CHRONIC OBSTRUCTIVE PULMONARY DISEASE RESPIRTORY DEPARTMENT RENJI HOSPITAL DEFINITION OF COPD Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease state characterized by air.
Download ReportTranscript CHRONIC OBSTRUCTIVE PULMONARY DISEASE RESPIRTORY DEPARTMENT RENJI HOSPITAL DEFINITION OF COPD Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease state characterized by air.
CHRONIC OBSTRUCTIVE PULMONARY DISEASE RESPIRTORY DEPARTMENT RENJI HOSPITAL DEFINITION OF COPD Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease state characterized by air flow limitation that is not fully reversible. Air flow limitation is usually progressive and is associated with an abnormal inflammatory response of lungs to noxious particles or gases,primarily caused by cigarette smoking. Component of COPD The definition Include chronic bronchitis ,emphysema with airflow limitation. The definition exclude other causes of chronic airflow obstruction such as Pulmonary cystic fibrosis , diffuse panbronchiolitis and bronchiectasis etc. COPD Component part : Process of copd Chronic Bronchitis 慢性支气管炎 Obstructive emphysema 阻塞性肺气肿 COPD airflow limitation Pulmonary artery hypertension 肺动脉高压 Col pulmonal heart disease 肺心病 Chronic Bronchitis Chronic Bronchitis Chronic bronchitis is defined clinically as the presence of a cough productive of sputum not attributable to other causes on most days for at least 3 months over 2 consecutive years. Clinical and epidemiological term Chronic Bronchitis Chronic nonspecific inflammation Symptoms of cough and sputum production with or without gasping Recurrent attacks Chronic proceeding Classification of Chronic Bronchitis Simple type of Chronic Bronchitis (without gasping) Chronic Bronchitis with gasping Cough Sputum expectoration Cough Sputum expectoration Gasping Stages of Chronic Bronchitis Stages Time Courses Exacerbation In a week Chronic lag phase One month or longer stable Lasts for two months Diagnosis of chronic bronchitis Cough & Sputum expectoration & Gasping Three months /per year or longer Continuously longer than two years Exclude other lung and heart disease If shorter than three months /per year then definite objective evidences are demanded (such as X-Ray and lung function et al.)to diagnose. Obstructive Emphysema Definition of Emphysema Pulmonary emphysema (a pathological term) is characterized by abnormal,permanent enlargement of air spaces distal to the terminal bronchioles ,accompanied by destruction of their walls and hyperdistension leading to reduction in lung elastics recoil and airway obstruction. Classification of Emphysema Obstructive Emphysema senile Emphysema emphysema(Physiological) without Interstitial Emphysema Obstruction Compensating Emphysema Scarred Emphysema Risk factor for COPD Genes Exposure to particles • Tobacco smoke • Occupational dusts, organic and inorganic • Indoor air pollution from heating and cooking with biomass in poorly vented dwellings • Outdoor air pollution Lung Growth and Development Oxidative stress Gender/ Age/ Respiratory infections /Socioeconomic status Nutrition Comorbidities Pathogenesis of COPD 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 Involve neutrophils, macrophages, and lymphocytes. These cells release inflammatory mediators and interact with structural cells in the airways and lung parenchyma. Inflammatory Mediators The 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. Protease-Antiprotease Imbalance Protease-mediated destruction of elastin, a major connective tissue component in lung parenchyma, is an important feature of emphysema and is likely to be irreversible. Difference in inflammation between COPD and asthma Although both COPD and asthma are associated with chronic inflammation of the respiratory tract, there are marked differences in the inflammatory cells and mediators involved in the two diseases, which in turn account for differences in physiological effects, symptoms, and response to therapy . ASTHMA COPD 致敏介质 有害介质 COPD 气道炎症 CD8+ T-淋巴细胞 巨噬细胞 中性粒细胞 哮喘气道炎症 CD4+ T-淋巴细胞 嗜酸性细胞 完全可逆 气流受限 完全不可逆 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 . •Proximal airways (trachea, bronchi > 2 mm internal diameter) Goblet cells, enlarged submucosal glands (both leading to mucus hypersecretion), squamous metaplasia of epithelium •Peripheral airways (bronchioles < 2mm i.d.) 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) 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 Normal distal lung acinus Centriacinar(centrilobular) emphysema Panacinar emphysema •Pulmonary vasculature Thickening of intima, endothelial cell dysfunction, smooth muscle pulmonary hypertension. PATHOPHYSIOLOGY Airflow Limitation and Air Trapping •The inflammation, fibrosis, and luminal exudates in small airways is correlated with the reduction in FEV1and FEV1/FVC ratio. •The peripheral airway obstruction traps air during expiration,resulting in hyperinflation. •Emphysema is more associated with gas exchange abnormalities than with reduced FEV1. 炎症 小气道疾病： 肺实质破坏： 气道炎症 气道重塑 失去肺泡支撑 弹性回缩降低 气流受限 Gas Exchange Abnormalities VA/Q imbalance Reduced pulmonary vascular bed Mucus Hypersecretion Pulmonary Hypertension •Hypoxic vasoconstriction of small pulmonary arteries eventually result in structural changes that include intimal hyperplasia and later smooth muscle hypertrophy/hyperplasia. •The loss of the pulmonary capillary bed in emphysema may also contribute to increased pressure in the pulmonary circulation. •Progressive pulmonary hypertension may lead to right ventricular hypertrophy and eventually to right-side cardiac failure (cor pulmonale). Systemic features They have a major impact on survival and comorbid diseases. •Cachexia • a loss of skeletal muscle mass and weakness •increased likeliness of having osteoporosis, depression and chronic anemia. •Increased concentrations of inflammatory mediators, including TNF-, IL-6, and oxygen-derived free radicals, • There is an increase in the risk of cardiovascular diseases. Clinical Manifestation History : History of exposure to risk factors, Tobacco smoke. Occupational dusts and chemicals Smoke from home cooking and heating fuels. Age of onset :After middle age Season:winter Clinical Manifestation Symptoms: Gradually progressive dyspnea is the most common presenting character. Dyspnea that is: Progressive (worsens over time) Usually worse with exercise Persistent (present every day) Described by the patient as an “increased effort to breathe,”“heaviness,” “air hunger,” or “gasping.” •Chronic Cough May be intermittent and may be unproductive. •Chronic sputum production: Recurrent respiratory infection Recurrent attacks leading to cor pulmonal heart disease Unexpected Decreased weigh loss food appetite Physical Signs: Earlier period:Minimal/Nonspecific signs Advanced Stage: *Inspection: Barrel-shaped chest , accessory respiratory muscle participate , prolonged expiration during quiet breathing. *Palpation: Weakened fremitus vocalis Clinical Manifestation *Percussion : Hyperresonant depressed diaphragm, dimination of the area of absolute cardiac dullness. *Auscultation: Prolonged expiration ； reduced breath sounds; The presence of wheezing during quiet breathing Crackle can be heard if infection exist. The heart sounds are best heard over the xiphoid area. Auxillary Examination Chronic bronchitis Chest Radiograph(X-Ray) Non apparent abnormality Or thickened and increased of the lung markings are noted. Auxiliary Examination Chest X-Ray --emphysema Chest findings are also varible. Marked over inflation is noted with flattend and low diaphragm Intercostal space becomes widen A horizontal pattern of ribs A long thin heart shadow Decreased markings of lung peripheral vessels Chest X-Ray Auxiliary Examination Pulmonary function Test Determination of a forced vital capacity and FEV1is necessary for the diagnosis and assessment of the severity of the disease and helpful in following its progress. FEV1 /FVC is the best index of airflow obstruction。 Auxiliary Examination Pulmonary function Test diagnostic criteria A post-bronchodilator (FEV1)/forced vital capacity(FVC) ≤70% confirm the presence of airflow limitation that is not fully reversible. FEV1 %pred is used for evaluation of the severity of pulmonary function status. The FEV1 and the FEV1/FVC ratio fall progressively as the severity of COPD increases. Pulmonary function Test Elevations of total lung capacity (TLC) Functional reserve capacity(FRC) Residual volume(RV) RV/TLC>40% for emphysema Vital capacity (VC) Peak expiratory flow(PEF) spirometric classification of COPD FEV1/FVC mild <70% moderate <70% severe disease <70% Very severe < 70% FEV1%pred ≥80% 50~80% 30~50% ≤ 30%or<50% following with respiratory failure & right heart failure Auxiliary Examination CT(Computed tomography) : greater sensitivity and specificity for emphysema than CXR , especially for the diagnosis of bronchiectasis and evaluation of bullous disease Computed Tomography Labortory Examination Blood examination In excerbation or acute infection in airway, leucocytosis may be detected. Sputum examination 肺炎链球菌 streptococcus pneumonia 流感嗜血杆菌 Haemophilus influenzae 卡他莫拉菌 Moraxella catarrhalis 肺炎克雷白杆菌 klebsiella pneumonia Auxiliary Examination Blood gas analysis: Arterial blood gas analysis may reveal hypoxemia,particularly advanced disease. In patients with severe hypoxemia ,CO2 retention,it shows low arterial PO2 and high arterial PCO2. Diagnosis of COPD Clinical manifestation Auxiliary examinations Significant importance of Pulmonary function test Spirometry should be obtained in all patients with : Exposure to cigarettes ; Environmental or occupational pollutants; presence of cough ,sputum production or dyspnea Stage： Exacerbation: Gradually progressive Cough and sputum & Dyspnea and gasping Increased purulence sputum followed by recurrent respiratory infection. Stable : Stable systoms of Cough and sputum ,gasping and dyspnea are alleviated. Differential Diagnosis of COPD Suggestive features Diagnosis 1. Mid-life onset COPD 2. Slowly progressing symptoms 3. Long history of smoking 4.Dyspnea during exercise 5.largely irreversible airflow limitation Asthma 1.Early onset 2. Symptoms vary from day to day ---哮喘 3. Symptoms at the night/early morning 4. A family history 5. Airflow limitation that is largely reversible 6.largely reversible airflow limitation 7.Allergy,rhinitis,eczema Differential Diagnosis of COPD Suggestive features Diagnosis Pulmonary carcinoma Commonly occurs in patients - --肺癌 over 40 years old with cigarette smoking. Obvious radiological abnormality Tuberculosis ---肺结核 Onset at all ages Tuberculosis toxic syndrome Lung infiltrate on chest radiography Microbiological confirmation Sputum examination of positive TB bacterium can confirms the diagnosis Differential Diagnosis of COPD Diagnosis Suggestive features Bronchiect 1. Large volume of purulent sputum asis— 2. Commonly associated with bacterial infection 支扩 3. Coarse crack/clubbing on auscultation 4. Bronchial dilation and bronchial wall thickening on X-ray /CT Nonobstructivee mphysema pulmonary function tests Complication •chronic respiratory failure •Pneumothorax •Chronic pulmonary heart disease TREATMENT Aim Based on the principles of prevention of further progress of disease preservation and enhancement of pulmonary functional capacity avoidance of exacerbations in order to improve the quality of life. TREATMENT Stop smoking Avoid environment pollution Antibiotic therapy Bronchodilators Glucocorticoids Expectorant Respiratory stimulant Oxygen therapy Rehabilitation care Lung volume reduction surgery stable COPD(I)： avoid risk factors Education and smoking cessation Smoking cessation has the greatest capacity to influence the natural history of COPD. Control the occupational and environmental pollution stable COPD(II)： Drug therapy: Prevent and control symptoms , increase exercise capacity, reduce the frequency and severity of exacerbations , improve health status. Drug Therapy 1.Bronchodilators—支气管舒张剂 Bronchodilators are central to the symptomatic management of COPD. improve emptying of the lungs,reduce dynamic hyperinflation and improve exercise performance . Drug Therapy Bronchodilators Three major classes of bronchodilators: β2 - agonists: Short acting: salbutamol & terbutaline Long acting :Salmeterol & formoterol Anticholinergic agents: Ipratropium,tiotropium Theophylline (a weak bronchodilator, which may have some anti-inflammatory properties) Drug Therapy 2.Glucocorticoids Regular treatment with inhaled glucocorticoids is appropriate for symptomatic patients with anFEV1<50%pred and repeated exacerbations. Chronic treatment with systemic glucocorticoids should be avoided because of an unfavorable benefit-torisk ratio. 3. COMBINATION THERAPY Combination therapy of long acting ß2-agonists and inhaled corticosteroids show a significant additional effect on pulmonary function and a reduction in symptoms. Mainly in patients with an FEV1<50%pred Drug Therapy 4.Others: Antioxidant agents---抗氧化剂 Immunoregulators---免疫调节剂 Vaccine---疫苗 Traditional Chinese medicine---中医中药 Alpha-1 antitrypsin augmentation Mucolytic(mucokinetic,mucoregulator) agents Antitussives Oxygen Therapy Oxygen -- >15 h /d Long-term oxygen therapy (LTOT) improves survival,exercise,sleep and cognitive performance in patients with respiratory failure. The therapeutic goal is to maintain SaO2 ≥ 90% and PaO2 ≥ 60mmHg at sea level and rest . Long-term Oxygen therapy LTOT Indication: For patients with a PaO2 ≤ 55 mmHg or SaO2≤88% , with or without hypercapnia For patients with a PaO2 of 55~70（60）mmHg or SaO2≤89% as well as pulmonary hypertension / heart failure / polycythemia (hematocrit >55%) Pulmonary rehabilitation Nutrition Surgery: Bullectomy Lung volume reduction surgery(肺减容） Lung transplantation （肺移植） Manage exacerbation Identify the cause of exacerbation: Virus or Bacteria or Other uncertain reasons Assessment of severity: The proceeding history and disease must be considered and comparison is very important. Oxygen therapy Controlled oxygen therapy. Supplemental oxygen should be titrated to improve the patient’s hypoxemia. Adequate levels of oxygenation (PaO2 > 8.0 kPa, 60 mm Hg, or SaO2 > 90%) are easy to achieve in uncomplicated exacerbations, but CO2 retention can occur insidiously with little change in symptoms. Once oxygen is started, arterial rrr blood gases should be checked 30-60 minutes later to ensure satisfactory oxygenation without CO2 retention or acidosis. Bronchodilators : Increase dose and times properly Atomization and inhalation Glucocorticoids: Oral or intravenous glucocorticosteroids are recommended. Thirty to 40 mg of oral prednisolone daily for 7-10 days is effective and safe. Antibiotics Respiratory infection is the usual predisposing factor. It is advocated to select antibiotics according to culture of sputum and drugsensitivity test. Mechanical Ventilation Noninvasive Invasive Others: mechanical ventilation mechanical ventilation Chronic Pulmonary Heart Disease Respiratory Department Renji Hospital DEFINITIONS Enlargement of the right ventricle (RV) due to pulmonary artery hypertension which arises from structural or functional abnormalities of the lungs, chest wall ,vascular. RV FAILURE Cor pulmonale may be acute or chronic. The most common cause of acute cor pulmonale --- thromembolism The most common cause of chronic cor pulmonale ---copd Bronchial pulmonary diseases: The main diseases : chronic bronchitis, copd,(80%~90%) Others: asthma, bronchiectasis, pulmonary fibrosis,sarcoidosis Severe thoracic deformity: cause compression of the lung Pulmonary vascular diseases: primary pulmonary hypertention; pulmonary embolism Neuromuscular disorder PATHOLOGY Primary lung : Chronic bronchitis & pulmonary emphysema Pulmonary vessel : 1. Stenosis of pulmonary artery & thicken of the vessel wall 2. Loss and fracture of the alveolar capillary 3. Distortion of the pulmonary vascular bed PATHOLOGY Heart : Increase of the heart weight Thicken of the heart muscle The enlarged right ventricle 肺心病：右心壁增厚，右心腔扩张 Cor pulmonale PATHOPHYSIOLOGY •Pulmonary arterial hypertension—肺动脉高压 1. Structural Smooth muscular thickening of the smaller arteries Anatomic reduction of the vascular bed Pulmonary vascular remodeling--肺血管重建 PATHOPHYSIOLOGY •Pulmonary arterial hypertension 2. Functional Pulmonary vasoconstriction secondary to alveolar hypoxia, acidosis, and hypercapnia. 1.humoral factor—体液因素 2.tissue factor---组织因素 3.nerve factor---神经因素 PATHOPHYSIOLOGY • Pulmonary arterial hypertension 3. The increase of pulmonary blood flow ， blood volume and blood viscosity。 （caused by polycythemia secondary to hypoxia.） PATHOPHYSIOLOGY Failure of right ventricle: Pulmonary hypertension Myocardial anoxia Repeatedly pulmonary infection : effect of bacterial toxin to the heart Acid base disorder : arrhythmia Clinical Manifestation • Historial information varies with the underlying etiology. For COPD patient • Productive cough and dyspnea, wheezing • Breathlessness limits the patient's ability . • Dyspnea and cardiopalmus after movement •A history of emergency hospital admissions because of respiratory infection. •Dyspnea on exertion is the most common presenting manifestation of pulmonary hypertension. Clinical Manifestation Physical examination Compensation period : For copd Pulmonary arterial hypertension signs (S3) and a systolic murmur of tricuspid regurgitant P2>A2 a right ventricular parasternale impulse Clinical Manifestation .Decompensation Physical period examination Respiratory failure Respiratory infection is the usual predisposing factor . Clinical manifestation hypercapnia and hypoxia : Such as dyspnea,cyanosis,increase in heart rate,peripheral venous dilation. Sweaty and nero-psychiatric symptoms ( headaches, letharfy,exciation,delirium,tremor,tic,papilloedema,etc). Clinical Manifestation Physical examination Right ventricular failure Tachynea, elevated jugular venous pressure, right ventricular parasternum impulse hepatomegaly, peripheral edema positive hepatojugular reflux total cardia failure with arrhythmia X-Ray Diagnostic Criteria (I) Distension of the low right pulmonary artery trunk: Diameter transversa ＞15mm Or diameter transversa (right hyoppulmonary artery /trachea) ＞1．07 Or widen ＞2mm(compare to the primary right pulmonary artery trunk) (II) Midrange projecture of pulmonary artery trunk or the altitude ≥3mm X-Ray Diagnostic Criteria (III) Significant projecture of the conus portion ≥7mm (IV) Enlargement of the main pulmonary artery,rapid tapering of pulmonary arterial branches toward lung periphery (V) Right ventricle enlarged Various pulmonary parenchymal,pleural,and/or thoracic abnormalities dependent on underlying etiology of cor pulmonale. One item can be diagnosed. Electrocardiogram Diagnostic Criteria Main Conditions: Mean QRS axis ＞十90。 Vl R／S≥1 Marked clockwise rotation of the electric axis(V5 R／S ≤ 1） P-pulmonary pattern (an increase in P-wave amplitude ) RV1十SV5＞1．05mV aVR R／S or R／Q≥1 (except for myocardial infarction) V1－3 :QS、Qr、qr pattern Electrocardiogram Diagnostic Criteria Secondary Conditions: Low-voltage ORS in Limb lead Right bundle-branch block (Incomplete or rarely complete) One item in main condition can be diagnosed; Two or more than two items in secondary condition is to suspect. Echocardiogram Diagnostic Criteria Main Conditons(I) Internal diameter of right ventricular outflow tract ≥30mm Right ventricular internal dimension ≥ 20mm The thickeness of right ventricular anterior wall ≥ 5．0mm Left/right ventricular internal dimension ＜2 Echocardiogram Diagnostic Criteria Main Conditons(II) Internal dimension of right pulmonary artery ≥ 18mm or pulmonary artery trunk ≥ 20mm Right ventricular outflow tract/internal dimension of left atrium ＞1．4 Pulmonary artery hypertension signs(low awave ＜2mm) or midsystolic closure Echocardiogram Diagnostic Criteria Reference conditions: Interventricular septal thickness ≥ 12mm Pulsation altitude ＜5mm or paradoxical motion Right atrium enlarged ≥ 25mm Curve DE EF of anterior tricuspid leaflet accelerate; E-peak sharp ;AC period prolong . Low curve amplitude of anterior leaflet of mitral valve ,CE＜18mm;CD section slowly upgrade and prolong as horizontal position;EF rate of decay ＜ 90mm／s Echocardiogram Diagnostic Criteria Notice: The diagnostic criteria is only fit for the Detection Position of praecordium Patient who has lung or chest disease,could be diagnosed if he or she has two items above (including one main condition at least) Auxiliary Examination echocardiogram Arterial blood gases Analysis of blood Diagnosis Chronic respiratory disease or thoracic cage disease: Pulmonary arterial hypertension Right ventricular hypertrophy or dilatation Right heart insufficienacy Other reason heart diseases must be ruled out Differential Diagnosis Coronary artery disease: ---冠心病 Angina cordis, Myocardial infarction history & Left ventricular hypertrophy (EKG) Rheumatic heart disease:---风湿性心脏病 History & echocardiogram Myocardial disease: ---原发性心肌病 Without chronic respiratory disease Echocardiogram The total heart enlarged Complication: •Pulmonary encephalopathy •Acid-base disorder and electrolyte disturbances •Shock •DIC •Arrhythmia •Gastrointestinal hemorrhage Treatment Acute exacerbation period Antibiotics Respiratory insufficiency therapy: * Airway Management (Oxygen,Bronchidilator ,secretion clean) *Respiratory stimulant *Mechanical ventilation Acid-base imbalance and electrolyte disturbance Treatment(I) Acute exacerbation period Therapeutic principle of heart failure: *Antibiotics: most important *Oxygen : low concentration and careful administration are essential to avoid depressing respiratory drive and causing hypercapnea. * Bronchodilator: can reduce the effort of breathing and decrease dyspnea. beta-adrenergic stimulants, theophylline compounds Treatment(II) *Diuretic agent: low dose ,short course *Cardiant: Low dose,fast effect, quick metabolism Hypoxemia,acidosis and catecholamine excess can increase the adverse effects of digitalis. indications: • left heart failure; • Infection has been controlled and diuretic agent has been used,heart failure still exist; • Right heart failure without severe infection; •Cardiac arrhythmia Vasodilating agent: Control the arhythmia: Corticosteroids: The value is depend on the likely responsiveness of the underlying ventilatory functional abnormality. Others: prevent complication Treatment(III) Compensation: Breath training Elevate the power of resistance: Chinese medicine and immunoenhancer Improve nutritional status Home oxygen therapy Long term oxygen therapy is indicated for patients with persistent arterial hypoxemia at rest or after exercise (arterial oxygen tension consistently below 55mmHg while breathing room air. Treatment Preventive measure: Prevent respiratory infection Physical exercise Environmental health Stop smoking Lung function monitoring