1. Your Name/Credentials
Understanding COPD
Your Name/Credentials
Job Title
Organization

2. © 2017 Global Initiative for Chronic Obstructive Lung Disease
COPD Definition
Chronic Obstructive Pulmonary Disease (COPD) is a common, preventable and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases.
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3. Definition and Overview
̵̵ With aging, the FEV1 naturally decreases. This graph shows that, with COPD, the FEV1 decreases more than usual.
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4. Definition and Overview
OVERALL KEY POINTS (1 of 2):
Chronic Obstructive Pulmonary Disease (COPD) is a common, preventable and treatable disease that is characterized by persistent respiratory symptoms and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases.
The most common respiratory symptoms include dyspnea, cough and/or sputum production. These symptoms may be under-reported by patients.
The main risk factor for COPD is tobacco smoking but other environmental exposures such as biomass fuel exposure and air pollution may contribute.
Key Points:
COPD is a progressive disease characterized by impaired airflow and includes both emphysema and chronic bronchitis.
Even on days that patients feel well, they experience breathlessness at levels of exercise that unaffected people could carry out without any breathing limitations.
Cough may start out intermittent but then becomes chronic, occurring every day and throughout the day, and often precedes airflow limitation by many years.
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5. Definition and Overview
OVERALL KEY POINTS (2 of 2):
Besides exposures, host factors predispose individuals to develop COPD. These include genetic abnormalities, abnormal lung development and accelerated aging.
COPD may be punctuated by periods of acute worsening of respiratory symptoms, called exacerbations.
In most patients, COPD is associated with significant concomitant chronic diseases, which increase its morbidity and mortality.
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6. Spectrum of Disease COPD Chronic Bronchitis Emphysema Mixed Disease
Key Points:
COPD is a progressive disease characterized by impaired airflow, which is not fully reversible, and by dyspnea on exertion.
It is associated with an abnormal inflammatory process of the lungs to tobacco smoke or other noxious particles or gases.
COPD includes chronic bronchitis and emphysema.
COPD is a disease of airflow obstruction with varying clinical presentations of the two components.
Asthma is also a disease of airflow obstruction, but is a different disease than COPD.
The airflow obstruction in asthma is generally intermittent and reversible; in COPD, the airflow limitation is only partially reversible.
A small percentage of patients have both COPD and asthma.
Asthma

7. Chronic Obstructive Pulmonary Disease (COPD)
COPD is currently the fourth leading cause of death in the world.1
COPD is projected to be the 3rd leading cause of death by
More than 3 million people died of COPD in 2012 accounting for 6% of all deaths globally.
Globally, the COPD burden is projected to increase in coming decades because of continued exposure to COPD risk factors and aging of the population.
Lozano R, Naghavi M, Foreman K, et al. 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 Lancet 2012; 380(9859):
Mathers CD, Loncar D. Projections of global mortality and burden of disease from 2002 to PLoS Med 2006; 3(11): e442.
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8. © 2017 Global Initiative for Chronic Obstructive Lung Disease
Prevalence
Estimated 384 million COPD cases in 2010.
Estimated global prevalence of 11.7% (95% CI 8.4%–15.0%).
Three million deaths annually.
With increasing prevalence of smoking in developing countries, and aging populations in high-income countries, the prevalence of COPD is expected to rise over the next 30 years.
By 2030 predicted 4.5 million COPD related deaths annually.
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9. Economic and Social Burden
COPD is associated with significant economic burden.
COPD exacerbations account for the greatest proportion of the total COPD burden.
European Union:
Direct costs of respiratory disease ~6% of the total healthcare budget
COPD accounting for 56% (38.6 billion Euros) of the cost of respiratory disease.
USA:
Direct costs of COPD are $32 billion
Indirect costs $20.4 billion.
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10. Factors that influence disease progression
Genetic factors
Age and gender
Lung growth and development
Exposure to particles
Socioeconomic status
Asthma & airway hyper-reactivity
Chronic bronchitis
Infections
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11. Risk Factors Cigarette smoking is major risk factor
80%-90% of patients have a smoking history of at least pk/yrs (Pk/yr=number of packs per day x number of years smoking)
Occupational and environmental exposures
Other:
Proteases/inflammation
Repetitive bacterial/viral infections
Genetics, especially 1-antitrypsin deficiency
Key Points:
The major risk factor for COPD is cigarette smoking
The calculation of pack years allows for a standard reference point reflecting smoking history
Most people who develop COPD have at least a pack-year history of smoking
There are other environmental and occupational exposures that are risk factors, especially living or working in the environment of a smoker (secondhand smoke)
NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease. April 2001; (Updated 2003).
American Thoracic Society Statement Statement. Am J Respir Crit Care Med. 1995;152(suppl 5):S77-S120.
Source: NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease. April 2001; (Updated 2003).
Source: American Thoracic Society Statement Statement. Am J Respir Crit Care Med. 1995;152(suppl 5):S77-S120.

12. Inflammatory Process in COPD
Macrophages in
respiratory
tract
activates
Neutrophils
release
release
Key Points:
Inflammation in COPD is associated with edema of the mucosa, hypersecretion of mucus, and fibrosis. The latter develops after chronic inhalation of toxic particles, the most important of these being from tobacco smoke.
The parenchymal destruction is characterized by loss of alveolar attachments, destruction of alveolar walls, and a decrease in the elastic recoil that keeps the airways open during expiration. Airways collapse.
NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease. Bethesda, Md: National Institutes of Health; April 2001 (updated 2003). NHLBI/WHO Workshop Report, NIH publication 2701.
American Thoracic Society Statement Statement. Standards for the diagnosis and care of patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1995;152(suppl 5):S77-S120.
The National Lung Health Education Program Executive Committee. Strategies in preserving lung health and preventing COPD and associated diseases: the National Lung Health Education Program (NLHEP). Chest. 1998;113(suppl 2):123S-163S.
Proteases
Parenchymal Destruction
result in
Source: Adapted with permission from NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease. April 2001(Updated 2003). Barnes PJ. Chronic Obstructive Pulmonary Disease. N Engl J Med. 2000;343:

13. Mechanisms of Airflow Limitation in COPD1
In the peripheral airways of patients with COPD, there is airflow limitation due to a variable mixture of loss of alveolar attachments, inflammatory obstruction of the airway, and luminal obstruction with mucus.
Barnes PJ. Chronic obstructive pulmonary disease. N Engl J Med. 2000; 343:
1Barnes PJ. Chronic obstructive pulmonary disease. N Engl J Med. 2000;343: Used with permission.

14. Consequences of Airflow Limitation
Lung Hyperinflation
Gas Trapping
Exacerbations
Dyspnea
The slide represents a summary of all the aforementioned concepts.
As destruction of the parenchyma and airflow limitation progresses, hyperinflation and gas trapping increase.
These mechanical derangements lead to breathlessness upon exertion and eventually while at rest, as well as diminished ability to participate in physical activities.
Patients decrease their activity as a result of the unpleasant sensation of dyspnea and as a result become deconditioned, which leads to further impairment in exercise tolerance because of the high oxygen requirements of deconditioned muscles.
As the effects on the lungs progress, dyspnea will become present with minimal effort or even at rest.
Ultimately, quality of life will deteriorate to the point at which patients may become oxygen-dependent and finally completely immobilized.
Exacerbations are periodic worsenings of COPD and are more common as the disease progresses.
Activity
Exercise Tolerance

15. Diagnosis and Initial Assessment
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16. Diagnosis and Initial Assessment
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17. COPDfoundation.org

18. Spirometry Spirometry is “the gold standard”
most reproducible, standardized, objective way of measuring airflow limitation
Expiratory airflow limitation is the hallmark physiologic change of COPD
FEV1, FVC, FEV1/FVC all decrease
FEV1 = forced expiratory volume in 1 second (the volume of air that is forcefully expelled in the first second of a forced expiration starting from full inspiration). A patient with unobstructed airflow should be able to exhale the majority of air (80%) from their lungs within the first second of forced expiration.
FVC = forced vital capacity. FVC is the maximum volume of air in liters that can be forcibly and rapidly exhaled following a maximum inspiration. A “normal” FVC in a healthy adult is approximately 80% of predicted or greater.
Predicted values are determined by a combination of factors including age, gender, height, and race.
Airway obstruction is characterized by a decrease in the FEV1/FVC ratio. A ratio of less than 70% in adults indicates airway obstruction.
If FEV1 returns to the predicted normal range after administration of a bronchodilator, the patient’s airflow limitation is likely caused by asthma.
Spirometry should be performed again after administering a bronchodilator such as albuterol to ascertain postbronchodilator readings and determine the amount of reversibility.
Patients with COPD commonly have significant improvements in spirometry following inhaling bronchodilators, but will not return to a normal range.
American Thoracic Society Statement Statement. Am J Respir Crit Care Med. 1995;152(suppl 5):S77-S120.
Source: NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease. April 2001 (Updated 2003).
Source: Petty TL, Enright PL. Simple office spirometry for primary care practitioners.
Source: American Thoracic Society Statement Statement. Am J Respir Crit Care Med. 1995;152(suppl 5):S77-S120.
Source: NHLBI/WHO Global Initiative for Chronic Obstructive Lung Disease. April 2001 (Updated 2003).
Source: Petty TL, Enright PL. Simple office spirometry for primary care practitioners. Available at

19. Diagnosis of COPD Role of Spirometry
Assessment of Severity of Airflow Obstruction
Follow-up Assessment
Therapeutic decisions
Pharmacogical in selected circumstances (e.g. discrepancy between spirometry and level of symptoms).
Consider alternative diagnoses when symptoms are disproportionate to degree of airflow obstruction.
Non-Pharmacological (e.g. interventional procedures).
Identification of rapid decline.
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20. © 2017 Global Initiative for Chronic Obstructive Lung Disease
Spirometry
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21. Classification of severity of airflow limitation
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22. Assessment of Exacerbation Risk
COPD exacerbations defined: An acute worsening of respiratory symptoms that result in additional therapy.
Classified as:
Mild (treated with SABDs only)
Moderate (treated with SABDs plus antibiotics and/or oral corticosteroids) or
Severe (patient requires hospitalization or visits the emergency room). Severe exacerbations may also be associated with acute respiratory failure.
Blood eosinophil count may also predict exacerbation rates (in patients treated with LABA without ICS).
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23. Differential Diagnosis
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24. Management of Stable COPD
No medication has been shown to reverse the decline in lung function
Pharmacotherapy aimed at reducing symptoms
Treatments that improve survival for COPD
Smoking cessation
Pulmonary rehabilitation
Oxygen
Beta Agonists short-acting: albuterol (proventil), levalbuterol (xopenex), bitolterol (tornalate), pirbuterol (Maxair), terbutaline (brethaire)
Beta agonists long-acting: salmeterol (serevent), formoterol (foradil)
Anticholinergics short-acting: ipatropium (atrovent), ipatropium + albuterol (combivent)
Anticholinergics long-acting: tiotropium (spiriva)
Steroids: flovent, pulmicort, azmacort
Combos: long-acting beta agonist w/steroid advair, symbicort
For patients with COPD, health education can play a role in improving skills, ability to cope with illness, and health status. All COPD patients benefit from exercise training programs, improving with respect to both exercise tolerance and symptoms of dyspnea and fatigue.

25. Evidence Supporting Prevention & Maintenance Therapy
OVERALL KEY POINTS (1 of 3):
Smoking cessation is key. Pharmacotherapy and nicotine replacement reliably increase long-term smoking abstinence rates.
The effectiveness and safety of e-cigarettes as a smoking cessation aid is uncertain at present.
Pharmacologic therapy can reduce COPD symptoms, reduce the frequency and severity of exacerbations, and improve health status and exercise tolerance.
Each pharmacologic treatment regimen should be individualized and guided by the severity of symptoms, risk of exacerbations, side-effects, comorbidities, drug availability and cost, and the patient’s response, preference and ability to use various drug delivery devices.
Inhaler technique needs to be assessed regularly.
© 2017 Global Initiative for Chronic Obstructive Lung Disease

26. Evidence Supporting Prevention & Maintenance Therapy
OVERALL KEY POINTS (2 of 3):
Influenza vaccination decreases the incidence of lower respiratory tract infections.
Pneumococcal vaccination decreases lower respiratory tract infections.
Pulmonary rehabilitation improves symptoms, quality of life, and physical and emotional participation in everyday activities.
In patients with severe resting chronic hypoxemia, long-term oxygen therapy improves survival.
In patients with stable COPD and resting or exercise-induced moderate desaturation, long-term oxygen treatment should not be prescribed routinely. However, individual patient factors must be considered when evaluating the patient’s need for supplemental oxygen.
© 2017 Global Initiative for Chronic Obstructive Lung Disease

27. Evidence Supporting Prevention & Maintenance Therapy
OVERALL KEY POINTS (3 of 3):
In patients with severe chronic hypercapnia and a history of hospitalization for acute respiratory failure, long-term non-invasive ventilation may decrease mortality and prevent re-hospitalization.
In select patients with advanced emphysema refractory to optimized medical care, surgical or bronchoscopic interventional treatments may be beneficial.
Palliative approaches are effective in controlling symptoms in advanced COPD.
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28. © 2017 Global Initiative for Chronic Obstructive Lung Disease
Smoking Cessation
Smoking cessation has the greatest capacity to influence the natural history of COPD.
If effective resources and time are dedicated to smoking cessation, long-term quit success rates of up to 25% can be achieved.
© 2017 Global Initiative for Chronic Obstructive Lung Disease

29. COPD: Smoking Cessation and FEV125 50 75
Age (y)
FEV1 (% of value at age 25)
100
Death
Disability
Stopped smoking at 65
Stopped smoking at 45
Smoked regularly and
susceptible to its effects
Never smoked or not
susceptible to smoke
As the graph on this slide illustrates, the rate of decline in FEV1 and progressions to disability and death are accelerated in smokers. Although the majority of lung function lost after years of smoking is never regained, progression to disability and death is delayed in people who stop smoking.
With smoking cessation before age 40, the subsequent loss in lung function is similar to that observed in healthy nonsmokers.
Higgins et al found that FEV1 levels were 7% lower in smokers who quit between the ages of 40 to 60 years and 14% lower in smokers older than 60 years compared with people who had never smoked. For example, in a smoker who quits smoking 10 years before diagnosis of COPD, the damage cannot be reversed, but it can slow the decline of lung function. Smokers who quit even after age 60 to 65 years have better pulmonary function than continuing smokers.
While pulmonary function as measured by FEV1 normally declines with age by about 30 mL per year from its peak at age 25 years, the rate of decline in smokers is on average 45 to 65 mL per year.
Some smokers may not lose lung function, while others may lose between 90 mL and 120 mL per year. About 20% of smokers are particularly sensitive to the effects of cigarette smoke and experience yearly declines in FEV1 of 150 mL to 200 mL.
In general, the more cigarettes one smokes, the greater the decline in respiratory function. Fortunately, those who quit smoking at any age have a slower rate of functional decline and better pulmonary function than those who continue to smoke.
Fletcher C, Peto R. The natural history of chronic airflow obstruction. B Med J. 1977;1: Used with permission from BMJ Publishing Group.
Source: Fletcher C. The natural history of chronic airflow obstruction. BMJ
Source: Used with permission from BMJ Publishing Group.

30. Pharmacologic Therapy
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31. Pharmacologic Therapy
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32. Bronchodilators in Stable COPD
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33. Anti-inflammatory Therapy in Stable COPD
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34. Non-Pharmacologic Treatment
Education and self-management
Physical activity
Pulmonary rehabilitation programs
Exercise training
Self-management education
End of life and palliative care
Nutritional support
Vaccination
Oxygen therapy
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35. © 2017 Global Initiative for Chronic Obstructive Lung Disease
Smoking Cessation
Smoking cessation has the greatest capacity to influence the natural history of COPD.
If effective resources and time are dedicated to smoking cessation, long-term quit success rates of up to 25% can be achieved.
© 2017 Global Initiative for Chronic Obstructive Lung Disease

36. Non-Pharmacologic Treatment
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37. Conclusions
COPD is a common disease for which morbidity and mortality continue to increase
COPD is increasing in women and being seen at a younger age
Smoking cessation, rehabilitation, and oxygen are effective in improving daily life and survival
Pharmacologic therapy is important for symptom relief
COPD is a common disease for which morbidity and mortality continue to increase. The disease is increasing in women and appearing at a younger age. The pathologic changes of COPD lead to physiologic impairment characterized by airflow limitation, gas trapping, and hyperinflation. The physiologic abnormalities are responsible for the clinical manifestations of COPD. Cholinergic mechanisms contribute to the physiologic changes in COPD, predominantly resting cholinergic tone, which can be effectively treated with inhaled anticholinergic therapy. The use of fixed combinations of anticholinergics and b-agonists provides improvements above the individual compounds in the treatment of COPD.