Copd 2012

MBBS en 34Heart Care
5 de May de 2015

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Copd 2012

  1. Department of Pulmonary Medicine Chronic Obstructive Pulmonary Disease (COPD) Dr. Rahul Magazine M.D. (Medicine); D.T.C.D. Dept. of Pulmonary Medicine
  2. Department of Pulmonary Medicine
  3. Department of Pulmonary Medicine
  4. Department of Pulmonary Medicine
  5. Department of Pulmonary Medicine DEFINITION COPD, a common preventable and treatable disease, is characterized by persistent airflow limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or gases.
  6. Department of Pulmonary Medicine Chronic bronchitis has been defined as the presence of chronic productive cough for 3 months during each of two successive years in a patient in whom other causes of chronic cough have been excluded. Emphysema is defined as a condition of the lung characterized by abnormal permanent enlargement of the air spaces distal to the terminal bronchioles accompanied by destruction of their walls and without obvious fibrosis.
  7. Department of Pulmonary Medicine EPIDEMIOLOGY • COPD ranked sixth as the cause of death in 1990, but will become the third leading cause of death worldwide by 2020. • The prevalence of COPD is appreciably higher in smokers and ex-smokers than in nonsmokers, in those over 40 years than those under 40, and in men than in women.
  8. Department of Pulmonary Medicine RISK FACTORS  Exposure to particles Tobacco smoke Indoor air pollution from heating and cooking with biomass in poorly vented dwellings (among women in developing countries) Occupational dusts (organic and inorganic) Outdoor air pollution  Genes (α1 anti-trypsin deficiency)  Airway hyperresponsiveness  Lung Growth and Development  Oxidative stress  Gender  Age  Respiratory infections  Socioeconomic status
  9. Department of Pulmonary Medicine PATHOLOGY • Large Airway Mucous gland enlargement and goblet cell hyperplasia. • Small Airways Airway wall thickening Peribronchial fibrosis Luminal inflammatory exudate Airway narrowing (obstructive bronchiolitis)
  10. Department of Pulmonary Medicine • Lung parenchyma Alveolar wall destruction Apoptosis of epithelial and endothelial cells • Pulmonary vasculature Thickening of intima Endothelial cell dysfunction, INFLAMMATORY CELLS: Macrophages, T lymphocytes, few neutrophils or eosinophils
  11. Department of Pulmonary Medicine PATHOPHYSIOLOGY Peripheral airway obstruction Air trapping during expiration Hyperinflation Functional Residual Capacity increased
  12. PATHOPHYSIOLOGY • Gas Exchange Abnormalities • Mucus Hypersecretion • Pulmonary Hypertension Department of Pulmonary Medicine
  13. Department of Pulmonary Medicine PATHOGENESIS The inflammation in the respiratory tract of COPD patients appears to be an amplification of the normal inflammatory response of the respiratory tract to chronic irritants such as cigarette smoke
  14. Department of Pulmonary Medicine Smoking Lung Inflammation Oxidative Stress COPD Pathology Proteinases
  15. Department of Pulmonary Medicine CLINICAL FEATURES Symptoms  Breathlessness Progressive (worsens over time) Usually worse with exercise Persistent (present every day)  Chronic cough, which is often, but not invariably, productive.  Wheeze
  16. Department of Pulmonary Medicine  History of exposures to risk factors: A smoking history of at least 20 pack years is usual before symptoms develop Smoke from home cooking and heating fuels Occupational dusts and chemicals  Family history of COPD  Weight loss and anorexia are features of severe COPD  Sleep quality is impaired in advanced COPD  Hemoptysis
  17. Department of Pulmonary Medicine Clinical signs General examination • Tachypnoea, • Prolonged forced expiratory time (more than 5 s) • Adopting pursed lipped breathing on expiration which reduces expiratory airway collapse.
  18. Department of Pulmonary Medicine • Use of the accessory muscles of respiration • Adopt the position of leaning forward, supporting themselves with their arms to fix the shoulder girdle • Tar-stained fingers • Cyanosis in advanced disease • Flapping tremor • Weight loss • Finger clubbing is not a feature of COPD
  19. Department of Pulmonary Medicine Examination of Chest Inspection and Palpation • Signs of overinflation: barrel-shaped with a kyphosis and an apparent increased anterior/posterior diameter, horizontal ribs, prominence of the sternal angle, and a wide subcostal angle. Distance between the suprasternal notch and the cricoid cartilage (normally three finger-breadths) may be reduced. • Pursed lip breathing, use of accessory muscles • An inspiratory tracheal tug • Hoover's sign
  20. Department of Pulmonary Medicine • Indrawing of the suprasternal and supraclavicular fossas and of the intercostal muscles Percussion • Hyper resonant note • Decreased hepatic and cardiac dullness Ausculatation • Breath sounds may have a prolonged expiratory phase, or may be uniformly diminished • Wheeze • Crackles may be heard particularly at the lung bases
  21. Department of Pulmonary Medicine Cardiovascular Examination • Difficulty in localizing the apex beat • Signs of pulmonary artery hypertension • Signs of right heart failure SYSTEMIC FEATURES: Skeletal muscle wasting Osteoporosis Anxiety and Depression Increased risk of cardiovascular disease, respiratory infections diabetes, lung cancer
  22. Type A: Pink Puffer (Emphysema Predominant) • Major complaint is dyspnea, • Cough is rare, with scant clear, mucoid sputum. • Patients are thin, with recent weight loss common. • They appear uncomfortable, with evident use of accessory muscles of respiration. • Chest is very quiet without adventitious sounds. • No peripheral edema. Department of Pulmonary Medicine
  23. Type B: Blue Bloater (Bronchitis Predominant) • Major complaint is chronic cough, productive of mucopurulent sputum • Dyspnea usually mild, though patients may note limitations to exercise. • Patients frequently overweight and cyanotic but seem comfortable at rest. • Peripheral edema is common. • Chest is noisy, with rhonchi invariably present Department of Pulmonary Medicine
  24. Department of Pulmonary Medicine MANAGEMENT
  25. Assessment • COPD Assessment Test (CAT): An 8-item measure of health status impairment in COPD • Breathlessness Measurement using the Modified British Medical Research Council (mMRC) Questionnairewell to other measures of health statusand predicts future mortality risk. Department of Pulmonary Medicine
  26. Department of Pulmonary Medicine INVESTIGATIONS Hematocrit Polycythemia can develop in the presence of arterial hypoxemia, especially in continuing smokers, and can be identified by hematocrit > 55%.
  27. Department of Pulmonary Medicine • Spirometry: The presence of a postbronchodilator FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation and thus COPD
  28. Spirometry: Normal Trace Showing FEV1 and FVC 1 2 3 4 5 6 1 2 3 4 Volume,liters Time, sec FVC5 1 FEV1 = 4L FVC = 5L FEV1/FVC = 0.8
  29. Spirometry: Obstructive Disease Volume,liters Time, seconds 5 4 3 2 1 1 2 3 4 5 6 FEV1 = 1.8L FVC = 3.2L FEV1/FVC = 0.56 Normal Obstructive
  30. Department of Pulmonary Medicine Classification of Severity of Airflow Limitation in COPD (Based on Post-Bronchodilator FEV1) In patients withFEV1/FVC < 0.70 GOLD I: Mild; FEV1 ≥ 80% predicted GOLD II: Moderate; 50% ≤ FEV1 < 80% predicted GOLD III: Severe; 30% ≤ FEV1 < 50% predicted GOLD IV: Very Severe; FEV1 < 30% predicted
  31. Department of Pulmonary Medicine • Imaging Chest X-ray Signs of hyperinflation (flattened diaphragm and an increase in the volume of the retrosternal air space), hyperlucency of the lungs, and rapid tapering of the vascular markings. Computed tomography (CT)
  32. Department of Pulmonary Medicine • Arterial blood gas measurement • Exercise testing • Alpha-1 antitrypsin deficiency screening (when COPD develops under 45 years or with a strong family history of COPD.)   • Other investigations, including electrocardiography, echocardiography, radionucleotide scintigraphy, and magnetic resonance imaging.
  33. Department of Pulmonary Medicine TREATMENT 1. Smoking Cessation • Counseling • Pharmacotherapy Nicotine replacement products (nicotine gum, inhaler, nasal spray, transdermal patch, sublingual tablet, or lozenge) Other pharmacotherapy:The antidepressants bupropion and nortriptyline. Varenicline, a nicotinic acetylcholine receptor partial agonist that aids smoking cessation by relieving nicotine withdrawal symptoms and reducing the rewarding properties of nicotine
  34. Department of Pulmonary Medicine Drugs Used in COPD β2-agonists Short-acting (Salbutamol, Terbutaline) Long-acting (Formoterol, Salmeterol)
  35. Department of Pulmonary Medicine Drugs Used in COPD Anticholinergics Short-acting Ipratropium bromide Oxitropium bromide Long-acting Tiotropium
  36. Drugs Used in COPD Combination short-acting β 2-agonists plus anticholinergic in one inhaler Salbutamol/Ipratropium Methylxanthines Aminophylline Theophylline (SR) Department of Pulmonary Medicine
  37. Department of Pulmonary Medicine Drugs Used in COPD Inhaled glucocorticosteroids Beclomethasone, Budesonide, Fluticasone, Triamcinolone Combination long-acting β 2-agonists plus glucocorticosteroids in one inhaler Formoterol/Budesonide Salmeterol/Fluticasone
  38. Drugs Used in COPD Phospodiesterase-4 inhibitor: Roflumilast Systemic glucocorticosteroids Prednisone, Methyl-prednisolone Department of Pulmonary Medicine
  39. Department of Pulmonary Medicine OTHER PHARMACOLOGIC TREATMENTS • Alpha-1 antitrypsin augmentation therapy. • Vaccines: Influenza vaccine (reduces serious illness and death) Pneumococcal vaccine (reduces incidence of CAP)
  40. OTHER PHARMACOLOGIC TREATMENTS • Mucolytic agents (ambroxol, carbocysteine, iodinated glycerol) Patients with viscous sputum may benefit from mucolytics; overall benefits are very small. • Antibioticsefits are very small • Antioxidant agents • Immunoregulators • Antitussives Department of Pulmonary Medicine
  41. Department of Pulmonary Medicine OTHER PHARMACOLOGIC TREATMENTS Oxygen Therapy Can be administered in three ways: longterm continuous therapy, during exercise, and to relieve acute dyspnea. The primary goal of oxygen therapy is to increase the baseline PaO2 to at least 8.0 kPa (60 mm Hg) at sea level and rest, and/or produce an SaO2 at least 90%, which will preserve vital organ function by ensuring adequate delivery of oxygen.
  42. Department of Pulmonary Medicine The long-term administration of oxygen(> 15 h/d) to patients with chronic respiratory failure has been shown to increase survival. Long-term oxygen therapy is generally introduced in patients with COPD, who have PaO2 at or below 55 mm Hg or SaO2 at or below 88%, with or without hypercapnia
  43. OTHER TREATMENTS • Non invasive ventilation with LTOT in a some selected patients may improve survival • Rehabilitation Department of Pulmonary Medicine
  44. Department of Pulmonary Medicine Surgical Treatments Bullectomy Lung volume reduction surgery Lung transplantation
  45. Only three interventions influence the natural history of patients with COPD. 1.Smoking cessation 2.Oxygen therapy in chronically hypoxemic patients 3.Lung volume reduction surgery in selected patients with emphysema. There is currently suggestive, but not definitive, evidence that the use of inhaled glucocorticoids may alter mortality rate. Department of Pulmonary Medicine
  46. Department of Pulmonary Medicine Patien t Characteristic Spirometric Classification Exacerbation s per year mMRC CAT A Low Risk Less Symptoms GOLD 1-2 ≤ 1 0-1 < 10 B Low Risk More Symptoms GOLD 1-2 ≤ 1 > 2 ≥ 10 C High Risk Less Symptoms GOLD 3-4 > 2 0-1 < 10 D High Risk More Symptoms GOLD 3-4 > 2 > 2 ≥ 10 Combined Assessment
  47. Management of Stable COPD Department of Pulmonary Medicine
  48. Managing Stable COPD Department of Pulmonary Medicine
  49. Department of Pulmonary Medicine MANAGE EXACERBATIONS An exacerbation of COPD is defined as an event in the natural 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.
  50. Department of Pulmonary Medicine  The most common causes of COPD exacerbations are viral upper respiratory tract infections and infection of the tracheobronchial tree. .  Streptococcus pneumoniae, Hemophilus influenzae, and Moraxella catarrhalis are the most common bacterial pathogens involved in COPD exacerbations.
  51. Department of Pulmonary Medicine Inhaled bronchodilators (particularly inhaled Β 2-agonists with or without anticholinergics) and oral glucocorticosteroids are effective treatments for exacerbations of COPD. Antibiotics if clinical signs of airway infection (e.g., increased sputum, purulence)
  52. Department of Pulmonary Medicine  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
  53. Department of Pulmonary Medicine OXYGEN THERAPY
  54. Department of Pulmonary Medicine INTRODUCTION Oxygen is the substrate that cells use in the greatest quantity and upon which aerobic metabolism and cell integrity depend. Since the tissues have no storage system for oxygen, a continuous supply at a rate that matches changing metabolic requirements is necessary to maintain aerobic metabolism and normal cellular function.
  55. Department of Pulmonary Medicine PRINCIPLES In general, maintain SaO2 >90%, though preferably >95%.
  56. Department of Pulmonary Medicine Devices For Providing Oxygen • Oxygen supply (cylinder or wall unit) • Nasal cannula • Face mask • Venturi mask
  57. Department of Pulmonary Medicine NASAL CANNULA • The nasal cannula is a low-flow oxygen administration system designed to add oxygen to room air when the patient inspires. • A nasal cannula provides up to 44% oxygen. • The ultimate inspired oxygen concentration is determined by the oxygen flow rate through the cannula and how deeply the patient breathes (tidal volume).
  58. Department of Pulmonary Medicine • Increasing the oxygen flow by 1 L/min (starting with 1 L/min) will increase the inspired oxygen concentration by approximately 4%: — 1 L/min: 21% to 24% — 2 L/min: 25% to 28% — 3 L/min: 29% to 32% — 4 L/min: 33% to 36% — 5 L/min: 37% to 40% — 6 L/min: 41% to 44%
  59. Department of Pulmonary Medicine
  60. Department of Pulmonary Medicine FACE MASK • A simple face mask delivers low oxygen flow to the patient’s nose and mouth. A partial rebreathing mask consists of a face mask with an attached reservoir bag
  61. Department of Pulmonary Medicine • A face mask can supply up to 60% oxygen with flow rates of 6 to 10 L/min. A face mask with oxygen reservoir nonrebreathing mask) provides up to 90% to 100% oxygen with flow rates of 9 to 15 L/min. In this system a constant flow of oxygen enters an attached reservoir.
  62. Department of Pulmonary Medicine Use a face mask with a reservoir for patients who Are seriously ill, responsive, and have adequate ventilation but require high oxygen concentrations
  63. Department of Pulmonary Medicine
  64. Department of Pulmonary Medicine VENTURI MASK • A Venturi mask enables a more reliable and controlled delivery of oxygen concentrations from 24% to 50%. Use the Venturi mask for patients who retain carbon dioxide (CO2). Patients who have chronic high levels of CO2 in their blood and moderate-to-severe hypoxemia may develop respiratory depression if the drive stimulating them to breathe (oxygen) is reduced.
  65. Department of Pulmonary Medicine • Delivered oxygen concentrations can be adjusted to 24%, 28%, 35%, and 40% using a flow rate of 4-8 L/min and 40% to 50% using a flow rate of 10-12 L/min.
  66. Department of Pulmonary Medicine MONITORING Adequacy and changes in arterial oxygen saturation can be continuously monitored by pulse oximetry and intermittent or continuous invasive blood gas analysis.
  67. Department of Pulmonary Medicine REFERENCES • Harrison's Principles of Internal Medicine, 18th Edition • GOLD. 2011 (revised) • Murray & Nadel's Textbook of Respiratory Medicine, 4th ed. • CMDT 2010
  68. Department of Pulmonary Medicine THANK YOU
  69. Department of Pulmonary Medicine
  70. Department of Pulmonary Medicine
  71. Department of Pulmonary Medicine

Notas del editor

  1. The GOLD definition refers to neither chronic bronchitis nor emphysema (see later), either of which may occur with or without airflow limitation. It contrasts with asthma, which by definition[2](see Chapter 37 ), is associated with reversible airflow limitation. The clinical distinction between asthma and COPD, however, is often difficult because the two entities may coexist ( Fig. 36.1 ), and asthma may progress to COPD (see later).
  2. The most important risk factor for the development of COPD is cigarette smoking, which is associated with 85-90% of all cases. Smokers exhibit a substantially greater rate of annual decline in forced expiratory volume in 1 sec (FEV1) than the normal age-related decline of 15–30 mL/yr. Cigar and pipe smokers are also at increased risk of developing COPD, albeit less than cigarette smokers. However, only a minority (~15%) of smokers develop clinically significant COPD, suggesting that genetic predisposition and other environmental factors may be required for the development of lung injury. Less than 1% of COPD cases are linked to alpha1-antitrypsin deficiency, Washington manual of pulmonary Med
  3. Genes COPD is a polygenic disease severe hereditary deficiency of alpha-1 antitrypsin4, a major circulating inhibitor of serine proteases. Premature and accelerated development of panlobular emphysema and decline in lung function occur in both smokers and nonsmokers with the severe deficiency, although smoking increases the risk appreciably Inhalational Exposures Tobacco Smoke: The most commonly encountered risk factor for COPD. Cigarette smokers have a higher prevalence of respiratory symptoms and lung function abnormalities, a greater annual rate of decline in FEV1, and a greater COPD mortality rate than nonsmokers. The risk for COPD in smokers is dose-related12. Age at starting to smoke, total pack-years smoked, and current smoking status are predictive of COPD mortality. Not all smokers develop clinically significant COPD, which suggests that genetic factors must modify each individual’s risk. Passive exposure to cigarette smoke may also contribute to respiratory symptoms19 and COPD 0 by increasing the lungs’ total burden of inhaled particles and gases. Occupational Dusts and Chemicals: Include organic and inorganic dusts and chemical agents and fumes. Indoor Air Pollution: From biomass cooking and heating in poorly ventilated dwellings is an important risk factor for COPD (especially among women in developing countries) Outdoor Air Pollution: Air pollution from fossil fuel combustion, primarily from motor vehicle emissions in cities, is associated with decrements of respiratory function Lung Growth and Development Any factor that affects lung growth during gestation and childhood has the potential for increasing an individual’s risk of developing COPD. Oxidative Stress Imbalance between oxidants and antioxidants is considered to play a role in the pathogenesis of COPD Gender Role of gender in determining COPD risk remains unclear Infections Infections (viral and bacterial) may contribute to the pathogenesis and progression of COPD Socioeconomic Status Risk of developing COPD is inversely related to socioeconomic status Nutrition It is estimated that 80% of patients seen for COPD have significant exposure to tobacco smoke. The remaining 20% frequently have a combination of exposures to environmental tobacco smoke, occupational dusts and chemicals, and indoor air pollution from biomass fuel used for cooking and heating in poorly ventilated buildings CMDT 2010
  4. PATHOLOGY Figure: Pathological Changes in COPD Proximal airways (trachea, bronchi &amp;gt; 2 mm internal diameter) Inflammatory cells: Macrophages, CD8+ (cytotoxic) T lymphocytes, few neutrophils or eosinophils Structural changes: Goblet cells, enlarged submucosal glands (both leading to mucus hypersecretion), squamous metaplasia of epithelium Peripheral airways (bronchioles &amp;lt; 2mm) Inflammatory cells: Macrophages, T lymphocytes (CD8+ &amp;gt; CD4+), B lymphocytes, lymphoid follicles, fibroblasts, few neutrophils or eosinophils Structural changes: Airway wall thickening, peribronchial fibrosis, luminal inflammatory exudate, airway narrowing (obstructive bronchiolitis) Increased inflammatory response and exudate correlated with disease severity Lung parenchyma (respiratory bronchioles and alveoli) Inflammatory cells: Macrophages, CD8+ T lymphocytes Structural changes: Alveolar wall destruction, apoptosis of epithelial and endothelial cells • Centrilobular emphysema: dilatation and destruction of respiratory bronchioles; most commonly seen in smokers • Panacinar emphysema: destruction of alveolar sacs as well as respiratory bronchioles; most commonly seen in alpha-1 antitrypsin deficiency Pulmonary vasculature Inflammatory cells: Macrophages, T lymphocytes Structural changes: Thickening of intima, endothelial cell dysfunction, smooth muscle pulmonary hypertension6. PATHOGENESIS The inflammation in the respiratory tract of COPD patients appears to be an amplification of the normal inflammatory response of the respiratory tract to chronic irritants such as cigarette smoke. Inflammatory Cells COPD is characterized by a specific pattern of inflammation involving neutrophils, macrophages, and lymphocytes Inflammatory Mediators Attract inflammatory cells from the circulation (chemotactic factors), amplify the inflammatory process (proinflammatory cytokines), and induce structural changes (growth factors). Oxidative Stress Oxidative stress may be an important amplifying mechanism in COPD. Oxidants are generated by cigarette smoke and other inhaled particulates, and released from activated inflammatory cells such as macrophages and neutrophils There may also be a reduction in endogenous antioxidants in COPD patients. Oxidative stress has several adverse consequences in the lungs, including activation of inflammatory genes, inactivation of antiproteases, stimulation of mucus secretion, and stimulation of increased plasma exudation. Protease-Antiprotease Imbalance There is compelling evidence for an imbalance in the lungs of COPD patients between proteases that break down connective tissue components and antiproteases that protect against this. PATHOPHYSIOLOGY Airflow Limitation and Air Trapping The extent of inflammation, fibrosis, and luminal exudates in small airways is correlated with the reduction in FEV1 and FEV1/FVC ratio, and probably with the accelerated decline in FEV1 characteristic of COPD. This peripheral airway obstruction progressively traps air during expiration, resulting in hyperinflation. Hyperinflation reduces inspiratory capacity such that functional residual capacity increases, particularly during exercise (when this abnormality is known as dynamic hyperinflation), and this results in dyspnea and limitation of exercise capacity. Gas Exchange Abnormalities Result in hypoxemia and hypercapnia Mucus Hypersecretion It is due to mucous metaplasia with increased numbers of goblet cells and enlarged submucosal glands in response to chronic airway irritation by cigarette smoke and other noxious agents. Pulmonary Hypertension Due to hypoxic vasoconstriction of small pulmonary arteries, eventually resulting in structural changes that include intimal hyperplasia and later smooth muscle hypertrophy/hyperplasia Progressive pulmonary hypertension may lead to right ventricular hypertrophy and eventually to right-side cardiac failure (cor pulmonale). Systemic features • Cachexia: loss of fat free mass • Skeletal muscle wasting: apoptosis, disuse atrophy • Osteoporosis • Depression • Increased risk of cardiovascular disease: associated with ↑ CRP
  5. Physical examination should always include an estimate of the forced expiratory time (FET).13 Measure the time taken by a patient to exhale forcefully and completely through the open mouth after taking a maximum inspiration. The normal forced expiratory time is 3 seconds or less. Note any audible wheeze or cough. An increased FET indicates airways obstruction. The combination of a significant smoking history and an FET of 9 seconds or more is predictive of chronic obstructive pulmonary disease (positive LR 9.6). A peak flow meter or spirometer, however, will provide a more accurate measurement. NJ Talley
  6. Some patients with advanced disease have paradoxical inward movement of the rib cage with inspiration (Hoover&amp;apos;s sign), the result of alteration of the vector of diaphragmatic contraction on the rib cage as a result of chronic hyperinflation.
  7. CMDT 2010
  8. Only three interventions—smoking cessation, oxygen therapy in chronically hypoxemic patients, and lung volume reduction surgery in selected patients with emphysema—have been demonstrated to influence the natural history of patients with COPD.
  9. Repeated exacerbations (for example, 3 in the last 3 years) GOLD 2006
  10. These exacerbations are commonly precipitated by infection (more often viral than bacterial) or environmental factors. CMDT 2010