2. 2008 Canadian COPD Guidelines Definition of COPD: “Chronic obstructive pulmonary disease (COPD) is a respiratory disorder largely caused by smoking which is characterized by progressive partially reversible airway obstruction, systemic manifestations, and increasing severity and frequency of exacerbations.”

3. Old Definitions: Chronic bronchitis= chronic cough and sputum production for at least 3 months in 2 consecutive years. Note: this is a clinical definition Emphysema= Pathological loss of lung tissue distal to the terminal bronchiole. Note: this is a pathologic definition

4. Emphysema Chronic bronchitis Asthma COPD- classification of patients:

5. Progressive Worsening (with exacerbations) Stable (with exacerbations) Disease Course PersistentIntermittent and VariableClinical Symptoms Never NormalizesOften NormalizesSpirometry InfrequentOftenAllergies OftenInfrequentSputum Production Smokers/past smokersUsually non-smokersSmoking History Usually > 40 yearsUsually < 40 yearsAge of Onset COPDAsthma Can Respir J 2003; 10(Suppl A): 11A-33A. 2003 Canadian COPD Guidelines COPD is Different From Asthma !

6. Percent Change in Age-Adjusted Death Rates, U.S., 1965-1998 0 0 0.5 1.0 1.5 2.0 2.5 3.0 Proportion of 1965 Rate 1965 - 1998 –59% –64% –35% +163% –7% Coronary Heart Disease Coronary Heart Disease Stroke Other CVD COPD All Other Causes All Other Causes

7. Facts About COPD  Cigarette smoking is the primary cause of COPD.  In the US 47.2 million people (28% of men and 23% of women) smoke.  The WHO estimates 1.1 billion smokers worldwide, increasing to 1.6 billion by 2025. In low- and middle-income countries, rates are increasing at an alarming rate.  Cigarette smoking is the primary cause of COPD.  In the US 47.2 million people (28% of men and 23% of women) smoke.  The WHO estimates 1.1 billion smokers worldwide, increasing to 1.6 billion by 2025. In low- and middle-income countries, rates are increasing at an alarming rate.

11. Facts About COPD  In India, it is estimated that 400-550 thousand premature deaths can be attributed annually to use of biomass fuels, placing indoor air pollution as a major risk factor in the country.

12. Exposure to Biomass Fuels is a Major Risk Factor For COPD in Developing Countries (especially in women).

14. Buist et al, Lancet 2006

17. Pathogenesis of COPD NOXIOUS AGENT (tobacco smoke, pollutants, occupational agent) COPD Genetic factors Respiratory infection Other

18. Lung inflammation in COPD, activation of neutrophils:

21. Normal Lung TissueEmphysema Large surface area, many alveoli, many capillaries, lots of supporting interstitial structures Destruction of tissue distal to the terminal bronchiole leaves large (emphysematous) air spaces, few capillaries, little supporting structures.

22. Emphysema Note that in emphysema there is destruction of the alveoli, the pulmonary capillaries, and the surrounding tissue distal to the terminal bronchiole. This means there is loss of the lung interstitium including loss of elastic fibers and other structures that support the alveoli and airways. This leads to diminished elastic recoil of the lung, (ie. increased lung compliance).

23. Emphysema on CT Scan Resp Med 2000; Murray & Nadel, Textbook of

24. Lung Compliance, Normal, Lung Fibrosis and Emphysema

25. The typical COPD patient: 1) Is elderly (usually at least 45 years old) 2) Has chronic symptoms of cough, wheeze or breathlessness- SOB is progressive over time. 3) Has airway obstruction documented by spirometry. 4) Is a smoker or has smoked in the past.

26. “Objective demonstration of airflow obstruction by spirometry is essential for the diagnosis of COPD.”

27. 2003 Canadian COPD Guidelines Definition of Airflow Obstruction “A post-bronchodilator FEV 1 < 100% of the predicted value associated with an FEV 1 /FVC < 0.70 indicates airflow obstruction, and both are necessary for the diagnosis of COPD to be established.”

28. Forced Vital Capacity Maneuver Netter FH, CIBA Collection of Medical Illustrations 1 st ed. 1979 vol.7, p. 58.

29. Spirometry - Flow/Volume Loop Volume (L) Flow (L/sec) 4 321 1 2 3 4 0 measured predicted Predicted FEV 1 = 3.0 L FVC = 4.0 L FEV 1 /FVC = 75% Measured FEV 1 = 2.0 L FVC = 3.6 L FEV 1 /FVC = 56% 0 2003 Canadian COPD Guidelines

30. Classification by Impairment of Lung Function

31. Causes of Airflow Obstruction: Irreversible –Loss of elastic recoil due to alveolar destruction –Destruction of alveolar support that maintains patency of small airways –Fibrosis and narrowing of the airways

32. Causes of Airflow Obstruction: Partially Reversible –Accumulation of inflammatory cells, mucus, and plasma exudate in bronchi –Smooth muscle contraction in peripheral and central airways

33. Forced Expiration with Pleural Pressure of 20 cm H2O

34. Emphysema, loss of small airway supporting structures: Small airways lack alveolar structural support. With expiration, +ve pleural and intrathoracic pressures create small airway closure. This traps air behind the equal pressure point Alveoli can’t empty Results in air trapping and hyperinflation.

35. Lung Function - Hyperinflation

36. Operating Lung Volumes During Exercise Adapted from O’Donnell DE, Revill SM, Webb KA. Am J Respir Crit Care Med. 2001;164:770-777. Ventilation (L/min) 0 20 40 60 80 100 120 Total Lung Capacity (% pred) EELV IRV VTVTVTVT Normal01020304050607080 IC COPD 010203040 50 IC Ventilation (L/min) EELV

37. COPD Classification by Symptoms and Disability

38. Survival in COPD – Relationship to Lung Function and Disability

39. Goals of COPD Management Prevent disease progression Relieve symptoms Improve exercise tolerance Improve health status Prevent and treat complications Prevent and treat exacerbations Reduce mortality Prevent or minimize side effects from treatment GOLD Workshop Report 2003

41. What Decreases Mortality? Non-Pharmacologic Smoking cessation Flu shot Pneumonia vaccine Pulmonary Rehab Pharmacologic Oxygen Systemic Steroids Antibiotics SABA (Ventolin) Anti-cholinergics Theophylline Inhaled Steroids LABAs Combo ICS/LABA Roflumilast  X  X

42. First step in COPD management: Patient education, education, education! Smoking Cessation! Exercise!

43. “Smoking causes 80-90% of COPD” 50% of smokers develop chronic bronchitis 15-20% of smokers develop airflow obstruction and COPD. Non-Smoker Smoker

44. Smoking Cessation

45. Decline of Lung Function in Susceptible Smokers:

46. Smoking Cessation Mean postbronchodilator FEV 1 : smoking intervention and placebo group; sustained quitters and continuous smokers  Office advice  Counselling  Nicotine replacements  Bupropion  Varenicline Anthonisen et al. JAMA 1994 Continuing Smokers Sustained Quitters

47. Dyspnea: Its importance in COPD Most common symptom Intensifies as the disease progresses Reason most patients seek medical attention

48. Dyspnea – Downward Spiral of Deconditioning Respiratory impairment Dyspnea during moderate exertion Abstention from exercise Physical deconditioning Dyspnea during mild exertion Further abstention Further deconditioning Dyspnea during ADL * * = stay at home. Depression, oxygen therapy etc.

49. Pulmonary Rehabilitation

50. Benefits of Pulmonary Rehabilitation

51. Summary: Epidemiology of COPD COPD is highly prevalent, it affects at least 8% of Canadians > 65 years old. After smoking, age is the second biggest independent risk factor for COPD. In the developing world exposure to pollution and biomass fuels is also an important risk factor. COPD is now an ‘equal-opportunity disease’ when it comes to gender. COPD is a poor person’s disease- more prevalent in patients of lower SES.

52. Summary: Treatment for COPD FEV1 relentlessly declines; only smoking cessation will halt progression. Education/pulmonary rehabilitation/smoking cessation are unsexy therapies but they work best! Long-acting BD’s are indicated for most patients to improve symptoms, exercise and QOL. For patients with severe COPD and hypoxemia at rest- home oxygen will prevent cor pulmonale and improve survival.