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Leading Causes of Deaths U.S. 1998
Cause of Death 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. Number
Cancer Cerebrovascular disease (stroke) 538,947 Respiratory Diseases (COPD) 158,060 Accidents 114,381 Pneumonia and influenza 94,828 Diabetes 93,207 Suicide Nephritis 29,264 liver disease Chronic 26,295 causes of death All other 24,936
Facts About COPD
COPD is the 4th leading cause of death in the United States (behind heart disease, cancer, and cerebrovascular disease). In 2000, the WHO estimated 2.74 million deaths worldwide from COPD. In 1990, COPD was ranked 12th as a burden of disease; by 2020 it is projected to rank 5th.
Percent Change in Age-Adjusted Death Rates, U.S., 1965-1998
Proportion of 1965 Rate 3.0 2.5 2.0 1.5 1.0 0.5 0
Coronary Heart Disease
All Other Causes
1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998 1965 - 1998
Facts About COPD
Between 1985 and 1995, the number of physician visits for COPD in the United States increased from 9.3 million to 16 million. The number of hospitalizations for COPD in 1995 was estimated to be 500,000. Medical expenditures amounted to an estimated $14.7 billion.
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.
Age-Adjusted Death Rates for COPD, U.S., 1960-1995
Deaths per 100,000 60 50 40 30 20 10 0 1960
It is unusual for a person to have clinically apparent COPD without a history of smoking for at least 20 pack years, and most patients have at least 40 pack years of exposure. A pack year is the equivalent of smoking 20 cigarettes per day for a year
Definition of COPD （ 1 ）
COPD 是可以治疗 和预防的疾病
COPD 是一种具有气流受限特征的可以预防和治疗的 疾病，气流受限不完全可逆、呈进行性发展，与肺部 对香烟烟雾等有害气体或有害颗粒的异常炎症反应有 关 ＣＯＰＤ不仅影响肺，也可以引起显著的全身反应。
Global initiative for Chronic Obstructive Lung Disease ， GOLD 2006
Definition of COPD(2)
支气管扩张药用后 FEV1/FVC <70% 证实存在 气道受限不完全可逆
Patients with COPD have varying degrees of three pathologic processes, each associated with smoking: chronic bronchitis, small airways obstruction, and emphysema.
Chronic Bronchitis Peripheral Airway Disease Emphysema Reduction in Maximum Expiratory Flow
Chronic bronchitis is a clinical diagnosis, defined as the presence of chronic cough and sputum production for at least 3 months of the year for at least 2 consecutive years in the absence of any other disease. The anatomic basis of chronic bronchitis is hypertrophy and hyperplasia of the mucussecreting glands normally found in the epithelium of larger airways.
These cells increase in size and number; as a consequence, they are found in smaller diameter airways than in nonsmokers chronic bronchitis may contribute to the progression of airways obstruction.
Peripheral Airway Disease
the most striking increase in the resistance to airflow occurs in peripheral airways or bronchioles. The degree of abnormality in these airways is correlated with lung function. The mechanisms involved in these changes are unknown.
the enlargement of air spaces distal to the conducting airways There are two important types of emphysema, centrilobular and panacinar. Centrilobular emphysema primarily involves the respiratory bronchioles , Panacinar emphysema involves the entire distal lung unit
α1-antitrypsin (AAT) deficiency
severe panacinar emphysema associated with α1-antitrypsin (AAT) deficiency. AAT is an acute phase serum protein that is secreted by the liver and that binds to and neutralizes neutrophil elastase; it is the most abundant antiprotease in the lung periphery. but it is not clear
Reduction in Maximum Expiratory Flow
Reduced expiratory flow is the hallmark of COPD the lung's elastic recoil is reduced by emphysema, and airways resistance is increased. Maximum expiratory flow is reduced, and even less effort than normal causes limitation of flow.
Tests of maximum expiratory flow, such as the flow-volume curve and the FEV1, are of clinical value because they reflect major pathologic processes in COPD and are relatively insensitive to a patient's effort and cooperation beyond a threshold minimum effort.
Lung Function Dyspnea
The decrease in maximum expiratory flow that characterizes COPD is most easily identified in terms of a reduction in FEV1 that is larger than the reduction in vital capacity, measured in the same forced expiratory maneuver and termed the forced vital capacity (FVC) lower ratios indicate airways obstruction <70%
Both the FEV1 and the FVC may increase after treatment with an inhaled bronchodilator, but the FEV1 does not attain normal values in COPD, whereas it can return to normal in patients with asthma
Hyperinflation of the lungs, which is often manifested as an increase in total lung capacity, is characteristic of COPD and reflects loss of lung recoil and limitation of expiratory flow. Residual volume often is increased even in mild cases of COPD. Functional residual capacityis routinely increased in moderate and severe COPD.
Arterial hypoxemia with or without carbon dioxide retention is common in severe COPD. Hypoxemia generally precedes carbon dioxide retention, rarely occurs in patients with an FEV1 in excess of 40% of the predicted normal value, and is common when the FEV1 is less than 30% of the predicted value. Gas exchange abnormalities in COPD are due to abnormally large differences in ventilationperfusion ratios among units in the lung.
Dyspnea is the major cause of disability in COPD. It arises from a sense of increased muscle effort to breathe in relation to the level of ventilation achieved
Normal subjects, even at the most strenuous levels of exercise, use only 60 to 70% of their maximum voluntary ventilation and never experience dyspnea comparable to that of diseased patients. Patients with obstructive airways disease usually characterize dyspnea as difficulty in inspiring because airways obstruction changes the shape of the chest wall and puts the inspiratory muscles at a mechanical disadvantage.
Expiratory flow limitation does not permit adequate expiration at normal lung volumes, so patients breathe at increased lung volumes This hyperinflation renders inspiratory muscles relatively ineffective, so that greater inspiratory effort is required to achieve the needed ventilation,
The degree of dyspnea in patients with COPD generally correlates inversely with the FEV1, but patients with similar degrees of airways obstruction may complain of different degrees of dyspnea. Careful assessment of dyspnea is a useful way to follow the progress of patients with COPD.
Diagnosis of COPD is based on a history of exposure to risk factors and the presence of airflow limitation that is not fully reversible, with or without the presence of symptoms.
Patients who have chronic cough and sputum production with a history of exposure to risk factors should be tested for airflow limitation, even if they do not have dyspnea.
Diagnosis of COPD
SYMPTOMS cough sputum dyspnea EXPOSURE TO RISK FACTORS tobacco occupation indoor/outdoor pollution
COPD is insidious . Dyspnea typically does not occur until the FEV1 is about 50% of normal, when the disease has usually been present for decades. Patients with COPD often have a history of chronic bronchitis that has antedated the onset of dyspnea
first experienced during episodes of acute bronchitis. Eventually, dyspnea becomes consistent being present at rest Wheezing is also common in COPD, usually with exertion, but may occur at rest in severe disease
Patients with COPD have periodic exacerbations, marked by increased dyspnea, wheezing, cough, and sputum production.. Exacerbations usually occur in the winter, often with upper respiratory infections, and are more common in patients with symptomatic chronic bronchitis and in those with severe obstruction. Exacerbations of COPD are the most common cause of hospitalization and result in substantial morbidity.
Some patients with COPD lose weight and muscle mass especially in the presence of severe emphysema. Weight loss is an ominous prognostic sign in COPD
the physical examination is usually normal. In severe disease, signs are often apparent The breathing rate is increased, often to more than 20 breaths per minute at rest in patients with hypoxemia or carbon dioxide retention.
Physical signs the appearance of a barrel chest with increased anteroposterior diameter, relatively low-lying diaphragms, and faint heart sounds. Patients with severe disease use the strap muscles of the neck during inspiration..
Breath sounds are often diminished, and both crackles and wheezes may be heard. Hypoxemic patients may be cyanotic In advanced disease, secondary pulmonary hypertension ,leads to right-sided heart failure
Spirometry, the measurement of the FEV1 and FVC, is the “gold standard” for diagnosis of COPD and is easy to perform in the office setting Airways obstruction (FEV1/FVC < 0.70) in a person with at least 20 pack years of tobacco exposure is a presumptive diagnosis of COPD.
Spirometry: Normal and COPD
0 1 2 Liter 3 FEV1 FEV1 FVC
80 % 60 %
4 5 1 2 FEV1
FVC 5 6 Seconds
Classification by Severity
0: At risk I: Mild II: Moderate
Normal spirometry Chronic symptoms (cough, sputum) FEV1/FVC < 70%; FEV1 ≥ 80% predicted With or without symptoms (cough, sputum) FEV1/FVC < 70%; 30% ≤ FEV1 < 80% predicted (IIA: 50% ≤ FEV1 < 80% predicted; IIB: 30% ≤ FEV1 < 50% predicted) With or without chronic symptoms (cough, sputum,
dyspnea) III: Severe
FEV1/FVC < 70%; FEV1 < 30% predicted or FEV1 < 50%predicted plus respiratory failure or clinical signs of right heart failure
Routine chest radiographs are insensitive for detecting COPD In advanced cases, patients develop hyperinflation with flattened diaphragms, increased retrosternal air space, and an apparently small, vertical heart ( Fig. 88-4 ). Increased or decreased lung markings and thin-walled bullae may be seen. Signs of pulmonary hypertension, including fullness of the main pulmonary arteries, are occasionally observed.
Computed tomographic (CT)
Computed tomographic (CT) scans are of considerable value in assessing the presence, distribution, and extent of emphysema. There are no standard grading systems. Emphysematous spaces are seen as “holes” in the lung
Patients thought to have COPD should undergo full pulmonary function testing at least once Testing should also include repeated spirometry at yearly intervals and when the patient is acutely ill. If the FEV1 is less than 40% of the predicted normal value, arterial blood gas analysis is advisable Annual chest radiographs should be performed only if the patient is a candidate for cancer surgery. Finally, the degree of dyspnea should be documented carefully, as should dietary intake, weight loss, and occurrence of exacerbations.
The most difficult disease to differentiate from COPD is asthma Asthma typically begins early in life with episodes of dyspnea and wheezing of rapid onset and that reverse rapidly and completely. However, patients with asthma can develop chronic airways obstruction that reverses little with therapy,
In these instances, the difference between asthma and COPD can become a matter of semantics.
Fortunately, the therapies for asthma and COPD are similar enough so that diagnostic uncertainties between these two entities should have little impact on management of the patient.
Management of COPD
Management of COPD (1)
The goals of COPD management include: • Relieve symptoms • Prevent disease progression • Improve exercise tolerance • Improve health status • Prevent and treat complications • Prevent and treat exacerbations • Reduce mortality • Prevent or minimize side effects from treatment. Cessation of cigarette smoking should be included as a goal throughout the management program.
Management of COPD (2)
These goals can be achieved through implementation of a COPD management program with four components:
1. Assess and Monitor Disease 2. Reduce Risk Factors 3. Manage Stable COPD 4. Manage Exacerbations
GOLD Workshop Report
Four Components of COPD Management
• Assess and monitor disease • Reduce risk factors • Manage stable COPD
q q q
Education Pharmacologic Non-pharmacologic
• Manage exacerbations
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 to reduce the risk of developing COPD and stop its progression (Evidence A).
Reduce Risk Factors Key Points
Brief tobacco dependence treatment is effective (Evidence A), and every tobacco user should be offered at least this treatment at every visit to a health care provider. Three types of counseling are especially effective: practical counseling, social support as part of treatment, and social support arranged outside of treatment (Evidence A).
Reduce Risk Factors Key Points
Several effective pharmacotherapies for tobacco dependence are available (Evidence A), and at least one of these medications should be added to counseling if necessary, and in the absence of contraindications.
Reduce Risk Factors Key Points
Progression of many occupationally-induced respiratory disorders can be reduced or controlled through a variety of strategies aimed at reducing the burden of inhaled particles and gases (Evidence B).
Brief Strategies To Help The Patient Willing To Quit Smoking
• ASK visit. • ADVISE • ASSESS • ASSIST Systematically identify all tobacco users at every Strongly urge all tobacco users to quit. Determine willingness to make a quit attempt. Aid the patient in quitting.
• ARRANGE Schedule follow-up contact.
Manage Stable COPD Key Points
The overall approach to managing stable COPD should be characterized by a stepwise increase in the treatment, depending on the severity of the disease. For patients with COPD, health education can play a role in improving skills, ability to cope with illness, and health status. It is effective in accomplishing certain goals, including smoking cessation (Evidence A).
Smoking cessation is the only treatment that has been shown to alter the course of COPD. Smoking cessation when the FEV1 exceeds 50% of the predicted normal value either averts or greatly delays the onset of symptomatic disease. It is probably never too late for patients with COPD to stop smoking.
Inhaled bronchodilators afford symptomatic relief in COPD and should be prescribed for all patients who find them helpful Bronchodilator medications are central to the symptomatic management of COPD (Evidence A). They are given on an as-needed basis or on a regular basis to prevent or reduce symptoms. The principal bronchodilator treatments are Beta2agonists, anticholinergics, theophylline, and a combination of these drugs (Evidence A).
Short-acting β2-agonists have rapid onset of action and are useful as rescue agents on a discretionary basis. Albuterol is the prototypical short-acting β2agonist; the normal dose is 200 μg (two puffs from a metered-dose inhaler). Ipratropium bromide is an inhaled anticholinergic drug that is as effective as β2agonists in COPD.
Because it has a slower onset of action, it is usually given on a schedule of three or four times a day at a dose of 36 μg (two puffs from a metered-dose inhaler). Higher doses of these drugs are of benefit in some patients, and many use both; a combination inhaler is available. Longer acting β2 agents, such as salmeterol (50 μg) and formoterol (12 μg), have durations of action up to 12 hours
Theophylline is less effective, although some patients receive symptomatic benefit when theophylline is added to inhaled agents, and a trial of theophylline is reasonable in patients with severe dyspnea. Serum levels should be measured, and a target of about 10 μg/mL is usually achieved with a dose of approximately 300 mg twice a day.
Inhaled steroids do not change the long-term rate of decline in lung function in COPD, but inhaled steroid therapy may produce a small (about 200 mL) onetime increase in FEV1. Of greater importance is evidence that inhaled steroids reduce the frequency and severity of exacerbations and reduce mortality in COPD. Patients with severe disease and multiple exacerbations should be given inhaled steroids in relatively high doses,
The combined use of a long-acting β-agonist with an inhaled steroid produces better control of symptoms without increased side effects compared with either used alone .
COPD patients benefit from pulmonary rehabilitation. The major component of rehabilitation programs is exercise training. Regular exercise improves exercise tolerance and quality of life in patients with COPD. In addition, rehabilitation programs teach coping skills and self-reliance, and they tend to reduce anxiety and depression.
home oxygen therapy
The long-term administration of oxygen (> 15 hours per day) to patients with chronic respiratory failure has been shown to increase survival (Evidence A).
stable patients with arterial Po2 below 60 mm Hg. Acceptable blood gas levels (Po2 of 65 to 80 mm Hg) can usually be achieved with oxygen flows of 2 L/min delivered by nasal cannula.
in such patients during sleep or exercise : some patients who are not hypoxemic during the day exhibit hypoxemia while asleep, many patients with severe COPD develop significant hypoxemia with exercise
Surgical approaches to COPD include lung transplantation and lung volume reduction surgery Lung transplantation is falling out of favor because it is not clear that it prolongs useful life. Lung volume reduction surgery involves removal of substantial amounts of emphysematous lung as identified by CT scan
Influenza vaccine should be administered annually to all patients with COPD to prevent exacerbations. Pneumococcal vaccination is also recommended because pneumococcal pneumonia is devastating in these patients
Management of COPD: All stages
Avoidance of noxious agents
- smoking cessation - reduction of indoor pollution - reduction of occupational exposure
Management of COPD Stage 0: At Risk
Characteristics Treatment • Chronic symptoms - cough - sputum • No spirometric abnormalities Recommended
Management of COPD Stage I: Mild COPD
Characteristics Treatment • FEV1/FVC < 70 % • FEV1 > 80 % predicted • With or without symptoms Recommended
bronchodilator as needed
Management of COPD Stage IIA: Moderate COPD
Characteristics Treatment •FEV1/FVC < 70% •50% < FEV1< 80% predicted •With or without symptoms Recommended •Regular treatment with one or more bronchodilators •Rehabilitation •Inhaled glucocorticosteroids if significant symptoms and lung function response
Management of COPD Stage IIB: Moderate COPD
Characteristics Treatment •FEV1/FVC < 70% •30% < FEV1 < 50% predicted •With or without symptoms Recommended Regular treatment with one or more bronchodilators •Rehabilitation •Inhaled glucocortico-steroids if significant symptoms and lung function response or if repeated
Management of COPD Stage III: Severe COPD
Characteristics Treatment •FEV1/FVC < 70% •FEV1 < 30% predicted or presence of respiratory failure or right heart failure Recommended
•Regular treatment with one or more bronchodilators •Inhaled glucocorticosteroids if significant symptoms and lung function response or if repeated exacerbations •Treatment of complications •Rehabilitation •Long-term oxygen therapy if respiratory failure •Consider surgical options
Manage ExacerbationsKey Points
Exacerbations of respiratory symptoms requiring medical intervention are important clinical events in COPD. 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 (Evidence B).
Manage Exacerbations Key Points
Inhaled bronchodilators (Beta2-agonists and/or anticholinergics), theophylline, and systemic, preferably oral, glucocorticosteroids are effective for the treatment of COPD exacerbations (Evidence A).
Manage Exacerbations Key Points
Patients experiencing COPD exacerbations with clinical signs of airway infection (e.g., increased volume and change of color of sputum, and/or fever) may benefit from antibiotic treatment (Evidence B)
Sputum smear and culture are not usually helpful, and empirical treatment is the rule. In low-risk patients, inexpensive antibiotics such as amoxicillin and trimethoprimsulfamethoxazole may be used for 10 days, but bacterial resistance to these agents is common.
In severe exacerbations, systemic steroid therapy has been shown to result in a relatively rapid recovery, and the equivalent of 40 mg of prednisone per day for 10 to 14 days is justifiable. It is reasonable to give compliant patients with COPD a supply of antibiotics and steroids so they self-treat exacerbations.
In severe exacerbations seen in the hospital or emergency department, other diagnoses must be considered. Exacerbations of COPD must be distinguished from pneumonia , pneumothorax and pulmonary embolism
Pneumonia and pneumothorax usually can be diagnosed by the chest radiograph. In patients with signs and symptoms typical of pneumonia, especially substantial fevers or elevated white blood cell counts, empirical treatment of pneumonia is appropriate until it can be excluded.
Pulmonary embolism can be difficult to diagnose in patients with COPD, and spiral CT angiography should be used if embolic disease is suspected
Exacerbations of COPD are often accompanied by hypoxemia, which can precipitate heart failure angina an acute coronary syndrome or hypoxic death in susceptible individuals. Hypoxemia may also cause an acute worsening of pulmonary hypertension or systemic hypertension It is essential to measure the arterial Po2 and to treat hypoxemia with oxygen.
Severe exacerbations of COPD require hospitalization and should be treated with bronchodilator therapy, intravenous antibiotics, and steroids. Arterial blood gases should be measured and oxygen therapy instituted. In COPD, uncontrolled high-flow oxygen carries the risk of precipitating carbon dioxide narcosis, and the initial goals should be to maintain arterial Po2 at levels of about 60 mm Hg In patients who can be discharged from the emergency department, a 10-day course of 40 mg of prednisone per day improves symptoms and reduces the relapse rate