Bill Pruitt, MBA, RRT, CPFT, AE-C

As people drift away from consciousness and into the state of sleep, a vast number of changes occur in the body. Sleep provides many benefits, including a restoration of energy levels, providing a coping mechanism for stress, help in solving problems through the subconscious mind, and aid in recovering from illness. The body undergoes repair during sleep, producing new tissues, bone, and muscle while tuning up the immune system. If people miss too much sleep time, they suffer the consequences of poor memory, distracted thought processes, depression, an increase in the perception of pain, and a lowered immune response.1 People with chronic obstructive pulmonary disease (COPD) are especially susceptible to sleep loss. Because COPD patients have a higher risk of decreased sleep quality and need special consideration for care as it relates to their sleep, special attention needs to be given to the pattern of sleep in this patient population.


COPD is the fourth leading cause of death in the United States, and it affects some 14 million adults. According to the Centers for Disease Control and Prevention (CDC), in the year 2000 COPD caused 119,000 deaths, 726,000 hospitalizations, and 1.5 million hospital emergency departments visits.2 In some 80% to 90% of the cases, COPD is caused by exposure to cigarette smoke over a period of time—sometimes as little as 10 years of smoking a pack per day can cause measurable changes in the lung, reflecting early COPD. COPD is described as a progressive and incurable disease that limits airflow, and this limitation is not fully reversible. COPD incorporates two diseases: chronic bronchitis and emphysema. Some patients also suffer from asthma along with COPD. Chronic bronchitis involves the airways and is characterized by a productive cough for at least 3 months of the year that has been present for at least 2 consecutive years. Emphysema involves the alveoli where there is destruction of alveolar walls and a permanent enlargement of the airspaces that occurs distal to the terminal bronchioles. In both diseases, patients complain of being short of breath, particularly with exertion. Patients have a cough (a dry cough with emphysema) and may have periodic wheezing. Pulmonary function studies reflect a decreased FEV1/FVC and a decreased expiratory airflow. Due to the expiratory airflow limitation, COPD patients have increased air trapping and over time develop lung hyperinflation. Arterial blood gases often show decreased oxygen measurements and increased carbon dioxide levels, which get progressively worse over time, particularly if the person continues to smoke. Long-term oxygen therapy is used in patients who meet certain criteria (such as a resting Pao2 of <55 mm Hg). Bronchodilator therapy is used to reduce work of breathing, relieve bronchospasm, and improve ventilation and oxygenation. Non-invasive positive pressure ventilation (NPPV) may be used to support these patients—sometimes on a long-term basis at home or on a short-term basis to help treat acute respiratory failure in the hospital. Acute failure may call for intubation and full mechanical ventilator support.2

Fatigue is a major problem in COPD patients. In a survey from 1986, it was ranked as the second most important symptom, with dyspnea being first.3 Fatigue affects a person’s functional status, and the level of fatigue is affected by anxiety, depression, and sleep problems. Fatigue may also be a sign that the person’s condition is getting worse. Fatigue may be the result of increased work of breathing due to a decline in lung function over time or due to an acute exacerbation of COPD. Poor sleep contributes to daytime fatigue, and conversely, fatigue has been proven to be responsive to rest and sleep. In a study 130 persons with moderate to severe COPD, 72.9% reported that their fatigue was reduced by rest and 75.2% reported that sleep reduced their fatigue.4

In an editorial published in 2003, the author states that “Sleep is the period of greatest physiologic disturbance in chronic obstructive pulmonary disease (COPD) and the time of greatest danger to these individuals.”5 Sleep in and of itself brings on many physiologic changes that do not present significant problems for persons with normal lungs but can be very detrimental to COPD patients due to their decreased pulmonary function.


In the respiratory center of the brain, there is reduced response to chemical, mechanical, and cortical input during sleep; this is even more pronounced during REM sleep.6 The normal (awake) response in the carotid body to low oxygen levels (hypoxemia) and increased carbon dioxide (hypercapnia) is to increase ventilation. This response is blunted during sleep and is even more apparent during REM sleep.7 The muscles of respiration have reduced responsiveness to respiratory center output (although less so in the diaphragm). This results in a decreased minute ventilation due to reduced tidal volume in all patients. The end result may be hypercapnia and hypoxemia (if the decrease is significant).

Many COPD patients have increased air trapping with hyperinflation and, as a result, a flattened diaphragm. In those patients, the rib cage and intercostal muscles play a bigger part in normal ventilation. Thus, with the reduced responsiveness to brain output for breathing, the COPD patient suffers a greater loss of minute ventilation as accessory muscles fade in their response to signals of respiration.6 Parasympathetic muscle tone is increased at night following circadian patterns. This brings on mild bronchoconstriction and results in a reduced airway diameter and decreased airflow. The lungs have a volume of gas in them at the normal resting point between breaths, which is called functional residual capacity (FRC). This volume is reduced during sleep, and this changes the normal ventilation-to-perfusion (V/Q) ratio in the lungs. As FRC drops to a lesser volume, the airways in the dependent lung zones close earlier, effectively stopping ventilation in the face of continued perfusion.8 As V/Q is altered, blood oxygen levels tend to drop. This is thought to be the mechanism that causes some patients to have major decreases in Spo2 during sleep, while others have only minor decreases. These two groups—major and minor “desaturators”—have a similar increase in carbon dioxide levels during sleep as measured by diffusion through the skin (transcutaneous Pco2 monitoring). This increase is the result of decreased ventilation. The similar drop in TcPco2 in both groups shows that in addition to hypoventilation as a cause of hypoxemia, other factors must have some influence—thus a possible indication of altered V/Q as a player in the drop in blood oxygen.

One other factor comes into play with COPD patients regarding oxygenation. Taking into account that COPD patients are often hypoxemic during their awake state, when the hypoxemia increases during sleep, they are more prone to an ever greater fall in Spo2 than patients with normal oxygen levels. This is due to the relative positioning of the COPD patients on the oxyhemoglobin dissociation curve. They are closer to the acute slope on this sigmoid-shaped curve than those with normal lungs so when oxygen levels begin to fall, there is a more significant drop in saturation as they move down the curve.6, 8 During research, defining significant nocturnal desaturation has been elusive with regard to the COPD patients with mild daytime hypoxemia (or no daytime hypoxemia).9 Proposed definitions include a) >30% of the recording time (bedtime) with Sao2 ¼ 90%; b) >5 minutes of sleep recording with Sao2 <90% and a nadir of at least 85%; and c) a mean nocturnal Sao2 <90%. Of the three, the last one seems to have support as being the best definition of significant desaturation.8

Researchers have also found dramatic increases in upper airway resistance during sleep in a small study of five patients with emphysema. By converting an old iron lung (used to ventilate polio patients in the 1950s) to become a body plethysmograph, they were able to confirm the drop in minute ventilation due to decreased tidal volume (a reduction in VE of some 35% during REM). Moreover, they found an increase in upper airway resistance of 163% during non-REM sleep and an incredible 264% increase during REM sleep.10

Given the negative impact of sleep (both non-REM and REM), researchers wondered if COPD patients would be more prone to having sleep apnea-hypopnea syndrome (SAHS). The Sleep Heart Health Study looked at this issue in a study involving 1,132 participants with mild COPD who were part of a larger group of some 5,954 participants. The results of their research showed that SAHS was no more prevalent in the COPD subset of the study group than in the general population.5 However; it has been found that patients with severe COPD have poor sleep quality. They have delayed sleep onset, a reduction in REM sleep, decreased sleep time, and three times more frequent changes in sleep stages.7, 8 Research looking at the impact of treatment for nocturnal desaturation has shown mixed results regarding improvement of sleep quality for COPD patients. While one study showed improvement in sleep time and the number and duration of episodes of REM sleep by adding oxygen therapy, another found no change in either sleep time or sleep-stage changes when oxygen desaturation was treated.7

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Continuous oxygen therapy is warranted for COPD patients with persistent daytime hypoxemia (Pao2 < 55 mm Hg or Sao2 < 89%). Use of isolated nocturnal oxygen therapy to treat desaturation during sleep has not been justified in those patients who do not qualify for continuous oxygen therapy.8, 9 For patients who have both COPD and obstructive sleep apnea, CPAP should be applied as indicated by full polysomnography. NPPV is indicated for those COPD patients with obesity hypoventilation syndrome, those who do not respond to or are not able to tolerate CPAP, those with marked hypercapnia (Paco2 > 55 mm Hg), and those with frequent hospitalizations.7, 8 Recommendations for pharmacologic therapy include use of anticholinergics such as ipratropium to block parasympathetic impulses and help decrease airway resistance. The effects on sleep of the longer-acting anticholinergic drug tiotropium have not been studied. Theophylline has been discussed as a possibility to increase central respiratory stimulation and improve contractions of the diaphragm, but theophylline tends to disrupt sleep and also has unwanted GI side effects of nausea and vomiting.2 Short-acting beta2 agonists such as albuterol or levalbuterol may be helpful in reducing work of breathing and airway resistance if given just before bedtime, but occasional side effects of tremor and tachycardia may affect the use of these medications. The effects on sleep of long-acting beta2 agonist such as salmeterol and formoterol have not been studied.6


Sleep brings many mysterious and sometimes detrimental changes to the body, particularly in regard to breathing. Healthy individuals generally have no problems related to these changes, but they can result in serious consequences for patients suffering from COPD. In addition, fatigue plays a role in the well-being of these individuals, either as a cause for increased risk (as it relates to respiratory failure) or as a result of increased disease. Treatment options for COPD patients are available, with particular strategies to help provide quality sleep and relieve symptoms. For the COPD patient who smokes, quitting is a number-one priority in order to stop doing more damage to the lungs. Health care professionals frequently deal with COPD in conjunction with inherent sleep disorders such as OSA and SAHS. Due to the added burden this pulmonary disease places on the body, professionals need to know and understand the impact of COPD on sleep. It is imperative to take time to study more on this topic and become well versed on the best treatment options to improve the quality of sleep and the quality of life for these patients.

Bill Pruitt, MBA, RRT, CPFT, AE-C, is a senior instructor in the Department of Cardiorespiratory Sciences, College of Allied Health Science, University of South Alabama in Mobile. He also works as a PRN therapist at Springhill Medical Center and at the Mobile Infirmary Medical Center. He has been in respiratory care since 1980 and has experience in many aspects of the profession including staff therapist, home care therapist, clinical specialist, department manager, and department director, researcher, and educator. He has written and published numerous articles for respiratory and nursing publications and is an accomplished speaker. He can be reached at .


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