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Chronic Obstructive Pulmonary Disease (COPD)

(Chronic Obstructive Bronchitis; Emphysema)


Robert A. Wise

, MD, Johns Hopkins Asthma and Allergy Center

Last full review/revision Jun 2020| Content last modified Jun 2020
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Chronic obstructive pulmonary disease (COPD) is airflow limitation caused by an inflammatory response to inhaled toxins, often cigarette smoke. Alpha-1 antitrypsin deficiency and various occupational exposures are less common causes in nonsmokers. Symptoms are productive cough and dyspnea that develop over years; common signs include decreased breath sounds, prolonged expiratory phase of respiration, and wheezing. Severe cases may be complicated by weight loss, pneumothorax, frequent acute decompensation episodes, right heart failure, and/or acute or chronic respiratory failure. Diagnosis is based on history, physical examination, chest x-ray, and pulmonary function tests. Treatment is with bronchodilators, corticosteroids, and, when necessary, oxygen and antibiotics. Lung volume reduction procedures or transplantation are used in advanced disease. About 50% of patients with severe COPD die within 10 years of diagnosis.

COPD comprises

  • Chronic obstructive bronchitis (clinically defined)

  • Emphysema (pathologically or radiologically defined)

Many patients have features of both.

Chronic obstructive bronchitis is chronic bronchitis with airflow obstruction. Chronic bronchitis is defined as productive cough on most days of the week for at least 3 months total duration in 2 successive years. Chronic bronchitis becomes chronic obstructive bronchitis if spirometric evidence of airflow obstruction develops. Chronic asthmatic bronchitis is a similar, overlapping condition characterized by chronic productive cough, wheezing, and partially reversible airflow obstruction; it occurs predominantly in smokers with a history of asthma Asthma Asthma is a disease of diffuse airway inflammation caused by a variety of triggering stimuli resulting in partially or completely reversible bronchoconstriction. Symptoms and signs include dyspnea... read more . In some cases, the distinction between chronic obstructive bronchitis and chronic asthmatic bronchitis is unclear and may be referred to as asthma COPD overlap (ACO).

Emphysema is destruction of lung parenchyma leading to loss of elastic recoil and loss of alveolar septa and radial airway traction, which increases the tendency for airway collapse. Lung hyperinflation, airflow limitation, and air trapping follow. Airspaces enlarge and may eventually develop blebs or bullae. Obliteration of small airways is thought to be the earliest lesion that precedes the development of emphysema.

Epidemiology of COPD

In the US, about 24 million people have airflow limitation, of whom about 16 million have a diagnosis of COPD. COPD is the 3rd leading cause of death, resulting in more than 140,000 deaths each year—compared with 52,193 deaths in 1980. From 1980 to 2000, the COPD mortality rate increased 64% (from 40.7 to 66.9/100,000) and has remained steady since then. Prevalence, incidence, and mortality rates increase with age. Prevalence is higher in women, but total mortality is similar in both sexes. COPD seems to aggregate in families independent of alpha-1 antitrypsin deficiency Alpha-1 Antitrypsin Deficiency Alpha-1 antitrypsin deficiency is congenital lack of a primary lung antiprotease, alpha-1 antitrypsin, which leads to increased protease-mediated tissue destruction and emphysema in adults.... read more (alpha-1 antiprotease inhibitor deficiency).

COPD is increasing worldwide because of the increase in smoking in developing countries, the reduction in mortality due to infectious diseases, and the widespread use of biomass fuels such as wood, grasses, or other organic materials. COPD mortality may also affect developing nations more than developed nations. COPD affects 64 million people and caused 3.2 million deaths worldwide in 2015 and is projected to become the 3rd leading cause of death globally by the year 2030.

Etiology of COPD

There are 2 main causes of COPD:

  • Smoking (and less often other inhalational exposures)

  • Genetic factors

Inhalational exposure

Of all inhalational exposures, cigarette smoking is the primary risk factor in most countries, although only about 15% of smokers develop clinically apparent COPD; an exposure history of 40 or more pack-years is especially predictive. Smoke from indoor cooking and heating is an important causative factor in developing countries. Smokers with preexisting airway reactivity (defined by increased sensitivity to inhaled methacholine), even in the absence of clinical asthma, are at greater risk of developing COPD than are those without.

Low body weight, childhood respiratory disorders, and exposure to passive cigarette smoke, air pollution, and occupational dust Overview of Environmental Pulmonary Disease Environmental pulmonary diseases result from inhalation of dusts, allergens, chemicals, gases, or environmental pollutants. The lungs are continually exposed to the external environment and... read more (eg, mineral dust, cotton dust) or inhaled chemicals (eg, cadmium) contribute to the risk of COPD but are of minor importance compared with cigarette smoking.

Genetic factors

More than 30 genetic alleles have been found to be associated with COPD or decline in lung function in selected populations, but none has been shown to be as consequential as alpha-1 antitrypsin.

Pathophysiology of COPD

Various factors cause the airflow limitation and other complications of COPD.


Inhalational exposures can trigger an inflammatory response in airways and alveoli that leads to disease in genetically susceptible people. The process is thought to be mediated by an increase in protease activity and a decrease in antiprotease activity. Lung proteases, such as neutrophil elastase, matrix metalloproteinases, and cathepsins, break down elastin and connective tissue in the normal process of tissue repair. Their activity is normally balanced by antiproteases, such as alpha-1 antitrypsin, airway epithelium–derived secretory leukoproteinase inhibitor, elafin, and matrix metalloproteinase tissue inhibitor. In patients with COPD, activated neutrophils and other inflammatory cells release proteases as part of the inflammatory process; protease activity exceeds antiprotease activity, and tissue destruction and mucus hypersecretion result.

Neutrophil and macrophage activation also leads to accumulation of free radicals, superoxide anions, and hydrogen peroxide, which inhibit antiproteases and cause bronchoconstriction, mucosal edema, and mucous hypersecretion. Neutrophil-induced oxidative damage, release of profibrotic neuropeptides (eg, bombesin), and reduced levels of vascular endothelial growth factor may contribute to apoptotic destruction of lung parenchyma.

The inflammation in COPD increases as disease severity increases, and, in severe (advanced) disease, inflammation does not resolve completely despite smoking cessation. This chronic inflammation does not seem to respond to corticosteroids.


Respiratory infection (which COPD patients are prone to) may amplify progression of lung destruction.

Bacteria, especially Haemophilus influenzae Haemophilus Infections The gram-negative bacteria Haemophilus species cause numerous mild and serious infections, including bacteremia, meningitis, pneumonia, sinusitis, otitis media, cellulitis, and epiglottitis... read more , colonize the lower airways of about 30% of patients with COPD. In more severely affected patients (eg, those with previous hospitalizations), colonization with Pseudomonas aeruginosa Pseudomonas and Related Infections Pseudomonas aeruginosa and other members of this group of gram-negative bacilli are opportunistic pathogens that frequently cause hospital-acquired infections, particularly in ventilator... read more or other gram-negative bacteria is common. Smoking and airflow obstruction may lead to impaired mucus clearance in lower airways, which predisposes to infection. Repeated bouts of infection increase the inflammatory burden that hastens disease progression. There is no evidence, however, that long-term use of antibiotics slows the progression of COPD.

Airflow limitation

The cardinal pathophysiologic feature of COPD is airflow limitation caused by airway narrowing and/or obstruction, loss of elastic recoil, or both.

Airway narrowing and obstruction are caused by inflammation-mediated mucus hypersecretion, mucus plugging, mucosal edema, bronchospasm, peribronchial fibrosis, and remodelling of small airways or a combination of these mechanisms. Alveolar septa are destroyed, reducing parenchymal attachments to the airways and thereby facilitating airway closure during expiration.

Enlarged alveolar spaces sometimes consolidate into bullae, defined as airspaces 1 cm in diameter. Bullae may be entirely empty or have strands of lung tissue traversing them in areas of locally severe emphysema; they occasionally occupy the entire hemithorax. These changes lead to loss of elastic recoil and lung hyperinflation.

Increased airway resistance increases the work of breathing. Lung hyperinflation, although it decreases airway resistance, also increases the work of breathing. Increased work of breathing may lead to alveolar hypoventilation with hypoxia and hypercapnia, although hypoxia and hypercarbia can also be caused by ventilation/perfusion (V/Q) mismatch.


In addition to airflow limitation and sometimes respiratory insufficiency, complications include

  • Pulmonary hypertension

  • Respiratory infection

  • Weight loss and other comorbidities

Viral or bacterial respiratory infections are common among patients with COPD and cause a large percentage of acute exacerbations. It is currently thought that acute bacterial infections are due to acquisition of new strains of bacteria rather than overgrowth of chronic colonizing bacteria.

Weight loss may occur, perhaps in response to decreased caloric intake and increased levels of circulating tumor necrosis factor (TNF)-alpha.

Other coexisting or complicating disorders that adversely affect quality of life and/or survival include osteoporosis Osteoporosis Osteoporosis is a progressive metabolic bone disease that decreases bone mineral density (bone mass per unit volume), with deterioration of bone structure. Skeletal weakness leads to fractures... read more Osteoporosis , depression Depressive Disorders Depressive disorders are characterized by sadness severe enough or persistent enough to interfere with function and often by decreased interest or pleasure in activities. Exact cause is unknown... read more , anxiety Overview of Anxiety Disorders Everyone periodically experiences fear and anxiety. Fear is an emotional, physical, and behavioral response to an immediately recognizable external threat (eg, an intruder, a car spinning on... read more , coronary artery disease Overview of Coronary Artery Disease Coronary artery disease (CAD) involves impairment of blood flow through the coronary arteries, most commonly by atheromas. Clinical presentations include silent ischemia, angina pectoris, acute... read more Overview of Coronary Artery Disease , lung cancer Overview of Lung Tumors Lung tumors may be Primary Metastatic from other sites in the body Primary tumors of the lung may be Malignant (see table Classification of Primary Malignant Lung Tumors) read more and other cancers, muscle atrophy, and gastroesophageal reflux Gastroesophageal Reflux Disease (GERD) Incompetence of the lower esophageal sphincter allows reflux of gastric contents into the esophagus, causing burning pain. Prolonged reflux may lead to esophagitis, stricture, and rarely metaplasia... read more Gastroesophageal Reflux Disease (GERD) . The extent to which these disorders are consequences of COPD, smoking, and the accompanying systemic inflammation is unclear.

Symptoms and Signs of COPD

COPD takes years to develop and progress. Most patients have smoked 20 cigarettes/day for > 20 years.

  • Productive cough usually is the initial symptom, developing among smokers in their 40s and 50s.

  • Dyspnea that is progressive, persistent, exertional, or worse during respiratory infection appears when patients are in their late 50s or 60s.

Symptoms usually progress quickly in patients who continue to smoke and in those who have a higher lifetime tobacco exposure. Morning headache develops in more advanced disease and signals nocturnal hypercapnia or hypoxemia.

Signs of COPD include wheezing, a prolonged expiratory phase of breathing, lung hyperinflation manifested as decreased heart and lung sounds, and increased anteroposterior diameter of the thorax (barrel chest). Patients with advanced emphysema lose weight and experience muscle wasting that has been attributed to immobility, hypoxia, or release of systemic inflammatory mediators, such as TNF-alpha.

Signs of advanced disease include pursed-lip breathing, accessory respiratory muscle use, paradoxical inward movement of the lower rib cage during inspiration (Hoover sign), and cyanosis. Signs of cor pulmonale include neck vein distention, splitting of the 2nd heart sound with an accentuated pulmonic component, tricuspid insufficiency murmur, and peripheral edema. Right ventricular heaves are uncommon in COPD because the lungs are hyperinflated.

Spontaneous pneumothorax may occur (possibly related to rupture of bullae) and should be suspected in any patient with COPD whose pulmonary status abruptly worsens.


Acute exacerbations

Acute exacerbations occur sporadically during the course of COPD and are heralded by increased symptom severity. The specific cause of any exacerbation is almost always impossible to determine, but exacerbations are often attributed to viral upper respiratory infections, acute bacterial bronchitis, or exposure to respiratory irritants. As COPD progresses, acute exacerbations tend to become more frequent, averaging about 1 to 3 episodes/year.

Diagnosis of COPD

  • Chest x-ray

  • Pulmonary function testing


Systemic disorders that may have a component of airflow limitation may suggest COPD; they include HIV infection Human Immunodeficiency Virus (HIV) Infection Human immunodeficiency virus (HIV) infection results from 1 of 2 similar retroviruses (HIV-1 and HIV-2) that destroy CD4+ lymphocytes and impair cell-mediated immunity, increasing risk of certain... read more Human Immunodeficiency Virus (HIV) Infection , abuse of IV drugs (particularly cocaine and amphetamines), sarcoidosis Sarcoidosis Sarcoidosis is an inflammatory disorder resulting in noncaseating granulomas in one or more organs and tissues; etiology is unknown. The lungs and lymphatic system are most often affected, but... read more Sarcoidosis , Sjögren syndrome Sjögren Syndrome Sjögren syndrome is a relatively common chronic, autoimmune, systemic, inflammatory disorder of unknown cause. It is characterized by dryness of the mouth, eyes, and other mucous membranes... read more Sjögren Syndrome , bronchiolitis obliterans Occupational Asthma Occupational asthma is reversible airway obstruction that develops after months to years of sensitization to an allergen encountered in the workplace. Symptoms are dyspnea, wheezing, cough,... read more , lymphangioleiomyomatosis Lymphangioleiomyomatosis Lymphangioleiomyomatosis (LAM) is an indolent, progressive growth of smooth muscle cells throughout the lungs, pulmonary blood vessels, lymphatics, and pleurae. It is rare and occurs in young... read more Lymphangioleiomyomatosis , and eosinophilic granuloma. COPD can be differentiated from interstitial lung diseases Overview of Interstitial Lung Disease Interstitial lung diseases are a heterogeneous group of disorders characterized by alveolar septal thickening, fibroblast proliferation, collagen deposition, and, if the process remains unchecked... read more by chest imaging, which shows increased interstitial markings in interstitial lung disease, and pulmonary function testing, which shows a restrictive ventilatory defect rather than an obstructive ventilatory defect. In some patients, COPD and interstitial lung disease coexist (combined pulmonary fibrosis and emphysema [CPFE]) in which lung volumes are relatively preserved, but gas exchange is severely impaired.

Pulmonary function tests

Patients suspected of having COPD should undergo pulmonary function testing Overview of Tests of Pulmonary Function Pulmonary function tests provide measures of airflow, lung volumes, gas exchange, response to bronchodilators, and respiratory muscle function. Basic pulmonary function tests available in the... read more to confirm airflow limitation, to quantify its severity and reversibility, and to distinguish COPD from other disorders. Pulmonary function testing is also useful for following disease progression and monitoring response to treatment. The primary diagnostic tests are

  • FEV1: The volume of air forcefully expired during the first second after taking a full breath

  • Forced vital capacity (FVC): The total volume of air expired with maximal force

  • Flow-volume loops: Simultaneous spirometric recordings of airflow and volume during forced maximal expiration and inspiration

Reductions of FEV1, FVC, and the ratio of FEV1/FVC are the hallmark of airflow limitation. Flow-volume loops show a concave pattern in the expiratory tracing (see figure Flow-volume loops Flow-volume loops Flow-volume loops ).

There are 2 basic pathways by which COPD can develop and manifest with symptoms in later life:

  • In the first pathway, patients may have normal lung function in early adulthood, which is followed by an increased decline in FEV1 (about ≥ 60 mL/year).

  • With the 2nd pathway, patients have impaired lung function in early adulthood, often associated with asthma or other childhood respiratory disease. In these patients, COPD may present with a normal age-related decline in FEV1 (about 30 mL/year).

Although this 2nd pathway model is conceptually helpful, a wide range of individual trajectories is possible (1 Diagnosis references Chronic obstructive pulmonary disease (COPD) is airflow limitation caused by an inflammatory response to inhaled toxins, often cigarette smoke. Alpha-1 antitrypsin deficiency and various occupational... read more Diagnosis references ). When the FEV1 falls below about 1 L, patients develop dyspnea during activities of daily living (although dyspnea is more closely related to the degree of dynamic hyperinflation [progressive hyperinflation due to incomplete exhalation] than to the degree of airflow limitation). When the FEV1 falls below about 0.8 L, patients are at risk of hypoxemia, hypercapnia, and cor pulmonale Cor Pulmonale Cor pulmonale is right ventricular enlargement secondary to a lung disorder that causes pulmonary artery hypertension. Right ventricular failure follows. Findings include peripheral edema, neck... read more Cor Pulmonale .

FEV1 and FVC are easily measured with office spirometry. Normal reference values are determined by patient age, sex, and height. Airflow limitation severity in patients with COPD and FEV1/FVC < 0.70 can be classified based on post-bronchodilator FEV1 (2 Diagnosis references Chronic obstructive pulmonary disease (COPD) is airflow limitation caused by an inflammatory response to inhaled toxins, often cigarette smoke. Alpha-1 antitrypsin deficiency and various occupational... read more Diagnosis references ):

  • Mild: ≥ 80% of predicted

  • Moderate: 50% to 79% of predicted

  • Severe: 30% to 49% of predicted

  • Very severe: < 30% of predicted

  • Increased total lung capacity

  • Increased functional residual capacity

  • Increased residual volume

  • Decreased vital capacity

  • Decreased single-breath diffusing capacity for carbon monoxide (DLCO)

Findings of increased total lung capacity, functional residual capacity, and residual volume can help distinguish COPD from restrictive pulmonary disease, in which these measures are diminished.

Decreased DLCO is nonspecific and is reduced in other disorders that affect the pulmonary vascular bed, such as interstitial lung disease, but can help distinguish emphysema from asthma, in which DLCO is normal or elevated.

Imaging tests

Chest x-ray may have characteristic findings. In patients with emphysema, changes can include lung hyperinflation manifested as a flat diaphragm (ie, increase in the angle formed by the sternum and anterior diaphragm on a lateral film from the normal value of 45° to > 90°), rapid tapering of hilar vessels, and bullae (ie, radiolucencies > 1 cm surrounded by arcuate, hairline shadows). Other typical findings include enlargement of the retrosternal airspace and a narrow cardiac shadow. Emphysematous changes occurring predominantly in the lung bases suggest alpha-1 antitrypsin deficiency Alpha-1 Antitrypsin Deficiency Alpha-1 antitrypsin deficiency is congenital lack of a primary lung antiprotease, alpha-1 antitrypsin, which leads to increased protease-mediated tissue destruction and emphysema in adults.... read more . The lungs may look normal or have increased lucency secondary to loss of parenchyma. Among patients with chronic obstructive bronchitis, chest x-rays may be normal or may show a bibasilar increase in bronchovascular markings as a result of bronchial wall thickening.

Chest CT may reveal abnormalities that are not apparent on the chest x-ray and may also suggest coexisting or complicating disorders, such as pneumonia, pneumoconiosis, or lung cancer. CT helps assess the extent and distribution of emphysema, estimated either by visual scoring or with analysis of the distribution of lung density. Indications for obtaining CT in patients with COPD include evaluation for lung volume reduction procedures, suspicion of coexisting or complicating disorders that are not clearly evident or excluded by chest x-ray, suspicion of lung cancer, and screening for lung cancer Screening Lung carcinoma is the leading cause of cancer-related death worldwide. About 85% of cases are related to cigarette smoking. Symptoms can include cough, chest discomfort or pain, weight loss... read more Screening . Enlargement of the pulmonary artery diameter greater than the ascending aorta diameter suggests pulmonary hypertension (3 Diagnosis references Chronic obstructive pulmonary disease (COPD) is airflow limitation caused by an inflammatory response to inhaled toxins, often cigarette smoke. Alpha-1 antitrypsin deficiency and various occupational... read more Diagnosis references ).

Adjunctive tests

Alpha-1 antitrypsin levels should be measured in patients < 50 years with symptomatic COPD and in nonsmokers of any age with COPD to detect alpha-1 antitrypsin deficiency Alpha-1 Antitrypsin Deficiency Alpha-1 antitrypsin deficiency is congenital lack of a primary lung antiprotease, alpha-1 antitrypsin, which leads to increased protease-mediated tissue destruction and emphysema in adults.... read more . Other indications of possible alpha-1 antitrypsin deficiency include a family history of premature COPD or unexplained liver disease, lower-lobe distribution of emphysema, and COPD associated with antineutrophil cytoplasmic antibody (ANCA)-positive vasculitis. If levels of alpha-1 antitrypsin are low, the diagnosis should be confirmed by genetic testing to establish the alpha-1 antitrypsin phenotype.

ECG Electrocardiography (ECG) in Pulmonary Disorders Electrocardiography (ECG) is a useful adjunct to other pulmonary tests because it provides information about the right side of the heart and therefore pulmonary disorders such as chronic pulmonary... read more , often done to exclude cardiac causes of dyspnea, typically shows diffusely low QRS voltage with a vertical heart axis caused by lung hyperinflation and increased P-wave voltage or rightward shifts of the P-wave vector caused by right atrial enlargement in patients with advanced emphysema. Findings of right ventricular hypertrophy include an R or R wave as tall as or taller than the S wave in lead V1; an R wave smaller than the S wave in lead V6; right-axis deviation >110° without right bundle branch block; or some combination of these. Multifocal atrial tachycardia Ectopic Supraventricular Rhythms Various rhythms result from supraventricular foci (usually in the atria). Diagnosis is by electrocardiography. Many are asymptomatic and require no treatment. (See also Overview of Arrhythmias... read more Ectopic Supraventricular Rhythms , an arrhythmia that can accompany COPD, manifests as a tachyarrhythmia with polymorphic P waves and variable PR intervals.

Echocardiography Echocardiography This photo shows a patient having echocardiography. This image shows all 4 cardiac chambers and the tricupsid and mitral valves. Echocardiography uses ultrasound waves to produce an image of... read more Echocardiography is occasionally useful for assessing right ventricular function and pulmonary hypertension, although air trapping makes it technically difficult in patients with COPD. Echocardiography is most often indicated when coexistent left ventricular or valvular heart disease is suspected.

Hemoglobin and hematocrit are of little diagnostic value in the evaluation of COPD but may show erythrocythemia (hematocrit > 48%) if the patient has chronic hypoxemia. Patients with anemia (for reasons other than COPD) have disproportionately severe dyspnea. The differential white blood cell count may be helpful. A growing body of evidence indicates that eosinophilia Eosinophilia Eosinophilia is defined as a peripheral blood eosinophil count > 500/mcL (> 0.5 × 109/L). Causes and associated disorders are myriad but often represent an allergic reaction... read more Eosinophilia predicts response to inhaled corticosteroids.

Serum electrolytes are of little value but may show an elevated bicarbonate level if patients have chronic hypercapnia. Venous blood gases are useful for diagnosis of acute or chronic hypercapnia.

Evaluation of exacerbations

Patients with acute exacerbations usually have combinations of increased cough, sputum, dyspnea, and work of breathing, as well as low oxygen saturation on pulse oximetry, diaphoresis, tachycardia, anxiety, and cyanosis. Patients with exacerbations accompanied by retention of carbon dioxide may be lethargic or somnolent, a very different appearance.

All patients requiring hospitalization for an acute exacerbation should undergo testing to quantify hypoxemia and hypercapnia. Hypercapnia may exist without hypoxemia.

Findings of PaO2< 50 mm Hg, or PaCO2 > 50 mm Hg, or partial pressure of carbon dioxide in venous blood (PvCO2) > 55 mm Hg in patients with respiratory acidemia define acute respiratory failure Acute Hypoxemic Respiratory Failure (AHRF, ARDS) Acute hypoxemic respiratory failure is severe arterial hypoxemia that is refractory to supplemental oxygen. It is caused by intrapulmonary shunting of blood resulting from airspace filling or... read more Acute Hypoxemic Respiratory Failure (AHRF, ARDS) . However, some patients chronically manifest such levels of PaO2 and PaCO2 in the absence of acute respiratory failure.

Yellow or green sputum is a reliable indicator of neutrophils in the sputum and suggests bacterial colonization or infection. Culture is usually done in hospitalized patients but is not usually necessary in outpatients. In samples from outpatients, Gram stain usually shows neutrophils with a mixture of organisms, often gram-positive diplococci (Streptococcus pneumoniae), gram-negative bacilli (H. influenzae), or both. Other oropharyngeal commensal organisms, such as Moraxella (Branhamella) catarrhalis, occasionally cause exacerbations. In hospitalized patients, cultures may show resistant gram-negative organisms (eg, Pseudomonas) or, rarely, Staphylococcus. During influenza season, a rapid influenza test will guide treatment with neuraminidase inhibitors, and a respiratory viral panel for respiratory syncytial virus (RSV), rhinovirus, and metapneumovirus may allow tailoring of antimicrobial therapy.

Diagnosis references

Prognosis for COPD

Severity of airway obstruction predicts survival in patients with COPD. The mortality rate in patients with an FEV1 50% of predicted is slightly greater than that of the general population. If the FEV1 is 0.75 to 1.25 L, 5-year survival is about 40 to 60%; if < 0.75 L, about 30 to 40%.

More accurate prediction of risk of death is possible by simultaneously measuring body mass index (B), the degree of airflow obstruction (O, which is the FEV1), dyspnea (D, which is measured using the Modified British Medical Research Council (mMRC) Questionnaire Breathlessness Measurement Using the Modified British Medical Research Council (mMRC) Questionnaire Breathlessness Measurement Using the Modified British Medical Research Council (mMRC) Questionnaire ), and exercise capacity (E, which is measured with a 6-minute walk test Six-minute walk test The two most common forms of exercise testing used to evaluate pulmonary disorders are the 6-minute walk test Cardiopulmonary exercise testing This simple test measures the maximal distance... read more ); this is the BODE index. Also, older age, heart disease, anemia, resting tachycardia, hypercapnia, and hypoxemia decrease survival, whereas a significant response to bronchodilators predicts improved survival. Risk factors for death in patients with acute exacerbation requiring hospitalization include older age, higher PaCO2, and use of maintenance oral corticosteroids. (Details for calculating the BODE index are available at Medical Criteria.)

Patients at high risk of imminent death are those with progressive unexplained weight loss or severe functional decline (eg, those who experience dyspnea with self-care, such as dressing, bathing, or eating). Mortality in COPD may result from intercurrent illnesses rather than from progression of the underlying disorder in patients who have stopped smoking. Death is generally caused by acute respiratory failure, pneumonia, lung cancer, heart disease, or pulmonary embolism.

Treatment of COPD

  • Smoking cessation

  • Inhaled bronchodilators, corticosteroids, or both

  • Supportive care (eg, oxygen therapy, pulmonary rehabilitation)

Treatment of chronic stable COPD aims to prevent exacerbations and improve lung and physical function. Relieve symptoms rapidly with primarily short-acting beta-adrenergic drugs and decrease exacerbations with inhaled corticosteroids, long-acting beta-adrenergic drugs, long-acting anticholinergic drugs, or a combination (see table Initial Treatment of COPD Initial Treatment of COPD Initial Treatment of COPD ).

Key Points

  • Cigarette smoking in susceptible people is the major cause of chronic obstructive pulmonary disease (COPD) in the developed world.

  • Diagnose COPD and differentiate it from disorders that have similar characteristics (eg, asthma, heart failure) primarily by routine clinical information, such as symptoms (particularly time course), age at onset, risk factors, and results of routine tests (eg, chest x-ray, pulmonary function tests).

  • Reductions of FEV1, FVC, and the ratio of FEV1/FVC are characteristic findings.

  • Categorize patients based on symptoms and exacerbation risk into one of 4 groups and use that category to guide drug treatment.

  • Relieve symptoms rapidly with primarily short-acting beta-adrenergic drugs and decrease exacerbations with inhaled corticosteroids, long-acting beta-adrenergic drugs, long-acting anticholinergic drugs, or a combination.

  • Encourage smoking cessation using multiple interventions.

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