxygen levels at night. Physical activity builds up your oxygen supply. Aim for 30 minutes of exercise a day, three times a week. Try not to do high energy or stressful activities 2 hours before bed.

Don’t take naps. If you must, don’t nap for longer than about 20 minutes.

Keep a sleep diary. Include what you ate, your medicines, and activities for the day as well as when you went to bed and woke up. Review it to see what helps you sleep better.

Go to bed at the same time every night, even on the weekends. A sleep routine programs your brain and internal clock to relax at the same time each evening.

Use Your Oxygen Mask

Your oxygen levels may drop at night and your breathing may slow down. If you use an oxygen mask, wear it when you go to bed.

Curb Caffeine

Changes to your diet may improve your sleep quality. Caffeine and caffeine products can keep you from falling asleep. Stay away from them after dinner. Alcohol may help you fall asleep quickly, but after it wears off, it keeps you wide awake.

It’s hard to sleep on a full stomach. So don’t eat large meals that are heavy on starchy or sugary carbohydrates too close to bedtime. Eat a well-balanced diet that includes fruits and vegetables as well as lean protein.

Get Ready for Bed

Before you’re tired, prepare for sleep by doing things that calm you. When you create a relaxing ritual, your mind and body follow. Try these tips for relaxation:

  • Take a warm bath to help your body reach a nice temperature for rest.
  • Journal or write a to-do list for the next day to clear your mind.
  • Relax your muscles with light stretching.
  • Listen to soothing music or a hypnosis recording.
  • Shut off your electronic devices an hour before bed.

Set Up for Sleep

Your bedroom should welcome and calm you. A dark room tells your brain it’s time for bed. Blackout curtains shut out any light from outside.

Create a comfortable and cool space with a temperature between 60-71 F. Get rid of clutter as it can cause stress. Aromatherapy with lavender can make it easier to fall asleep.

Keep electronics such as your smartphone, computer, and TV out of your bedroom.

Sleep Position

Your lung capacity is lower when you’re flat on your back. Sleep with your head slightly higher than the rest of your body.

If you prefer lying on your side, place a pillow between your legs and keep your back straight. When you sleep on your back, bend your knees slightly with a pillow placed under them.

Sleeping Tips for Better COPD Management

Living Healthy

September 16, 2019

Sleeping Tips for Better COPD Management


People with chronic obstructive pulmonary disease (COPD) face special challenges when it comes to getting a good night’s sleep. COPD causes coughing, pain and shortness of breath, which can make it difficult to sleep. But sleep is important for resting pulmonary muscles — and for making it possible to simply function the next day. There are a number of reasons beyond direct COPD symptoms that you might be having sleeping problems. Understanding what these are could help you find your way to a better night’s sleep.


How COPD Can Complicate Sleep

Sleep can be a complicated process. We all can have trouble sleeping from time to time. However, people with COPD can have added difficulties. Factors that can contribute to COPD sleeping problems include:

  • Medications. Common COPD medications, such as albuterol and prednisone, can have insomnia as a side effect.
  • Sleeping position. Breathing is often easier sitting up than lying down when you have COPD. However, trying to sleep in a sitting position can interfere with the ability to sleep. But lying flat also poses problems. Blood oxygen levels fall, and lung function slows, when you lie flat. This can exacerbate shortness of breath. Lying flat also can make acid reflux problems worse — this is a common problem for people with COPD.
  • Sleep apnea. Sleep apnea is common in people who have COPD. If you or a bed partner notice you frequently snore, this might be the case for you, as well.

  • Anxiety and depression. These mental health conditions are common for people suffering from chronic health problems. Both can interfere with your ability to sleep.

How Your Doctor Can Help

While you might be napping during the day to make up for lost sleep, this isn’t a good idea. Sleeping during the day can throw off your body’s natural sleep patterns. Instead, it’s better to have a conversation with your doctor. During this visit, you’ll want to:

  • Review your medications. Bring a list of the prescriptions and over-the-counter drugs you now take. Ask if any might be disrupting your sleep. Timing also might be a problem. It could be possible to adjust when you take certain medications to help you sleep more easily.

  • Ask about other medications. If pain is keeping you awake at night, there might be medications that can help manage that problem. You also might want to ask about safe sleeping aids. Some sleep medication can slow down your breathing, though, so it’s important to talk with your doctor before taking anything new.

  • Discuss oxygen therapy. Using oxygen at night can help some people with COPD sleep more soundly. It’s possible this could be an option for you, as well.

  • Talk about sleep apnea solutions. CPAP is a common method to address sleep apnea. It could help you improve your oxygen levels both day and night.

How Sleep Habits Matter

There also are some simple adjustments you can make to your schedule and bedroom that could help improve your sleep.

  • Limit napping. Too much sleeping during the day can disrupt regular sleeping patterns. Limit naps to 20 minutes or less to support nighttime rest.

  • Stick to a routine. Try to go to bed and get up at the same time every day. This will help reinforce natural sleep/wake cycles.

  • Elevate yourself. Sleeping in a slightly upright position helps reduce stress on your lungs. It also can reduce acid reflux symptoms.

Sleep disorders in COPD: the forgotten dimension


Sleep in chronic obstructive pulmonary disease (COPD) is commonly associated with oxygen desaturation, which may exceed the degree of desaturation during maximum exercise, both subjectively and objectively impairing sleep quality. The mechanisms of desaturation include hypoventilation and ventilation to perfusion mismatching. The consequences of this desaturation include cardiac arrhythmias, pulmonary hypertension and nocturnal death, especially during acute exacerbations. Coexistence of COPD and obstructive sleep apnoea (OSA), referred to as overlap syndrome, has been estimated to occur in 1% of the general adult population. Overlap patients have worse sleep-related hypoxaemia and hypercapnia than patients with COPD or OSA alone. OSA has a similar prevalence in COPD as in a general population of similar age, but oxygen desaturation during sleep is more pronounced when the two conditions coexist. Management of sleep-related problems in COPD should particularly focus on minimising sleep disturbance via measures to limit cough and dyspnoea; nocturnal oxygen therapy is not generally indicated for isolated nocturnal hypoxaemia. Treatment with continuous positive airway pressure alleviates hypoxaemia, reduces hospitalisation and pulmonary hypertension, and improves survival.


Sleep has several effects on breathing, which include changes in central respiratory control, lung mechanics and muscle contractility, that do not have an adverse effect in healthy individuals but may result in significant hypoxaemia and hypercapnia in patients with chronic obstructive pulmonary disease (COPD), particularly during rapid eye movement (REM) sleep [1]. Gas exchange in sleeping normal subjects is largely a consequence of hypoventilation, although ventilation/perfusion (V′/Q′) abnormalities may also contribute. In COPD patients this hypoventilation is more pronounced, particularly during REM-sleep, due to a number of factors that include: airflow obstruction, hyperinflation, respiratory muscle dysfunction, blunted ventilatory responses to hypercapnia and/or hypoxia, V′/Q′ mismatching and medications such as loop diuretics and oral steroids. Sleep disturbance is also common in COPD [2, 3] and this is likely a consequence of the underlying lung disease, although adverse effects of drug therapy on sleep quality may also contribute. Sleep disturbance is one of the most common symptoms reported by COPD patients, occurring in ∼40% of patients in one large study [4]. These patients have problems initiating or maintaining sleep, and have increased light sleep and reduced REM sleep, frequent sleep stage shifts and micro-arousals. Sleep efficiency is low, in the range of 50–70%, in the majority of this patient population. Sleep disturbance likely contributes to the non-specific daytime symptoms of chronic fatigue, lethargy and overall impairment in quality of life described by these patients. Night-time symptoms in COPD patients frequently go unnoticed by physicians and/or are not reported by patients themselves [2].

The present review discusses the pathophysiological basis of sleep and breathing disturbances in patients with COPD, reviews the overlap syndrome where COPD and obstructive sleep apnoea (OSA) coexist, and finally discusses the management of sleep-related disorders in patients with COPD.

Pathophysiology of sleep-related breathing disturbances in COPD

Alterations in respiratory mechanics and ventilatory control during sleep related to COPD

A combination of factors can contribute to disturbances in ventilation and gas exchange during sleep in COPD, relating to accentuated physiological adaptations, such as hypoventilation, which are summarised in figure 1] [5]. People who are hypoxaemic during wakefulness have resting oxygen saturation levels on the steep portion of the oxyhaemoglobin dissociation curve, which can result in disproportionately greater falls in oxygen saturation at night. In addition, V′/Q′ mismatch and a reduced functional residual capacity (FRC) may also play a role in nocturnal hypoxaemia in COPD.

Figure 1.

Pathophysiology of sleep-related respiratory changes in chronic obstructive pulmonary disease. Sleep has negative effects on various aspects of respiration resulting in worsening hypoxaemia. FRC: functional residual capacity; FEV1: forced expiratory volume in 1 s; V′/Q′: ventilation/perfusion ratio.

Accentuated physiological hypoventilation due to central respiratory effects

Ventilatory control in patients with COPD follows the same basic principles as in normal subjects. During all sleep stages, respiratory centre responses to chemical and other inputs are diminished and respiratory muscle responses to respiratory centre outputs are also diminished, particularly during REM sleep, especially those involving accessory muscles of respiration [6, 7]. During REM sleep, in healthy individuals, ventilation may be 40% lower than during wakefulness. This is predominantly caused by a reduction in tidal volume, to which increased upper airway resistance and diminished inspiratory drive contribute, and results in a slight fall in arterial oxygen saturation (SaO2) that is not clinically significant in normal subjects [8]. A similar breathing pattern is present during sleep in patients with COPD. However, the physiological hypoventilation normally present during sleep is accentuated, resulting in profound hypoxaemia in patients with respiratory insufficiencies such as COPD [9]. This is likely a result of the increased physiological dead space in COPD, which leads to an even greater decrease in alveolar ventilation with lower tidal volumes than in normal subjects [10]. Because many COPD patients have hypoxaemia while awake, they are especially prone to nocturnal oxygen desaturation as a result of being on the steep portion of the oxyhaemoglobin dissociation curve [1].

In addition, during non-REM sleep, the basal metabolic rate and ventilatory drive are decreased. These effects may result in a decreased central respiratory drive in non-REM sleep. In REM sleep, the respiratory centre has a diminished response to chemical and mechanical inputs [11]. Studies performed in COPD patients have demonstrated that a lower response of minute ventilation to CO2 can already be present during wakefulness. However, the response measured from parameters that are less influenced by respiratory mechanics, such as mouth occlusion pressure 0.1 s after onset of inspiration (P0.1), appear to be less impaired, if not normal [5]. Thus, although the receptor and respiratory centre response to hypercapnia may be normal, this response cannot be translated into ventilation due to peripheral mechanisms relating to airflow obstruction, in addition to the hyperinflation and/or respiratory muscle dysfunction affecting such patients [11, 12].

Altered airway resistance and respiratory muscle contractility

Upper airway resistance increases during sleep compared to wakefulness [13, 14] due to a loss of tone in the upper pharyngeal muscles. This may also alter the ventilatory responses to hypoxia and hypercapnia, and may contribute to hypoventilation. Consequently, the resistance of the supraglottic airways increases from wakefulness to sleep to a similar degree in normal subjects as in COPD patients. However, the dilatory response of the supraglottic airways to increases in arterial carbon dioxide tension (PaCO2) is significantly lower in COPD patients, which indicates an impaired response of lowering the upper airway resistance, which can further contribute to nocturnal hypercapnia and hypoxaemia [15]. Moreover, there is mild bronchoconstriction during sleep as a feature of the normal circadian change in airway calibre, which may be exaggerated in patients with COPD, thus resulting in an increase in lower airway resistance as well, as previously demonstrated in patients with bronchial asthma [16].

In addition, there is hypotonia of skeletal muscles (tongue, pharyngeal, laryngeal and intercostal muscles) during sleep and a change in the relative contribution of rib cage and abdominal compartment to breathing [17, 18]. During REM sleep, there is a marked loss of tonic activity in the intercostal muscles, due to supraspinal inhibition of γ-motoneurons (and to a lesser extent α-motoneurons), in addition to presynaptic inhibition of afferent terminals from muscle spindles. The diaphragm, being driven almost entirely by α-motoneurons and with far fewer spindles than in the intercostal muscles, has little tonic (postural) activity and, therefore, escapes the reduction of this particular drive during REM sleep [8]. This reduction in accessory respiratory muscle activity during REM sleep may contribute to hypoventilation, especially in COPD patients who are particularly reliant on accessory muscle activity to maintain ventilation. One of the pathological consequences of COPD is stretching of the diaphragm due to lung hyperinflation, which may reduce the efficiency of diaphragmatic contraction, thus necessitating an increased accessory muscle contribution to breathing [19]. Subjects with severe COPD may be totally dependent on a poorly functioning diaphragm for ventilation during sleep [5]. Skeletal muscle atrophy and dysfunction are common in advanced COPD, which may further compromise the contribution made by accessory muscles [20]. Diaphragmatic efficiency is further compromised by the supine position, since the pressure of abdominal contents against the diaphragm exerted by gravitational force contrasts with the effect of gravity in the erect position, which tends to move the abdominal contents away from the diaphragm. Since the diaphragm is virtually the only respiratory muscle that is active during REM sleep, this will lead to paradoxical breathing and further hypoventilation. This probably explains why significant correlations have been observed between variables relating to respiratory muscle strength (maximal inspiratory mouth pressure) and mean nocturnal SaO2 in COPD patients.

Respiratory mechanics during sleep in COPD

V′/Q′ mismatch in COPD results from progressive airflow limitation and emphysematous destruction of the pulmonary capillary bed. A small, but statistically significant, reduction in FRC occurs during sleep, principally because of a reduction in tonic muscle activity and an increase in airway resistance, which may augment V′/Q′ mismatch [21]. In addition, the supine position is associated with a 10% decrease in FRC in normal subjects. These physiological changes in pulmonary function, when imposed on subjects with COPD, may adversely affect the V′/Q′ mismatch, by closing small airways in the dependent lung zones [22]. This results in lower oxygen reserves, in addition to lower carbon dioxide buffering capacity, which contributes to nocturnal oxygen desaturation and hypercapnia. Furthermore, cephalad displacement of the diaphragm and a decrease in lung compliance are other possible mechanisms contributing to this reduction in FRC [19]. Evidence for a role of V′/Q′ mismatch in the pathophysiology of nocturnal oxygen desaturation in COPD comes from the observation that PaCO2 levels rise to a similar extent in those patients who develop major nocturnal oxygen desaturation as in those who develop only a minor degree of desaturation, which suggests a similar degree of hypoventilation in both groups [23]. Moreover, cardiac output is maintained during these episodes of hypoventilation, indicating changes in global V′/Q′ matching [24, 25].

Worsening of V′/Q′ mismatch during sleep in COPD has also been explained by a decreased mucociliary clearance. V′/Q′ mismatch due to pulmonary emphysema and small airways disease is measurable even in subjects with mild COPD, but appears to increase in line with disease progression. However, there is evidence based on body plethysmographic studies that FRC does not change during sleep in patients with COPD, but these data were only gathered in five patients [26].

Impact of COPD on sleep quality

Sleep quality is often impaired in patients with COPD, which is likely to be an important factor in the chronic fatigue, sleepiness and overall impairment in quality of life reported by these patients [27, 28]. There is an increased prevalence of insomnia, use of hypnotic medications and an increase in daytime sleepiness in subjects with COPD compared with the general population [29]. Klink et al. [29] reported that 39% of patients with nocturnal cough or wheezing reported difficulty initiating or maintaining sleep. If cough and wheeze were both present, 53% reported difficulty initiating or maintaining sleep, and 23% reported excessive daytime sleepiness [29]. It seems that in patients with mild obstructive airways disease, there is little impact on sleep quality [30]. However, as COPD becomes more severe, there are an increasing number of sleep complaints with possibly more deleterious physiological effects [3, 28].

Sleep tends to be fragmented, with frequent arousals and diminished amounts of deep sleep and REM sleep [3, 31]. Kwon et al. [32] reported a strong relationship between hyperinflation and lower sleep efficiency in patients with the overlap syndrome, but the effect was independent of OSA after correction for the apnoea/hypopnoea index (AHI).

The cause of this poor sleep quality is not entirely clear. The role of hypoxaemia as a respiratory stimulant is rather weak, since quality of sleep is not improved by adding oxygen, and thus, hypercapnia is considered as a much stronger stimulant in provoking arousals [33]. Also, increased inspiratory loads, due to hyperinflation and intrinsic positive end-expiratory pressure, can substantially add to the work of breathing and, hence, elicit arousals by stimulation of mechanoreceptors in the chest wall and lower airways. The arousal response is lowest for hypercapnia and hypoxia during REM sleep, but the arousal response to inspiratory loading is relatively preserved [28]. Nocturnal cough may disturb sleep in these patients, as may the use of drugs like theophylline that are frequently used as a bronchodilator. Last but not least, cigarette smokers manifest disturbances in the sleep electroencephalogram that are not evident in conventional measures of sleep architecture. Nicotine in cigarette smoke and withdrawal from it during sleep may contribute to a higher alpha power and the subjective experience of non-restorative sleep [34]. Unfortunately, sleep impairment is an aspect of COPD that is frequently neglected by many physicians, and in trials designed to assess the impact of COPD on quality of life [2]. Moreover, it has been shown that sleep deprivation is associated with a mild decrease in forced vital capacity (FVC) (-5%) and forced expiratory volume in 1 s (FEV1) (-6%) [35]. When extrapolating these data towards COPD patients with sleep fragmentation, it could be speculated that disturbed sleep quality may lead to worse outcomes in COPD. This was confirmed by Omachi et al. [36] who demonstrated that disturbed sleep is predictive of COPD exacerbations, emergency healthcare utilisation and mortality. However, Ito et al. [37] proved that depression but not sleep disturbance itself is an independent factor affecting exacerbations and hospitalisation in COPD.

Overlap syndrome of COPD and OSA

The coexistence of COPD and obstructive sleep apnoea was first described as the “Overlap Syndrome” by David Flenley almost 30 years ago [38]. He pointed out that a sleep study should be considered in obese COPD patients, in those who snore, or those who complain of headache following nocturnal oxygen therapy to determine the presence of associated OSA. He questioned nocturnal oxygen administration in these patients and believed that the clinical course and prognosis of overlap patients was worse than patients suffering from COPD or OSA alone. These opinions remain valid today.

Definitions and epidemiology

The latest version of the Global Initiative for Chronic Obstructive Lung Disease strategy document defined COPD as a common preventable and treatable disease, characterised by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases. It underlines that “exacerbations and comorbidities contribute to the overall severity in individual patients” [39]. Clearly, the coexistence of OSA is one of these comorbidities. The diagnosis of COPD should be considered in any patient who has chronic respiratory symptoms, mainly exertional dyspnoea, chronic cough and/or sputum production, and a history of exposure to risk factors for the disease (mainly cigarette smoking). Spirometry is required to make the diagnosis in this clinical context and the presence of a post-bronchodilator FEV1/FVC <0.70 confirms the presence of persistent airflow limitation and, thus, of COPD.

At sleep onset, patients with OSA suffer recurrent pharyngeal collapse and temporary cessation of breathing (apnoea). Such apnoea events cause repetitive hypoxia and carbon dioxide retention, and provoke awakenings (i.e. arousals) that restore airflow. However, once sleep resumes, pharyngeal obstruction and subsequent apnoea recurs. An OSA disorder is generally defined as an AHI >5 events·h−1 [40, 41]. Patients may present with daytime and/or nocturnal complaints, but frequently close companions are the first to push for medical attention because of concerns regarding snoring and/or witnessed apnoea. The presence and severity of the sleep disordered breathing is confirmed by a sleep study.

In pulmonary clinics, OSA, COPD and asthma are the most prevalent chronic respiratory disorders. The prevalence of COPD is directly related to the prevalence of tobacco smoking, but 10% of the general population around the world have moderate-to-severe COPD (FEV1/FVC <0.7 plus FEV1 <80% predicted) [42]. As defined above, the prevalence of OSA was more than 20% of males and 9% of females [43, 44]. Obesity is one of the main risk factors for OSA and obesity rates have risen since these population studies were performed. Therefore, it is logical to think that current rates of prevalence of OSA are much higher.

There are some indirect data about the prevalence of overlap syndrome. In the Sleep Heart Health Study, a large community-based cohort study which included polysomnography and spirometry, 0.5% of the participants had airflow obstruction [30]. In a European study with predominantly mild COPD patients, OSA occurred in 3% [45].

Sleep in patients with COPD and OSA

In a recent European survey, 78.1% of patients with COPD reported some degree of night-time symptoms [46]. They also reported that as the severity of airflow limitation increased so did the prevalence of night-time symptoms. Patients reporting bothersome symptoms at night experienced more daytime breathlessness, had more exacerbations within the previous 12 months and were receiving more maintenance medications than those who did not report bothersome night-time symptoms. Unfortunately, in this survey OSA symptoms or sleep studies were not recorded. Therefore, the potential impact of the coexistence of OSA in the night-time symptoms of COPD patients is unknown. The presence of COPD symptoms, such as dyspnoea, cough, sputum or wheezing, is associated with arousals and difficulty with maintenance of sleep. Decreased total sleep time and sleep efficiency have been confirmed in sleep studies [47], which likely contributes to the complaint of daytime hypersomnolence by many patients.

Patients with COPD develop significant nocturnal oxygen desaturation, and daytime gas exchange abnormalities, particularly a low PaO2, are predictive of nocturnal desaturation [23]. Nevertheless, more than 50% of COPD patients with daytime SaO2 >90% without sleep apnoea experience significant desaturation during sleep [48]. This phenomenon has been largely ignored, although an increased mortality in these patients compared to those who do not desaturate has previously been described.

The prevalence of OSA is not greater in COPD patients compared with the non-COPD population. Nevertheless some predisposing factors such as age, active smoking, peripheral oedema and oral corticosteroids, increase the risk of obstructive apnoea events. Obesity, when present among COPD patients, is a key contributor for sleep disordered breathing, accelerated pulmonary hypertension and obesity hypoventilation syndrome irrespective of airflow obstruction severity [49]. These patients particularly resemble the so-called “blue bloater” COPD phenotype. By contrast, some patients with advanced COPD can lose weight and consequently reduce the risk for upper airway obstruction (fig. 2).

Figure 2.

Pathophysiological interactions between chronic obstructive pulmonary disease (COPD), sleep and obstructive sleep apnoea syndrome (OSAS). Interactions between COPD, sleep and OSAS are shown, highlighting factors relating to COPD that may promote or inhibit the development of obstructive apnoea and hypopnoea (OAH). BMI: body mass index; REM: rapid eye movement. Reproduced from [50] with permission from the publisher.

Clinical features of the overlap syndrome

Nocturnal hypoxaemia is one of the most important sleep abnormalities in COPD and OSA. The overlap syndrome causes more severe nocturnal hypoxaemia than either disease alone (fig. 3). Hypoxaemic events are associated with both systemic and pulmonary increases in blood pressure and arrhythmias [51, 52]. A well-established chronic effect of these events is the development of cor pulmonale. In patients with the overlap syndrome, surrogates of OSA severity such AHI, seem to play a minor role for developing pulmonary hypertension compared with variables that reflect the severity of COPD. For example, daytime hypoxaemia, hypercapnia and reduced FEV1, were found to be predictors of right-heart failure [53].

Figure 3.

Arterial oxygen saturation (SaO2) patterns during sleep in obstructive sleep apnoea (OSA) alone and the overlap syndrome. SaO2 patterns in a patient with a) OSA alone and b) overlap syndrome demonstrating the persisting pattern of desaturation in the overlap patient whereas the OSA patient returns to normal SaO2 between apnoea events.

Nocturnal death appears to increase in COPD exacerbations [54] and OSA compared with non-COPD, non-OSA [55]. No data are available on this issue in the overlap syndrome, although in the report by McNicholas and FitzGerald [54] nocturnal death was highest amongst “blue-bloater” type patients with type 2 respiratory failure, a COPD phenotype commonly associated with sleep disordered breathing. Overall, the evidence indicates that mortality is increased in overlap patients. In OSA patients studied at sleep clinics, the coexistence of COPD increased risk of death [56]. We have recently confirmed this data in our cohort of patients referred with suspected sleep disordered breathing. In addition to a sleep study all patients underwent spirometry. After a median follow-up of >9 years, all-cause mortality was higher in the untreated overlap group (42.2%) than in the COPD-only group (24.2%). Comorbid OSA remained a risk factor for death after adjusting for COPD severity [57]. Continuous positive airway pressure (CPAP) was offered to all patients to treat OSA following local guidelines and among those who accepted and adhered to the treatment, CPAP eliminated the additional mortality risk of OSA in overlap patients, compared with the COPD-only patients (fig. 4). In a Brazilian cohort of patients with overlap syndrome and daytime hypoxaemia, CPAP was offered in addition to long-term oxygen therapy (LTOT) [58]. Among those that could not afford the CPAP, did not adhere to or refused treatment, the 5-year survival was only 26% versus 71% with CPAP and LTOT, versus 26% with LTOT alone. In both studies, CPAP was not provided in a randomised, blinded manner, so a definitive conclusion on the protective effect of CPAP among overlap patients cannot be given. In our series, death in the untreated overlap group was most commonly attributed to cardiovascular diseases [57]. There is no clear mechanistic explanation for this finding. Since we also found an increase in severe COPD exacerbations in the untreated group, we can speculate that in overlap syndrome the increased incidence of COPD exacerbations may accelerate lung-function decline, which is associated with greater mortality [59].

Figure 4.

Kaplan–Meier survival curves for outcomes among chronic obstructive pulmonary disease (COPD) patients without obstructive sleep apnoea (OSA) (COPD group), patients with COPD and coexisting OSA (overlap group), and patients with overlap syndrome treated with continuous positive airway pressure (CPAP) since enrolment (overlap with CPAP group). a) Survival and b) severe COPD exacerbation-free survival curves among the three study groups. The differences between curves from the COPD only and COPD with OSA treated with CPAP groups are statistically significant from the curve of patients with COPD and untreated OSA (p<0.001). Reproduced from [57] with permission from the publisher.

Management of sleep disorders in COPD

Since patients with COPD experience disturbed sleep quality in addition to worsening gas exchange during sleep, management should consider each aspect of the disorder. However, the first management principle of sleep-related breathing disturbances in COPD should be to optimise the underlying condition, which will almost invariably benefit breathing while asleep. Correction of hypoxaemia is particularly important and in recent years considerable interest has focussed on the potential benefits of noninvasive ventilation (NIV).

Oxygen therapy

The most serious consequence of hypoventilation, particularly during sleep, is hypoxaemia, and appropriate oxygen therapy plays an important part in the management of any disorder associated with respiratory insufficiency during sleep. Care must be taken that correction of hypoxaemia is not complicated by hypercapnia in patients with COPD, since respiratory drive in such patients may be partly dependent on the stimulant effect of hypoxaemia. Therefore, the concentration of added oxygen should be carefully titrated to bring the arterial oxygen tension (PaO2) up into the mildly hypoxaemic range in order to minimise the tendency towards carbon dioxide retention, particularly during sleep. However, the risk of carbon dioxide retention with supplemental oxygen therapy in such patients may have been overstated in the past, and there is evidence that carbon dioxide retention with oxygen supplementation during sleep is often modest, and usually non-progressive [60]. In particular, there appears to be a low risk of serious carbon dioxide retention with carefully controlled oxygen therapy during exacerbations of COPD even when relatively high flow oxygen supplementation is required to bring the SaO2 into the region of 90–92% [61]. Thus, the priority in oxygen supplementation should be to provide sufficient oxygen to bring the SaO2 level above 90%, but doing so in a controlled fashion to avoid excessive supplementation. Oxygen supplementation during sleep is best delivered via nasal cannulae, since face masks are more likely to become dislodged during sleep [62].

In the chronic setting, indications for supplemental oxygen are best determined by measures that indicate the overall magnitude of hypoxaemia during sleep, such as the cumulative time spent with SaO2 <90%. Furthermore, the potential benefits of nocturnal oxygen therapy in patients with moderate daytime hypoxaemia (PaO2 55–60 mmHg) remain unclear and are the subject of ongoing large prospective studies.

Pharmacological therapy

Considerations of pharmacological therapy in the setting of sleep in patients with COPD should address the impact of conventional therapeutic agents, such as bronchodilators and anti-inflammatory agents, on sleep and gas exchange, and also the impact on ventilation and gas exchange of pharmacological agents that are designed to improve sleep quality.

Conventional bronchodilator and anti-inflammatory agents used in COPD

Cholinergic tone is increased at night and it has been proposed that this contributes to airflow obstruction and deterioration in gas exchange during sleep in patients with obstructive airways disease. One report demonstrated significant improvements in both sleep quality and gas exchange in patients with COPD treated with ipratropium [63]. Another study demonstrated significant improvements in nocturnal SaO2 with the once-daily anticholinergic agent, tiotropium, without significant changes in sleep quality [64]. Improvements in SaO2 were particularly significant during REM sleep, which is clinically significant since REM sleep is associated with the most severe oxygen desaturation.

There are only limited data on the efficacy of beta-agonists in the management of sleep-related breathing abnormalities in COPD. However, a recent report demonstrated improvements in gas exchange during sleep with the long-acting beta-agonist salmeterol to a similar degree to that seen with tiotropium [65].

The effects of theophylline have also been studied during sleep in patients with COPD. In addition to being a bronchodilator, theophylline has important effects on respiration that may be particularly beneficial in patients with sleep-related respiratory disturbance, including central respiratory stimulation and improved diaphragmatic contractility [66]. Beneficial effects on SaO2 and arterial carbon dioxide levels in COPD during sleep have also been demonstrated [67]. Theophylline has an added advantage in that there is evidence of beneficial effects in OSA [68]. The mechanism of this effect in COPD appears to be mainly due to a reduction in trapped gas volume rather than bronchodilation. However, the principal limiting effect of theophyllines in this context is an adverse effect on sleep quality, in contrast to the anticholinergic agents, discussed above. There are no data on the potential for newer phosphodiesterase 4 agents, such as rofumilast, to benefit sleep-related variables in COPD.

Other medications with potential to improve sleep-disordered breathing in COPD

Historically almitrine was used as a therapy, it is a powerful carotid body agonist that stimulates ventilation and improves ventilation/perfusion relationships within the lung, probably via enhancement of hypoxic pulmonary vasoconstriction. The overall effect is to lessen hypoxaemia, which could potentially be a useful addition in the management of conditions associated with nocturnal hypoxaemia, particularly COPD. Significant improvements in nocturnal SaO2 have been reported compared with placebo, which were most pronounced during REM sleep [69]. However, important side-effects include pulmonary hypertension, dyspnoea and peripheral neuropathy, which resulted in almitrine being withdrawn and the agent is no longer available.

Tricyclic antidepressants and selective serotonin reuptake inhibitors have also been studied in the context of sleep disordered breathing in COPD. These agents produce a fragmentation of REM sleep, and thus, may reduce the severity of oxygen desaturation in this sleep stage. There appears to be a short-term benefit to nocturnal SaO2 levels in COPD [70], although this benefit may not persist with long-term use of the drug [71]. Therefore, despite its theoretical role, this agent is rarely used in the management of sleep-related breathing disturbances in COPD.

Therapies used to promote sleep

Benzodiazepine and non-benzodiazepine hypnotics shorten sleep latency, improve sleep efficiency and decrease arousal frequency, but have adverse effects on ventilation that include hypoventilation with associated hypoxaemia and hypercapnia, in addition to diminished arousal response to hypercapnia and increased apnoea frequency [72]. Thus, these agents should be avoided, if possible, in patients with severe COPD, although there is evidence that some hypnotics, such as zolpidem, can be used in less severe COPD without significant adverse effects on gas exchange [73].

Melatonin receptor antagonists, such as ramelteon, also shorten sleep latency and improve sleep efficiency, and have been reported to have no adverse effects on apnoea frequency or PaO2 levels in patients with COPD [74]. There is also evidence that cognitive behavioural therapy for insomnia in COPD results in positive sleep and fatigue effects [75].

Noninvasive pressure support

Patients with COPD associated with respiratory insufficiency who fail to respond to pharmacological therapy should be considered for some form of assisted ventilation. In an acute setting, this may require intubation and ventilation, but in the past two decades increasing attention has been directed towards noninvasive methods of ventilatory support, particularly during sleep [76, 77]. NIV is particularly indicated in patients with hypercapnic respiratory failure. Long-term nocturnal NIV can also be considered in COPD patients with chronic respiratory failure where improvements in gas exchange during wakefulness have been reported [78], in addition to improvements in respiratory muscle strength and endurance [79]. Sleep quality and diurnal PaO2 and PaCO2 levels are better with NIV plus supplemental oxygen than with supplemental oxygen alone [80]. Several mechanisms are likely to play a role in these improvements, including the resting of chronically fatigued respiratory muscles thereby improving daytime respiratory muscle function [81]. Lung compliance is also improved by reversing microatelectasis and preventing collapse of the airways leading to a reduction in the work of breathing. Furthermore, over time, home mechanical ventilation is thought to lead to resetting of the chemoreceptor drive to breathe, as a direct result of reversal of nocturnal hypoventilation [78]. Patients with severe awake blood gas derangement appear to tolerate NIV relatively well. Although long-term NIV therapy is associated with sustained improvements in waking gas exchange, improvements in long-term survival have not been clearly documented [82–87].

Patients with the overlap syndrome should also be treated by nocturnal pressure support and the choice between CPAP or bilevel positive airway pressure can be determined based on the pattern of sleep disordered breathing. In cases where OSA predominates, CPAP may be most appropriate, whereas in cases where there is evidence of significant nocturnal hypoventilation with associated periods of sustained hypoxaemia, bilevel positive airway pressure may be more appropriate. Newer modalities of pressure support, such as adaptive servo ventilation, may be particularly suited to patients with the overlap syndrome.

Sleep Abnormalities and Treatment in Emphysema

Proc Am Thorac Soc. 2008 May 1; 5(4): 536–542.

Samuel Krachman

1Sleep Disorders Center, Division of Pulmonary and Critical Care, Temple University School of Medicine, Philadelphia, Pennsylvania; 2Division of Pulmonary, Allergy, and Critical Care, Cleveland Clinic, Cleveland, Ohio; and 3Sleep Disorders Center, Division of Pulmonary and Critical Care, University of Maryland, Baltimore, Maryland

Omar A. Minai

1Sleep Disorders Center, Division of Pulmonary and Critical Care, Temple University School of Medicine, Philadelphia, Pennsylvania; 2Division of Pulmonary, Allergy, and Critical Care, Cleveland Clinic, Cleveland, Ohio; and 3Sleep Disorders Center, Division of Pulmonary and Critical Care, University of Maryland, Baltimore, Maryland

Steven M. Scharf

1Sleep Disorders Center, Division of Pulmonary and Critical Care, Temple University School of Medicine, Philadelphia, Pennsylvania; 2Division of Pulmonary, Allergy, and Critical Care, Cleveland Clinic, Cleveland, Ohio; and 3Sleep Disorders Center, Division of Pulmonary and Critical Care, University of Maryland, Baltimore, Maryland

1Sleep Disorders Center, Division of Pulmonary and Critical Care, Temple University School of Medicine, Philadelphia, Pennsylvania; 2Division of Pulmonary, Allergy, and Critical Care, Cleveland Clinic, Cleveland, Ohio; and 3Sleep Disorders Center, Division of Pulmonary and Critical Care, University of Maryland, Baltimore, Maryland

Correspondence and requests for reprints should be addressed to Samuel Krachman, D.O., Temple University School of Medicine, 3401 North Broad Street, Philadelphia, PA 19140. E-mail: [email protected]

Received 2007 Aug 22; Accepted 2007 Oct 23.

This article has been cited by other articles in PMC.


Sleep abnormalities are common in severe emphysema, and include poor sleep quality, the development of nocturnal oxygen desaturation, and the presence of coexistent obstructive sleep apnea. With lower baseline oxygenation and abnormal respiratory mechanics in patients with severe emphysema, alterations in ventilatory control and respiratory muscle function that normally occur during sleep can have profound effects, and contribute to the development of sleep abnormalities. The impact on quality of life, cardiopulmonary hemodynamics, and overall survival remains uncertain. In addition, treatment for chronic obstructive pulmonary disease and its effect on sleep abnormalities have demonstrated conflicting results. More recently, as part of the National Emphysema Treatment Trial, lung volume reduction surgery has been shown to improve both sleep quality and nocturnal oxygenation in emphysema. Although indications for performing an overnight polysomnogram in patients with emphysema have been debated, recommendations have been presented. Future studies investigating disease mechanism and response to therapy in patients with sleep abnormalities and severe emphysema are warranted.

Keywords: emphysema, sleep, hypoventilation, apnea, oxygenation

Patients with severe emphysema commonly have distinct abnormalities related to sleep that include poor sleep quality (1–4) and the development of nocturnal oxygen desaturation (NOD) (1, 3–8). Patients with emphysema often complain of difficulty with initiating and maintaining sleep (3), and objective measurements have demonstrated increased sleep latency, decreased total sleep time, and an increased number of nocturnal arousals (1–4). These findings contribute to the excessive daytime sleepiness and early morning awakenings reported in these patients (9–11). As part of the National Emphysema Treatment Trial (NETT), sleep quality and nocturnal oxygenation have been examined in patients with severe emphysema who were being evaluated for lung volume reduction surgery (LVRS) (4, 12).

Episodes of NOD are more pronounced during REM sleep (2, 5–7), and can develop despite an awake PaO2 > 60 mm Hg. Although predictors for the development of NOD have been identified (3, 7, 8, 13–18), its effect on pulmonary hemodynamics and overall survival are still uncertain. In addition, patients with emphysema with coexistent obstructive sleep apnea (OSA), often referred to as the “overlap syndrome,” also demonstrate NOD. This review examines the physiological variables that affect sleep quality and nocturnal oxygenation in severe emphysema. In addition, therapeutic interventions, including LVRS, and their impact on sleep quality and overall survival are reviewed. Finally, limitations in the current literature and open questions that remain to be answered are discussed.


Ventilation is normally controlled by a combination of two systems: a metabolic system responsible for the automatic changes directly related to gas exchange, and a behavioral system responsible for the voluntary changes originating from cortical and forebrain structures. At sleep onset, input from the behavioral system decreases, and the metabolic control system, which was active but influenced by the behavioral control system during wakefulness, acts as the primary controller of the respiratory system. There are associated changes in ventilatory control and thoracoabdominal muscle activity that are sleep stage specific. Ventilatory responses to both hypoxia and hypercapnia are decreased, with the largest decrease noted during REM sleep (19, 20). In addition, during non-REM sleep, intercostal muscle activity and thus rib cage contribution to breathing, as well as diaphragmatic muscle activity, are increased (21). Despite an increase in respiratory muscle activity, minute ventilation decreases during non-REM sleep because of a decrease in tidal volume. A decrease in upper airway dilator muscle activity, resulting in an increase in upper airway resistance, appears to be responsible (22). As a result, PaCO2 increases 3 to 10 mm Hg, and PaO2 decreases 2 to 8 mm Hg (23).

During REM sleep, there is a decrease in rib cage contribution to breathing due to a marked decrease in intercostal muscle activity (21). Tidal volume is maintained by an increase in diaphragmatic muscle activity. Upper airway resistance, which would be expected to be highest during REM sleep because of pharyngeal dilator muscle atonia, has been less investigated. Results suggest an increase in upper airway resistance similar to that seen during non-REM sleep (24). The breathing pattern during REM sleep is irregular, with sudden changes in respiratory amplitude and frequency observed (23). Overall, tidal volume and minute ventilation are decreased during what is referred to as phasic REM sleep, when rapid eye movements are noted to be abundant.


Alterations in ventilatory control and respiratory muscle function during sleep become important in patients with chronic obstructive pulmonary disease (COPD) who have lower baseline oxygenation and abnormal respiratory mechanics. These factors contribute to the development of NOD and poor sleep quality, which may lead to the long-term sequelae of polycythemia, cor pulmonale, arrhythmias, myocardial stress, and possibly decreased survival (). However, evidence to support many of these relationships is still lacking.

Potential consequences due to changes in ventilatory control and respiratory muscle function during sleep when they occur in patients with underlying chronic obstructive pulmonary disease (COPD). A/W = airways; OSA = obstructive sleep apnea; d/t = ratio of dead space volume to tidal volume.


Prevalence of NOD in Emphysema

Patients with emphysema can develop significant NOD despite adequate oxygenation during wakefulness. This effect is more pronounced among those with low baseline oxygenation (1, 16), can be more severe than desaturation during maximal exercise (16), and may be seen more commonly in patients with the “blue bloater” than the “pink puffer” phenotype (25). However, significant NOD has also been reported in patients with COPD with mild daytime hypoxia. Koo and coworkers (5) studied 15 patients with COPD with a mean FEV1 of 0.96 L and found a mean decrease in PaO2 of 13.5 mm Hg and an increase in PaCO2 of 8.3 mm Hg during sleep, despite an awake PaO2 exceeding 60 mm Hg. Other studies have shown decreases in SaO2 during sleep, with the most severe episodes occurring during REM sleep (2, 6, 7). In one of the largest of these studies, Fletcher and coworkers (7) showed that 27% of 135 patients with COPD with awake PaO2 exceeding 60 mm Hg had REM-associated NOD. Although patients with REM-associated NOD had a lower awake PaO2 and higher awake PaCO2, these parameters were not predictive in identifying patients with NOD. In our study of 16 NETT patients (4), the mean SaO2 was 90 ± 6% and the lowest SaO2 during the night was 83 ± 8%. The percentage total sleep time (TST) with an SaO2 less than 90% was 37 ± 45%.

Mechanisms of NOD in Emphysema

Several mechanisms have been proposed to explain the development of NOD in emphysema (26–30). Alveolar hypoventilation appears to play a major role, especially during REM sleep. This was demonstrated by Becker and coworkers (26) in a study of nine patients with underlying emphysema. Compared with wakefulness, minute ventilation decreased 16% during non-REM sleep and 32% during REM sleep, predominantly because of a decrease in tidal volume, measured with a pneumotachograph. Hudgel and Devodatta (27) noted that desaturators had a greater decrease in functional residual capacity compared with nondesaturators, suggesting that a maldistribution of ventilation may be a contributing factor. However, Ballard and coworkers (28) reported no change in lung volume during sleep in patients with emphysema, and believed that the decrease in minute ventilation was related to an increase in upper airway resistance and a decrease in respiratory neuromuscular output. More recently, O’Donoghue and coworkers (29) noted a similar preservation of lung volume during sleep in hypercapnic patients with COPD, despite a decrease in tidal volume and minute ventilation. Finally, changes in the distribution of ventilation–perfusion ratios may contribute to NOD, suggested by the fact that mild increases in PaCO2 (and thus hypoventilation) could not account for the more significant decreases in PaO2 during sleep (30). However, changes in ventilation–perfusion ratios were not measured during the night. Therefore, a number of mechanisms may be responsible for the development of NOD, with hypoventilation, as occurs normally during sleep, playing an important role in patients with abnormal respiratory mechanics and lower baseline awake oxygenation.

Consequences of NOD in Emphysema

Potential consequences of NOD include the development of cor pulmonale. In other patient populations, pulmonary hypertension has been associated with NOD (31). In patients with emphysema, Coccagna and Lugaresi (32) noted a progressive acute increase in mean pulmonary artery pressures across all sleep stages in 12 patients with COPD, with the most significant increase noted in REM sleep. The increase in pulmonary artery pressure was associated with the decrease in PaO2 and less so with the increase in PaCO2. Whether these acute changes lead to the development of chronic pulmonary hypertension is still controversial. Fletcher and coworkers (33) demonstrated that systolic and mean pulmonary artery pressures, as well as pulmonary vascular resistance, were higher in patients with NOD compared with those without NOD. However, in a larger study, Chaouat and coworkers (17) noted no difference in mean pulmonary artery pressure in patients with and without NOD, and nocturnal oxygenation was not predictive of the presence or absence of pulmonary hypertension. The presence of coexisting obstructive sleep apnea (overlap syndrome), may increase the risk of developing cor pulmonale.

The relationship between NOD and sleep quality remains poorly defined. Because of the decrease in output from the reticular activating system and responsiveness to hypercapnia and especially hypoxia during sleep, subjects can remain asleep even when arterial saturation decreases to approximately 70% (19). We studied 16 patients with COPD with an emphysema-predominant phenotype as part of the NETT and found no significant correlation between changes in sleep quality (as measured by TST and sleep efficiency, respectively) and changes in nocturnal oxygenation during the night, including mean oxygen saturation (r = 0.1, P = 0.8 and r = 0.1, P = 0.9), lowest oxygen saturation (r = 0.4, P = 0.3 and r = 0.1, P = 0.9), and percentage TST with an oxygen saturation less than 90% (r = 0.1, P = 0.8 and r = 0.2, P = 0.6) (4).

Survival may also be affected by the presence of NOD in emphysema. In a retrospective study of 169 patients with emphysema, Fletcher and coworkers (34) noted significantly decreased survival among patients with NOD compared with those without NOD. However, this retrospective study was based on two different definitions of NOD, and this and other studies have not demonstrated improved survival on correction of the NOD (see below). Therefore, a definite relationship between NOD and the development of chronic pulmonary hypertension, sleep quality, and survival is yet to be determined.

Predictors of NOD in Emphysema

Because of the complexity of measuring NOD, many investigators have attempted to determine which physiological parameters measured during wakefulness might predict NOD (3, 7, 8, 12, 13, 15–18). Cormick and coworkers noted that NOD was related to waking values of SaO2 and PaCO2, but not to any other measurements of daytime lung function (3). Fletcher and coworkers found a combination of high daytime PaCO2 and low PaO2 to be significantly related, but not very predictive of NOD in 135 patients with emphysema (7), with similar findings noted in a subset of patients who were followed up a mean of 40 months later (15). Connaughton and coworkers studied 97 patients with severe emphysema and noted that both the daytime PaCO2 and PaO2 were significantly related to NOD (13). Bradley and coworkers identified awake SaO2 and PaCO2 as independent variables related to NOD; these variables accurately predicted NOD in a group of 26 patients with COPD (8). Mulloy and McNicholas (16) found that PaO2, and Chaouat and coworkers (17) identified PaCO2, as predictive of NOD in similar groups of patients. Heijdra and coworkers (18) demonstrated that, in addition to awake gas exchange, FEV1 and maximal inspiratory muscle strength correlated with NOD. Despite a noted relationship, the clinical utility of these awake physiological variables as they relate to NOD remains uncertain.


Prevalence and Characteristics

Patients with emphysema have low quality of life scores compared with normative samples (35). These findings apply to both general and disease-specific quality of life measures. However, few studies have examined the extent to which disturbed sleep contributes to these low quality of life scores (3, 36). Indicators of poor sleep quality include the subjective complaints of difficulty falling and staying asleep, morning tiredness, early awakenings, and excessive daytime sleepiness (3, 9–11). Cormick and coworkers (3) queried 50 patients with emphysema about their perception of sleep quality over a 6-month period and found that 72% complained of daytime sleepiness, 32% reported impaired daytime concentration, and 28% complained of early morning headaches. In a survey of more than 2,000 emphysema patients, Klink and coworkers (10) noted that the presence of respiratory symptoms, specifically cough or sputum production and wheezing, was associated with disturbed sleep, including difficulty initiating and maintaining sleep, as well as daytime sleepiness. If both symptoms were present, 53% of patients reported insomnia symptoms and 23% complained of daytime sleepiness. A similar association between insomnia complaints and the presence of respiratory symptoms was noted by Dodge and coworkers (11) in a survey of more than 1,600 patients with obstructive lung disease. Insomnia was more prevalent in those patients with reported cough, dyspnea, or wheezing. Finally, in a questionnaire to 734 patients greater than 65 years of age, Bellia and coworkers (9) noted that nocturnal awakening, morning tiredness, and early awakenings were more frequent in patients with either asthma or emphysema, as compared with age-matched control subjects who were free of respiratory disease.

Assessment of Sleep Quality in Emphysema

Objective measurement of sleep quality includes determination of sleep latency, the TST during the night, sleep efficiency (total sleep time/time in bed), and the arousal index. Other variables assessed objectively include the percentage spent in each sleep stage, including slow wave sleep (SWS) and REM sleep. Objective assessment of sleep quality by polysomnography has been performed predominantly in small cohorts of patients with severe emphysema. Calverley and coworkers (2) studied 20 patients with severe COPD and found increased sleep latency, a decreased amount of uninterrupted sleep, and decreases in SWS and REM sleep, when compared with healthy control subjects. Fleetham and coworkers (6) found decreased TST, an increased number of arousals, and decreased SWS and REM sleep in 15 patients with severe COPD compared with historical control subjects. Wynne and coworkers (1) studied seven patients with severe COPD, and noted similar findings of a decreased TST, with 30% of the night spent awake. In 16 patients with severe COPD, Cormick and coworkers (3) found that subjective complaints of difficulty initiating and maintaining sleep were in significant agreement with objective measurements of poor sleep quality as indicated by a TST of only 208 minutes and increased arousal index. More recently, we studied 16 patients (10 males; age [mean ± SD], 63 ± 6 yr) with severe COPD (FEV1% predicted, 28 ± 10%) who were evaluated for LVRS as part of the NETT (4). Patients underwent a full-night polysomnogram while on room air following an acquaintance night study to compensate for a “first night” effect. As compared with historical age-matched control subjects, sleep quality was poor, with a TST of 203 ± 100 minutes (mean ± SD), and a sleep efficiency of only 50 ± 24%. There was an increase in the number of arousals during the night and an increase in stage 1 sleep and decreases in SWS and REM sleep.

Consequences of Poor Sleep Quality in Emphysema

Despite subjective and objective findings of poor sleep quality in emphysema, Orr and coworkers (36) noted no evidence of daytime sleepiness, as measured with a multiple sleep latency test (mean sleep latency, 11 ± 4 min), in 14 patients with severe COPD. However, the study involved only a small number of patients, and none of the patients had any subjective complaints of daytime sleepiness. Other studies have noted a lack of subjective daytime sleepiness, despite the presence of objectively measured poor sleep quality (37). In addition, it is unknown at the present time whether poor sleep quality in patients with emphysema has an effect on other parameters of daytime function, such as neurocognition, or psychomotor vigilance.

Mechanisms Responsible for Poor Sleep Quality

In a survey of patients 65 years and older with obstructive airway disease due to asthma or COPD, Bellia and coworkers (9) found no correlation between sleep scores associated with insomnia complaints and severity of airflow obstruction (percent predicted FEV1). The only independent correlates for sleep scores were having underlying depression or arthritis. However, the study included patients with underlying asthma, with no comparison made between the control subjects who were free of respiratory disease and those with strictly COPD. Therefore, whether there is a relationship between sleep quality and the severity of underlying disease is yet to be determined (12).

A number of medications used in the treatment of COPD could affect sleep quality. Veale and coworkers (38) noted no change in sleep quality in 14 patients with COPD treated with a sustained-release form of salbutamol. The effects of theophylline on sleep quality have been more variable, with some studies demonstrating an impairment in sleep quality (39), whereas others have noted no significant effect (40–42). Anticholinergics such as ipratropium may improve sleep quality (43). More recently, McNicholas and coworkers (44) demonstrated that the long-acting anticholinergic tiotropium did not affect sleep quality after 4 weeks of treatment.

Therefore, although sleep quality appears to be poor in patients with emphysema, the mechanism responsible, and the association between nighttime findings and daytime function, has yet to be determined.


Because of the prevalence of both COPD and OSA in the general population, both disorders are bound to occur together, what has been coined the “overlap syndrome.” Chaouat and coworkers (45) found an obstructive pattern on spirometry in 11% of patients with a known diagnosis of OSA. PaO2 was lower and PaCO2 higher in the overlap group and mean nocturnal SaO2 was significantly lower despite a lack of difference in the apnea–hypopnea index. A blunted central respiratory response in these patients, as measured by CO2 rebreathing, may explain some of these findings (46). More recently, as part of the Sleep Heart Health Study, Sanders and coworkers (47) reported that 22 and 14% of patients with mild obstructive airway disease (mean FEV1/FVC, 64%) had an apnea–hypopnea index greater than 10 and greater than 15, respectively. However, the prevalence of OSA was similar in the groups with and without obstructive airway disease. In addition, the risk for NOD in patients with coexistent obstructive airway disease and OSA was equal to the combined risk from each disorder alone (47). Regarding prognosis, patients with OSA who fall into the overlap group experience higher mortality despite treatment with continuous positive airway pressure therapy (48).

NOD is theorized to be worse in patients with OSA and COPD. This may be because oxygen stores are lower in diseased lungs than in normal lungs. Thus, for a given apnea period, desaturation should be worse in patients with overlap syndrome than in patients with only OSA but normal lungs. Therefore, in patients with overlap syndrome, the consequences of NOD might be expected to be greater. However, there are few data to address this concern.


Oxygen Therapy

Both the British Medical Research Council (MRC) Long-Term Domiciliary Oxygen Therapy Trial (49) and the Nocturnal Oxygen Therapy Trial (NOTT) (50) evaluated the effects of oxygen therapy in patients with COPD with severe hypoxemia (mean PaO2, 49–51 and 51–52 mm Hg, respectively). In the British study, patients were assigned to continuous oxygen (at least 15 h/d) versus no oxygen therapy, and in the NOTT, patients received continuous oxygen (average, 18 h/d) versus nocturnal oxygen (average, 12 h/d). The continuous oxygen therapy groups in both studies demonstrated improved survival, but the number of patients in each study was small.

In a relatively small study of patients with moderate hypoxemia (PaO2, 56–69 mm Hg), Gorecka and coworkers (51) noted no difference in survival at 3 years between patients prescribed supplemental oxygen (average, 14 h/d) compared with a control group. In addition, Fletcher and coworkers (52) noted no difference in survival in patients with COPD with NOD and an awake PaO2 > 60 mm Hg, who were randomized to nocturnal oxygen at 3 L/minute or a sham control for 36 months. However, there was an improvement in pulmonary hemodynamics noted in the oxygen therapy group. Similar results regarding survival were noted by Chaouat and coworkers (53) in patients with mild to moderate hypoxemia (PaO2, 56–69 mm Hg) who were randomized to nocturnal oxygen therapy versus control and monitored for up to 60 months. In addition to no difference in survival, there was no difference in developing a need for conventional long-term oxygen therapy, or in the degree of change in pulmonary hemodynamics. A similar lack of change in pulmonary hemodynamics has been reported in an uncontrolled study (54).

The effect of oxygen therapy on sleep quality has been examined in only a limited number of studies. Calverley and coworkers (2) noted that the addition of oxygen led to a decrease in sleep latency, an increase in the duration of uninterrupted sleep, and an increase in REM sleep. However, Fleetham and coworkers (6) noted no change in TST, distribution of sleep stages, or frequency of arousals during the night with the addition of oxygen. Therefore, beneficial effects of nocturnal oxygen therapy on sleep quality, pulmonary hemodynamics, and survival remain unproven at the present time.


As noted above, bronchodilator medications have shown mixed results regarding their effects on sleep quality, with some demonstrating improvement (43), no significant effect (40–42, 44), or deterioration in sleep quality (39). However, despite their diverse effects on sleep quality, the majority have demonstrated an improvement in nocturnal oxygen saturation (39, 41, 43, 44) and lung function (39–44). Regarding treatment of insomnia symptoms in patients with emphysema, benzodiazepines should be avoided, even in normocapnic patients, because of their effect on ventilatory drive and worsening nocturnal hypoxemia (55). However, some of the newer nonbenzodiazepine imidazopyridine compounds, such as zolpidem, have been shown to be safer in patients with less severe COPD (56, 57).

Respiratory Muscle Training

Because of the presence of nocturnal hypoventilation, Heijdra and coworkers (18) hypothesized that respiratory muscle weakness may be contributing to the decrease in minute ventilation. They found a significant correlation between measurements of nocturnal oxygenation and both maximal inspiratory mouth and transdiaphragmatic pressures. As a result, Heijdra and coworkers (58) evaluated the effects of inspiratory muscle training on nocturnal oxygenation. Compared with a sham control group, patients in the inspiratory muscle–training group demonstrated an improvement in inspiratory muscle strength, which correlated with a noted improvement in nocturnal oxygenation. However, these studies involved only a small number of patients, and the improvement in mean nocturnal SaO2 was minimal (1.9 ± 2.2%).

Noninvasive Positive-Pressure Ventilation

The use of noninvasive positive-pressure ventilation (NIPPV) has been shown to be beneficial both during an acute exacerbation of COPD (59) as well as in selected groups of patients with stable chronic emphysema (60, 61). We previously demonstrated that NIPPV in a group of stable hypercapnic patients with COPD, as compared with a sham control group, improved sleep quality without an associated improvement in nocturnal gas exchange (60). These findings suggested that factors other than improvement in gas exchange, such as unloading inspiratory muscles or effects on central drive, might play a role. Other long-term trials have demonstrated improvements in sleep quality (62) and gas exchange (61, 62) and a decrease in hospital admissions and office visits (61). As a result, guidelines have been developed for the use of NIPPV in patients with stable COPD (63).


Before the NETT, LVRS had been demonstrated to improve a number of awake physiologic parameters, including respiratory mechanics, gas exchange, and exercise tolerance. We hypothesized that, in association with improvements in respiratory mechanics, LVRS would result in improvement in sleep quality and NOD in severe emphysema. Therefore, as an ancillary study for the NETT, we conducted a prospective, randomized controlled trial, with 6 patients randomized to optimal medical therapy and 10 patients randomized to LVRS and continued optimal medical therapy (4). All patients had an acquaintance night and baseline polysomnogram, with repeat testing at 6 months. The LVRS group, but not the medical group, demonstrated a significant improvement in sleep quality, as measured by TST, sleep efficiency, and arousal index (). In addition, nocturnal oxygenation, as measured by the mean and lowest oxygen saturation, as well as the percentage TST with an SaO2 less than 90%, improved only in the LVRS group. The mechanism by which LVRS improved sleep quality was not conclusively determined. Improvements in nocturnal oxygenation were noted to correlate with improvements in airflow obstruction and inversely with improvements in air trapping and hyperinflation (). However, improvement in nocturnal oxygenation did not appear to be responsible for the improvement in sleep quality, suggesting that other mechanisms, such as a decrease in hyperinflation and improvement in respiratory muscle function, may be responsible.

Effects of lung volume reduction surgery (LVRS) and medical therapy on total sleep time and sleep efficiency after 6 months. There was a significant improvement in total sleep time and sleep efficiency in the LVRS group, with no change noted in the medical therapy group. Reprinted by permission from Reference 4.

There was a significant inverse correlation between the change in lowest SaO2 during the night (from baseline to 6 mo) and changes in residual volume and functional residual capacity (n = 16; r = −0.5, P = 0.04 and r = −0.6, P = 0.03, respectively). Reprinted by permission from Reference 4.


An American Thoracic Society and European Respiratory Society task force published a position paper on standards for the diagnosis and treatment in COPD (64). The group recommended that sleep studies be performed only under special circumstances, including when there a clinical suspicion for OSA, or if there are complications from hypoxemia that are unexplained on the basis of the awake arterial oxygen level, or if there is pulmonary hypertension that is out of proportion to the degree of airflow obstruction.

Limitations and Unanswered Questions

The current literature regarding sleep abnormalities in patients with emphysema has a number of limitations, with small numbers of patients being studied and often conflicting results. Therefore, a number of unanswered important questions remain, including determining whether NOD contributes to the development of chronic pulmonary hypertension and poor sleep quality, as well as whether NOD affects survival. In addition, it is yet to be determined whether poor sleep quality in these patients affects daytime function, including psychomotor vigilance and neurocognitive function. Other mechanistic issues include determining how interventions such as NIPPV and LVRS improve both sleep quality and nocturnal oxygenation. Finally, evaluating whether nocturnal oxygen therapy has an effect on sleep quality and survival will require a relatively large trial. It is hoped that some of these important questions can be answered in the upcoming multicenter National Institutes of Health–sponsored Long-term Oxygen Treatment Trial (LOTT).


In severe emphysema, sleep is often disturbed and of poor quality, both subjectively and objectively. In addition, nocturnal oxygen desaturation is common, even in patients who do not require oxygen as determined on the basis of awake values. The causes for disturbed sleep are probably multiple, with the severity of underlying disease possibly playing a role. In patients with mild to moderate hypoxemia, the effects of oxygen therapy are mixed, in terms of its effects on both pulmonary hemodynamics and sleep quality. More recently, LVRS has been shown to improve both sleep quality and nocturnal oxygenation in severe emphysema. However, the mechanism by which LVRS improves sleep quality is yet to be determined. A number of questions regarding NOD in COPD remain unanswered. These and other questions of interest will be answered only in future larger and well-controlled clinical trials.


The National Emphysema Treatment Trial (NETT) is supported by contracts with the National Heart, Lung, and Blood Institute (N01HR76101, N01HR76102, N01HR76103, N01HR76104, N01HR76105, N01HR76106, N01HR76107, N01HR76108, N01HR76109, N01HR76110, N01HR76111, N01HR76112, N01HR76113, N01HR76114, N01HR76115, N01HR76116, N01HR76118, and N01HR76119), the Centers for Medicare and Medicaid Services (CMS), and the Agency for Healthcare Research and Quality (AHRQ).

Conflict of Interest Statement: None of the authors has a financial relationship with a commercial entity that has an interest in the subject of this manuscript.


1. Wynne JW, Block AJ, Hemenway J, Hunt LA, Flick MR. Disordered breathing and oxygen desaturation during sleep in patients with chronic obstructive lung disease. Am J Med 1979;66:573–579. [PubMed] [Google Scholar]2. Calverley PMA, Brezinova V, Douglas NJ, Catterall JR, Flenley DC. The effect of oxygenation on sleep quality in chronic bronchitis and emphysema. Am Rev Respir Dis 1982;126:206–210. [PubMed] [Google Scholar]3. Cormick W, Olson LG, Hensley MJ, Suadners NA. Nocturnal hypoxaemia and quality of sleep in patients with chronic obstructive lung disease. Thorax 1986;41:846–854. [PMC free article] [PubMed] [Google Scholar]4. Krachman SL, Chatila W, Martin UJ, Nugent T, Crocetti J, Gaughan J, Criner GJ. Effects of lung volume reduction surgery on sleep quality and nocturnal gas exchange in patients with severe emphysema. Chest 2005;128:3221–3228. [PubMed] [Google Scholar]5. Koo KW, Sax DS, Snider GL. Arterial blood gases and pH during sleep in chronic obstructive pulmonary disease. Am J Med 1975;58:663–670. [PubMed] [Google Scholar]6. Fleetham J, West P, Mezon B, Conway W, Roth T, Kryger M. Sleep, arousals, and oxygen desaturation in chronic obstructive pulmonary disease: the effect of oxygen therapy. Am Rev Respir Dis 1982;126:429–433. [PubMed] [Google Scholar]7. Fletcher EC, Miller J, Divine GW, Fletcher JG, Miller T. Nocturnal oxyhemoglobin desaturation in COPD patients with arterial oxygen tensions above 60 mmHg. Chest 1987;92:604–608. [PubMed] [Google Scholar]8. Bradley TD, Mateika J, Li D, Avendano M, Goldstein RS. Daytime hypercapnia in the development of nocturnal hypoxemia in COPD. Chest 1990;97:308–312. [PubMed] [Google Scholar]9. Bellia V, Catalano F, Scichilone N, Incalzi RA, Spatafora M, Vergani C, Rengo F. Sleep disorders in the elderly with and without chronic airflow obstruction: the SARA Study. Sleep 2003;26:318–323. [PubMed] [Google Scholar]10. Klink ME, Dodge R, Quan SF. The relation of sleep complaints to respiratory symptoms in the general population. Chest 1994;105:151–154. [PubMed] [Google Scholar]11. Dodge R, Cline MG, Quan SF. The natural history of insomnia and its relationship to respiratory symptoms. Arch Intern Med 1995;155:1797–1800. [PubMed] [Google Scholar]12. Krachman SL, Criner GJ, Nugent T, Martin UJ, Chatila WM. Physiologic determinants of sleep quality in patients with severe emphysema [abstract]. Am J Respir Crit Care Med 2003;167:A234. [Google Scholar]13. Connaughton JJ, Catterrall JR, Elton RA, Stradling JR, Douglas NJ. Do sleep studies contribute to the management of patients with severe chronic obstructive pulmonary disease? Am Rev Respir Dis 1988;138:341–344. [PubMed] [Google Scholar]14. Fletcher EC, Luckett RA, Miller T, Fletcher JG. Exercise hemodynamics and gas exchange in patients with chronic obstruction pulmonary disease, sleep desaturation and daytime PaO2 above 60 mmHg. Am Rev Respir Dis 1989;140:1237–1245. [PubMed] [Google Scholar]15. Fletcher EC, Scott D, Qian W, Luckett RA, Miller CC, Goodnight-White S. Evolution of nocturnal oxyhemoglobin desaturation in patients with chronic obstructive pulmonary disease and a daytime PaO2 above 60 mmHg. Am Rev Respir Dis 1991;144:401–405. [PubMed] [Google Scholar]16. Mulloy E, McNicholas WT. Ventilation and gas exchange during sleep and exercise in severe COPD. Chest 1996;109:387–394. [PubMed] [Google Scholar]17. Chaouat A, Weitzenblum E, Kessler R, Charpentier C, Ehrhart M, Levi-Valensi P, Zielinski J, Delaunois L, Cornudella R, Moutinho dos Santos J. Sleep-related O2 desaturation and daytime pulmonary haemodynamics in COPD patients with mild hypoxaemia. Eur Respir J 1997;10:1730–1735. [PubMed] [Google Scholar]18. Heijdra YF, Dekhuijzen PNR, van Herwaarden CLA, Folgering HTM. Nocturnal saturation and respiratory muscle function in patients with chronic obstructive pulmonary disease. Thorax 1995;50:610–612. [PMC free article] [PubMed] [Google Scholar]19. Berthon-Jones M, Sullivan CE. Ventilatory and arousal responses to hypoxia in normal sleeping humans. Am Rev Respir Dis 1982;125:632–639. [PubMed] [Google Scholar]20. Berthon-Jones M, Sullivan CE. Ventilatory and arousal responses to hypercapnia in normal sleeping humans. J Appl Physiol 1984;57:59–67. [PubMed] [Google Scholar]21. Tabachnik E, Muller NL, Bryan AC, Levison H. Changes in ventilation and chest wall mechanics during sleep in normal adolescents. J Appl Physiol 1981;51:557–564. [PubMed] [Google Scholar]22. Berger RJ. Tonus of extrinsic laryngeal muscles during sleep and dreaming. Science 1961;134:840. [PubMed] [Google Scholar]

23. Krieger J. Breathing during sleep in normal subjects. In: Kryger MH, Roth T, Dement WC, editors. Principles and practices of sleep medicine. Philadelphia, PA: W.B. Saunders; 2005. pp. 232–244.

24. Wiegand DA, Latz B, Zwillich CW, Wiegand L. Geniohyoid muscle activity in normal men during wakefulness and sleep. J Appl Physiol 1990;69:1262–1269. [PubMed] [Google Scholar]25. De Marco FJ Jr, Wynne JW, Block AJ, Boysen PG, Tassan VC. Oxygen desaturation during sleep as a determinant of the blue bloated syndrome. Chest 1981;79:621–625. [PubMed] [Google Scholar]26. Becker HF, Piper AJ, Flynn WE, McNamara SG, Grunstein RR, Peter JH, Sullivan CE. Breathing during sleep in patients with nocturnal desaturation. Am J Respir Crit Care Med 1999;159:112–118. [PubMed] [Google Scholar]27. Hudgel DW, Devodatta P. Decrease in functional residual capacity during sleep in normal humans. J Appl Physiol 1984;57:1319–1322. [PubMed] [Google Scholar]28. Ballard RD, Clover CW, Suh BY. Influence of sleep on respiratory function in emphysema. Am J Respir Crit Care Med 1995;151:945–951. [PubMed] [Google Scholar]29. O’Donoghue FJ, Catcheside PG, Eckert DJ, McEvoy RD. Changes in respiration in NREM sleep in hypercapnic chronic obstructive pulmonary disease. J Physiol 2004;559:663–673. [PMC free article] [PubMed] [Google Scholar]30. Catterall JR, Calverley PMA, MacNee W, Warren PM, Shapiro CM, Douglas NJ, Flenley DC. Mechanism of transient nocturnal hypoxemia in hypoxic chronic bronchitis and emphysema. J Appl Physiol 1985;59:1698–1703. [PubMed] [Google Scholar]31. Minai OA, Pandya CM, Golish JA, Avecillas JF, McCarthy K, Marlow S, Arrolida AC. Predictors of nocturnal oxygen desaturation in pulmonary arterial hypertension. Chest 2007;131:109–117. [PubMed] [Google Scholar]32. Coccagna G, Lugaresi E. Arterial blood gases and pulmonary and systemic arterial pressure during sleep in chronic obstructive pulmonary disease. Sleep 1978;1:117–124. [PubMed] [Google Scholar]33. Fletcher EC, Luckett RA, Miller T, Costarangos C, Kutka N, Fletcher JG. Pulmonary vascular hemodynamics in chronic lung disease patients with and without oxyhemoglobin desaturation during sleep. Chest 1989;95:757–766. [PubMed] [Google Scholar]34. Fletcher EC, Donner CF, Midgren B, Zielinski J, Levi-Valensi P, Braghiroli A, Rida Z, Miller CC. Survival in COPD patients with daytime PaO2 > 60 mmHg with and without nocturnal oxyhemoglobin desaturation. Chest 1992;101:649–655. [PubMed] [Google Scholar]35. Kaplan RM, Ries AL, Reilly J. Mohsenifar: measurement of health-related quality of life in the National Emphysema Treatment Trial. Chest 2004;126:781–789. [PubMed] [Google Scholar]36. Orr WC, Shamma-Othman Z, Levin D, Lthman J, Rundell OH. Persistent hypoxemia and excessive daytime sleepiness in chronic obstructive pulmonary disease (COPD). Chest 1990;97:583–585. [PubMed] [Google Scholar]37. Saaresranta T, Irjala K, Aittokallio T, Polo O. Sleep quality, daytime sleepiness and fasting insulin levels in women with chronic obstructive pulmonary disease. Respir Med 2005;99:856–863. [PubMed] [Google Scholar]38. Veale D, Cooper BG, Griffiths CJ, Corris PA, Gibson GJ. The effect of controlled-release salbutamol on sleep and nocturnal oxygenation in patients with asthma and chronic obstructive pulmonary disease. Respir Med 1994;88:121–124. [PubMed] [Google Scholar]39. Mulloy E, McNicholas WT. Theophylline improves gas exchange during rest, exercise and sleep in severe chronic obstructive pulmonary disease. Am Rev Respir Dis 1993;148:1030–1036. [PubMed] [Google Scholar]40. Martin RJ, Pak J. Overnight theophylline concentrations and effects on sleep and lung function in chronic obstructive pulmonary disease. Am Rev Respir Dis 1992;145:540–544. [PubMed] [Google Scholar]41. Berry RB, Desa MM, Branum JP, Light RW. Effect of theophylline on sleep and sleep-disordered breathing in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis 1991;143:245–250. [PubMed] [Google Scholar]42. Mann GCW, Chapman KR, Ali SH, Darke AC. Sleep quality and nocturnal respiratory function with once-daily theophylline (Uniphyl) and inhaled salbutamol in patients with COPD. Chest 1996;110:648–653. [PubMed] [Google Scholar]43. Martin RJ, Bucher Bartelson B, Smith P, Hudgel DW, Lewis D, Pohl G, Koker P, Souhrada JF. Effect of ipratropium bromide treatment on oxygen saturation and sleep quality in COPD. Chest 1999;115:1338–1345. [PubMed] [Google Scholar]44. McNicholas WT, Calverley PM, Lee A, Edwards JC. Long-acting inhaled anticholinergic therapy improves sleeping oxygen saturation in COPD. Eur Respir J 2004;23:825–831. [PubMed] [Google Scholar]45. Chaouat A, Weitzenblum E, Krieger J, Ifoundza T, Oswald M, Kessler R. Association of chronic obstructive pulmonary disease and sleep apnea syndrome. Am J Respir Crit Care Med 1995;151:82–86. [PubMed] [Google Scholar]46. Radwan L, Maszczyk Z, Koziorowski A, Koziej M, Cieslicki J, Sliwinski P, Zielinski J. Control of breathing in obstructive sleep apnoea and in patients with the overlap syndrome. Eur Respir J 1995;8:542–545. [PubMed] [Google Scholar]47. Sanders MH, Newman AB, Haggerty CL, Redline S, Lebowitz M, Samet J, O’Connor GT, Punjabi NM, Shahar E. Sleep and sleep-disordered breathing in adults with predominantly mild obstructive airway disease. Am J Respir Crit Care Med 2003;167:7–14. [PubMed] [Google Scholar]48. Chaouat A, Wetzenblum E, Krieger J, Sforza I, Hammad H, Oswald M, Kessler R. Prognostic value of lung function and pulmonary haemodynamics in OSA patients treated with CPAP. Eur Respir J 1999;13:1091–1096. [PubMed] [Google Scholar]49. Medical Research Council Working Party. Long-term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema. Lancet 1981;1:681–686. [PubMed] [Google Scholar]50. Nocturnal Oxygen Therapy Trial Group. Continuous or nocturnal oxygen therapy in hypoxemic chronic obstructive lung disease: a clinical trial. Ann Intern Med 1980;93:391–398. [PubMed] [Google Scholar]51. Gorecka D, Gorzelak K, Sliwinski P, Tobiasz M, Zielinski J. Effect of long-term oxygen therapy on survival in patients with chronic obstructive pulmonary disease with moderate hypoxemia. Thorax 1997;52:674–679. [PMC free article] [PubMed] [Google Scholar]52. Fletcher EC, Luckett RA, Goodnigth-White S, Miller CC, Qian W, Costarangos-Galarza C. A double-blind trial of nocturnal supplemental oxygen for sleep desaturation in patient with chronic obstructive pulmonary disease and a daytime PaO2 above 60 mmHg. Am Rev Respir Dis 1992;145:1070–1076. [PubMed] [Google Scholar]53. Chaouat A, Weitzenblum E, Kessler R, Charpentier C, Ehrahart M, Schott R, Levi-Valensi P, Zielinski J, Delaunois L, Cornudella R, et al. A randomized trial of nocturnal oxygen therapy in chronic obstructive pulmonary disease patients. Eur Respir J 1999;14:1002–1008. [PubMed] [Google Scholar]54. Zielenski J, Tobiasz M, Hawrylkiewicz I, Sliwinski P, Palasiewicz G. Effects of long-term oxygen therapy on pulmonary hemodynamics in COPD patients. Chest 1998;113:65–70. [PubMed] [Google Scholar]55. Block AJ, Dolly FR, Slayton PC. Does flurazepam ingestion affect breathing and oxygenation during sleep in patients with chronic obstructive lung disease? Am Rev Respir Dis 1984;129:230–233. [PubMed] [Google Scholar]56. Girault C, Muir JF, Mihaltan F, Borderies P, De La Giclais B, Verdure A, Samson-Dollfus D. Effects of repeated administration of zolpidem on sleep, diurnal and nocturnal respiratory function, vigilance, and physical performance in patients with COPD. Chest 1996;110:1203–1211. [PubMed] [Google Scholar]57. Steens R, Pouliot Z, Millar T, Kryger M, George C. Effects of zolpidem and triazolam on sleep and respiration in mild to moderate chronic obstructive pulmonary disease. Sleep 1993;16:318–326. [PubMed] [Google Scholar]58. Heijdra YF, Dekhuijzen PN, van Herwaarden CL, Folgering HT. Nocturnal saturation improves by target-flow inspiratory muscle training in patients with COPD. Am J Respir Crit Care Med 1996;153:260–265. [PubMed] [Google Scholar]59. Antonelli M, Conti G, Rocco M, Bufi M, De Blasi RA, Vivino G, Gasparetto A, Meduri GU. A comparison of noninvasive positive pressure ventilation and conventional mechanical ventilation in patients with acute respiratory failure. N Engl J Med 1998;339:429–435. [PubMed] [Google Scholar]60. Krachman SL, Quaranta AJ, Berger TJ, Criner GJ. Effects of noninvasive positive pressure ventilation on gas exchange and sleep in COPD patients. Chest 1997;112:623–628. [PubMed] [Google Scholar]61. Jones SE, Packham S, Hebden M, Smith AP. Domiciliary nocturnal intermittent positive pressure ventilation in patients with respiratory failure due to severe COPD: long-term follow-up and effect on survival. Thorax 1998;53:495–498. [PMC free article] [PubMed] [Google Scholar]62. Elliott MW, Simonds AK, Carroll MP, Wedzicha JA, Branthwaite MA. Domiciliary nocturnal nasal intermittent positive pressure ventilation in hypercapnic respiratory failure due to chronic obstructive lung disease: effects on sleep and quality of life. Thorax 1992;47:342–348. [PMC free article] [PubMed] [Google Scholar]63. Goldberg A, conference facilitator; Leger P, Hill N, Criner G. Clinical indications for noninvasive positive pressure ventilation in chronic respiratory failure due to restrictive lung disease, COPD, and nocturnal hypoventilation: a consensus conference report. Chest 1999;116:521–534. [PubMed] [Google Scholar]64. Celli BR, Mac Nee W, Agusti A, Anzueto A, Berg B, Buist AS, Calverley PMA, Chavannes N, Dillard T, Fahy B, et al. Standards for the diagnosis and treatment of patients with COPD: a summary of the ATS/ERS position paper. Eur Respir J 2004;23:932–946. [PubMed] [Google Scholar]

Sleeping Positions with COPD | Centers for Respiratory Health

Do you ever wake up in the middle of the night struggling for breath? Does it ever feel like the agonizing pain will never go away?

Having a good night’s sleep is vital to maintaining good health. Without sufficient sleep, the body cannot begin to heal itself, which weakens the immune system. It also can lead to mood swings and affect your capability to maintain a healthy weight. Unfortunately, these issues are often shared among people with lung disease. When people with lung disease do not get an effective amount of sleep, it can cause their condition to worsen over time.

COPD Sleeping Disturbance

Sleep disturbance is one of the most common symptoms reported by patients with chronic obstructive pulmonary disease (COPD). According to the Confronting COPD International Survey about 40 percent of patients experience trouble sleeping. Having COPD is directly associated with oxygen desaturation, which results in impaired sleep quality, particularly during the end of REM sleep. This stage can last up to about an hour, and throughout this time both breathing and heart rate increase. Patients with COPD experience the most interruption during this period, causing intense hyperventilation.

Sleep Better With COPD

Luckily, there are a few small changes that those with COPD can make for easier breathing while sleeping. One of those small changes is adjusting your sleeping position. It is often said that the best way to keep the airways open is to avoid lying down, but rather sitting in an upright position. Although this method is extremely effective, it does not mean that is comfortable. Trying to sleep straight up can seem more like a hassle than an escape. Sleeping on your side is more of a comfortable alternative that avoids any tension in the throat, which can hinder breathing. Sleeping on your side opens up the airways and can tremendously decrease the risk of breathing problems.

Your head position is another factor that needs to be considered. When you are lying on your side, making sure that your head is propped in an upright position and not lying flat is key. When your head is completely flat, your airways are restricted which can cause hyperventilation. It is extremely important to pay attention to the amount of head support you use. Too many pillows can cause just as much tension as using no pillow at all. Using at least one to two pillows is best when trying to focus on maintaining an opening of the airways.

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At the Lung Health Institute, we understand the difficultly of not just COPD itself, but the troubles of sleeping that come with it. If you or a loved one is suffering from a chronic lung disease like COPD, the Lung Health Institute might be able to help. Give the gift of a better quality of life through cellular therapy at the Lung Health Institute. Contact one of our Patient Coordinators today by calling 888-745-6697 for a free consultation.



COPD / Adjusting Sleep Position To Breathe Better

Chronic obstructive pulmonary disease (COPD) is an umbrella term for group of progressive lung diseases, such as emphysema and chronic bronchitis –

 but what does COPD actually mean?

Over 17 million people in North America have been diagnosed with COPD but many others are living with it every day undiagnosed. It is a serious illness that affects breathing, which drastically impacts the lifestyle of those suffering with this common condition.

The symptoms of COPD can vary from person to person. Typically, this disease develops over time and most people are around 40 years old when they start experiencing consistent symptoms, including:

shortness of breath
a chronic cough that may produce mucus
swelling in ankles, feet or legs
chest tightness.

There are ways to manage the symptoms of COPD but currently no way to cure it. Specialists recommend medication, supplemental oxygen and surgery as three viable clinical methods of treatment. Additionally, lifestyle changes can help prevent worsening of the symptoms including avoiding smoking or second-hand smoke, eating healthy & moderate exercise.

As previously mentioned, COPD can make it difficult to get quality, restful sleep. This is partly because of the medications that are prescribed to treat the symptoms of this illness, but also changes in breathing patterns that occur during normal sleep which may worsen and complicate COPD since they reduce blood oxygen. According to the Cleveland Clinic and other Medical institutions, sleeping in certain positions can help ease the symptoms of COPD, including shortness of breath and a build of mucus in your lungs. Positioning yourself with your head and knees slightly elevated is suggested. Adjustable beds with the ability to raise the head and knees sections with the touch of a button can help simplify the proper positioning for comfort with ease.


We’re here to help! Send us a message and someone will be in contact with you as soon as possible! To book your appointment to see SonderCare beds in person please call us at 1.833.649.7772

90,000 What position is it recommended to sleep in? answer from Sonit experts

As a rule, a person does not think at all what position for sleeping is considered the most useful, and sometimes he does not even know in which of the many positions he usually falls asleep. However, doctors say that a correctly chosen resting position is the key to good health and the prevention of numerous diseases.

Let’s figure out which of the poses has more advantages over the others, as well as what the pros and cons are in each of them.This information will help you take a different look at your sleep and choose exactly the position that suits your body.

Supine position.

Sleeping on the back is considered the most natural and beneficial, and therefore recommended by doctors. It is in this position that a person relaxes as much as possible, and his spine is in an even, comfortable position, not twisting anywhere. It is in this position that a person is able to restore his strength as much as possible after a day’s load.

If you suffer from heartburn , then the ideal option for you would be to sleep on your back with a slightly raised headboard. This position will eliminate squeezing of the stomach and will not allow acid to rise to the esophagus.
Sleeping on your back is also very beneficial for people with scoliosis and heart disease. Such rest is good for the prevention of osteochondrosis, and, surprisingly, for the prevention of wrinkles!

The thing is that lying on your back, your face does not come into contact with the pillow in any way, as a result of which wrinkles, creases and folds do not form on it.

However, there are some nuances here. The main one is snoring. Unfortunately, it is in this position that a person is prone to snoring. This is due to the fact that in this position the jaw tends to sink in, which interferes with proper breathing. That is why people with bronchial asthma or obstructive pulmonary disease should not sleep on their backs.

It is not recommended to sleep in this position and pregnant women for a period of 20 weeks or more . At this time, the uterus already has a fairly large size and in the supine position is capable of pinching the lower artery of the expectant mother, which will impede blood circulation.It becomes more difficult for the heart to pump blood and not only the mother, but also her unborn baby is exposed to discomfort.

How to choose a pillow for sleeping on your back?

The pillow should be of medium height and moderately soft. It is important that she supports her head, but in no case lifts her too high. The choice of your optimal pillow height should be approached very carefully, because if your pillow is too high, you have every chance of earning osteochondrosis , if it is too flat, this will lead to straightening of the cervical lordosis.

Lateral position.

This is the ideal position for pregnant women at any stage of pregnancy. On the side, a person is also not susceptible to snoring, since the airways in this position do not close.

Speaking about the benefits of such a dream, one should make a reservation: it is important to take into account exactly the position that you take while sleeping on your side. Some people press their chin tightly to their chest, as a result of which the neck is overextended, others lie in such a way that their spine takes a twisted shape.

One of the favorite poses of young children is sleeping on their side with their head thrown back sharply. Be careful – this position contributes to the formation of a malocclusion.

As for the posture of the embryo, it is the most natural and favorable for a person, however, not everything is so smooth here either. Sitting on the side has a negative effect on female beauty. Many wrinkles form in the décolleté, neck and shoulders. But it will be especially bad for your face.

Lying on the side, a fold appears under the lower eyelid, on the bridge of the nose, on the cheeks near the nose. All these small and inconspicuous folds eventually turn into deep wrinkles, which we mistake for expression lines. However, these imperfections appear not due to active facial expressions, but due to an incorrectly chosen sleeping position.

How to choose a pillow for sleeping on your side?

The right side rest pillow is a piece that is lush and thick. Ideal – orthopedic pillow with rollers to support the cervical vertebrae.The right pillow should fill the entire space from the neck to the mattress, otherwise your neck will be very tense during sleep and you will have a headache.

Position on the stomach.

Many doctors call this posture the most unhealthy and wrong. During sleep on the stomach, the face is pressed into a pillow, and the neck is in a semi-folded state, due to which one of the arteries is pinched and the blood supply to the brain is noticeably impaired.

It is worth mentioning breathing during sleep.In the prone position, the lungs are compressed, which cannot open completely when inhaling. Less oxygen enters the bloodstream and your heart, instead of getting rest, works in an enhanced mode.

If you have osteochondrosis or atherosclerosis, the position on your stomach is also far from the best option for you.

The pressure on the bladder, which occurs when sleeping on your stomach, will not allow you to get quality sleep, and constant squeezing of your breasts will lead to the fact that over time it will lose its elasticity and attractiveness.

However, in defense of this position, it should be said that in this position, as in the position on the side, a person is not susceptible to snoring. It is worth adding to this that it is recommended to sleep on the stomach for people with intestinal colic and increased gas production. Also, lying on your stomach, you exclude the squeezing of the kidneys, due to which the body is cleansed much better and more efficiently. It is believed that sleeping on the stomach creates favorable conditions for straightening the intervertebral cartilage, and is recommended for the prevention of ulcers and gastritis.

The main rule is not to sleep on your stomach on a full stomach.

How to choose a pillow for sleeping on your stomach?

The pillow for sleeping on the stomach should be soft, elastic, as thin and flat as possible. The head should lie flat, and the fragile cervical vertebrae should in no case bend.


As it turns out, any sleeping position has its advantages and disadvantages. And if it is convenient for you to sleep in one position or another, you do not need to immediately relearn to fall asleep in a different position.

If you often roll over from one side to the other, and then change positions that are convenient for you several times and this helps you to wake up refreshed, fresh and full of energy, then trust your body – there is no single clear recipe for health for all people at the same time. If in the morning you are not tormented by pain in your back or neck, your muscles do not swell, and your head does not hurt, this once again confirms that you sleep exactly as your body needs.


9 Tips For Better Sleep When You Have COPD

Sleeping is important for everyone – but people with

chronic obstructive pulmonary disease



) you need to get a good night’s sleep in order to calm your lungs and be able to function the next day, says

Joseph M.Ojil, md

The Clayton Spin Institute in Maplewood and Farmington, Missouri and the National Sleep Foundation Chair. The problem is that it can be difficult to boil when you are short of breath, cough, and in pain.

It can become a vicious cycle, he says. In addition, there are other reasons why you may be having trouble sleeping, including:

  • You can have


    which can be caused by medications such as




    According to the National Sleep Foundation.
  • You try to sleep to sit; Although it might be easier for you


    In this position, it can interfere with your ability to fall asleep.
  • When you lie flat, the amount of oxygen in your blood decreases because breathing slows down, says

    E. Neil Schachter, MD

    pulmonologist and

    Sleep medicine

    Specialist at Mount Sinai Hospital in New York City. Also some alveoli, air sacs in your lungs that help move oxygen into your bloodstream, go to sleep and also fall out of the Medical Center, according to the University of California San Francisco Medical Center.This phenomenon “happens to some degree in every degree, but the degree and the consequences are greater” if you have COPD, says Shakhtar.

  • You have anxiety or depression, which can occur in people who have chronic conditions.
  • You may also have undiagnosed

    Sleep apnea

    , a state in which you stop or almost stop breathing several times during the night.

Sleep tips for people with COPD

The good news: There are ways to improve the quality of your sleep.Here’s What You Can Do

If you have COPD


Adjust your sleeping position.

Sleeping in a slightly upright position will take a little strain from your lungs, says

Meilan King Han, MD

Spokesperson for the American Lung Association, Assistant Professor of Internal Medicine in the Division of Pulmonary and Critical Medicine in Health Medicine at the University of Michigan Health System and Director of the Women’s Respiratory Clinic.Having your head slightly taller also helps prevent acid reflux from waking you up at night. Also known as

gastroesophageal reflux disease

, or


This condition, in which stomach acid enters your esophagus, is a common problem for people with COPD. (Staying awake on the left side may also help prevent acid reflux, according to a review published in

International Journal of Chronic Obstructive Pulmonary Disease

In September 2015.)

Avoid nopping during the day.

You cannot fight

increased daytime sleepiness

Taking NAPS – You Should Know That


Your sleepiness speaks

Martha Cortés, DDS

Sleep Medicine Biological Dental Medicine Expert and Founder of Sleep Fitness, New York Branch of CORTÉS Advanced Dentistolation. If you must take a nap, keep it short – no more than 20 minutes, she says.

Drive electronics out of the bedroom.

The light emitted from laptops, tablets, mobile phones and e-readers can keep you awake, Dr. Cortez says.

Get moving. ”

Exercise is what improves COPD in general, ”says Dr. Schachter. “It improves your endurance so you can do more during the day, and if you do more during the day, you will sleep better at night.”

Establish a sleep routine.

Going to bed and waking up at the same time every day – even on weekends – can help keep your circadian rhythm (approximately 24-25 hour cycles) in sync with your mother’s schedule, Cortés says.

Talk to your doctor about using oxygen therapy.

If your oxygen saturation levels drop, your doctor may prescribe oxygen for you to use at night. “If you need it, it’s important that you are prescribed overnight oxygen,” says Shakhtar.

Keep your bedroom sleeping.

This means that he is not watching TV or answering emails in bed. Goal: Train yourself to fall asleep as soon as you are in bed. Keep the room calm, dark, and cool; it also helps to nod.

Living for sleep apnea.

If you have any signs and

Sleep apnea symptoms

– For example, say, for example, your bed partner notes that you dare a lot – ask your doctor about scheduling a test.Sleep apnea and COPD often overlap, according to the underlying COPD.

Review your medications.

Talk to your doctor about all the medications you are taking and ask if any of them are causing you to lose sleep. You can adjust the time you take them to prevent them from staying awake at night, Miner says. Plus, pain is very damaging to sleep, Dr. Ogil says, so talk to your doctor about ways to control your pain.

If you don’t get enough sleep, your immune system can weaken, increasing your risk for infections, Ojile says. It is important that you solve your sleep problems with your health care team.

How to work with COPD – Question to the pulmonologist

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Good to know about COPD (kols)

Facts about chronic obstructive pulmonary disease (COPD) ( kols )

An estimated 370,000 people in Norway suffer from COPD. It is estimated that as many as 280,000 of them are unaware of their illness. COPD is a disease that is rapidly progressing around the world and by 2020 it is expected that this disease will be the third leading cause of death in the world.

What is COPD?

Chronic obstructive pulmonary disease (COPD) is characterized by a progressive deterioration in lung function. This leads to a forced increase in respiratory movements and a feeling of shortness of breath. There is a chronic narrowing of the airways and breathing becomes heavy. In addition, chest whistling, coughing, and sputum are typical symptoms. Symptoms worsen with physical activity. With a serious degree of the disease, it becomes difficult to breathe even in a calm environment.

Who can get COPD?

Tobacco smoking is the leading cause of COPD and accounts for two out of three cases in Norway. Six to eight percent of patients have never smoked and at least 15 percent of cases would never have occurred if it were not for exposure to irritants in the respiratory tract in a working environment. Heredity also plays a separate role.

World statistics show that 95% of patients with chronic obstructive pulmonary disease are smokers, often with more than 20 years of daily smoking experience.

Current research also shows that the likelihood of acquiring COPD in adulthood is three times higher among people with childhood asthma than among people who smoked daily but did not have asthma.

At this link you can read the results of the research.

Diagnosis of COPD

COPD develops gradually, and it may take 30-40 years before the first symptoms appear. Inflammation of the airways leads to narrowing and scarring that cannot be detected with conventional x-rays.The presence of COPD can be easily determined by examining lung function by a physician. The symptoms of COPD are similar to those of asthma, which can make a diagnosis difficult.

The intensity of COPD symptoms can vary. For some, the disease may proceed easily, without much discomfort in everyday life, while others may be disabled and dependent on constant oxygen supply. In some cases, patients can suffer from both COPD and asthma.


It is estimated that over 370,000 Norwegians over 18 years of age have COPD, with 20,000 new cases each year.Less than half of the patients were diagnosed. The number of patients increases significantly with age. Worldwide, the rate of increase in the incidence of COPD is the fastest. The World Health Organization has ranked COPD as the fourth leading cause of death in the world. According to calculations, it is expected that by 2020 this particular disease will be the third in the list of causes of death in the world.

What happens in the respiratory tract?

  • The amount of mucus in the bronchi increases.
  • Inflammatory changes (inflammation) in the mucous membrane.
  • Spasms (contraction) of muscle tissue around the bronchi.
  • Destruction of elastic fibers of tissues of small and large airways. In COPD, there is damage and gradual destruction of the elastic tissue around the bronchi. This leads to a tendency for the airway to collapse on expiration.

This illustration shows a breathing tube in the lungs. The upper figure shows the normal version.The bottom picture shows the thickened tissue that causes the tube to narrow, which is a typical symptom of COPD. In addition, the elements whose task is to keep the airways open have lost their rigidity, which leads to a tendency to collapse on exhalation.

In this illustration, you see an illustration of a normal airway tube above and on the right. Shown below is a breathing tube with COPD – thickened tissue that narrows the tube, weakened elements that are common in COPD.In addition, a large amount of mucus is produced. The mucus further narrows the pathways, promotes the development of coughing, which, in turn, leads to even more difficult breathing.

The difference between asthma and COPD

In asthma, symptoms occur in the form of attacks, often with changes in lung function throughout the day. With COPD, symptoms develop gradually and with less variation than with asthma. Between attacks, the lungs of an asthmatic are normal. The lung function of a COPD patient gradually deteriorates from year to year.

Training and education

Education is essential for increasing the amount of COPD knowledge needed to improve the condition of patients. This type of education is provided in COPD schools or during rehabilitation. Training centers located throughout the country conduct such courses. Some centers also offer courses for relatives of people with COPD. These centers are often located in hospitals. There is no single register of centers, you should go to the hospital where you live.