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Chronic Obstructive Pulmonary Disease
Chen xin M.D., Pulmonary Medicine zhujiang hospital, southern medical university Introduce Myself Describe what we are going to try and accomplish This will not be comprehensive, we will skip pathogenesis on purpose for instance We will be trying to bring COPD into the appropriate spotlight and focus on what’s new
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Introduction Chronic Obstructive Pulmonary Disease (COPD) is a major cause of chronic morbidity and mortality throughout the world. Many people suffer from this disease for years and die prematurely from it or its complications. COPD is the fourth leading cause of death in the world, and further increases in its prevalence and mortality can be predicted in the coming decades.
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Definition COPD is a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with the chronic inflammatory response of the lung to noxious particles or gases. acute exacerbations and It's complications influence the severity of the disease
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Definition Airflow limitation Not completely reversible Progressive
Inflammation “Bronchitis” & “Emphysema” no longer in definition The most common form of COPD is a combination of chronic bronchitis and emphysema.
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Burden of COPD COPD is a leading cause of morbidity and mortality worldwide and results in an economic and social burden that is both substantial and increasing. COPD prevalence, morbidity, and mortality vary across countries and across different groups within countries. The burden of COPD is projected to increase in the coming decades due to continued exposure to COPD risk factors and the changing age structure of the world’s population.
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Percent Change in Age-Adjusted Death Rates, U.S., 1965-1998
Proportion of 1965 Rate 3.0 Coronary Heart Disease Stroke Other CVD COPD All Other Causes 2.5 2.0 1.5 1.0 0.5 –59% –64% –35% +163% –7%
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Of the six leading causes of death in the United States, only COPD has been increasing steadily since 1970 Source: Jemal A. et al. JAMA 2005
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Disease Trajectory of a Patients with COPD
Symptoms Exacerbations Deterioration End of Life
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Risk Factors Genes Exposure to particles Tobacco smoke
Occupational dusts, organic and inorganic Indoor air pollution from heating and cooking with biomass in poorly ventilated dwellings Outdoor air pollution Lung growth and development Oxidative stress Gender Age Respiratory infections Socioeconomic status Nutrition Comorbidities
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Aging Populations Risk Factors Nutrition Infections
Socio-economic status Aging Populations
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Pathology Pathological changes characteristic of COPD are found in the proximal airways, peripheral airways, lung parenchyma, and pulmonary vasculature. These changes include chronic inflammation, and structural changes resulting from repeated injury and repair. Inhaled cigarette smoke and other noxious particles cause lung inflammation, a normal response which appears to be amplified in patients who develop COPD.
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Lung inflammation is further amplified by oxidative stress and an excess of proteases in the lung.
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Amplifying mechanisms
Pathogenesis of COPD Cigarette smoke Biomass particles Particulates Host factors Amplifying mechanisms LUNG INFLAMMATION Anti-oxidants Anti-proteinases Oxidative stress Proteinases Repair mechanisms COPD PATHOLOGY Source: Peter J. Barnes, MD
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PROTEASES Fibrosis Inflammatory Cells Involved in COPD CD8+ Neutrophil
Cigarette smoke (and other irritants) Epithelial cells Alveolar macrophage Chemotactic factors CD8+ lymphocyte Fibroblast Neutrophil Monocyte Neutrophil elastase Cathepsins MMPs PROTEASES Fibrosis (Obstructive bronchiolitis) Alveolar wall destruction Mucus hypersecretion (Emphysema) Source: Peter J. Barnes, MD
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↓ HDAC2 ↑Inflammation Steroid resistance
Oxidative Stress in COPD Macrophage Neutrophil Anti-proteases SLPI 1-AT NF-B Proteolysis IL-8 TNF- ↓ HDAC2 ↑Inflammation Steroid resistance O2-, H202 OH., ONOO- Neutrophil recruitment Isoprostanes Bronchoconstriction Plasma leak Mucus secretion Source: Peter J. Barnes, MD
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Squamous metaplasia of epithelium No basement membrane thickening
Changes in Large Airways of COPD Patients Mucus hypersecretion Neutrophils in sputum Squamous metaplasia of epithelium No basement membrane thickening Goblet cell hyperplasia ↑ Macrophages ↑ CD8+ lymphocytes Mucus gland hyperplasia Little increase in airway smooth muscle Source: Peter J. Barnes, MD
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Changes in Small Airways in COPD Patients
Inflammatory exudate in lumen Disrupted alveolar attachments Thickened wall with inflammatory cells - macrophages, CD8+ cells, fibroblasts Peribronchial fibrosis Lymphoid follicle Source: Peter J. Barnes, MD
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Alveolar wall destruction
Changes in Lung Parenchyma in COPD Alveolar wall destruction Loss of elasticity Destruction of pulmonary capillary bed ↑ Inflammatory cells macrophages, CD8+ lymphocytes Source: Peter J. Barnes, MD
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Endothelial dysfunction Smooth muscle hyperplasia
Changes in Pulmonary Arteries in COPD Patients Endothelial dysfunction Intimal hyperplasia Smooth muscle hyperplasia ↑ Inflammatory cells (macrophages, CD8+ lymphocytes) Source: Peter J. Barnes, MD
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COPD ASTHMA Airflow Limitation Small airway narrowing
Alv macrophage Ep cells CD8+ cell (Tc1) Neutrophil Cigarette smoke Small airway narrowing Alveolar destruction COPD ASTHMA Allergens Y Ep cells Mast cell CD4+ cell (Th2) Eosinophil Bronchoconstriction AHR Airflow Limitation Reversible Irreversible Source: Peter J. Barnes, MD
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Pulmonary Hypertension in COPD
Chronic hypoxia Pulmonary vasoconstriction Muscularization Intimal hyperplasia Fibrosis Obliteration Pulmonary hypertension Cor pulmonale Edema Death Source: Peter J. Barnes, MD
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Air Trapping in COPD Mild/moderate COPD Normal Severe COPD ↓ Health
Inspiration small airway alveolar attachments loss of elasticity loss of alveolar attachments Expiration closure ↓ Health status Dyspnea ↓ Exercise capacity Air trapping Hyperinflation Source: Peter J. Barnes, MD
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Inflammation in COPD Exacerbations
Bacteria Viruses Non-infective Pollutants Macrophages Epithelial cells TNF- IL-8 IL-6 Neutrophils Oxidative stress Source: Peter J. Barnes, MD
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Chronic bronchitis Chronic bronchitis is an inflammation and eventual scarring of the lining of the bronchial tubes. Symptoms of chronic bronchitis include chronic cough, increased mucus, frequent clearing of the throat and shortness of breath.
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Emphysema Emphysema causes irreversible lung damage. The walls between the air sacs within the lungs lose their ability to stretch and recoil. They become weakened and break. Elasticity of the lung tissue is lost, causing air to be trapped in the air sacs and impairing the exchange of oxygen and carbon dioxide. Also, the support of the airways is lost, allowing for obstruction of airflow.
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Emphysema Symptoms of emphysema include cough, shortness of breath and a limited excercise tolerance. Diagnosis is made by pulmonary function tests, along with the patient’s history, examination and other tests.
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COPD病理学特点 气道 结构 改变 气道 阻塞 气道 炎症 粘膜纤毛 功能障碍 肺泡破坏 平滑肌收缩 上皮增生 粘液过度分泌
增加炎症细胞数量/活性 - 中性粒细胞, - 巨噬细胞, - CD8+ 淋巴细胞 提高 IL-8, TNF, LTB4 蛋白酶/抗蛋白酶失衡 粘膜水肿 平滑肌收缩 增加胆碱能释放 支气管 高反应性? 弹性收缩降低 肺泡破坏 上皮增生 腺体过度增大 杯状细胞变形 气道纤维化 粘液过度分泌 粘液粘性增加 减少纤毛转运 粘膜损伤
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Pathophysiology Increased mucus production and reduced mucociliary clearance - cough and sputum production Loss of elastic recoil - airway collapse Increase smooth muscle tone Pulmonary hyperinflation Gas exchange abnormalities - hypoxemia and/or hypercapnia
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Chronic bronchitis Emphysema COPD asthma
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GOALS of COPD MANAGEMENT UPDATED 2011
Relieve symptoms Prevent disease progression Improve exercise tolerance Improve health status Prevent and treat complications Prevent and treat exacerbations Reduce mortality
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Four Components of COPD Management
Assess and monitor disease Reduce risk factors Manage stable COPD Education Pharmacologic/Non-pharmacologic Manage exacerbations Diagnosis and Assessment of Severity Home/Hospital Management
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Assess and Monitor COPD: Key Points
A clinical diagnosis of COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and/or a history of exposure to risk factors for the disease. The diagnosis should be confirmed by spirometry. A post-bronchodilator FEV1/FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible. Comorbidities are common in COPD and should be actively identified.
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indoor/outdoor pollution
Diagnosis of COPD EXPOSURE TO RISK FACTORS SYMPTOMS cough tobacco sputum occupation shortness of breath indoor/outdoor pollution clinical diagnosis SPIROMETRY diagnosis è
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Key Indicators for COPD Diagnosis
Chronic cough Present intermittently or every day often present throughout the day; seldom only nocturnal Chronic sputum production Present for many years, worst in winters. Initially mucoid – becomes purulent with exacerbation Dyspnoea that is Progressive (worsens over time) Persistent (present every day) Worse on exercise Worse during respiratory infections Acute bronchitis Repeated episodes History of exposure to risk factors Tobacco smoke (including beedi) occupational dusts and chemical smoke from home cooking and heating fuel
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Physical signs Large barrel shaped chest (hyperinflation)
Prominent accessory respiratory muscles in neck and use of accessory muscle in respiration Low, flat diaphragm Diminished breath sound
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Spirometry Diagnosis Assessing severity Assessing prognosis
Monitoring progression
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Spirometry FEV1 – Forced expired volume in the first second
FVC – Total volume of air that can be exhaled from maximal inhalation to maximal exhalation FEV1/FVC% - The ratio of FEV1 to FVC, expressed as a percentage.
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Flow-volume curve Flow Normal obstruction restrictions Mixed Volum RV
TLC
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Chest X-rays Emphysema Hyperinflation Flattened diaphragms
Decreased vascular markings Chronic Bronchitis Usually normal
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Chest X-rays Hyper- inflated Flat diaphragm Increased Retrosternal air
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Assess and Monitor COPD: Spirometry GOLD 2006
Spirometry should be performed after the administration of an adequate dose of a short-acting inhaled bronchodilator to minimize variability. A post-bronchodilator FEV1/FVC < 0.70 confirms the presence of airflow limitation that is not fully reversible. Where possible, values should be compared to age-related normal values to avoid overdiagnosis of COPD in the elderly.
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COPD classification based on spirometry GOLD 2006
Severity Postbronchodilator FEV1/FVC Postbronchodilator FEV1% predicted Mild COPD <0.7 >80 Moderate COPD 50-80 Severe COPD 30-50 Very severe COPD <30 SPIROMETRY is not to substitute for clinical judgment in the evaluation of the severity of disease in individual patients.
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Assess and Monitor COPD: GOLD 2011
Clinical symptoms Spirometry risk of acute exacerbations complications Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease Revised 2011
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Assess and Monitor COPD: Clinical symptoms
COPD assessment test (CAT) including eight common clinical problem, to evaluate the health damage of patients with COPD modified british medical research council (mMRC) Having a good correlation with health condition and can predict the future risk of death
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mMRC CAT
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Assess and Monitor COPD: risk of acute exacerbations
History of acute exacerbations : the number of acute exacerbations is more than 2 times in the last year Spirometry: FEV1 < 50 % Pred as a high risk index
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Comprehensive Assessment
Risk Risk (GOLD) ≥ 2 (AE) mMRC mMRC 2+ CAT< CAT> 10+ symptoms（mMRC or CAT） C D A B A:Fewer symptoms, lower risk B: more symptoms, lower risk C: Fewer symptoms,higher risk D: more symptoms, higher risk
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Arterial Blood Gas (ABGs)
An ABG is done from a sample drawn from one of your arteries. The blood is then analyzed by a special machine, which records the amount of carbon dioxide (waste gas) and oxygen in your blood. One of the uses of this test is to determine whether or not you need any extra oxygen.
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Parameters and Predictions
Normal Values Predictions Arterial PO2 95 mmHg decrease Arterial PCO2 40 mmHg increases Aterial pH approx. 7.4 decreases Arterial HCO3-content 22-26 mEq/L Total Arterial O2 content 20 ml/dL
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Differential Diagnosis: COPD and Asthma
Onset early in life (often childhood) Symptoms vary from day to day Symptoms at night/early morning Allergy, rhinitis, and/or eczema also present Family history of asthma Largely reversible airflow limitation Onset in mid-life Symptoms slowly progressive Long smoking history Dyspnea during exercise Largely irreversible airflow limitation
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COPD and Co-Morbidities
COPD patients are at increased risk for: Myocardial infarction, angina Osteoporosis Respiratory infection Depression Diabetes Lung cancer
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COPD and Co-Morbidities
COPD has significant extrapulmonary (systemic) effects including: Weight loss Nutritional abnormalities Skeletal muscle dysfunction
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Management of Stable COPD Reduce Risk Factors: Key Points
Reduction of total personal exposure to tobacco smoke, occupational dusts and chemicals, and indoor and outdoor air pollutants are important goals to prevent the onset and progression of COPD. Smoking cessation is the single most effective — and cost effective — intervention in most people to reduce the risk of developing COPD and stop its progression.
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Reducing the risk from indoor and outdoor air pollution is feasible and requires a combination of public policy and protective steps taken by individual patients. Reduction of exposure to smoke from biomass fuel, particularly among women and children, is a crucial goal to reduce the prevalence of COPD worldwide.
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Management of Stable COPD Manage Stable COPD: Key Points
Bronchodilator medications are central to the symptomatic management of COPD. They are given on an as-needed basis or on a regular basis to prevent or reduce symptoms and exacerbations. The principal bronchodilator treatments are ß2-agonists, anticholinergics, and methylxanthines used singly or in combination. Regular treatment with long-acting bronchodilators is more effective and convenient than treatment with short-acting bronchodilators.
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Management of Stable COPD Pharmacotherapy: Bronchodilators
Bronchodilator medications are central to the symptomatic management of COPD .They are given on an as-needed basis or on a regular basis to prevent or reduce symptoms and exacerbations. The principal bronchodilator treatments are ß2-agonists, anticholinergics, and methylxanthines used singly or in combination. Regular treatment with long-acting bronchodilators is more effective and convenient than treatment with short-acting bronchodilators.
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Algorithm for the management of COPD
Mild Short acting bronchodilator – as required Tiotropium Long acting beta agonist assess with symptoms and spirometry Tiotropium+LABA LABA + tiotropium Add -Inhaled steroids -Theophylline Severe
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Pharmacotherapy: Glucocorticosteroids
Management of Stable COPD Pharmacotherapy: Glucocorticosteroids The addition of regular treatment with inhaled glucocorticosteroids to bronchodilator treatment is appropriate for symptomatic COPD patients with an FEV1 < 50% predicted (Stage III: Severe COPD and Stage IV: Very Severe COPD) and repeated exacerbations. An inhaled glucocorticosteroid combined with a long-acting ß2-agonist is more effective than the individual components .
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Pharmacotherapy for Stable COPD
Steroids Oral – Prednisolone Inhaled - Fluticasone, Budesonide Bronchodilators Short-acting b2-agonist – Salbutamol Long-acting b2-agonist - Salmeterol and Formoterol Anticholinergics – Ipratropium, Tiiotropium Methylxanthines - Theophylline
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Pharmacotherapy: Vaccines
Management of Stable COPD Pharmacotherapy: Vaccines In COPD patients influenza vaccines can reduce serious illness. Pneumococcal polysaccharide vaccine is recommended for COPD patients 65 years and older and for COPD patients younger than age 65 with an FEV1 < 40% predicted.
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Management of Stable COPD All Stages of Disease Severity
Avoidance of risk factors - smoking cessation - reduction of indoor pollution - reduction of occupational exposure Influenza vaccination
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Therapy at Each Stage of COPD (GOLD2006)
I: Mild II: Moderate III: Severe IV: Very Severe FEV1/FVC < 70% FEV1 < 30% predicted or FEV1 < 50% predicted plus chronic respiratory failure FEV1/FVC < 70% 30% < FEV1 < 50% predicted FEV1/FVC < 70% 50% < FEV1 < 80% predicted FEV1/FVC < 70% FEV1 > 80% predicted Active reduction of risk factor(s); influenza vaccination Add short-acting bronchodilator (when needed) This provides a summary of the recommended treatment at each stage of COPD. Add regular treatment with one or more long-acting bronchodilators (when needed); Add rehabilitation Add inhaled glucocorticosteroids if repeated exacerbations Add long term oxygen if chronic respiratory failure. Consider surgical treatments
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Therapy at Each Stage of COPD (GOLD2011)
First chonice Second chonice Alternative chonice A SABA /SAMA prn LAMA/LABA or SAMA＆SABA Theophylline B LABA / LAMA LAMA ＆ LABA SABA ＆ /orSAMA； Theophylline C ICS/LABA or LAMA PDE-4 inhibitors ； SABA ＆ /orSAMA； Theophylline D ICS ＆ LAMA ICS/LABA ＆ LAMA；ICS/LABA ＆ PDE-4 inhibitors LAMA ＆ LABA；LAMA ＆ PDE-4 inhibitors Carbocisteine； SABA ＆ /orSAMA； Theophylline Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease Revised 2011
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The Future of COPD：Phenotypes
Clinical Manifestations Age, smoking history, sex, ethnicity Physiological Manifestations Radiologic Characterization frequent COPD Exacerbations Systemic Inflammation
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Other Pharmacologic Treatments
Management of Stable COPD Other Pharmacologic Treatments Antibiotics: Only used to treat infectious exacerbations of COPD Antioxidant agents: No effect of n-acetylcysteine on frequency of exacerbations, except in patients not treated with inhaled glucocorticosteroids Mucolytic agents, Antitussives, Vasodilators: Not recommended in stable COPD
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Non-Pharmacologic Treatments
Management of Stable COPD Non-Pharmacologic Treatments Rehabilitation: All COPD patients benefit from exercise training programs, improving with respect to both exercise tolerance and symptoms of dyspnea and fatigue. Oxygen Therapy: The long-term administration of oxygen (> 15 hours per day) to patients with chronic respiratory failure has been shown to increase survival.
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Key Points An exacerbation of COPD is defined as:
Management COPD Exacerbations Key Points An exacerbation of COPD is defined as: “An acute event in the course of the disease characterized by a change in the patient’s baseline dyspnea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication in a patient with underlying COPD.”
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Key Points Management COPD Exacerbations
The most common causes of an exacerbation are infection of the tracheobronchial tree and air pollution, but the cause of about one-third of severe exacerbations cannot be identified . Patients experiencing COPD exacerbations with clinical signs of airway infection (e.g., increased sputum purulence) may benefit from antibiotic treatment .
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Key Points Manage COPD Exacerbations
Inhaled bronchodilators (particularly inhaled ß2-agonists with or without anticholinergics) and oral glucocortico- steroids are effective treatments for exacerbations of COPD.
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Manage COPD Exacerbation cause and mechanism
Viruses Bacteria Aerial pollution COPD airway inflammation is, the more serious, pathological physiology change is, the more evident. leading to a symptom aggravating, so patients much to seek for medical help, usually diagnosed of acute exacerbation Cardiovascular Co-Morbidities Dynamic hyperinflation The deterioration of airway inflammation Symptoms of AECOPD Expiratory Airflow limitation Bronchial inflammation Hydroncus, mucous Systemic inflammation COPD airway inflammation Wedzicha JA. Lancet 2007；370： Antonio Anzueto. Proc Am Thorac Soc 2007；4：554–564
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Key Points Management COPD Exacerbations
Noninvasive mechanical ventilation in exacerbations improves respiratory acidosis, increases pH, decreases the need for endotracheal intubation, and reduces PaCO2, respiratory rate, severity of breathlessness, the length of hospital stay, and mortality. Medications and education to help prevent future exacerbations should be considered as part of follow-up, as exacerbations affect the quality of life and prognosis of patients with COPD.
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COPD is increasing in prevalence in many countries of the world.
Global Strategy for Diagnosis, Management and Prevention of COPD: Summary COPD is increasing in prevalence in many countries of the world. COPD is treatable and preventable. The GOLD program offers a strategy to identify patients and to treat them according to the best medications available.
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Global Strategy for Diagnosis, Management and Prevention of COPD: Summary
COPD can be prevented by avoidance of risk factors, the most notable being tobacco smoke. Patients with COPD have multiple other conditions (comorbidities) that must be taken into consideration. GOLD has developed a global network to raise awareness of COPD and disseminate information on diagnosis and treatment.
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The End
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