Copd Patient Essay

This assignment will explain the pathophysiology of the disease process chronic obstructive pulmonary disease (COPD). It will examine how this disease affects an individual looking at the biological, psychological and social aspects. It will accomplish this by referring to a patient who was admitted to a medical ward with an exacerbation of COPD. Furthermore with assistance of Gibbs model of reflection (as cited in Bulman & Schutz, 2004) it will demonstrate how an experience altered an attitude. In accordance with the Nursing and Midwifery Council, (NMC) Code of Professional Conduct (NMC, 2005) regarding safeguarding patient information no names or places will be divulged. Therefore throughout the assignment the patient will be referred to as John. John is a 57 year old gentleman who has been married to Mavis for two years. John was admitted to the ward with severe breathlessness cough and excessive sputum production. By looking through John’s notes it was discovered this was an exacerbation of COPD.

To understand John’s condition it is useful to look at how the normal respiratory system works. The function of the respiratory System is to supply the body with oxygen and remove carbon dioxide (Marieb, 2004). According to Waugh and Grant (2004) it also helps maintain body temperature and eliminate excess water from the body. The Respiratory system consists of the mouth, nasal cavity, pharynx, larynx, trachea, bronchi and the lungs (Seeley, Stephens & Tate, 2000). Air enters through either the mouth or nose which humidifies and cleans the air. (Cohen & Wood, 2000) merging into a common chamber called the oropharynx (Watson, 2000). Air then leaves to the pharynx, a short, funnel-shaped tube that transports air to the larynx (Waugh & Grant, 2004). The air enters the larynx which is lined with mucous membrane and proceeds to the trachea, which is formed of semi-circular cartilage rings. The inner membrane of the trachea contains hair cells and mucous cells which trap particles and sweeps them toward the bronchi. The bronchi are also lined with mucous membrane and ringed with cartilage (Marieb, 2004).

Each bronchus is lined with mucous membrane. (Martini, 2000) and extends into a lung where it subdivides forming smaller bronchioles (Watson, 2000). Bronchioles terminate with the alveoli which are the functional units for gas exchange and are thin, moist and surrounded by capillaries (Clancy & McVicar 2001). Inhaled air travels through these airways to the alveoli. Blood is pumped out of the heart through the pulmonary arteries to the capillaries surrounding the alveoli. (Shaw, 2005) The oxygen of the inhaled air diffuses out of the alveoli into the blood, while carbon dioxide in the blood moves into the alveoli to be exhaled (Tortora & Grabowskie, 2003). The oxygen-rich blood is returned to the heart through the pulmonary veins.

The lungs can expand and contract without friction during breathing due to the pleura, a thin membranous structure (Tamir, 2002). The visceral pleura surround the lungs, while the parietal pleura line the wall of the thoracic cavity. These pleura are separated by a small fluid-filled space called the pleural cavity. Ventilation requires work and before the lungs can become inflated, a pressure change must take place. The elastic properties of the lung allow ventilation to take place more efficiently and the fluid in the pleural cavity serves as a lubricant that allows the lungs to slide against the chest wall (Marieb, 2004).

John notified the staff that he was diagnosed with COPD twelve months ago by his general practitioner (G.P.). He added that he repeatedly went to his G.P. as he had been feeling breathless, which was becoming worse and was present every day, more so when he exercised. This breathlessness he revealed was accompanied by a cough alongside sputum production. John’s G.P inquired if he smoked and how many, John informed him he has smoked around 30 cigarettes a day for 42 years. The doctor then gave John a lung function test using a spirometer. John was notified by his GP that he had COPD which, John was informed, was both chronic bronchitis and emphysema (National Lung Health Education Program, 2005).

The World Health Organization (WHO) (2006A) defines COPD as a disease state characterized by airflow limitation that is not wholly reversible. The airflow limitation is usually both progressive and associated with abnormal inflammatory response of the lungs to noxious particles or gases. John’s chronic bronchitis is defined, clinically, as the presence of a chronic productive cough for 3 months in each of 2 successive years, provided other causes of chronic cough have been ruled out. (Mannino, 2003). The British lung Foundation (BLF) (2005) announces that chronic bronchitis is the inflammation and eventual scarring of the lining of the bronchial tubes which is the explanation for John’s dyspnea. The BLF (2005) believe that when the bronchi become inflamed less air is able to flow to and from the lungs and once the bronchial tubes have been irritated over a long period of time, excessive mucus is produced. This increased sputum results from an increase in the size and number of goblet cells (Jeffery, 2001) resulting in John’s excessive mucus production. The lining of the bronchial tubes becomes thickened and an irritating cough develops, (Waugh & Grant 2004) which is an additional symptoms that john is experiencing.

Emphysema affects the parenchyma of the lung through destruction of the alveolar walls, leading to permanent enlargement of air spaces distal to the terminal bronchioles (Sandford, Weir & Pare, 1997). The walls between adjacent alveoli break down, the alveoli ducts dilate and there is loss of interstitial elastic tissue (Watson, 2000) This results in distention of the lungs and loss of normal elastic recoil, therefore trapping and stagnation of alveolar air (National Emphysema Foundation, 2006). As alveoli merge there is loss of surface area for gaseous exchange (Alexander, Fawcett & Runciman, 2004) resulting in less oxygen. This loss of area for gaseous exchange is an additional explanation for John’s dyspnea.

John was referred to the physiotherapist to help alleviate his breathlessness and mucus production. Turner Foster & Johnson (2005) pronounce physiotherapists are key members of the intervention team, can education and give John practical guidance on how he can breathe comfortably and effectively. (United Kingdom Parliament, 2005). Van der Schans, Postma, Koeter & Rubin (1999) suggest physiotherapists facilitate John’s mucus transport by using breathing techniques, percussion and postural drainage. Moreover they can educate John on body positioning as this is fundamental with people with COPD (Gosselink, 2003).

Additionally John was referred to the Occupational Therapist (OT) who assessed his current level of fitness and then formulated a program of activities which will improve his overall strength and stamina. The OT can also give advice to John to manage his condition with the least distress and disruption of daily living (Turner Foster & Johnson 2005). Furthermore the National Institute of Health and Clinical Excellence (NICE) (2004) recommend patient with COPD should be regularly asked about their ability to undertake activities of daily living and how breathless they become when doing these.

John was informed that his COPD was possibly caused by smoking. Kanner (1996) believes that the major environmental factor of COPD is tobacco smoke. The Global Initiative for Chronic Obstructive Lung Disease (GOLD) (2005) concurs and states cigarette smoking is by far the most important risk factor for COPD. This according to the National Heart Blood and Lung Institute (NHLBI) (2006) is because smoking irritates the lungs, which causes the airways to become inflamed and narrowed. Additionally Verra, Escudier, Lebargy, Bernaudin, De Cremoux & Bignon (1995) adds that enzymes released because of the inflammation breaks down elastin, the protein important for structural integrity of the lungs, creating breathing air in and out of the lungs more difficult (NHLBI, 2006)

However D’hulst, Maes, Bracke, Demedts, Tournoy, Joos & Brusselle (2005) states not all smokers develop clinically significant COPD, which suggests that genetic factors must modify each individual’s risk (WHO, 2006B). John continues to smoke although he has reduced his intake; however NICE (2004) guidelines suggest all COPD patents who continue to smoke should be encouraged to stop, and offered help to do so, at every opportunity because, smoking cessation is the single most effective way to reduce the risk of developing COPD and stop its progression (WHO, 2006B). John was encouraged to stop, given guidance on how to stop, was informed about a smoking cessation group that he could attend and in addition offered nicotine patches; however he refused and told staff that he would quit in his own time.

John explained to the nurse that for the past few months he has been feeling low, can not concentrate and has a lack of interest in anything, he says he does not understand why he is feeling this way. Gross (2001) believes these symptoms could be a sign of depression. According to Kunik, Roundy, Veazey, Souchek, Richardson, Wray & Stanley (2005) many CODP patients develop psychological symptoms in addition to physical complaints. According to Kunik & Densmore (2002) this is because of the nature of the disease and the fear of being breathless. The BLF (2005) concur and believe breathing difficulty can instigate anxiety and depression. Other causes stated by Ohri & Steiner (2004) include body image, increased loneliness, lack of social support, and low self-esteem. Kunik et al (2005) report that depression and anxiety are two to three times more prevalent in COPD patients than in the general population and the explanation for this is because of the sustained and persistent feelings of frustration, hopelessness and helplessness.

John’s depressed mood could lower his level of energy needed to cope with his chronic illness, which, in turn, could make his symptoms less tolerable. (Singer, Ruchinskas, Riley, Broshek & Barth, 2001) Depression also can lead to increased severity of John’s medical symptoms since feelings of depression can cause a person to be less active, and, in turn, may exacerbate physical deterioration, which can intensify the psychosocially crippling effects of COPD (Van Ede, Yzermans & Brouwer, 1999). However a study by Engstrom, Persson, Larsson, Ryden & Sullivan (1996) found that quality of life is not significantly affected in patients with mild to moderate COPD, possibly due to coping and/or pulmonary reserve capacity.

John was given the opportunity to talk to a psychiatrist since mental health specialist can diagnose depression and provide appropriate treatment. One treatment that was suggested was pulmonary rehabilitation. Mahler (1998) states these programs incorporate psychosocial and behavioral components. Emery, Leatherman, Burker & MacIntyre (1991) agree and suggests that it can also enhance cognitive functioning and psychological well-being. Studies by Withers, Rudkin & White (1999) reiterate this and show that levels of anxiety and depression were significantly enhanced by pulmonary rehabilitation.

John was 56 when he was diagnosed with COPD. He stated he was forced to take early retirement from his employment where he assisted in the repair, installation and maintenance of water and sewer lines. This, he believes was because of the time lost at work caused by his dyspnea. Mavis declared she also had to resign from her part time job as a cleaner to take care of John since she is his only carer and is exhausted. Their income is from government benefits and a small pension and they say they are finding it difficult to manage on the amount of money they receive. Strassels, Smith, Sullivan, & Mahajan (1987) reported that the typical COPD patient was more than 65 years old and had limited work loss directly related to his or her disease. However a study by Tinkelman & Corsello (2003) indicated that COPD is not just a disease of the elderly. They state a large percentage of patients with COPD are unable to work, and those who do work miss days as a result of their disease. This situation they believe is of great concern to the individual worker who may lose his job as a consequence of excessive absenteeism.

Chronic illness and disability are strongly class related (Taylor & Field 1993) and those in the lower socio-economic groups are the most affected. Smoking, the greatest risk factor for COPD and exposure to occupational factors from manual unskilled jobs, such as mining and foundry working are highest amongst males in the lower socio-economic groups (Parnell, 2000). COPD patients and their families tend to be members of this group and are often elderly as symptoms become intrusive in the fifth and sixth decades of life which is John’s situation. Webb & Tossell (1999) maintain that pensions often reflect an individual’s class and social status and as a result more women, retired manual workers and ethnic minorities are disproportionately represented in old age as being on the margins of poverty.

A reliance on state benefits may be a consequence if forced to retire early and carers may not be entitled to benefits in their own right. The financial burden is increased by the costs of disability such as home alterations and help in the home or transport (Young, 1995). To help John and Mavis a social worker was involved who assisted with home care help when John was discharged so Mavis could have some time for herself. Additionally the OT was involved and provided equipment to help John maintain his independence (Trombly & Radomski 2000).

Although I was conscious, through study, other health professionals and through nurse training, that smoking can be detrimental to health and can cause diseases such as cancer (Newcomb & Carbone 1992) atherosclerotic diseases (McBride, 1992) and COPD (British Thoracic Society, 1997) I was unwilling to give health promotion and smoking cessation advice since I smoke myself. Several studies show that I am not alone in this thinking. Studies by Dore & Hoey (1998) and Adriaanse, Van Reek, Zandbelt & Evers (1991) show that high smoking rates among some populations of nurses may diminish their willingness and effectiveness as potential providers of smoking cessation care. An additional study by Nardini, Bertoletti, Rastelli , Ravelli & Donner (1998) demonstrated that smoking habits influence the attitude of health staff toward patient counseling about tobacco smoking. I considered that it was not my place and felt hypocritical if I attempted to give advice on stopping smoking. On meeting John my feelings did not change despite the fact that I could see the effects that COPD had on John’s breathing.

However on spending time with John and Mavis my attitude altered. I realized that if John stopped smoking then his condition, although his lost lung function would not be regained, (Booker, 2005) will be slowed down (Osman & Hyland, 2005). I became aware of the fact that I was in a prime position to aid John in maintaining his independence, to educate and to help improve John’s quality of life through health promoting and advice on smoking cessation. Although John decided not to give up this did not deter me on giving health promotion advice on smoking. On talking to other patients I took the opportunity to talk about stopping smoking although I did not do this aggressively (Seedhouse, 2004). This experience with John changed my feelings regarding health promotion and smoking. Although I still feel somewhat hypocritical, I acknowledge the importance of my position and how it can facilitate patients and their lives. I believe I understand the difficulties patients face when attempting to quit, perhaps more than a lifelong non smoker. I will continue to provide smoking cessation advice throughout my training and also throughout my career.

In conclusion this assignment has explained the pathophysiology of COPD through introducing a patient. It examined how this individual has been affected holistically. Finally it demonstrated how an experience encountered altered an opinion with help from a reflective model.


Alexander, M. F., Fawcett, J. M., & Runciman, P. J. (Eds.). (2004). Nursing practice hospital and home – The adult (2nd ed.). Edinburgh: Churchill Livingstone.

Adriaanse, H., Van Reek, J., Zandbelt, L., & Evers, G. (1991). Nurses’ smoking worldwide. A review of 73 surveys on nurses’ tobacco consumption in 21 countries in the period 1959-1988. International Journal of Nursing Studies, 28, 361-375.

Booker, R. (2005). Chronic obstructive pulmonary disease and nice guidelines. Nursing standard, 19(22).

British Lung Foundation (2005). COPD. Retrieved March 14, 2006, from Thoracic Society (1997). BTS guidelines for the management of chronic obstructive pulmonary disease. Thorax, 52(5).

Bulman, C., & Scultz, S. (2004). Reflective practice in nursing (3rd ed.). Oxford: Blackwell.

Clancy, J., & McVicar, A. (2001). Physiology and anatomy: a homeostatic approach (2nd ed.). London: Arnold.

Cohen, B. J., & Wood, D. L. (2000). Memmler’s the human body in health and disease (9th ed.). Philadelphia: Lippincott Williams & Wilkins.

D’hulst, A., Maes, T., Bracke, K., Demedts, L Tournoy, K., Joos G., & Brusselle G. (2005). Cigarette smoke-induced pulmonary emphysema in scid-mice is the acquired immune system required?. Respiratory Research, 6(147).

Dore, K., & Hoey, J. (1998). Smoking practices, knowledge and attitudes regarding smoking of university hospital nurses. Canadian Journal of Public Health, 4(79).

Emery, E. F., Leatherman, N. E., Burke, E. J., & MacIntyre, N. R. (1991). Psychological outcomes of a pulmonary rehabilitation program. American college of chest physicians, 42(7).

Engstrom, C., Persson, L., Larsson, S., Ryden, A., & Sullivan, M. (1996). Functional status and well being in chronic obstructive pulmonary disease with regard to clinical parameters and smoking: a descriptive and comparative study. Thorax, 51(30).

Gosselink, R. (2003). Controlled breathing and dyspnea in patients with chronic obstructive pulmonary disease. Journal of rehabilitation research and development, 40(5).

Global Initiative for Chronic Obstructive Lung Disease (2005). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease. Retrieved February 19, 2006, from, R. (2001). Psychology: the science of mind and behavior (4th ed.). London: Hodder and Stoughton.

Jeffery, P. K. (2001). Remodeling in asthma and chronic obstructive lung disease. American Journal of Respiratory and Critical Care Medicine , 164(28).

Kanner, R. (1996). Early intervention in chronic obstructive pulmonary disease: a review of the lung health study results. Medical Clinics of North America, 80(4).

Kunik, M., & Densmore, D. (2002). Depression and COPD. Geriatrics, 7(4).

Kunik, M., Roundy, K., Veazey, C., Souchek, J., Richardson, P., Wray, N., & Stanley, M. (2005). Surprisingly high prevalence of anxiety and depression in chronic breathing disorders. American college of chest physicians, 127(4).

Mahler, D. A. (1998). Pulmonary rehabilitation. Chest , 113(26).

Mannino, D. M. (2003). Chronic obstructive pulmonary disease: definition and epidemiology. Respiratory care journal, 48(12).

Marieb, E. (2004). Human anatomy & physiology. San Francisco: Pearson Education.

Martini, F. (2000). Fundamentals of anatomy and physiology. New Jersey:

McBride, P. E. (1992). The health consequences of smoking. Cardiovascular diseases. Medical Clinics of North America, 76(2).

Nardini, S., Bertoletti , R., Rastelli, V., & Ravelli, L., & Donner, C. (1998). Personal smoking habit and attitude toward smoking among the health staff of a general hospital. Monaldi Archive for Chest disease, 53(1).

National Emphysema Foundation (2006). COPD – What is it?. Retrieved March 11, 2006, from Heart Blood and Lung Institute (2006). What Causes COPD?. Retrieved March 8, 2006, from Institute for Health and Clinical Excellence (2004). Management of chronic obstructive pulmonary disease in adults in primary and secondary care. Retrieved February 12, 2006, from Lung Health Education Program (2005). What is COPD? Retrieved March 19, 2006, from, P. A., & Carbone, P. P. (1992). The health consequences of smoking: Cancer. Medical Clinics of North America, 76(2).

Nursing & Midwifery council. (2004). Code of professional conduct. London: Nursing & Midwifery council.

Ohri, C., & Steiner, M. (2004). COPD: the disease and non drug treatment. Hospital pharmacist, 11.

Osman, L. M., & Hyland, M. E. (2005). Patient needs and medication styles in COPD. The European Respiratory Society, 14(7).

Parnell, H. (2000). Respiratory disease: Caring for the carers of chronic lung disease sufferers in the community. Retrieved February 23, 2006, from
cleID=346Seedhouse, D. (2004). Health promotion: philosophy, prejudice, and practice (2nd ed.). Chichester: J. Wiley.

Seeley, R.R., Stephens, T. D., & Tate, P. (2000). Anatomy and physiology (5th ed.). USA: McGraw- Hill higher education.

Sandford, A. J., Weir, T. D., & Pare, P. D. (1997). Genetic risk factors for chronic obstructive pulmonary disease. European Respiratory Journal , 10(42).

Shaw, L. (2005). Anatomy and physiology. Cheltenham: Nelson ThornesSinger, H., Ruchinskas , R., Riley, K., Broshek, D., & Barth, J. (2001). The psychological impact of end-stage lung disease. American college of chest physicians, 120(4).

Strassels, S. A., Smith, D. H., Sullivan, S. D., & Mahajan, P. (1987). The costs of treating COPD in the United States. American college of chest physicians, 119(9).

Tamir, E. (2002). The human body made simple : a guide to anatomy, physiology, and disease. Edinburgh: Churchill Livingstone.

Taylor, S., & Field, D. (Eds.). (1993). Sociology of health and health care: an introduction for nurses (3rd ed.). London: Blackwell Scientific Publications.

Tinkelman, O., & Corsello, P. (2003). Chronic obstructive pulmonary disease: the impact occurs earlier than we think. American Journal of Managed Care, 9(6).

Tortora, G. J., & Grabowski, S. R. (2003). Principals of anatomy and physiology. New York: HarperCollins College Publishers.

Turner, A., Foster, M., & Johnson, S. E. (2005). The practice of occupational therapy: an introduction to the treatment of physical dysfunction (5th ed.). London: Churchill Livingstone.

Trombly, C. A., & RadomskI, M. V. (Eds.). (2000). Occupational therapy for physical dysfunction . Philadelphia: Lippincott Williams & Wilkins.

United Kingdom parliament (2005). Memorandum by the Chartered Society of Physiotherapy. Retrieved March 9, 2006, from Ede, L., Yzermans, C. J., & Brouwer, H. J. (1999). Prevalence of depression in patients with chronic obstructive pulmonary disease: a systematic review. Thorax, 17(4).

Van der Schans , C. P., Postma, D. S., Koeter, G. H., & Rubin, B. K. (1999). Physiotherapy and bronchial mucus transport. European Respiratory Journal, 13(8).

Verra, F., Escudier, E., Lebargy, F., Bernaudin, J. F., De Cremoux, H., & Bignon. J. (1995). Ciliary abnormalities in bronchial epithelium of smokers, ex- smokers, and nonsmokers. American Journal of Respiratory Critical Care Medicine, 151.

Watson , R. (2000). Anatomy and physiology for nurses . Edinburgh: Bailliere Tindall.

Waugh, A., & Grant, A. (2004). Ross and Wilson anatomy and physiology in health and health care. (9th ed.). Edinburgh; New York: Churchill Livingstone.

Webb, R., & Tossell, D. (1999). Social Issues for Carers: Towards Positive Practice (2nd ed.). London: Arnold.

World Health Organization. (2006A).COPD: A definition. Retrieved February 21, 2006, from Health Organization. (2006B). COPD: Causes. Retrieved February 19, 2006, from, N. J., Rudkin, S. T., & White RJ, R. J. (1999). Anxiety and depression in severe
chronic obstructive pulmonary disease: the effects of pulmonary rehabilitation. Journal of Cardiopulmonary Rehabilitation, 19(6).

Young, P. (1995). Mastering social welfare (3rd ed.). London: Macmillan Press.

Recently, chronic obstructive pulmonary disease (COPD) has gained interest as a major public health concern. It is currently the focus of intense research because of its persistently increasing prevalence, mortality, and disease burden. COPD was responsible for more than 2.5 million deaths worldwide in 2000 alone.1 It currently ranks as the third leading cause of death in the United States (U.S.).2-3 COPD is projected to have the fifth leading burden of disease worldwide by the year 2020.4 It is one of the leading causes of disability worldwide and is the only disease for which the prevalence and mortality rates continue to rise.

This chapter presents a concise review of COPD. We address its definition, prevalence and epidemiology, pathology and pathophysiology, diagnosis, therapy, and outcomes. Also, because of recent developments, we have included a discussion of the relationship between COPD and sleep disorders.


COPD is broadly defined and encompasses several clinical and pathologic entities, primarily emphysema and chronic bronchitis. Evidence of airflow obstruction that is chronic, progressive, and for the most part fixed, characterizes COPD. Notwithstanding the presence of irreversible airflow obstruction in COPD, most people with the disease (~60%-70%) demonstrate a reversible component of airflow obstruction when tested repeatedly.5-8

Emphysema is specifically defined5-8 in pathologic terms as "alveolar wall destruction with irreversible enlargement of the air spaces distal to the terminal bronchioles and without evidence of fibrosis." Chronic bronchitis is defined as "productive cough that is present for a period of 3 months in each of 2 consecutive years in the absence of another identifiable cause of excessive sputum production."

The American Thoracic Society (ATS), British Thoracic Society (BTS), and European Respiratory Society (ERS) definitions of COPD emphasize chronic bronchitis and emphysema, but the Global Initiative for Chronic Obstructive Lung Disease (GOLD) proposes a definition of COPD that focuses on the progressive nature of airflow limitation and its association with abnormal inflammatory response of the lungs to various noxious particles or gases.5-8 According to the GOLD document, COPD is defined as "a disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases."8 The current definition also emphasizes the importance of exacerbations and of systemic comorbidities (eg, cardiovascular disease) in framing the clinical course of COPD.

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Prevalence and Epidemiology

The prevalence of COPD is increasing. Recent estimates suggest that there are approximately 23.6 million men and women with COPD in the U.S. and more than 52 million sufferers around the world.1,2,8 The worldwide prevalence is likely to be underestimated for several reasons, including delays in establishing the diagnosis, the variability in defining COPD, and the lack of age-adjusted estimates. The BOLD study, a recent multinational population-based study, placed the worldwide overall prevalence of stage-II or higher COPD at 10.1% with a higher prevalence rate for men (11.8%) than for women (8.5 %). The rates and severity of spirometrically confirmed COPD were higher than those previously reported.9 Age adjustment is important because the prevalence of COPD in people aged <45 years is low and the prevalence is highest in patients aged >65 years. In 1995, 553,000 patients were treated for COPD in the U.S., two-thirds of them were aged >65 years. The prevalence of COPD in those aged >65 years was 4 times that among those aged 45-64 years.10-11 The gender distribution of COPD is also changing and, since 2000, the number of COPD deaths in women has exceeded those in men.2

Because of its chronic and progressive nature, COPD represents a massive and growing burden in direct and indirect costs. In developing countries where smoking continues to be extremely prevalent, the health and economic burdens are higher than in developed nations. The disability caused by COPD in such countries further magnifies the problem.

Although it has been difficult to estimate the costs associated with COPD, they include direct costs relating to outpatient and inpatient care expenses, the indirect costs resulting from the loss of productivity caused by premature disability and death, and the additional cost of disability. In the U.S., hospitalization accounts for the bulk of all COPD-related health costs. In 2007, direct health costs of COPD were $23.6 billion, and the overall cost burden was estimated at more than $42 billion.1,2,11

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Pathogenesis and Pathology

As indicated in the definition of emphysema, the pathologic hallmark is elastin breakdown with resultant loss of alveolar wall integrity. This process is triggered by the exposure of a susceptible person to noxious particles and gases. Cigarette smoke remains the main causative agent, implicated in >90% of cases. However, other gases and particles have been shown to play a role in causing COPD,12 which results from an inflammatory process. In contrast to the eosinophilic inflammation seen in asthma, the predominant inflammatory cell in COPD is the neutrophil. Macrophages and CD8+ T lymphocytes are increased in the various parts of the lungs, and several mediators, including leukotriene B4, interleukin 8, and tumor necrosis factor, contribute to the inflammatory process.6

Recent observations by McDonough et al have challenged the traditional understanding of the pathogenesis of emphysema. Whereas the accepted wisdom has placed the initial insult at alveolar wall destruction, a more recent study by this group suggests that the narrowing and disappearance of terminal bronchioles precede and lead to the alveolar destruction that occurs in centrilobular and panlobular emphysema. Specifically, the authors applied microcomputer tomography to assess the terminal bronchioles of 78 patients with various stages of COPD in addition to lungs explanted from COPD transplant patients and control normal lungs. Comparing the numbers and dimensions of terminal bronchioles in the different groups led the authors to postulate that narrowing and loss of terminal bronchioles precede the emphysematous destruction observed in patients with COPD.13

Oxidative stress is regarded as another important process in the pathogenesis of COPD, and altered protease-antiprotease balance, at least in individuals with severe deficiency of α1-antitrypsin, has been shown to predispose to panacinar emphysema. Individuals with severe deficiency of α1-antitrypsin can develop emphysema at an early age (eg, by the fourth or fifth decade) in contrast to the “usual” emphysema, which typically begins in the sixth to seventh decades of life.

The pathologic hallmark of chronic bronchitis is an increase in goblet cell size and number that leads to excessive mucus secretion. Airflow obstruction and emphysematous change are common but not universal accompaniments. When COPD is complicated by hypoxemia, intimal and vascular smooth muscle thickening can cause pulmonary hypertension, which is a late and poor prognostic development in COPD.5-8,14,15

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The diagnosis of COPD is suggested by findings on history or physical examination, or both, and is confirmed by laboratory tests, usually with a supportive risk factor (eg, familial COPD or cigarette exposure, or both). Spirometry is indispensable in establishing the diagnosis because it is a standardized and reproducible test that objectively confirms the presence of airflow obstruction. Characteristically, spirometry shows a decreased forced expiratory volume in 1 second (FEV1) and a decreased FEV1/FVC (forced vital capacity) ratio, the latter defined as being abnormal if below 0.70 or the fifth predicted percentile.5-8 Evidence of reversible airflow obstruction, defined as a post-bronchodilator rise of FEV1 and/or FVC by 12% and 200 mL, is present in up to two-thirds of patients with serial testing. Measurement of the diffusing capacity for carbon monoxide (DLCO) can help differentiate between emphysema and chronic bronchitis. Specifically, in the context of fixed airflow obstruction, a decreased diffusing capacity indicates a loss of alveolar-capillary units, which is consistent with (but does not establish) emphysema.

Deficiency of α1-antitrypsin is an uncommon cause of emphysema that continues to be under-recognized by practicing clinicians.16-18 Guidelines from the American Thoracic Society/European Respiratory Society (ATS/ERS) suggest testing all symptomatic adults with fixed airflow obstruction for α1-antitrypsin deficiency. These guidelines also call for heightened suspicion under specific clinical circumstances. These include: emphysema occurring in a young person (aged ≤45 years) or without obvious risk factors (eg, smoking or occupational exposure) or with prominent basilar emphysema on imaging, necrotizing panniculitis, antineutrophil cytoplasmic antibody (C-ANCA)-positive vasculitis, bronchiectasis of undetermined etiology, otherwise unexplained liver disease, or a family history of any one of these conditions, especially siblings of individuals who are positive for theα1-antitrypsin variant (Pi-ZZ).16

The most common symptoms and signs of COPD include cough, dyspnea on exertion, and increased phlegm production. Additional signs and symptoms include wheezing, prolonged expiration with pursed-lip breathing, barrel chest, use of accessory muscles of breathing and, in advanced cases, cyanosis, evidence of right heart failure, and peripheral edema. A chest x-ray is usually obtained to exclude other etiologies but might show hyperinflation and flattening of the diaphragm with increased retrosternal space on the lateral view and hyperlucency reflecting oligemia. The chest x-ray is an insensitive test for diagnosing emphysema and is abnormal only when the disease is relatively advanced. In contrast, high-resolution computed tomography (CT) scanning is far more sensitive and specific than chest x-ray for diagnosing emphysema and readily identifies bullae and blebs that are the consequences of alveolar breakdown. Chest CT is essential for identifying proper candidates for lung volume reduction surgery, though its role in clinical management of COPD otherwise is still evolving.5-8

Classification of Severity

Because the degree of FEV1 reduction carries prognostic implications and correlates with mortality and morbidity, a staging system based on the degree of airflow obstruction has been proposed by different societal guidelines. As reviewed in Table 1, 4 groups — the ATS, the ERS, the British Thoracic Society (BTS), and GOLD — have developed staging systems for COPD based on the value of FEV1 percent predicted. All systems propose 3- or 4-stage classifications of COPD, although the FEV1 criteria vary among systems.5-8

Table 1: Staging of Disease Severity
Disease Severity FEV1 PredictedATSERSBTSGOLD
Stage 0: at riskNormal;
Chronic symptoms (cough, sputum production)
Stage I: mild≥50%≥70%>80%≥80% with or without chronic symptoms
Stage II: moderate35%-49%50%-69%31%-80%50%-79% with or without chronic symptoms
Stage III: severe<35%<50%≤3030%-49% with or without chronic symptoms
Stage IV: very severe<30%

ATS, American Thoracic Society; BTS, British Thoracic Society; ERS, European Respiratory Society; FEV1, forced expiratory volume in 1 second; GOLD, Global Initiative for Chronic Obstructive Lung Disease.

In the context that one major purpose of a staging system is to establish prognosis, attention has focused on the value of including weight (ie, body mass index [BMI]), dyspnea, and exercise capacity (ie, the 6-minute walk distance), with FEV1 in staging COPD.19 Indeed, the resultant index, called BODE (for BMI, obstruction, dyspnea, and exercise capacity) has been shown to better predict survival in COPD than FEV1 alone. BODE scores of 0 to 10 (most impaired) are stratified into 4 quartiles, which discriminate mortality risk better than FEV1 alone. Other multifactorial prognostic systems (eg, ADO [for age, dyspnea, and obstruction] and DOSE [for dyspnea, obstruction, smoking, and exercise capacity]) have also been proposed.20,21

In the most recent revision of the GOLD strategy document, the concept of spirometric stages has been replaced by spirometric grades because the level of FEV1 alone has been found to incompletely predict disease status. A composite measure of level of symptoms and frequency of exacerbations has been added to FEV1 to categorize patients into 4 groups:

In the context that one major purpose of a staging system is to establish prognosis, attention has focused on the value of including weight (ie, body mass index [BMI]), dyspnea, and exercise capacity (ie, the 6-minute walk distance), with FEV1 in staging COPD.19 Indeed, the resultant index, called BODE (for BMI, obstruction, dyspnea, and exercise capacity) has been shown to better predict survival in COPD than FEV1 alone. BODE scores of 0 to 10 (most impaired) are stratified into 4 quartiles, which discriminate mortality risk better than FEV1 alone. Other multifactorial prognostic systems (eg, ADO [for age, dyspnea, and obstruction] and DOSE [for dyspnea, obstruction, smoking, and exercise capacity]) have also been proposed.20,21

In the most recent revision of the GOLD strategy document, the concept of spirometric stages has been replaced by spirometric grades because the level of FEV1 alone has been found to incompletely predict disease status. A composite measure of level of symptoms and frequency of exacerbations has been added to FEV1 to categorize patients into 4 groups:

  • Group A: (low risk, fewer symptoms) includes patients with an FEV1 >50% (grade 1 or 2) and low level of symptoms as judged by a COPD Assessment Test (CAT) score <10, or a modified Medical Research Council Dyspnea Scale (mMRC) score <2 and 0-1 exacerbations in the previous year
  • Group B: (low risk, more symptoms) includes patients with an FEV1 >50% and 0-1 exacerbations in the previous year but symptomatic with CAT score >10, or mMRC score >2
  • Group C: (high risk, fewer symptoms) includes patients with an FEV1 <50% and CAT score <10, or mMRC score <2 but with ≥2 exacerbations in the previous year
  • Group D: (high risk, more symptoms) includes patients with an FEV1 <50%, CAT score >10, or mMRC >2 and ≥2 exacerbations in the previous year.8

The CAT and the mMRC are validated tools that assess symptoms and correlate well with the Saint George’s Respiratory Questionnaire (SGRQ), a widely used quality of life instrument in COPD research. The CAT is an 8-item questionnaire with scores ranging from 0-5 for each question (total range 0-40) with a score >10 being abnormal.22 This test is easier to administer and correlates more strongly with outcome measures in COPD patients than does FEV1. These characteristics have led to its adoption in the new GOLD strategy approach to assessing severity and grading patients with COPD.23

Natural History and Prognosis

Several factors influence the natural history and affect survival in patients with COPD. These factors include age, smoking status, pulmonary artery pressure, resting heart rate, BMI, airway responsiveness, hypoxemia, dyspnea, exercise capacity, exacerbation frequency, and most importantly, the level of FEV1, which remains the single best indicator of prognosis.

Few interventions have been shown to change the natural history of COPD. For patients who are hypoxemic on room air, survival can be improved by use of supplemental oxygen.24 Smoking cessation can improve survival in smokers,25,26 and lung volume reduction surgery can improve survival in selected patients.27

Acute exacerbations of COPD (AECOPD) are a significant contributor to mortality. For example, in the SUPPORT study28 of 1,016 patients with AECOPD admitted to the hospital with hypercapnic respiratory failure, 89% survived the acute hospitalization, but only 51% were alive at 2 years. Patient characteristics associated with mortality at 6 months included increased severity of illness, lower body mass index, older age, poor prior functional status, lower PaO2/Fio2 (inspired fraction of oxygen), and lower serum albumin. However, congestive heart failure and cor pulmonale were associated with longer survival time at 6 months, and this was attributed to the effective therapy available for the management of these conditions. The overall severity of illness on the third day of hospitalization, as measured by the APACHE III score, was the most important independent predictor of survival at 6 months.28

Notably, in another study of patients with AECOPD, the development of hypercapnia during an acute exacerbation of COPD appeared not to affect the risk of death with AECOPD.29  Specifically, in a prospective study involving 85 patients admitted with acute exacerbation and followed for 5 years, the mortality rate was not significantly different between hypercapnic and eucapnic patients. In contrast, patients with chronic hypercapnia demonstrated a much poorer outcome, with only an 11% rate of 5-year survival.30

To better understand the impact of exacerbations on the natural history of COPD, a large 3-year observational cohort study has been performed (the ECLIPSE study). Results from ECLIPSE showed that the rate and severity of exacerbations increased with disease severity. More importantly, ECLIPSE showed that the best single predictor of future exacerbations, a major factor influencing outcome, was a history of exacerbations, suggesting a distinct phenotype for patients with frequent exacerbations. Furthermore, patients with frequent exacerbations demonstrated a poorer outcome over the study period.31

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Sleep and COPD

In the context of a growing understanding of sleep and the interactions between disorders of sleep and COPD, this section reviews the mechanism of hypoxemia in sleep and the overlap between COPD and obstructive sleep apnea syndrome (OSAS).

Hypoxemia During Sleep in COPD

Under normal circumstances, sleep results in a decrease in ventilation and in chemo-responsiveness to the arterial partial pressure of carbon dioxide (PaCO2).32,33 The decreased ventilation appears to be almost entirely related to a drop in tidal volume. Normally, this decrease in tidal volume does not result in hypoxemia, because the drop in the arterial partial pressure of oxygen (PaO2) occurs on the flat portion of the oxyhemoglobin dissociation curve, thereby preserving the oxygen saturation (SaO2). However, in patients with COPD whose oxygenation during wakefulness may already be on the steep portion of the oxyhemoglobin dissociation curve, hypoxemia during sleep can occur as tidal volume falls.

The most pronounced hypoxemia occurs during the rapid eye movement (REM) stage of sleep because of the generalized muscle hypotonia that accompanies this stage. REM-associated hypoxemia can reach critically low levels, especially in patients with already borderline waking oxygenation, with potentially deleterious clinical consequences such as cardiac dysrhythmias, pulmonary hypertension, and polycythemia.

Hypoxemia during sleep in COPD is primarily a result of hypoventilation, but it is also caused by a decrease in functional residual capacity (FRC) and a worsening ventilation/perfusion (V/Q) mismatch.

COPD and Obstructive Sleep Apnea Syndrome

The co-occurrence of COPD and OSAS, also referred to as the overlap syndrome, involves a minority of COPD patients, but identifying these patients is important because their nocturnal hypoxemia tends to be more pronounced, leading to a greater likelihood of adverse clinical events. It follows that in patients with the overlap syndrome, therapy must be directed at both the COPD and the OSAS.

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Stable COPD

Once the diagnosis of COPD is established and the stage of the disease is determined, attention should turn to patient education and modification of risk factors, to pharmacologic and non-pharmacologic methods needed to ameliorate the signs and symptoms of COPD, and to optimizing patients’ longevity and functional status.34,35

Patient education is an essential component of treatment because it facilitates reduction of risk factors and improves the individual patient’s ability to cope with the disease. Education requires a team approach that includes, in addition to the physician and the patient, home health nurses, social workers, physical therapists, occupational therapists, and others. In addition to risk factor reduction, education should provide a basic, simple-to-understand overview of COPD, its pathophysiology, medications and their proper use, and instructions on when to seek help. The educational process, especially when applied in the setting of pulmonary rehabilitation, facilitates discussing end-of-life issues and establishing advance directives.36,37 Several randomized trials have demonstrated the value of an education and management program for patients with COPD, including development of a home action plan for the patient to initiate an antibiotic and course of systemic corticosteroids in the event of an exacerbation.38-40 However, results of a recent trial suggest the need for additional study of self-management strategies in COPD.41

Smoking cessation is a cornerstone of patient education and confers many benefits, including slowing the rate of FEV1 decline among smokers, improvements in symptoms, and lessening the risk of lung cancer. For example, data from the Lung Health Study (LHS) show that in the sustained nonsmokers over that 11-year study, the rate of FEV1 decline slowed to 30 mL per year in men and 22 mL per year in women compared with the 66 mL per year and 54 mL per year decline in continuing male and female smokers, respectively. The result was that 38% of continuing smokers had an FEV1 <60% of predicted normal at 11 years compared with only 10% of sustained quitters. Aggressive smoking cessation intervention with counseling and nicotine patch allowed 22% of LHS participants to achieve sustained smoking cessation over 5 years, and 93% of these participants were still abstinent at 11 years.25,26,34

Available strategies for smoking cessation include nicotine replacement (available in gum, patch, lozenge, inhaler and nasal spray), bupropion (an antidepressant), smoking-cessation programs, varenicline,42 counseling, and combinations of these. Randomized, controlled trials suggest that the combination of nicotine replacement and bupropion confers greater likelihood of achieving smoke-free status than either therapy alone.43 Use of the partial acetylcholine receptor agonist varenicline appears to allow higher rates of smoking cessation than does buproprion.42

Beyond education and smoking cessation, the goals of pharmacologic and non-pharmacologic treatments are to enhance survival, quality of life, and functional status, and to lessen mortality. As reviewed in Table 2, available treatments include bronchodilators, corticosteroids, immunizations, antibiotics, mucokinetics, and others.

Table 2: Recommendations by Professional Societies for Management of Stable COPD
American Thoracic Society 1995 ConsensusEuropean Respiratory Society 1995 ConsensusBritish Thoracic Society 1997 ConsensusGlobal Initiative for Chronic Obstructive Lung Disease 2011 Evidence-Based Review
Diagnostic Testing
Pre- and post-BDPre- and post-BDPre- and post-BDPre- and post-BD
Pre- and post-corticosteroids only if inadequate response to treatmentPre- and post-corticosteroids in stages 2 and 3Pre- and post-corticosteroids in stages 2 and 3Pre- and post-corticosteroids in stages 2 and 3
CXRCXRCXR in moderate or severe diseaseCXR to exclude alternative Dx and establish presence of significant comorbidities
CT: not routinely, but helpful in predicting the benefit of pulmonary resection for giant bullous diseaseCT assessment of bullaeRestricted to assessment of bullous emphysemaCT when Dx is in doubt or if LVRS is contemplated
ABG in stages 2 and 3ABG in stages 2 and 3 or SaO2 <92%ABG in severe diseaseABG if pulse oximetry <92%
α1-AT deficiency in early, severe diseaseα1-AT deficiency in early, severe diseaseNot discussedα1-AT deficiency in early COPD (age <45) or strong family history
Bronchodilator Therapy
β2 Agonist first line PRN use; anticholinergic first line for regular use; theophylline and/or sustained release albuterol for persistent symptomsβ2 Agonist or anticholinergic as needed; combination if needed; theophylline if no response to other BD; long-acting inhaled β2-agonist or oral if neededShort-acting β2 agonist or inhaled anticholinergic as needed; regular β2 agonist and/or anticholinergics and/or combination for advanced stages; long-acting β2 agonist if evidence of improvement; theophylline is of limited valueShort-acting BD as needed
Regular treatment with one or more BD in advanced stages; long-acting inhaled BD more convenient; combination BD and anticholinergics is better than either agent alone
PDE-4 inhibitor may be useful in properly selected patients
If corticosteroid response established:If corticosteroid response established:If corticosteroid response established:If corticosteroid response established:
  • Lowest effective oral dose used
  • Insufficient data to support use of aerosolized steroid
  • Inhaled steroids
  • Inhaled steroids in patients with mild disease but “fast decline” of FEV1 (>50 mL per yr)
  • Inhaled steroids
  • Inhaled steroids in stages 2 and 3
  • Long-term monotherapy with oral or inhaled steroids not recommended
Not recommendedNot recommendedNot recommendedNot recommended
Not recommendedNot recommendedNot recommendedNot recommended
α-1 Antitrypsin Augmentation Therapy
In appropriate patientsNot recommendedNot discussedIn appropriate patients
Influenza recommended; pneumococcal recommendedInfluenza recommended; pneumococcal, insufficient dataInfluenza and pneumococcal recommendedInfluenza and pneumococcal recommended
Smoking Cessation
Recommended; smoking cessation protocolRecommendedRecommendedRecommended
Lung Volume Reduction Surgery
In appropriately selected patientsIn appropriately selected patientsIn appropriately selected patientsNot recommended, insufficient data
Lung Transplantation
In appropriately selected patientsIn appropriately selected patientsIn appropriately selected patientsIn appropriately selected patients
Home Mechanical Ventilation
Non-elective ventilation supported; elective ventilation not supportedNo recommendation providedElective and non-elective ventilation modestly supportedNot supported
Long-Term Oxygen Therapy
Recommended in patients with chronic hypoxemiaRecommended in patients with chronic hypoxemiaRecommended in patients with chronic hypoxemiaRecommended in patients with chronic hypoxemia
Pulmonary Rehabilitation
Recommended; upper extremity training and breathing retraining supportedRecommendedRecommendedRecommended along with nutritional counseling, and education

ABG, arterial blood gas; α1-AT, Alpha-1 antitrypsin; BD, bronchodilator; COPD, chronic obstructive pulmonary disease; CXR, chest x-ray; CT, computed tomography; Dx, diagnosis; FEV1, forced expiratory volume in 1 second; LVRS, lung volume reduction surgery; RHF, right heart failure. ©2002 The Cleveland Clinic Foundation.


Bronchodilators are a mainstay of COPD treatment and include β-adrenergic agonists, anticholinergics, and methylxanthines. β-adrenergic agonists are effective in alleviating symptoms and improving exercise capacity, and they can produce significant increases in FEV1.5,6 Their effect is achieved through smooth-muscle relaxation, resulting in improved lung emptying, reduced thoracic gas volume and residual volume, and lessened dynamic hyperinflation. It is believed that the increase in exercise tolerance and reduction in symptoms of breathlessness are primarily a result of an improvement in inspiratory capacity rather than an increase in FEV1. Oral theophylline has been shown to lessen dyspnea and improve the health-related quality of life despite lack of significant rise in FEV1, with improvements believed to be a result of increased respiratory muscle performance. However, the narrow therapeutic index of older methylxanthines (which are phosphodiesterase inhibitors) and their potential for adverse drug-drug interactions have hindered their widespread use. The more specific phosphodiesterase-4 inhibitor, roflumilast (see below), has been approved on the strength of evidence that it confers some bronchodilation and can avert exacerbations in patients with advanced COPD who have had frequent exacerbations.44

Phosphodiesterase-4 Inhibitors

Newly developed oral, highly selective phosphodiesterase-4 (PDE-4) inhibitors roflumilast45 and cilomilast,46 have shown promise in the management of stable COPD. Specifically, a randomized, double-blind study involving more than 1400 patients with moderate-to-severe COPD compared patients assigned to receive 250 mcg of roflumilast, 500 mcg of roflumilast, or placebo over a period of 24 weeks. The primary end points were post-bronchodilator FEV1 and health-related quality of life. Secondary end points included the rate of COPD exacerbations. Although there was no significant difference in the post-bronchodilator FEV1 in the treatment arms, both were superior to placebo (P < 0.0001). Similar findings were reported in the health-related quality of life and rate of exacerbations with an acceptable safety profile.45 In 2011, the U.S. Food and Drug Administration (FDA) approved roflumilast for the treatment of stable COPD in patients with frequent exacerbations.44 In the most recent GOLD strategy document, roflumilast is listed as an alternative treatment option in group D patients.8

β-Adrenergic Agonists and Antimuscarinic Agents

In the early stages of COPD (eg, stage I), a short-acting β-adrenergic agonist (eg, albuterol, terbutaline) or an anticholinergic is used on an as-needed basis. As the disease progresses (eg, stages II and III), regular use of one or more bronchodilators is often recommended. Some data suggest that a combination of albuterol and ipratropium bromide provides better bronchodilation than does either agent alone.5,47-49

In 2004, the FDA approved a new anticholinergic agent, tiotropium, for the long-term, once daily, maintenance treatment of bronchospasm associated with stable COPD, including chronic bronchitis and emphysema.50 Although this is the same indication granted to ipratropium, tiotropium has shown significant advantages over ipratropium, both pharmacologically and clinically. Specifically, tiotropium blocks the M1 to M5 muscarinic receptors with a 6- to 20-fold greater affinity than ipratropium and for a longer period51-53 and dissociates more rapidly from the M2 receptor associated with acetylcholine release, thereby conferring theoretical mechanistic advantages over ipratropium.

These advantages were shown in clinical trials comparing the 2 agents. Specifically, tiotropium demonstrated significantly greater bronchodilation than ipratropium, and users experienced less dyspnea, fewer acute exacerbations, reduced albuterol use, and improved nocturnal oxygen saturation.52-55 When compared with long-acting β2-agonists, tiotropium provided greater bronchodilation and more-reduced dyspnea than salmeterol. A large double-blind, placebo-controlled trial showed a significantly greater reduction in yearly incidence as well as delay to first COPD exacerbation compared with either salmeterol or placebo.55 With the approval in the U.S. of a once-daily β-agonist (indacaterol) and early comparisons with tiotropium,56 it is likely that further clarification of the relative roles of these long-acting agents, especially in concert with other agents, will be the subject of ongoing study and forthcoming recommendations. Other long-acting agents (eg, vilanterol57) are also currently under investigation.

Results of a large randomized, controlled trial (called UPLIFT) assessing the efficacy of tiotropium (compared with placebo) have shown that tiotropium conferred benefits of a lower exacerbation frequency but neither slowed the rate of FEV1 decline nor lowered the mortality rate.58

In the 2011 GOLD document, β-adrenergic agonists are recommended in all 4 COPD groups (A-D). In group A, short-acting beta-agonist (SABA) agents or short-acting muscarinic agents (SAMA) are first-line therapies with long-acting beta agonists) (LABA) or long-acting muscarinic agents (LAMA) as alternatives. In groups B, C, and D, LABA, LAMA, or a combination are deemed either first- or second-line therapies.8


Inhaled corticosteroids play an important role in managing patients with stable COPD though systemic steroids should generally be reserved for managing acute exacerbations. Several groups suggest brief trials of oral corticosteroids for patients with stable COPD. For example, the BTS suggests a course of oral prednisone (eg, 30 mg daily) taken for 2 weeks or a course of inhaled steroid (eg, beclomethasone 500 mcg twice daily or the equivalent) taken for 6 weeks.7 Similarly, the ERS suggests a trial of corticosteroids (eg, 0.4-0.6 mg/kg/day) taken for 2 to 4 weeks. Patients with significant FEV1 responses are considered candidates for long-term inhaled corticosteroids.6 The weight of evidence from randomized, placebo-controlled trials of inhaled corticosteroids in patients with COPD shows no effect on the rate of FEV1 decline,35,59-62 although one study (TORCH) did show a slowed rate of FEV1 decline in patients who received inhaled steroids.63 Several other randomized, controlled clinical trials have also assessed the role of inhaled corticosteroids (eg, called Euroscop [European Respiratory Society study on chronic obstructive pulmonary disease], ISOLDE, Copenhagen City, Lung Health Study, and OPTIMAL) and of inhaled steroids combined with LABAs regarding exacerbation frequency, quality of life, rate of change of FEV1, and, in one study (TORCH), mortality.63 The weight of evidence, including from meta-analyses,64,65 suggested that inhaled corticosteroids can lessen the frequency of acute exacerbations of COPD, but (with the exception of the TORCH trial) inhaled corticosteroids do not appear to affect the rate of FEV1 decline. The combination of inhaled fluticasone and salmeterol appears better than placebo in enhancing health-related quality of life and lessening exacerbation frequency. The one trial (TORCH) that examined mortality as a primary outcome measure showed that the combination of inhaled fluticasone and salmeterol (500 mcg/50 mcg, respectively, twice daily) conferred a 2.6% absolute reduction in mortality (15.2%-12.6%; 17.5% relative reduction), although this difference missed statistical significance (P = 0.052).

Regarding the effects of combined LABA-inhaled steroid, the TORCH trial was conducted to compare the effect of the salmeterol-fluticasone combination with either agent alone and with placebo. The trial found that the combination therapy was significantly more effective than sole therapy with the long-acting bronchodilator, or fluticasone, or placebo in patients with COPD.63 Another similar trial, the so-called TRISTAN study, was a 52-week, randomized, placebo-controlled study involving 1,465 patients with moderate-to-severe COPD. This trial showed significant improvement in FEV1 in the salmeterol-fluticasone combination versus salmeterol (treatment difference of 73 mL, P < 0.0001), fluticasone (treatment difference of 95 mL, P < 0.0001),64 and placebo (treatment difference of 133 mL, P < 0.0001). Other benefits included a decrease in the use of rescue medications in the combination group and a significant improvement in health status as defined by the St. George's Respiratory Questionnaire compared with the fluticasone group but not the salmeterol group. The rate of moderate and severe exacerbations was reduced by 25% in the combination group compared with placebo.64

This finding becomes all the more significant in the context that severe acute exacerbations have an independent adverse impact on prognosis, with increased mortality associated with the frequency of severe exacerbations.65 In a prospective cohort of 304 men with severe COPD (mean FEV1, 46% of predicted), older age, PCO2, and acute exacerbation of COPD represented independent indicators of poor prognosis, and patients with 3 or more exacerbations showed the greatest mortality risk.65 In the ECLIPSE study, the "frequent exacerbator" phenotype was associated with a poorer quality of life, higher frequency of gastroesophageal reflux, and a higher white blood cell count, suggesting ongoing inflammation in addition to the worsened disease severity.31 Currently, inhaled corticosteroids are widely used, especially for patients with frequent exacerbations of COPD, although recent concerns about excess pneumonia risk in users of inhaled steroids have spurred some controversy and will certainly receive prospective scrutiny.


Yearly prophylactic immunization with the influenza vaccine has been shown to reduce the incidence of influenza by 76% and is strongly recommended.66-68 Immunization once with the 23- polyvalent pneumococcal vaccine in patients with COPD or, in the special case of patients with immunodeficiency or those with splenectomy, every 5 years, is also recommended.67


Although many studies of prophylactic antibiotics have not shown benefit in the management of stable COPD, recent studies of regular macrolide use (ie, azithromycin and erythromycin) have shown benefit, with fewer exacerbations and/or longer times to a first exacerbation.69,70 The precise role of long-term use macrolides in the face of existing drugs to decrease exacerbation frequency (eg, inhaled corticosteroids, roflumilast, etc.) warrants further study.

Mucokinetic Agents

Mucoactive agents are varied and include ambroxol, erdosteine, carbocysteine, iodinated glycerol, N-acetylcysteine, surfactant, and others, all of which have been studied with conflicting results. However, a Cochrane systematic review of 23 randomized, controlled trials in Europe and the U.S. associates the long-term use (>2 months) of oral mucolytics with a reduction in acute COPD exacerbations and days of illness and suggests considering these agents in patients with recurrent, prolonged, severe COPD exacerbations.71 Still, the latest guidelines by the ATS and BTS do not recommend the routine use of mucoactive agents in the management of chronic COPD.5-8


Antitussives containing narcotics and other therapies, such as inhaled nitric oxide, may be harmful. Their use in COPD is relatively contraindicated.5-8 In the specific case of α1-antitrypsin deficiency, intravenous augmentation therapy with pooled human plasma antiprotease can raise serum levels of α1-antitrypsin above a serum protective threshold value (11 micro molar or ~57 mg/dL using nephelometry).16 Available observational studies show that augmentation therapy can slow the rate of FEV1 decline in patients with severe deficiency of α1-antitrypsin (eg, with the Pi-ZZ phenotype) and established airflow obstruction of moderate severity (eg, FEV1 30%-65% of predicted). Also, 2 randomized controlled trials of augmentation therapy have shown trends toward slower rates of lung density loss in augmentation therapy recipients.72 Currently, 4 preparations of pooled human plasma antiprotease have received FDA approval and appear generally similar in effect, with some variation in product formulation.72

Non-pharmacologic treatment of COPD includes pulmonary rehabilitation, long-term oxygen therapy, ventilatory support, and lung volume reduction procedures, both surgical (LVRS) and bronchoscopic. Pulmonary rehabilitation is recommended at all stages by all available guidelines (see Table 2).5-8,73-74 Aerobic lower extremity training can improve exercise endurance, dyspnea, use of health care, and overall quality of life. Upper extremity-exercise and respiratory muscle training also appear helpful.5,73

Long-term oxygen therapy for patients with hypoxemia has been shown to improve survival in eligible patients with COPD.24 Criteria for prescribing long-term oxygen therapy include a PaO2 <55mm Hg or SaO2 <88% with or without increased PaCO2, or PaO2 between 55 and 59mm Hg or SaO2 <89%, with right-sided failure reflected by evidence of pulmonary hypertension or polycythemia (eg, hematocrit >55%). Because the evidence of benefit of supplemental oxygen is scant in COPD patients with moderate resting hypoxemia (ie, SpO2 between 89% to 92%) or desaturation solely with exercise, a large multicenter controlled trial of oxygen versus no oxygen sponsored by the National Institutes of Health (Long-term Oxygen Treatment Trial [LOTT]) is currently examining the survival benefits of supplemental oxygen for patients with COPD with these specific characteristics, ie, moderate hypoxemia (pulse oximetry saturation of 89%-92% on room air at rest) and/or desaturation only with activity.74

Nocturnal noninvasive ventilatory support still has an unproven role in managing patients with stable COPD. Lung volume reduction surgery (LVRS) involves resecting 20% to 35% of the emphysematous lung to improve lung mechanics. The procedure was first proposed by Brantigan and Mueller in the late 1940s,75 but it was abandoned then because of unacceptably high associated mortality. More recently, randomized, controlled trials show that LVRS is contraindicated in patients with severely impaired lung function (eg, FEV1 <20% predicted, homogeneous emphysema and/or lung diffusing capacity for carbon monoxide <20% predicted)27,76-80 but that patients with moderate degrees of airflow obstruction who undergo LVRS might experience an improved FEV1, walking distance, and quality of life.27,76-80 In the results of the National Emphysema Treatment Trial (NETT), a randomized, controlled trial of LVRS versus medical therapy (including rehabilitation) in which 1218 subjects with moderate COPD (FEV1 <45% predicted) were enrolled, the LVRS group overall experienced improved disease-specific quality of life and exercise capacity compared with the medically managed group.27,79 On the other hand, the LVRS group had rates of survival similar to those of the medically managed group. In prespecified subsets, a survival advantage was observed in the subgroup of patients with predominantly upper lobe emphysema and low baseline (ie, post-rehabilitation) exercise capacity (defined as a maximal workload at <25 watts for women and 40 watts for men).27,79 A longer-term overall survival benefit was demonstrated in those allocated to LVRS.

The high short-term mortality (5%) and more importantly the increased morbidity from LVRS coupled with the strict selection criteria of LVRS candidates has led to several innovative bronchoscopic techniques targeting outcomes similar to LVRS.81,82 These novel approaches include endobronchial blockers, airway bypass, endobronchial valves, thermal vapor ablation, biological sealants, and airway implants. To date, the clinical benefit of these options remains incompletely characterized with a few available studies. For example, the VENT study randomly assigned 220 patients with heterogeneous emphysema to receive an endobronchial valve and 101 controls to receive standard medical care and demonstrated a 6%-7% increase in FEV1 and a significant improvement in 6-minute walk test (6MWT) at 6 months. However, the benefit was offset by an increased incidence of hemoptysis and COPD exacerbations.82 Further studies are awaited to better identify subsets of COPD patients who can benefit from these promising techniques.

Lung transplantation is an option for patients with severe airflow obstruction and functional impairment. The 5-year actuarial survival rate for patients undergoing single-lung transplantation for COPD is 43.2%.83-85 Selection criteria include an FEV1 <25% predicted or a PaCO2 >55 mm Hg or cor pulmonale, or both.

Acute Exacerbations of COPD

Acute exacerbation of COPD (AECOPD) represents an acute worsening of the patient's baseline condition, generally characterized by worsened dyspnea and increased volume and purulence of sputum.5-8,86-88 Depending on the severity of baseline COPD, additional derangements can occur, including hypoxemia, worsening hypercapnia, cor pulmonale with worsening lower extremity edema, or altered mental status.

The main goals of treating AECOPD are to restore the patient to his or her previous stable baseline and to prevent or reduce the likelihood of recurrence. This requires identifying the precipitating factor or condition and reversing or ameliorating it while optimizing gas exchange and improving the patient's symptoms. Treatment modalities similar to the ones used in stable COPD are used in managing acute exacerbations (Table 3), with the notable exception that systemic corticosteroids may play a role in managing patients with AECOPD. Other treatments for AECOPD include oxygen therapy, bronchodilators, antibiotics, mechanical ventilation, and others.

Table 3: Recommendations by Professional Societies for Management of Acute Exacerbations of COPD
American Thoracic SocietyEuropean Respiratory SocietyBritish Thoracic SocietyGlobal Initiative for Chronic Obstructive Lung Disease
Recommended: β2 agonists ± anticholinergics; IV aminophylline if inadequate responseRecommended: β2 agonists ± anticholinergics; methylxanthines if needed as second-line therapy in severe exacerbationsRecommended: β2 agonists ± anticholinergics; IV aminophylline if inadequate responseRecommended: β2 agonist dose increase ± anticholinergics ± IV aminophylline depending on disease severity
Oral or systemicOral or systemic empirically7-14 days of systemic steroidsSystemic steroids
Narrow-spectrum antibiotic; broad spectrum if no responseInexpensive antibiotic empirically for 7-14 days; if ineffective, choice guided by sputum cultureCommon oral antibiotics usually adequate; Broader spectrum if no response or if more severe exacerbationEmpirically with increased sputum volume and purulence based on local sensitivity patterns to usual pathogens
Oxygen Therapy
Raise PaO2 > 60mm HgKeep SaO2 ≥90% and/or PaO2 ≥60mm Hg. Avoid PaCO2 rise by >10mm Hg or pH drop to <7.25Raise PaO2 to ≥50mm Hg while avoiding pH <7.26Keep SaO2 between 88%-92%
Ventilatory Support
NIPPV or invasive mechanical ventilation based on criteriaNIPPV in appropriate patientsNIPPV or invasive mechanical ventilation if pH <7.26 with rising PaCO2 despite controlled oxygen therapyNIPPV or invasive mechanical ventilation based on selection and exclusion criteria.
Chest Physiotherapy
Only if sputum volume is >25 mL/dayHelp in clearance of secretionsNot recommendedMay be beneficial in certain circumstances

COPD, chronic obstructive pulmonary disease; NIPPV, noninvasive positive pressure ventilation. ©2002 The Cleveland Clinic Foundation.

Oxygen Therapy

The role of oxygen therapy is to correct the hypoxemia that usually accompanies the AECOPD. The end point is to maintain oxygen tension at approximately 60 to 65mm Hg, thereby assuring near-maximal hemoglobin saturation while minimizing the potential for deleterious hypercapnia. Hypercapnia complicating supplemental oxygen is mainly a result of ventilation-perfusion mismatch, with generally smaller contributions of depression of the respiratory drive and the Haldane effect.


Bronchodilators are widely used in AECOPD, and β-adrenergic agonists and anticholinergics are first-line therapies. As in stable COPD, both can improve airflow in AECOPD, and although recommendations vary, combined therapy is often recommended. β-Adrenergic agonists generally have a quicker onset of action, whereas anticholinergics have a more favorable side-effect profile. Because of their potential side effects, as well as their limited benefit, older methylxanthines have been reserved as second-line therapy.5-8


Antibiotics play a favorable role in treating AECOPD, especially in the setting of increased volume and purulence of phlegm.87-89 A narrow-spectrum antibiotic (eg, amoxicillin, trimethoprim-sulfamethoxazole, doxycycline) is often recommended as first-line therapy, although use of a beta-lactam/beta-lactamase combination has been recommended in patients with severe AECOPD, and fluoroquinolones have been used in patients suspected to be colonized with Pseudomonas aeruginosa.8 The optimal duration of treatment is still unclear, although most guidelines recommend treating for between 7 and 14 days.85,86


Randomized clinical trials generally support the use of systemic corticosteroids to enhance airflow and to lessen treatment failure in AECOPD. Prolonged therapy beyond 2 weeks confers no additional benefits, with 5 to 10 days being the likeliest optimal duration.93-95

Noninvasive Positive Pressure Ventilation and Mechanical Ventilation

Noninvasive positive pressure ventilation (NIPPV) is emerging as a preferred method of ventilation in adequately selected patients with acute respiratory acidemia.90-93 This mode is used in the treatment of acute respiratory failure of many causes, including COPD. Appropriate patient selection is critical to ensure the success of NIPPV. Poor candidates are those with acute respiratory arrest, altered mental status with agitation or lack of cooperation, distorted facial anatomy preventing proper application of the mask, cardiovascular instability, or excessive secretions. NIPPV improves symptomatic and physiologic variables; reduces the need for intubation, hospital stay, and mortality; and does not use additional resources.93-95

For patients who do not qualify for NIPPV or who show evidence of worsening respiratory failure and life-threatening acidemia despite NIPPV, intubation and mechanical ventilation are indicated. This method of ventilation carries numerous risks and complications, including ventilator-acquired pneumonia and barotrauma. Adequate ventilator management is necessary, and every effort should be undertaken to minimize the duration of mechanical ventilation.


Mucolytics, expectorants, and chest physiotherapy have not been shown to improve the outcome and are not recommended.5-8

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Overall, COPD poses a common, growing, and significant clinical challenge for patients and clinicians alike. Clinicians' expert knowledge regarding diagnosis and management can enhance patients' longevity and quality of life. Results of emerging studies will likely lead to enhancements in current management and new paradigms in managing patients with COPD.

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  • COPD is emerging as a major cause of morbidity and mortality in the U.S. and is currently is the third leading cause of death among Americans.
  • COPD is under-recognized overall, as is α1-antitrypsin deficiency, a genetic predisposition to COPD.
  • The frequency of exacerbations and the presence of co-morbidities (eg, cardiovascular disease, musculoskeletal disease, etc.) affect the clinical course of COPD.
  • Among the available therapies for COPD, many can improve symptoms (eg, bronchodilators, pulmonary rehabilitation). Three treatments-smoking cessation, supplemental oxygen used 24 hours a day, and lung volume reduction surgery-have been shown to prolong life in appropriately selected COPD patients.

Suggested Readings

  • AACP/AACVPR Pulmonary Rehabilitation Guidelines Panel. Pulmonary rehabilitation: Joint ACCP/AACVPR evidence-based guidelines. Chest 1997;112:1363-1396.
  • American Thoracic Society. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease., accessed May 30, 2008.
  • Qaseem A, MD, PhD, MHA, Wilt TJ, MD, MPH et al: Diagnosis and Management of Stable Chronic Obstructive Pulmonary Disease: A Clinical Practice Guideline Update from the American College of Physicians, American College of Chest Physicians, American Thoracic Society, and European Respiratory Society. Ann Intern Med. 2011;155:179-191.
  • American Thoracic Society/European Respiratory Society Statement: Standards for the diagnosis and management of individuals with α1-antitrypsin deficiency. Am J Respir Crit Care Med 2003;168:818-900.
  • Anthonisen NR, Connett JE, Murray RP: Smoking and lung function of Lung Health Study participants after 11 years. The Lung Health Study Research Group. Am J Respir Crit Care Med 2002;166:675-679.
  • Maurer JR, Frost AE, Estenne M, et al: International guidelines for the selection of lung transplant candidates. The International Society for Heart and Lung Transplantation, the American Thoracic Society, the American Society of Transplant Physicians, the European Respiratory Society. Transplantation 1998;66:951-956.
  • Calverley PM, Anderson JA, Celli B, et al. Salmeterol and fluticasone propionate and survival in chronic obstructive pulmonary disease. N Engl J Med 2007; 356: 775-789.
  • Aaron SD, Vandemheen KL, Ferguson D, et al. Tiotropium in combination with placebo, salmeterol, or fluticasone-salmeterol for treatment of chronic obstructive pulmonary disease: a randomized trial. Ann Intern Med 2007; 146: 545-555.
  • National Emphysema Treatment Trial Research Group. A randomized trial comparing lung-volume-reduction surgery with medical therapy for severe emphysema. N Engl J Med 2003;348:2059-2073.
  • Pauwels RA, Buist AS, Calverley PM, et al: GOLD Scientific Committee. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease (GOLD) Workshop summary. Am J Respir Crit Care Med 2001;163:1256-1276.
  • Pauwels RA, Lofdahl CG, Laitinen LA, et al: Long-term treatment with inhaled budesonide in persons with mild chronic obstructive pulmonary disease who continue smoking. European Respiratory Society Study on Chronic Obstructive Pulmonary Disease. N Engl J Med 1999;340:1948-1953.
  • Sutherland ER, Cherniack RM: Management of chronic obstructive pulmonary disease. N Engl J Med 2004;350:2689-2697.
  • The Lung Health Study Research Group. Effect of inhaled triamcinolone on the decline in pulmonary function in chronic obstructive pulmonary disease. N Engl J Med 2000;343:1902-1909.

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  1. Murray CJL, Lopez AD, Mathers CD, Stein C: The global burden of disease 2000 project: Aims, methods and data sources. Global Programme on Evidence for Health Policy Discussion Paper No. 36. Geneva: World Health Organization, 2001.
  2. National Heart, Lung, and Blood Institute: 2007 NHLBI Morbidity and Mortality Chartbook. Available at (accessed March 20, 2009).
  3. Kochanek KD, Xu JQ, Murphy SL, Miniño AM, Kung HC: Deaths: preliminary data for 2009. Natl Vital Stat Rep 2011;59(4). Hyattsville, MD: US Department of Health and Human Services, CDC, National Center for Health Statistics; 2011. Available at Accessed February 21, 2012.
  4. Murray CJ, Lopez AD: Alternative projections of mortality and disability by cause 1990-2020: Global Burden of Disease Study. Lancet 1997;349:1498-1504.
  5. American Thoracic Society/European Respiratory Society Task Force: Standards for the diagnosis and management of patients with COPD. Version 1.2. New York: American Thoracic Society, 2004. PDF available for download at (accessed March 20, 2009).
  6. Siafakas NM, Vermeire P, Pride NB, et al.: for the European Respiratory Society Task Force: Optimal assessment and management of chronic obstructive pulmonary disease (COPD). Eur Respir J 1995;8:1398-1420.
  7. The COPD Guidelines Group of the Standards of Care Committee of the BTS. BTS guidelines for the management of chronic obstructive pulmonary disease. Thorax 1997;52(suppl 5):S1-S28.
  8. From the Global Strategy for the Diagnosis, Management and Prevention of COPD, Global Initiative for Chronic Obstructive Lung Disease (GOLD) 2011. Available from: Accessed online July 12, 2012.
  9. Buist AS, McBurnie MA, Vollmer WM, et al.: BOLD Collaborative Research Group. International variation in the prevalence of COPD (the BOLD Study): a population-based prevalence study. Lancet 2007;370(9589):741-50.
  10. Hurd S: The impact of COPD on lung health worldwide: Epidemiology and incidence. Chest 2000;117(suppl 2):1S-4S.
  11. Sullivan SD, Ramsey SD, Lee TA: The economic burden of COPD. Chest 2000;117(suppl 2):5S-9S.
  12. Liu S, Zhou Y, Wang X, et al: Biomass fuels are the probable risk factor for chronic obstructive pulmonary disease in rural South China. Thorax 2007;62(10):889-97.
  13. McDonough JE. Small-Airway Obstruction and Emphysema in Chronic Obstructive Pulmonary Disease. N Engl J Med 2011; 365: 1567-75.
  14. Keatings VM, Collins PD, Scott DM, Barnes PJ: Differences in interleukin-8 and tumor necrosis factor-alpha in induced sputum from patients with chronic obstructive pulmonary disease or asthma. Am J Respir Crit Care Med 1996;153:530-534.
  15. Repine JE, Bast A, Lankhorst I: Oxidative stress in chronic obstructive pulmonary disease. Oxidative Stress Study Group. Am J Respir Crit Care Med 1997;156:341-357.
  16. American Thoracic Society/European Respiratory Society Statement: Standards for the diagnosis and management of individuals with α1-antitrypsin deficiency. Am J Respir Crit Care Med 2003;168:818-900.
  17. Stoller JK, Sandhaus RA, Turino G, et al.: Delay in diagnosis of α1-antitrypsin deficiency: A continuing problem. Chest 2005;128:1989-1994.
  18. Campos MA, Wanner A, Zhang G, Sandhaus RA: Trends in the diagnosis of symptomatic patients with α1-antitrypsin deficiency between 1968 and 2003. Chest 2005;128:1179-1186.
  19. Celli BR, Cote CG, Marin JM, et al.: The body-mass index, airflow obstruction, dyspnea, and exercise capacity index in chronic obstructive pulmonary disease. N Engl J Med 2004;350:1005-1012.
  20. Puhan MA, Garcia-Aymerich J, Frey M, et al.: Expansion of the prognostic assessment of patients with chronic obstructive pulmonary disease: The updated BODE index and the ADO index. Lancet 2009;374:704–711.
  21. Jones RC, Donaldson GC, Chavannes NH, et al.: Derivation and validation of a composite index of severity in chronic obstructive pulmonary disease: the DOSE Index. Am J Respir Crit Care Med 2009;180(12):1189–1195.
  22. Jones PW, Harding G, Berry P, et al.: Development and first validation of the COPD Assessment Test. Eur Respir J 2009;34(3):648-54.
  23. Agusti A, Calverley PM, Celli B, et al.: Characterisation of COPD heterogeneity in the ECLIPSE cohort. Resp Res 2010;11:122.
  24. 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.
  25. Anthonisen NR, Connett JE, Kiley JP, et al.: Effects of smoking intervention and the use of an inhaled anticholinergic bronchodilator on the rate of decline of FEV1. The Lung Health Study. JAMA 1994;272:1497-1505.
  26. Anthonisen NR, Skeans MA, Wise RA, et al.: Lung Health Study Research Group: The effects of a smoking cessation intervention on 14.5-year mortality: A randomized clinical trial. Ann Intern Med 2005;142:233-239.
  27. National Emphysema Treatment Trial Research Group: A randomized trial comparing lung-volume-reduction surgery with medical therapy for severe emphysema. N Engl J Med 2003;348:2059-2073.
  28. Connors AF Jr, Dawson NV, Thomas C, et al. for the SUPPORT Investigators (Study to Understand Prognoses and Preferences for Outcomes and Risks of Treatments): Outcomes following acute exacerbation of severe chronic obstructive lung disease. Am J Respir Crit Care Med 1996;154:959-967.
  29. Costello R, Deegan P, Fitzpatrick M, McNicholas WT: Reversible hypercapnia in chronic obstructive pulmonary disease: A distinct pattern of respiratory failure with a favorable prognosis. Am J Med 1997;102:239-244.
  30. Roberts CM, Barnes S, Lowe D, et al.: Evidence for a link between mortality in acute COPD and hospital type and resources. Thorax 2002;57: 137-141.
  31. Hurst JR, Vestbo J, Anzueto A, et al.: Susceptibility to exacerbation in chronic obstructive pulmonary disease. N Engl J Med 2010;363:1128-38.
  32. Gay PC: Chronic obstructive pulmonary disease and sleep. Respir Care 2004;49(1):39-51.
  33. McNicholas WT: Impact of sleep on ventilation and gas exchange in chronic lung disease. Monaldi Arch Chest Dis 2003;59(3):212-215.
  34. Anthonisen NR, Connett JE, Murray RP: Smoking and lung function of Lung Health Study participants after 11 years. The Lung Health Study Research Group. Am J Respir Crit Care Med 2002;166:675-679.
  35. Sutherland ER, Cherniack RM: Management of chronic obstructive pulmonary disease. N Engl J Med 2004;350:2689-2697.
  36. Celli BR: Pulmonary rehabilitation in patients with COPD. Am J Respir Crit Care Med 1995;152:861-864.
  37. Heffner JE, Fahy B, Hilling L, Barbieri C: Outcomes of advance directive education of pulmonary rehabilitation patients. Am J Respir Crit Care Med 1997;155:1055-1059.
  38. Bourbeau J, Collet JP, Schwartzman K, et al.: Economic benefits of self-management education in COPD. Chest 2006;130(6):1704-11.
  39. Dewan NA, Rice KL, Caldwell M, et al.: Economic evaluation of a disease management program for chronic obstructive pulmonary disease. COPD 2011;8(3):153-9.
  40. Trappenburg JC, Monninkhof EM, Bourbeau J, et al.: Effect of an action plan with ongoing support by a case manager on exacerbation-related outcome in patients with COPD: A multicentre randomised controlled trial. Thorax 2011;66(11):977-84.
  41. Fan VS, Gaziano JM: A comprehensive care management program to prevent chronic obstructive pulmonary disease hospitalizations: a randomized, controlled trial. Ann Intern Med 2012;156(10):673-83.
  42. Gonzales D, Rennard SI, Nides M, et al.: Varenicline Phase 3 Study Group. Varenicline, an α4β2 nicotinic acetylcholine receptor partial agonist, vs. sustained-release bupropion and placebo for smoking cessation: A randomized controlled trial. JAMA 2006;296:47-55.
  43. Jorenby DE, Leischow SJ, Nides MA, et al.: A controlled trial of sustained-release bupropion, a nicotine patch, or both for smoking cessation. N Engl J Med 1999;340:685-691.
  44. Calverley PM, Rabe KF, Goehring UM, et al.: Roflumilast in symptomatic chronic obstructive pulmonary disease: two randomised clinical trials. Lancet 2009;374(9691):685-94.
  45. Rabe KF, Bateman ED, O'Donnell D, et al.: Roflumilast-an oral anti-inflammatory treatment for chronic obstructive pulmonary disease: A randomized controlled trial. Lancet 2005;366(9485):563-571.
  46. Rennard SI, Schachter N, Strek M, et al.: Cilomilast for COPD: Results of a 6-month, placebo-controlled study of a potent, selective inhibitor of phosphodiesterase 4. Chest 2006;129:56-66.
  47. Ferguson GT, Cherniack RM: Management of chronic obstructive pulmonary disease. N Engl J Med 1993;328:1017-1022.
  48. Combivent Inhalation Aerosol Study Group: In chronic obstructive pulmonary disease, a combination of ipratropium and albuterol is more effective than either agent alone. An 85-day multicenter trial. Chest 1994;105:1411-1419.
  49. The Combivent Inhalation Solution Study Group: Routine nebulized ipratropium and albuterol together are better than either alone in COPD. Chest 1997; 112:1514-1521.
  50. The Pink Sheet. FDC Reports 2004;66(6):18.
  51. Panning CA, DeBisschop M: Tiotropium: An inhaled, long-acting anticholinergic drug for chronic obstructive pulmonary disease. Pharmacotherapy 2003; 23:183-189.
  52. van Noord JA, Bantje TA, Eland ME, et al.: A randomised controlled comparison of tiotropium and ipratropium in the treatment of chronic obstructive pulmonary disease. Thorax 2000;55:289-294.
  53. Vincken W, van Noord JA, Greefhorst AP, et al.: Improved health outcomes in patients with COPD during 1 year's treatment with tiotropium. Eur Respir J 2002; 19:209-216.
  54. 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.
  55. Brusasco V, Hodder R, Miravitlles M, et al.: Health outcomes following treatment for six months with once daily tiotropium compared with twice daily salmeterol in patients with COPD. Thorax 2003;58: 399-404.
  56. Ribeiro M, Chapman KR. Comparative efficacy of indacaterol in chronic obstructive pulmonary disease. Intl J COPD 2012; 7:145-152.
  57. Hanania NA, Feldman G, Zachgo W et al.: The efficacy and safety of the novel, long-acting beta 2 agonist vilanterol in patients with COPD: A randomized placebo-controlled trial. Chest 2012; 142:119–127.
  58. Tashkin DP, Celli B, Senn S, et al.: UPLIFT Study Investigators. A 4-year trial of tiotropium in chronic obstructive pulmonary disease. N Engl J Med 2008; 35a:1543-1554.
  59. Pauwels RA, Lofdahl CG, Laitinen LA, et al.: Long-term treatment with inhaled budesonide in persons with mild chronic obstructive pulmonary disease who continue smoking. European Respiratory Society Study on Chronic Obstructive Pulmonary Disease. N Engl J Med 1999;340:1948-1953.
  60. Burge PS, Calverley PM, Jones PW, et al.: Randomised, double blind, placebo controlled study of fluticasone propionate in patients with moderate to severe chronic obstructive pulmonary disease: The ISOLDE trial. BMJ 2000;320:1297-1303.
  61. Vestbo J, Sorensen T, Lange P, et al.: Long-term effect of inhaled budesonide in mild and moderate chronic obstructive pulmonary disease: A randomised controlled trial. Lancet 1999;353:1819-1823.
  62. The Lung Health Study Research Group: Effect of inhaled triamcinolone on the decline in pulmonary function in chronic obstructive pulmonary disease. N Engl J Med 2000;343:1902-1909.
  63. Vestbo J, TORCH Study Group: The TORCH (towards a revolution in COPD health) survival study protocol. Eur Respir J. 2004;24(2):206-10.
  64. Calverley P, Pauwels R, Vestbo J, et al.: Trial of Inhaled Steroids and Long-acting β2-Agonists Study Group: Combined salmeterol and fluticasone in the treatment of chronic obstructive pulmonary disease: A randomised controlled trial. Lancet 2003 Feb 8;361(9356):449-456.
  65. Soler-Cataluna JJ, Martinez-Garcia MA, Roman Sanchez P, et al: Severe acute exacerbations and mortality in patients with chronic obstructive pulmonary disease. Thorax 2005;60:925-931.
  66. Nichol KL, Margolis KL, Wuorenma J, Von Sternberg T: The efficacy and cost effectiveness of vaccination against influenza among elderly persons living in the community. N Engl J Med 1994;331:778-784.
  67. Koivula I, Sten M, Leinonen M, Makela PH: Clinical efficacy of pneumococcal vaccine in the elderly: A randomized, single-blind population-based trial. Am J Med 1997;103:281-290.
  68. Centers for Disease Control and Prevention: Prevention and control of influenza: Recommendations of the Advisory Committee on Immunization Practices (ACIP). MMWR Morb Mortal Wkly Rep 1999;48:1-28.
  69. Seemungal TA, Wilkinson TM, Hurst JR, et al.: Long-term erythromycin therapy is associated with decreased chronic obstructive pulmonary disease exacerbations. Am J Respir Crit Care Med 2008;178(11):1139-47.
  70. Albert RK, Connett J, Bailey WC, et al.: Azithromycin for prevention of exacerbations of COPD. N Engl J Med. 2011;365(8):689-98.
  71. Poole PJ, Black PN: Mucolytic agents for chronic bronchitis or chronic obstructive pulmonary disease. Cochrane Database Syst Rev 2006;(3):CD001287.
  72. Stoller JK, Aboussouan L. Concise clinical review: Alpha-1 antitrypsin deficiency. Am J Respir Crit Care Med 2012;185:246-259.
  73. AACP/AACVPR Pulmonary Rehabilitation Guidelines Panel: Pulmonary rehabilitation: Joint ACCP/AACVPR evidence-based guidelines. Chest 1997; 112:1363-1396.
  74. Stoller JK, Panos R, Krachman S, Doherty D, Make B. Oxygen therapy for patients with COPD: Evidence for current therapy and the Long-term Oxygen Treatment Trial (LOTT). Chest 2010;38:179-187.
  75. Brantigan OC, Mueller E: Surgical treatment of pulmonary emphysema. Am Surg 1957;23:789-794.
  76. National Emphysema Treatment Trial Research Group: Patients at high risk of death after lung-volume-reduction surgery. N Engl J Med 2001;345:1075-1083.
  77. Geddes D, Davies M, Koyama H, et al.: Effect of lung-volume-reduction surgery in patients with severe emphysema. N Engl J Med 2000;343: 239-245.
  78. Goldstein RS, Todd TRJ, Guyatt G, et al.: Influence of lung volume reduction surgery (LVRS) on health related quality of life in patients with chronic obstructive pulmonary disease. Thorax 2003;58:405-410.
  79. Fishman A, Martinez F, Naunheim K et al.: A randomized trial comparing lung-volume-reduction surgery with medical therapy for severe emphysema. N Engl J Med 2003;348(21):2059–2073.
  80. DeCamp MM, McKenna RJ, Deschamps CC, et al.: Lung volume reduction surgery: technique, operative mortality, and morbidity. Proc Amer Thor Soc 2008;5(4):442–446.
  81. Ernst A, Anantham D: Bronchoscopic lung volume reduction. Pulm Med. 2011;2011:610802.
  82. Sciurba FC, Ernst A, Herth F et al.: VENT study. Endobronchial valves. A randomized study of endobronchial valves for advanced emphysema. N Engl J Med 2010;363(13):1233–1244.
  83. Bennett LE, Keck BM, Daily OP, et al.: Worldwide thoracic organ transplantation: A report from the UNOS/ISHLT International Registry for Thoracic Organ Transplantation. Clin Transpl 2000:31-44.
  84. Maurer JR, Frost AE, Estenne M, et al.: International guidelines for the selection of lung transplant candidates. The International Society for Heart and Lung Transplantation, the American Thoracic Society, the American Society of Transplant Physicians, the European Respiratory Society. Transplantation 1998;66:951-956.
  85. International Society for Heart and Lung Transplantation. Available at, accessed August 1, 2012.
  86. McCrory DC, Brown C, Gelfand SE, Bach PB: Management of acute exacerbations of COPD: A summary and appraisal of the published evidence. Chest 2001; 119:1190-1209.
  87. Stoller JK: Acute exacerbations of chronic obstructive pulmonary disease. N Engl J Med 2002;346:988-994.
  88. Anthonisen NR, Manfreda J, Warren CP, et al.: Antibiotic therapy in exacerbations of chronic obstructive pulmonary disease. Ann Intern Med. 1987;106:196-204.
  89. Stockley RA, O'Brien C, Pye A, Hill SL: Relationship of sputum color to nature and outpatient management of acute exacerbation of COPD. Chest 2000; 117:1638-1645.
  90. Niewoehner DE, Erbland ML, Deupree RH, et al.: Effect of systemic glucocorticoids on exacerbations of chronic obstructive pulmonary disease. Department of Veterans Affairs Cooperative Study Group. N Engl J Med 1999;340:1941-1947.
  91. Davies L, Angus RM, Calverley PM: Oral corticosteroids in patients admitted to hospital with exacerbations of chronic obstructive pulmonary disease: A prospective randomised controlled trial. Lancet 1999;354:456-460.
  92. Thompson WH, Nielson CP, Carvalho P, et al.: Controlled trial of oral prednisone in outpatients with acute COPD exacerbation. Am J Respir Crit Care Med 1996;154:407-412.
  93. Mehta S, Hill NS: Noninvasive ventilation. Am J Respir Crit Care Med 2001;163:540-577.
  94. International Consensus Conferences in Intensive Care Medicine: Noninvasive positive pressure ventilation in acute respiratory failure. Am J Respir Crit Care Med 2001;163:283-291.
  95. Kramer N, Meyer TJ, Meharg J, et al.: Randomized, prospective trial of noninvasive positive pressure ventilation in acute respiratory failure. Am J Respir Crit Care Med 1995;151:1799-1806.

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