Chronic obstructive pulmonary disease (COPD) is a type of obstructive lung disease characterized by long-term breathing problems and poor airflow. The main symptoms include shortness of breath and cough with sputum production. COPD is a progressive disease, meaning it typically worsens over time. Eventually everyday activities, such as walking or getting dressed, become difficult.Chronic bronchitis and emphysema are older terms used for different types of COPD. The term "chronic bronchitis" is still used to define a productive cough that is present for at least three months each year for two years.
As of 2015, COPD affected about 174.5 million (2.4%) of the global population. It typically occurs in people over the age of 40. Males and females are affected equally commonly. In 2015, it resulted in 3.2 million deaths, up from 2.4 million deaths in 1990. More than 90% of these deaths occur in the developing world. The number of deaths is projected to increase further because of higher smoking rates in the developing world, and an aging population in many countries. It resulted in an estimated economic cost of $2.1 trillion in 2010.
The most common symptoms of COPD are sputum production, shortness of breath, and a productive cough. These symptoms are present for a prolonged period of time and typically worsen over time. It is unclear whether different types of COPD exist. While previously divided into emphysema and chronic bronchitis, emphysema is only a description of lung changes rather than a disease itself, and chronic bronchitis is simply a descriptor of symptoms that may or may not occur with COPD.
A chronic cough is often the first symptom to develop. When it persists for more than three months each year for at least two years, in combination with sputum production and without another explanation, it is by definition chronic bronchitis. This condition can occur before COPD fully develops. The amount of sputum produced can change over hours to days. In some cases, the cough may not be present or may only occur occasionally and may not be productive. Some people with COPD attribute the symptoms to a "smoker's cough". Sputum may be swallowed or spat out, depending often on social and cultural factors. Vigorous coughing may lead to rib fractures or a brief loss of consciousness. Those with COPD often have a history of "common colds" that last a long time.
Shortness of breath
Shortness of breath is often the symptom that most bothers people. It is commonly described as: "my breathing requires effort," "I feel out of breath," or "I can't get enough air in". Different terms, however, may be used in different cultures. Typically the shortness of breath is worse on exertion of a prolonged duration and worsens over time. In the advanced stages, or end stage pulmonary disease it occurs during rest and may be always present. It is a source of both anxiety and a poor quality of life in those with COPD. Many people with more advanced COPD breathe through pursed lips and this action can improve shortness of breath in some.
In COPD, breathing out may take longer than breathing in. Chest tightness may occur, but is not common and may be caused by another problem. Those with obstructed airflow may have wheezing or decreased sounds with air entry on examination of the chest with a stethoscope. A barrel chest is a characteristic sign of COPD, but is relatively uncommon.Tripod positioning may occur as the disease worsens.
The primary cause of COPD is tobacco smoke, with occupational exposure and pollution from indoor fires being significant causes in some countries. Typically, these exposures must occur over several decades before symptoms develop. A person's genetic makeup also affects the risk.
Percentage of females smoking tobacco as of the late 1990s early 2000s
Percentage of males smoking tobacco as of the late 1990s and early 2000s. Note the scales used for females and males differ.
The primary risk factor for COPD globally is tobacco smoking. Of those who smoke, about 20% will get COPD, and of those who are lifelong smokers, about half will get COPD. In the United States and United Kingdom, of those with COPD, 80–95% are either current smokers or previously smoked. The likelihood of developing COPD increases with the total smoke exposure. Additionally, women are more susceptible to the harmful effects of smoke than men. In nonsmokers, secondhand smoke is the cause of about 20% of cases. Other types of smoke, such as, marijuana, cigar, and water-pipe smoke, also confer a risk. Water-pipe smoke appears to be as harmful as smoking cigarettes. Problems from marijuana smoke may only be with heavy use. Women who smoke during pregnancy may increase the risk of COPD in their child. For the same amount of cigarette smoking, women have a higher risk of COPD than men.
Poorly ventilated cooking fires, often fueled by coal or biomass fuels such as wood and dung, lead to indoor air pollution and are one of the most common causes of COPD in developing countries. These fires are a method of cooking and heating for nearly 3 billion people, with their health effects being greater among women due to more exposure. They are used as the main source of energy in 80% of homes in India, China and sub-Saharan Africa.
People who live in large cities have a higher rate of COPD compared to people who live in rural areas. While urban air pollution is a contributing factor in exacerbations, its overall role as a cause of COPD is unclear. Areas with poor outdoor air quality, including that from exhaust gas, generally have higher rates of COPD. The overall effect in relation to smoking, however, is believed to be small.
Intense and prolonged exposure to workplace dusts, chemicals, and fumes increases the risk of COPD in both smokers and nonsmokers. Workplace exposures are believed to be the cause in 10–20% of cases. In the United States, they are believed to be related to more than 30% of cases among those who have never smoked and probably represent a greater risk in countries without sufficient regulations.
A number of industries and sources have been implicated, including high levels of dust in coal mining, gold mining, and the cotton textile industry, occupations involving cadmium and isocyanates, and fumes from welding. Working in agriculture is also a risk. In some professions, the risks have been estimated as equivalent to that of one-half to two packs of cigarettes a day.Silica dust and fiberglass dust exposure can also lead to COPD, with the risk unrelated to that for silicosis. The negative effects of dust exposure and cigarette smoke exposure appear to be additive or possibly more than additive.
Genetics play a role in the development of COPD. It is more common among relatives of those with COPD who smoke than unrelated smokers. Currently, the only clearly inherited risk factor is alpha 1-antitrypsin deficiency (AAT). This risk is particularly high if someone deficient in alpha 1-antitrypsin also smokes. It is responsible for about 1–5% of cases and the condition is present in about three to four in 10,000 people. Other genetic factors are being investigated, of which many are likely.
A number of other factors are less closely linked to COPD. The risk is greater in those who are poor, although if this is due to poverty itself or other risk factors associated with poverty, such as air pollution and malnutrition, is not clear. Tentative evidence indicates those with asthma and airway hyperreactivity are at increased risk of COPD. Birth factors such as low birth weight may also play a role, as do a number of infectious diseases, including HIV/AIDS and tuberculosis.Respiratory infections such as pneumonia do not appear to increase the risk of COPD, at least in adults.
An acute exacerbation (a sudden worsening of symptoms) is commonly triggered by infection or environmental pollutants, or sometimes by other factors such as improper use of medications. Infections appear to be the cause of 50 to 75% of cases, with bacteria in 30%, viruses in 23%, and both in 25%. Environmental pollutants include both poor indoor and outdoor air quality. Exposure to personal smoke and secondhand smoke increases the risk. Cold temperature may also play a role, with exacerbations occurring more commonly in winter. Those with more severe underlying disease have more frequent exacerbations: in mild disease 1.8 per year, moderate 2 to 3 per year, and severe 3.4 per year. Those with many exacerbations have a faster rate of deterioration of their lung function.Pulmonary emboli (blood clots in the lungs) can worsen symptoms in those with pre-existing COPD. Signs of PE in COPD include pleuritic chest pain and heart failure without signs of infection.
On the left is a diagram of the lungs and airways with an inset showing a detailed cross-section of normal bronchioles and alveoli. On the right are lungs damaged by COPD with an inset showing a cross-section of damaged bronchioles and alveoli.
COPD is a type of obstructive lung disease in which chronic, incompletely reversible poor airflow (airflow limitation) and inability to breathe out fully (air trapping) exist. The poor airflow is the result of breakdown of lung tissue (known as emphysema) and small airways disease (known as obstructive bronchiolitis). The relative contributions of these two factors vary between people. Severe destruction of small airways can lead to the formation of large air pockets—known as bullae—that replace lung tissue. This form of disease is called bullous emphysema.
COPD develops as a significant and chronic inflammatory response to inhaled irritants. Chronic bacterial infections may also add to this inflammatory state. The inflammatory cells involved include neutrophil granulocytes and macrophages, two types of white blood cells. Those who smoke additionally have Tc1lymphocyte involvement and some people with COPD have eosinophil involvement similar to that in asthma. Part of this cell response is brought on by inflammatory mediators such as chemotactic factors. Other processes involved with lung damage include oxidative stress produced by high concentrations of free radicals in tobacco smoke and released by inflammatory cells, and breakdown of the connective tissue of the lungs by proteases that are insufficiently inhibited by protease inhibitors. The destruction of the connective tissue of the lungs leads to emphysema, which then contributes to the poor airflow, and finally, poor absorption and release of respiratory gases. General muscle wasting that often occurs in COPD may be partly due to inflammatory mediators released by the lungs into the blood.
Micrograph showing emphysema (left – large empty spaces) and lung tissue with relative preservation of the alveoli (right)
Narrowing of the airways occurs due to inflammation and scarring within them. This contributes to the inability to breathe out fully. The greatest reduction in air flow occurs when breathing out, as the pressure in the chest is compressing the airways at this time. This can result in more air from the previous breath remaining within the lungs when the next breath is started, resulting in an increase in the total volume of air in the lungs at any given time, a process called hyperinflation or air trapping. Hyperinflation from exercise is linked to shortness of breath in COPD, as breathing in is less comfortable when the lungs are already partly filled. Hyperinflation may also worsen during an exacerbation.
Low oxygen levels, and eventually, high carbon dioxide levels in the blood, can occur from poor gas exchange due to decreased ventilation from airway obstruction, hyperinflation, and a reduced desire to breathe. During exacerbations, airway inflammation is also increased, resulting in increased hyperinflation, reduced expiratory airflow, and worsening of gas transfer. This can also lead to insufficient ventilation, and eventually, low blood oxygen levels. Low oxygen levels, if present for a prolonged period, can result in narrowing of the arteries in the lungs, while emphysema leads to breakdown of capillaries in the lungs. Both of these changes result in increased blood pressure in the pulmonary arteries, which may cause cor pulmonale.
A person blowing into a spirometer: Smaller handheld devices are available for office use.
The diagnosis of COPD should be considered in anyone over the age of 35 to 40 who has shortness of breath, a chronic cough, sputum production, or frequent winter colds and a history of exposure to risk factors for the disease.Spirometry is then used to confirm the diagnosis. Screening those without symptoms is not recommended.
Spirometry measures the amount of airflow obstruction present and is generally carried out after the use of a bronchodilator, a medication to open up the airways. Two main components are measured to make the diagnosis, the forced expiratory volume in one second (FEV1), which is the greatest volume of air that can be breathed out in the first second of a breath, and the forced vital capacity (FVC), which is the greatest volume of air that can be breathed out in a single large breath. Normally, 75–80% of the FVC comes out in the first second and a FEV1/FVC ratio less than 70% in someone with symptoms of COPD defines a person as having the disease. Based on these measurements, spirometry would lead to over-diagnosis of COPD in the elderly. The National Institute for Health and Care Excellence criteria additionally require a FEV1 less than 80% of predicted. People with COPD also exhibit a decrease in diffusing capacity of the lung for carbon monoxide (DLCO) due to decreased surface area in the alveoli, as well as damage to the capillary bed.
A number of methods can determine how much COPD is affecting a given individual. The modified British Medical Research Council questionnaire or the COPD assessment test (CAT) are simple questionnaires that may be used to determine the severity of symptoms. Scores on CAT range from 0–40 with the higher the score, the more severe the disease. Spirometry may help to determine the severity of airflow limitation. This is typically based on the FEV1 expressed as a percentage of the predicted "normal" for the person's age, gender, height, and weight. Both the American and European guidelines recommended partly basing treatment recommendations on the FEV1. The GOLD guidelines suggest dividing people into four categories based on symptoms assessment and airflow limitation. Weight loss and muscle weakness, as well as the presence of other diseases, should also be taken into account.
A chest X-ray and complete blood count may be useful to exclude other conditions at the time of diagnosis. Characteristic signs on X-ray are overexpanded lungs, a flattened diaphragm, increased retrosternal airspace, and bullae, while it can help exclude other lung diseases, such as pneumonia, pulmonary edema, or a pneumothorax. A high-resolution computed tomography scan of the chest may show the distribution of emphysema throughout the lungs and can also be useful to exclude other lung diseases. Unless surgery is planned, however, this rarely affects management. A saber-sheath trachea deformity may also be present. An analysis of arterial blood is used to determine the need for oxygen; this is recommended in those with an FEV1 less than 35% predicted, those with a peripheral oxygen saturation less than 92%, and those with symptoms of congestive heart failure. In areas of the world where alpha-1 antitrypsin deficiency is common, people with COPD (particularly those below the age of 45 and with emphysema affecting the lower parts of the lungs) should be considered for testing.
Chest X-ray demonstrating severe COPD: Note the small heart size in comparison to the lungs.
A lateral chest X-ray of a person with emphysema: Note the barrel chest and flat diaphragm.
Lung bulla as seen on chest X-ray in a person with severe COPD
A severe case of bullous emphysema
Axial CT image of the lung of a person with end-stage bullous emphysema
Very severe emphysema with lung cancer on the left (CT scan)
COPD may need to be differentiated from other causes of shortness of breath such as congestive heart failure, pulmonary embolism, pneumonia, or pneumothorax. Many people with COPD mistakenly think they have asthma. The distinction between asthma and COPD is made on the basis of the symptoms, smoking history, and whether airflow limitation is reversible with bronchodilators at spirometry. Tuberculosis may also present with a chronic cough and should be considered in locations where it is common. Less common conditions that may present similarly include bronchopulmonary dysplasia and obliterative bronchiolitis. Chronic bronchitis may occur with normal airflow and in this situation it is not classified as COPD.
Keeping people from starting smoking is a key aspect of preventing COPD. The policies of governments, public health agencies, and antismoking organizations can reduce smoking rates by discouraging people from starting and encouraging people to stop smoking.Smoking bans in public areas and places of work are important measures to decrease exposure to secondhand smoke, and while many places have instituted bans, more are recommended.
In those who smoke, stopping smoking is the only measure shown to slow down the worsening of COPD. Even at a late stage of the disease, it can reduce the rate of worsening lung function and delay the onset of disability and death. Often, several attempts are required before long-term abstinence is achieved. Attempts over 5 years lead to success in nearly 40% of people.
Some smokers can achieve long-term smoking cessation through willpower alone. Smoking, however, is highly addictive, and many smokers need further support. The chance of quitting is improved with social support, engagement in a smoking cessation program, and the use of medications such as nicotine replacement therapy, bupropion, or varenicline. Combining smoking-cessation medication with behavioral therapy is more than twice as likely to be effective in helping people with COPD stop smoking, compared with behavioral therapy alone.
A number of measures have been taken to reduce the likelihood that workers in at-risk industries—such as coal mining, construction, and stonemasonry—will develop COPD. Examples of these measures include the creation of public policy, education of workers and management about the risks, promoting smoking cessation, checking workers for early signs of COPD, use of respirators, and dust control. Effective dust control can be achieved by improving ventilation, using water sprays and by using mining techniques that minimize dust generation. If a worker develops COPD, further lung damage can be reduced by avoiding ongoing dust exposure, for example by changing the work role.
Both indoor and outdoor air quality can be improved, which may prevent COPD or slow the worsening of existing disease. This may be achieved by public policy efforts, cultural changes, and personal involvement.
A number of developed countries have successfully improved outdoor air quality through regulations. This has resulted in improvements in the lung function of their populations. Those with COPD may experience fewer symptoms if they stay indoors on days when outdoor air quality is poor.
One key effort is to reduce exposure to smoke from cooking and heating fuels through improved ventilation of homes and better stoves and chimneys. Proper stoves may improve indoor air quality by 85%. Using alternative energy sources such as solar cooking and electrical heating is also effective. Using fuels such as kerosene or coal might be less bad than traditional biomass such as wood or dung.
No cure for COPD is known, but the symptoms are treatable and its progression can be delayed. The major goals of management are to reduce risk factors, manage stable COPD, prevent and treat acute exacerbations, and manage associated illnesses. The only measures that have been shown to reduce mortality are smoking cessation and supplemental oxygen. Stopping smoking decreases the risk of death by 18%. Other recommendations include influenza vaccination once a year, pneumococcal vaccination once every five years, and reduction in exposure to environmental air pollution. In those with advanced disease, palliative care may reduce symptoms, with morphine improving the feelings of shortness of breath.Noninvasive ventilation may be used to support breathing. Providing people with a personalized action plan, an educational session, and support for use of their action plan in the event of an exacerbation, reduces the number of hospital visits and encourages early treatment of exacerbations. When self-management interventions, such as taking corticosteriods and using supplemental oxygen, is combined with action plans, health-related quality of life is improved compared to usual care.
Pulmonary rehabilitation is a program of exercise, disease management, and counseling, coordinated to benefit the individual. In those who have had a recent exacerbation, pulmonary rehabilitation appears to improve the overall quality of life and the ability to exercise. If pulmonary rehabilitation improves mortality rates or hospital readmission rates is unclear. Pulmonary rehabilitation has been shown to improve the sense of control a person has over their disease, as well as their emotions.
The optimal exercise routine, use of noninvasive ventilation during exercise, and intensity of exercise suggested for people with COPD, is unknown. Performing endurance arm exercises improves arm movement for people with COPD, and may result in a small improvement in breathlessness. Performing arm exercises alone does not appear to improve quality of life. Breathing exercises in and of themselves appear to have a limited role.Pursed lip breathing exercises may be useful.Tai chi exercises appear to be safe to practice for people with COPD, and may be beneficial for pulmonary function and pulmonary capacity when compared to a regular treatment program. Tai Chi was not found to be more effective than other exercise intervention programs. Inspiratory and expiratory muscle training (IMT, EMT) is an effective method for improving activities of daily living (ADL). A combination of IMT and walking exercises at home may help limit breathlessness in cases of severe COPD. Additionally, the use of low amplitude high velocity joint mobilization together with exercise improves lung function and exercise capacity. The goal of spinal manipulation therapy (SMT) is to improve thoracic mobility in an effort to reduce the work on the lungs during respiration, to in turn increase exercise capacity as indicated by the results of a systemic medical review.
Being either underweight or overweight can affect the symptoms, degree of disability, and prognosis of COPD. People with COPD who are underweight can improve their breathing muscle strength by increasing their calorie intake. When combined with regular exercise or a pulmonary rehabilitation program, this can lead to improvements in COPD symptoms. Supplemental nutrition may be useful in those who are malnourished.
Inhaled bronchodilators are the primary medications used, and result in a small overall benefit. The two major types are β2 agonists and anticholinergics; both exist in long-acting and short-acting forms. They reduce shortness of breath, wheeze, and exercise limitation, resulting in an improved quality of life. It is unclear if they change the progression of the underlying disease.
In those with mild disease, short-acting agents are recommended on an as needed basis. In those with more severe disease, long-acting agents are recommended. Long-acting agents partly work by improving hyperinflation. If long-acting bronchodilators are insufficient, then inhaled corticosteroids are typically added. With respect to long-acting agents, if tiotropium (a long-acting anticholinergic) or long-acting β2 agonists (LABAs) are better is unclear, and trying each and continuing the one that worked best may be advisable. Both types of agent appear to reduce the risk of acute exacerbations by 15–25%. While both may be used at the same time, any benefit is of questionable significance.
Several short-acting β2 agonists are available, including salbutamol (albuterol) and terbutaline. They provide some relief of symptoms for four to six hours. LABAs such as salmeterol, formoterol, and indacaterol are often used as maintenance therapy. Some feel the evidence of benefits is limited, while others view the evidence of benefit as established. Long-term use appears safe in COPD with adverse effects include shakiness and heart palpitations. When used with inhaled steroids they increase the risk of pneumonia. While steroids and LABAs may work better together, it is unclear if this slight benefit outweighs the increased risks. There is some evidence that combined treatment of LABAs with long-acting muscarinic antagonists (LAMA), an anticholinergic, may result in less exacerbations, less pneumonia, an improvement in forced expiratory volume (FEV1%), and potential improvements in quality of life when compared to treatment with LABA and an inhaled corticosteriod. Indacaterol requires an inhaled dose once a day, and is as effective as the other long-acting β2 agonist drugs that require twice-daily dosing for people with stable COPD.
Two main anticholinergics are used in COPD, ipratropium and tiotropium. Ipratropium is a short-acting agent, while tiotropium is long-acting. Tiotropium is associated with a decrease in exacerbations and improved quality of life, and tiotropium provides those benefits better than ipratropium. It does not appear to affect mortality or the overall hospitalization rate. Anticholinergics can cause dry mouth and urinary tract symptoms. They are also associated with increased risk of heart disease and stroke.Aclidinium, another long-acting agent, reduces hospitalizations associated with COPD and improves quality of life. The LAMA umeclidinium bromide is another anticholinergic alternative. When compared to tiotropium, the LAMAs aclidinium, glycopyrronium, and umeclidinium appear to have a similar level of efficacy; with all four being more effective than placebo. Further research is needed comparing aclidinium to tiotropium.
Corticosteroids are usually used in inhaled form, but may also be used as tablets to treat and prevent acute exacerbations. While inhaled corticosteroids (ICSs) have not shown benefit for people with mild COPD, they decrease acute exacerbations in those with either moderate or severe disease. By themselves, they have no effect on overall one-year mortality. Whether they affect the progression of the disease is unknown. When used in combination with a LABA, they may decrease mortality compared to either ICSs or LABA alone. Inhaled steroids are associated with increased rates of pneumonia. Long-term treatment with steroid tablets is associated with significant side effects.
Supplemental oxygen is recommended in those with low oxygen levels at rest (a partial pressure of oxygen less than 50–55 mmHg or oxygen saturations of less than 88%). In this group of people, it decreases the risk of heart failure and death if used 15 hours per day and may improve people's ability to exercise. In those with normal or mildly low oxygen levels, oxygen supplementation may improve shortness of breath when given during exercise, but may not improve breathlessness during normal daily activities or affect the quality of life. A risk of fires and little benefit exist when those on oxygen continue to smoke. In this situation, some recommend against its use. During acute exacerbations, many require oxygen therapy; the use of high concentrations of oxygen without taking into account a person's oxygen saturations may lead to increased levels of carbon dioxide and worsened outcomes. In those at high risk of high carbon dioxide levels, oxygen saturations of 88–92% are recommended, while for those without this risk, recommended levels are 94–98%.
For those with very severe disease, surgery is sometimes helpful and may include lung transplantation or lung volume-reduction surgery, which involves removing the parts of the lung most damaged by emphysema, allowing the remaining, relatively good lung to expand and work better. It seems to be particularly effective if emphysema predominantly involves the upper lobe, but the procedure increases the risks of early death and adverse events. Lung transplantation is sometimes performed for very severe COPD, particularly in younger individuals.
Acute exacerbations are typically treated by increasing the use of short-acting bronchodilators. This commonly includes a combination of a short-acting inhaled beta agonist and anticholinergic. These medications can be given either via a metered-dose inhaler with a spacer or via a nebulizer, with both appearing to be equally effective. Nebulization may be easier for those who are more unwell.Oxygen supplementation can be useful. Excessive oxygen; however, can result in increased CO2 levels and a decreased level of consciousness.
Corticosteroids by mouth improve the chance of recovery and decrease the overall duration of symptoms. They work equally well as intravenous steroids but appear to have fewer side effects. Five days of steroids work as well as ten or fourteen. In those with a severe exacerbation, antibiotics improve outcomes. A number of different antibiotics may be used including amoxicillin, doxycycline and azithromycin; whether one is better than the others is unclear. The FDA recommends against the use of fluoroquinolones when other options are available due to higher risks of serious side effects. There is no clear evidence for those with less severe cases.
COPD usually gets gradually worse over time and can ultimately result in death. It is estimated that 3% of all disability is related to COPD. The proportion of disability from COPD globally has decreased from 1990 to 2010 due to improved indoor air quality primarily in Asia. The overall number of years lived with disability from COPD, however, has increased.
The rate at which COPD worsens varies with the presence of factors that predict a poor outcome, including severe airflow obstruction, little ability to exercise, shortness of breath, significant underweight or overweight, congestive heart failure, continued smoking, and frequent exacerbations. Long-term outcomes in COPD can be estimated using the BODE index which gives a score of zero to ten depending on FEV1, body-mass index, the distance walked in six minutes, and the modified MRC dyspnea scale. Significant weight loss is a bad sign. Results of spirometry are also a good predictor of the future progress of the disease but not as good as the BODE index.
Globally, as of 2010, COPD affected approximately 329 million people (4.8% of the population). The disease affects men and women almost equally, as there has been increased tobacco use among women in the developed world. The increase in the developing world between 1970 and the 2000s is believed to be related to increasing rates of smoking in this region, an increasing population and an aging population due to fewer deaths from other causes such as infectious diseases. Some developed countries have seen increased rates, some have remained stable and some have seen a decrease in COPD prevalence. The global numbers are expected to continue increasing as risk factors remain common and the population continues to get older.
Between 1990 and 2010 the number of deaths from COPD decreased slightly from 3.1 million to 2.9 million and became the fourth leading cause of death. In 2012 it became the third leading cause as the number of deaths rose again to 3.1 million. In some countries, mortality has decreased in men but increased in women. This is most likely due to rates of smoking in women and men becoming more similar. COPD is more common in older people; it affects 34–200 out of 1000 people older than 65 years, depending on the population under review.
In England, an estimated 0.84 million people (of 50 million) have a diagnosis of COPD; this translates into approximately one person in 59 receiving a diagnosis of COPD at some point in their lives. In the most socioeconomically deprived parts of the country, one in 32 people were diagnosed with COPD, compared with one in 98 in the most affluent areas. In the United States approximately 6.3% of the adult population, totaling approximately 15 million people, have been diagnosed with COPD. 25 million people may have COPD if currently undiagnosed cases are included. In 2011, there were approximately 730,000 hospitalizations in the United States for COPD. In the United States, COPD is estimated to be the third leading cause of death in 2011.
The word "emphysema" is derived from the Greekἐμφυσᾶνemphysan meaning "inflate" -itself composed of ἐν en, meaning "in", and φυσᾶν physan, meaning "breath, blast". The term chronic bronchitis came into use in 1808 while the term COPD is believed to have first been used in 1965. Previously it has been known by a number of different names, including chronic obstructive bronchopulmonary disease, chronic obstructive respiratory disease, chronic airflow obstruction, chronic airflow limitation, chronic obstructive lung disease, nonspecific chronic pulmonary disease, and diffuse obstructive pulmonary syndrome. The terms chronic bronchitis and emphysema were formally defined in 1959 at the CIBA guest symposium and in 1962 at the American Thoracic Society Committee meeting on Diagnostic Standards.
Early descriptions of probable emphysema include: in 1679 by T. Bonet of a condition of "voluminous lungs" and in 1769 by Giovanni Morgagni of lungs which were "turgid particularly from air". In 1721 the first drawings of emphysema were made by Ruysh. These were followed with pictures by Matthew Baillie in 1789 and descriptions of the destructive nature of the condition. In 1814 Charles Badham used "catarrh" to describe the cough and excess mucus in chronic bronchitis. René Laennec, the physician who invented the stethoscope, used the term "emphysema" in his book A Treatise on the Diseases of the Chest and of Mediate Auscultation (1837) to describe lungs that did not collapse when he opened the chest during an autopsy. He noted that they did not collapse as usual because they were full of air and the airways were filled with mucus. In 1842, John Hutchinson invented the spirometer, which allowed the measurement of vital capacity of the lungs. However, his spirometer could measure only volume, not airflow. Tiffeneau and Pinelli in 1947 described the principles of measuring airflow.
In 1953, Dr. George L. Waldbott, an American allergist, first described a new disease he named "smoker's respiratory syndrome" in the 1953 Journal of the American Medical Association. This was the first association between tobacco smoking and chronic respiratory disease.
Early treatments included garlic, cinnamon and ipecac, among others. Modern treatments were developed during the second half of the 20th century. Evidence supporting the use of steroids in COPD was published in the late 1950s. Bronchodilators came into use in the 1960s following a promising trial of isoprenaline. Further bronchodilators, such as salbutamol, were developed in the 1970s, and the use of LABAs began in the mid-1990s.
COPD has been referred to as "smoker's lung". People with emphysema have been known as "pink puffers" or "type A" due to their frequent pink complexion, fast respiratory rate and pursed lips, and people with chronic bronchitis have been referred to as "blue bloaters" or "type B" due to the often bluish color of the skin and lips from low oxygen levels and their ankle swelling. This terminology is no longer accepted as useful as most people with COPD have a combination of both emphysema and chronic bronchitis.
Many health systems have difficulty ensuring appropriate identification, diagnosis and care of people with COPD; Britain's Department of Health has identified this as a major issue for the National Health Service and has introduced a specific strategy to tackle these problems.
Globally, as of 2010, COPD is estimated to result in economic costs of $2.1 trillion, half of which occurring in the developing world. Of this total an estimated $1.9 trillion are direct costs such as medical care, while $0.2 trillion are indirect costs such as missed work. This is expected to more than double by the year 2030. In Europe, COPD represents 3% of healthcare spending. In the United States, costs of the disease are estimated at $50 billion, most of which is due to exacerbation. COPD was among the most expensive conditions seen in U.S. hospitals in 2011, with a total cost of about $5.7 billion.
Infliximab, an immune-suppressing antibody, has been tested in COPD; there was a possibility of harm with no evidence of benefit.
Roflumilast, cilomilast, and phosphodiesterase 4 inhibitors act as a bronchodilator and as an anti-inflammatory. They show promise in decreasing the rate of exacerbations, but do not appear to change a persons quality of life. Roflumilast and cilomilast may be associated with side effects such as gastrointestinal issues and weight loss. Sleep disturbances and mood disturbances related to roflumilast have also been reported. PDE4 is recommended to be used as an add-on therapy in case of failure of the standard COPD treatment during excerpations.
Several new long-acting agents are under development. Treatment with stem cells is under study. While there is tentative data that it is safe, and the animal data is promising, there is little human data as of 2017. The human data has shown poor results.
Research continues into the use of telehealthcare to treat people with COPD when they experience episodes of shortness of breath; treating people remotely may reduce the number of emergency-room visits and improve the person's quality of life.
Chronic obstructive pulmonary disease may occur in a number of other animals and may be caused by exposure to tobacco smoke. Most cases of the disease, however, are relatively mild. In horses it is known as recurrent airway obstruction, can be quite severe, and most often is linked to an allergic reaction to a fungus contained in contaminated hay or straw. COPD is also commonly found in old dogs.
^Mahler DA (May 2006). "Mechanisms and measurement of dyspnea in chronic obstructive pulmonary disease". Proceedings of the American Thoracic Society. 3 (3): 234–8. doi:10.1513/pats.200509-103SF. PMID16636091.
^Levack WM, Poot B, Weatherall M, Travers J, Levack WM (2015). "Interventions for sexual dysfunction in people with chronic obstructive pulmonary disease (COPD)". Reviews. doi:10.1002/14651858.CD011442.pub2.
^Brulotte CA, Lang ES (May 2012). "Acute exacerbations of chronic obstructive pulmonary disease in the emergency department". Emergency Medicine Clinics of North America. 30 (2): 223–47, vii. doi:10.1016/j.emc.2011.10.005. PMID22487106.
^ abKennedy SM, Chambers R, Du W, Dimich-Ward H (December 2007). "Environmental and occupational exposures: do they affect chronic obstructive pulmonary disease differently in women and men?". Proceedings of the American Thoracic Society. 4 (8): 692–4. doi:10.1513/pats.200707-094SD. PMID18073405.
^Halbert RJ, Natoli JL, Gano A, Badamgarav E, Buist AS, Mannino DM (September 2006). "Global burden of COPD: systematic review and meta-analysis". The European Respiratory Journal. 28 (3): 523–32. doi:10.1183/09031936.06.00124605. PMID16611654.
^ abcdefgVestbo J (2013). "Management of Exacerbations"(PDF). Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease. Global Initiative for Chronic Obstructive Lung Disease. pp. 39–45.[dead link]
^Aleva FE, Voets LW, Simons SO, de Mast Q, van der Ven AJ, Heijdra YF (March 2017). "Prevalence and Localization of Pulmonary Embolism in Unexplained Acute Exacerbations of COPD: A Systematic Review and Meta-analysis". Chest. 151 (3): 544–554. doi:10.1016/j.chest.2016.07.034. PMID27522956.
^Murphy DM, Fishman AP (2008). "Chapter 53". Fishman's Pulmonary Diseases and Disorders (4th ed.). McGraw-Hill. p. 913. ISBN0-07-145739-9.
^ abCalverley PM, Koulouris NG (January 2005). "Flow limitation and dynamic hyperinflation: key concepts in modern respiratory physiology". The European Respiratory Journal. 25 (1): 186–99. doi:10.1183/09031936.04.00113204. PMID15640341.
^O'Donnell DE (April 2006). "Hyperinflation, dyspnea, and exercise intolerance in chronic obstructive pulmonary disease". Proceedings of the American Thoracic Society. 3 (2): 180–4. doi:10.1513/pats.200508-093DO. PMID16565429.
^ abCooper CB (October 2006). "The connection between chronic obstructive pulmonary disease symptoms and hyperinflation and its impact on exercise and function". The American Journal of Medicine. 119 (10 Suppl 1): 21–31. doi:10.1016/j.amjmed.2006.08.004. PMID16996896.
^Kopsaftis, Z; Wood-Baker, R; Poole, P (26 June 2018). "Influenza vaccine for chronic obstructive pulmonary disease (COPD)". The Cochrane Database of Systematic Reviews. 6: CD002733. doi:10.1002/14651858.CD002733.pub3. PMID29943802.
^Teo, E; Lockhart, K; Purchuri, SN; Pushparajah, J; Cripps, AW; van Driel, ML (19 June 2017). "Haemophilus influenzae oral vaccination for preventing acute exacerbations of chronic bronchitis and chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews. 6: CD010010. doi:10.1002/14651858.CD010010.pub3. PMID28626902.
^Jiménez-Ruiz CA, Fagerström KO (March 2013). "Smoking cessation treatment for COPD smokers: the role of counselling". Monaldi Archives for Chest Disease = Archivio Monaldi Per Le Malattie Del Torace. 79 (1): 33–7. doi:10.4081/monaldi.2013.107. PMID23741944.
^van Eerd EA, van der Meer RM, van Schayck OC, Kotz D (August 2016). "Smoking cessation for people with chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews (8): CD010744. doi:10.1002/14651858.CD010744.pub2. PMID27545342.
^ abDrummond MB, Dasenbrook EC, Pitz MW, Murphy DJ, Fan E (November 2008). "Inhaled corticosteroids in patients with stable chronic obstructive pulmonary disease: a systematic review and meta-analysis". JAMA. 300 (20): 2407–16. doi:10.1001/jama.2008.717. PMID19033591.
^ abCarlucci A, Guerrieri A, Nava S (December 2012). "Palliative care in COPD patients: is it only an end-of-life issue?". European Respiratory Review. 21 (126): 347–54. doi:10.1183/09059180.00001512. PMID23204123.
^Howcroft M, Walters EH, Wood-Baker R, Walters JA (December 2016). "Action plans with brief patient education for exacerbations in chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews. 12: CD005074. doi:10.1002/14651858.CD005074.pub4. PMID27990628.
^Lenferink A, Brusse-Keizer M, van der Valk PD, Frith PA, Zwerink M, Monninkhof EM, van der Palen J, Effing TW (August 2017). "Self-management interventions including action plans for exacerbations versus usual care in patients with chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews. 8: CD011682. doi:10.1002/14651858.CD011682.pub2. PMID28777450.
^ abPuhan MA, Gimeno-Santos E, Cates CJ, Troosters T (December 2016). "Pulmonary rehabilitation following exacerbations of chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews. 12: CD005305. doi:10.1002/14651858.CD005305.pub4. PMID27930803.
^ abZainuldin R, Mackey MG, Alison JA (November 2011). "Optimal intensity and type of leg exercise training for people with chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews (11): CD008008. doi:10.1002/14651858.CD008008.pub2. PMID22071841.
^McCarthy B, Casey D, Devane D, Murphy K, Murphy E, Lacasse Y (February 2015). "Pulmonary rehabilitation for chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews. 2 (2): CD003793. doi:10.1002/14651858.CD003793.pub3. PMID25705944.
^McNamara RJ, McKeough ZJ, McKenzie DK, Alison JA (December 2013). "Water-based exercise training for chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews (12): CD008290. doi:10.1002/14651858.CD008290.pub2. PMID24353107.
^Menadue C, Piper AJ, van 't Hul AJ, Wong KK (May 2014). "Non-invasive ventilation during exercise training for people with chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews (5): CD007714. doi:10.1002/14651858.CD007714.pub2. PMID24823712.
^Ferreira IM, Brooks D, White J, Goldstein R (December 2012). Ferreira IM, ed. "Nutritional supplementation for stable chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews. 12: CD000998. doi:10.1002/14651858.CD000998.pub3. PMID23235577.
^van Dijk WD, van den Bemt L, van Weel C (2013). "Megatrials for bronchodilators in chronic obstructive pulmonary disease (COPD) treatment: time to reflect". Journal of the American Board of Family Medicine. 26 (2): 221–4. doi:10.3122/jabfm.2013.02.110342. PMID23471939.
^Kew KM, Dias S, Cates CJ (March 2014). "Long-acting inhaled therapy (beta-agonists, anticholinergics and steroids) for COPD: a network meta-analysis". The Cochrane Database of Systematic Reviews (3): CD010844. doi:10.1002/14651858.CD010844.pub2. PMID24671923.
^ abFarne HA, Cates CJ (October 2015). "Long-acting beta2-agonist in addition to tiotropium versus either tiotropium or long-acting beta2-agonist alone for chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews (10): CD008989. doi:10.1002/14651858.CD008989.pub3. PMID26490945.
^ abcdefghVestbo J (2013). "Therapeutic Options"(PDF). Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease. Global Initiative for Chronic Obstructive Lung Disease. pp. 19–30.[dead link]
^ abCave AC, Hurst MM (May 2011). "The use of long acting β₂-agonists, alone or in combination with inhaled corticosteroids, in chronic obstructive pulmonary disease (COPD): a risk-benefit analysis". Pharmacology & Therapeutics. 130 (2): 114–43. doi:10.1016/j.pharmthera.2010.12.008. PMID21276815.
^Spencer S, Karner C, Cates CJ, Evans DJ (December 2011). Spencer S, ed. "Inhaled corticosteroids versus long-acting beta(2)-agonists for chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews (12): CD007033. doi:10.1002/14651858.CD007033.pub3. PMID22161409.
^Wang J, Nie B, Xiong W, Xu Y (April 2012). "Effect of long-acting beta-agonists on the frequency of COPD exacerbations: a meta-analysis". Journal of Clinical Pharmacy and Therapeutics. 37 (2): 204–11. doi:10.1111/j.1365-2710.2011.01285.x. PMID21740451.
^ abGeake JB, Dabscheck EJ, Wood-Baker R, Cates CJ (January 2015). "Indacaterol, a once-daily beta2-agonist, versus twice-daily beta₂-agonists or placebo for chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews. 1: CD010139. doi:10.1002/14651858.CD010139.pub2. PMID25575340.
^Horita N, Goto A, Shibata Y, Ota E, Nakashima K, Nagai K, Kaneko T (February 2017). "Long-acting muscarinic antagonist (LAMA) plus long-acting beta-agonist (LABA) versus LABA plus inhaled corticosteroid (ICS) for stable chronic obstructive pulmonary disease (COPD)". The Cochrane Database of Systematic Reviews. 2: CD012066. doi:10.1002/14651858.CD012066.pub2. PMID28185242.
^Cheyne L, Irvin-Sellers MJ, White J (September 2015). "Tiotropium versus ipratropium bromide for chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews (9): CD009552. doi:10.1002/14651858.CD009552.pub3. PMID26391969.
^Singh S, Loke YK, Furberg CD (September 2008). "Inhaled anticholinergics and risk of major adverse cardiovascular events in patients with chronic obstructive pulmonary disease: a systematic review and meta-analysis". JAMA. 300 (12): 1439–50. doi:10.1001/jama.300.12.1439. PMID18812535.
^Jones P (April 2013). "Aclidinium bromide twice daily for the treatment of chronic obstructive pulmonary disease: a review". Advances in Therapy. 30 (4): 354–68. doi:10.1007/s12325-013-0019-2. PMID23553509.
^Cazzola M, Page CP, Matera MG (June 2013). "Aclidinium bromide for the treatment of chronic obstructive pulmonary disease". Expert Opinion on Pharmacotherapy. 14 (9): 1205–14. doi:10.1517/14656566.2013.789021. PMID23566013.
^Ni H, Htet A, Moe S (June 2017). "Umeclidinium bromide versus placebo for people with chronic obstructive pulmonary disease (COPD)". The Cochrane Database of Systematic Reviews. 6: CD011897. doi:10.1002/14651858.CD011897.pub2. PMID28631387.
^Chinet T, Dumoulin J, Honore I, Braun JM, Couderc LJ, Febvre M, Mangiapan G, Maurer C, Serrier P, Soyez F, Terrioux P, Jebrak G (December 2016). "[The place of inhaled corticosteroids in COPD]". Revue Des Maladies Respiratoires. 33 (10): 877–891. doi:10.1016/j.rmr.2015.11.009. PMID26831345.
^Dong YH, Lin HH, Shau WY, Wu YC, Chang CH, Lai MS (January 2013). "Comparative safety of inhaled medications in patients with chronic obstructive pulmonary disease: systematic review and mixed treatment comparison meta-analysis of randomised controlled trials". Thorax. 68 (1): 48–56. doi:10.1136/thoraxjnl-2012-201926. PMID23042705.
^Nannini LJ, Poole P, Milan SJ, Kesterton A (August 2013). "Combined corticosteroid and long-acting beta(2)-agonist in one inhaler versus inhaled corticosteroids alone for chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews. 8 (8): CD006826. doi:10.1002/14651858.CD006826.pub2. PMID23990350.
^Kew KM, Seniukovich A (March 2014). "Inhaled steroids and risk of pneumonia for chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews. 3 (3): CD010115. doi:10.1002/14651858.CD010115.pub2. PMID24615270.
^Mammen MJ, Sethi S (2012). "Macrolide therapy for the prevention of acute exacerbations in chronic obstructive pulmonary disease". Polskie Archiwum Medycyny Wewnetrznej. 122 (1-2): 54–9. PMID22353707.
^ abHerath SC, Poole P (November 2013). "Prophylactic antibiotic therapy for chronic obstructive pulmonary disease (COPD)". The Cochrane Database of Systematic Reviews. 11 (11): CD009764. doi:10.1002/14651858.CD009764.pub2. PMID24288145.
^Simoens S, Laekeman G, Decramer M (May 2013). "Preventing COPD exacerbations with macrolides: a review and budget impact analysis". Respiratory Medicine. 107 (5): 637–48. doi:10.1016/j.rmed.2012.12.019. PMID23352223.
^Barr RG, Rowe BH, Camargo CA (2003). Barr RG, ed. "Methylxanthines for exacerbations of chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews (2): CD002168. doi:10.1002/14651858.CD002168. PMID12804425.
^Poole P, Chong J, Cates CJ (July 2015). "Mucolytic agents versus placebo for chronic bronchitis or chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews. 7 (7): CD001287. doi:10.1002/14651858.CD001287.pub5. PMID26222376.
^ abSalpeter S, Ormiston T, Salpeter E (October 2005). "Cardioselective beta-blockers for chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews (4): CD003566. doi:10.1002/14651858.CD003566.pub2. PMID16235327.
^Ni Y, Shi G, Wan H (2012). "Use of cardioselective β-blockers in patients with chronic obstructive pulmonary disease: a meta-analysis of randomized, placebo-controlled, blinded trials". The Journal of International Medical Research. 40 (6): 2051–65. doi:10.1177/030006051204000602. PMID23321161.
^Bradley JM, O'Neill B (October 2005). Bradley JM, ed. "Short-term ambulatory oxygen for chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews. 4 (4): CD004356. doi:10.1002/14651858.CD004356.pub3. PMID16235359.
^Ekström M, Ahmadi Z, Bornefalk-Hermansson A, Abernethy A, Currow D (November 2016). "Oxygen for breathlessness in patients with chronic obstructive pulmonary disease who do not qualify for home oxygen therapy". The Cochrane Database of Systematic Reviews. 11: CD006429. doi:10.1002/14651858.CD006429.pub3. PMID27886372.
^Walters JA, Tan DJ, White CJ, Wood-Baker R (March 2018). "Different durations of corticosteroid therapy for exacerbations of chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews. 3: CD006897. doi:10.1002/14651858.CD006897.pub4. PMID29553157.
^ abVollenweider DJ, Jarrett H, Steurer-Stey CA, Garcia-Aymerich J, Puhan MA (December 2012). Vollenweider DJ, ed. "Antibiotics for exacerbations of chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews. 12: CD010257. doi:10.1002/14651858.CD010257. PMID23235687.
^ abMurray CJ, Vos T, Lozano R, Naghavi M, Flaxman AD, Michaud C, et al. (December 2012). "Disability-adjusted life years (DALYs) for 291 diseases and injuries in 21 regions, 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet. 380 (9859): 2197–223. doi:10.1016/S0140-6736(12)61689-4. PMID23245608.
^ abVos T, Flaxman AD, Naghavi M, Lozano R, Michaud C, Ezzati M, et al. (December 2012). "Years lived with disability (YLDs) for 1160 sequelae of 289 diseases and injuries 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet. 380 (9859): 2163–96. doi:10.1016/S0140-6736(12)61729-2. PMID23245607.
^Lozano R, Naghavi M, Foreman K, Lim S, Shibuya K, Aboyans V, et al. (December 2012). "Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: a systematic analysis for the Global Burden of Disease Study 2010". Lancet. 380 (9859): 2095–128. doi:10.1016/S0140-6736(12)61728-0. PMID23245604.
^McQualter JL, Anthony D, Bozinovski S, Prêle CM, Laurent GJ (November 2014). "Harnessing the potential of lung stem cells for regenerative medicine". The International Journal of Biochemistry & Cell Biology. 56: 82–91. doi:10.1016/j.biocel.2014.10.012. PMID25450456.
^Tzouvelekis A, Ntolios P, Bouros D (2013). "Stem cell treatment for chronic lung diseases". Respiration; International Review of Thoracic Diseases. 85 (3): 179–92. doi:10.1159/000346525. PMID23364286.
^Tzouvelekis A, Laurent G, Bouros D (February 2013). "Stem cell therapy in chronic obstructive pulmonary disease. Seeking the Prometheus effect". Current Drug Targets. 14 (2): 246–52. doi:10.2174/1389450111314020009. PMID23256721.
^Gompelmann D, Eberhardt R, Herth FJ (August 2015). "Novel Endoscopic Approaches to Treating Chronic Obstructive Pulmonary Disease and Emphysema". Seminars in Respiratory and Critical Care Medicine. 36 (4): 609–15. doi:10.1055/s-0035-1555614. PMID26238645.
^Gøtzsche PC, Johansen HK (September 2016). "Intravenous alpha-1 antitrypsin augmentation therapy for treating patients with alpha-1 antitrypsin deficiency and lung disease". The Cochrane Database of Systematic Reviews. 9: CD007851. doi:10.1002/14651858.CD007851.pub3. PMID27644166.
^McLean S, Nurmatov U, Liu JL, Pagliari C, Car J, Sheikh A (July 2011). "Telehealthcare for chronic obstructive pulmonary disease". The Cochrane Database of Systematic Reviews (7): CD007718. doi:10.1002/14651858.CD007718.pub2. PMID21735417.