Chronic Obstructive Pulmonary Disease

Gerald W. Staton, Jr., MD

Part 1: Epidemiology, Etiology, Pathophysiology, and Diagnosis

Clinical Case

A new patient visiting the office this morning is a 50-year-old white woman whose chief symptom is dyspnea. She says that it has been slowly increasing over the past 5 years to the point that she cannot keep up with her husband on their daily walks. She adds that she has an occasional morning cough that produces a small amount of white phlegm. On further questioning, she mentions that each winter she has what she refers to as "month-long chest colds" that are associated with worsened dyspnea on exertion. After each of these colds, she has difficulty attaining her previous baseline tolerance for exercise. She has smoked a pack of cigarettes a day since college. She has no other medical problems and currently takes no medications.

On physical examination, she appears somewhat thin but otherwise looks well and is in no respiratory distress. Her vital signs are normal. Likewise, there is no neck vein distention, and heart sounds are normal. The chest examination shows slightly diminished breath sounds, but no rales, rhonchi, or wheezes are heard. The remainder of the examination is normal.

A chest radiograph is normal, and an electrocardiogram shows no abnormalities. What should be done next to determine the cause of her dyspnea?

Introduction

Definition

The most recent guidelines issued by the American Thoracic Society (ATS) and the European Respiratory Society (ERS) define COPD as follows[1]:

Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles and gases, primarily caused by cigarette smoking. Although COPD affects the lungs, it also produces significant systemic consequences.

It should be noted that this definition emphasizes that COPD is preventable and treatable, cigarette smoking is an important cause, inflammation is a characteristic component, and the disease is not confined to the lungs.

Clinical Patterns

The ATS/ERS definition does not mention the 2 clinical patterns of COPD -- namely, chronic bronchitis and emphysema. Chronic bronchitis is defined as a chronic, productive cough 3 months or longer in duration in each of 2 successive years in a patient in whom other causes of chronic cough have been eliminated. Emphysema is defined as abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles that is accompanied by destruction of the air space walls and no obvious fibrosis.

These 2 disease patterns are accompanied by different clinical presentations: Chronic bronchitis is associated with cough and sputum production, and emphysema with dyspnea.

It is important to note that, in an individual patient, COPD often manifests as a combination of chronic bronchitis and emphysema. In addition, COPD may coexist with other diseases, such as asthma, and these overlapping disease processes sometimes cause distinct clinical syndromes. For example, the syndrome arising from an overlap between chronic bronchitis and asthma is referred to as asthmatic or wheezy bronchitis (Figure 1).[2]

Figure 1. Subsets and overlap of obstructive lung disease.

Disease Severity

The severity of COPD is gauged by the extent of airway obstruction, as determined by spirometry. Spirometry involves a forced expiratory maneuver after a patient has inhaled to total lung capacity. The volume of air exhaled in the first second of this maneuver is the forced expiratory volume in 1 second (FEV1), and the total volume of air exhaled during the maneuver is the forced vital capacity (FVC). Airflow obstruction is defined as a reduction in the ratio of FEV1 to FVC. On the basis of airflow obstruction, COPD is classified as mild, moderate, severe, and very severe (Table 1).

Table 1. Classification of COPD Severity

FEV1 = forced expiratory volume in 1 second; FVC = forced vital capacity

Epidemiology

Prevalence

In 2006, an estimated 12.1 million Americans were diagnosed with COPD,[3] but studies have suggested that as many as 24 million Americans have chronic airflow obstruction, which suggests that COPD is greatly underdiagnosed.[4] COPD affects more women than men, and the prevalence in women has risen steadily over several decades as smoking rates among women have increased. For several consecutive years, more women than men died of COPD (Figure 2).[5] Evidence suggests that women may be more susceptible to COPD than men.[3,6] Before 1995, the prevalence of COPD in African Americans was lower than that in whites. However, because of increased cigarette smoking in African Americans in the past 20 years, more recent analyses show no difference between the 2 groups.[7]

Figure 2. Forced expiratory volume in 1 second (FEV1) can be used to demonstrate the accelerated decline in lung function that leads to COPD in susceptible persons. The benefit of smoking cessation is evident in the graph: Deterioration in lung function slows and parallels that of a nonsmoker, even in late stages of the disease.

COPD is the fourth leading cause of death in the United States and claimed the lives of 127,049 Americans in 2005. The other 3 leading causes of death are in decline, but the death rate for COPD continues to rise. It is expected that COPD will become the third leading cause of death by 2020.[8]

Economic Cost

Although costly in terms of morbidity and mortality, COPD is no less costly in terms of annual expenditure. In 2007, the cost to the nation attributed to COPD was approximately $42.6 billion; of that figure, $26.7 billion was healthcare expenditures and $15.9 were indirect costs as a result of lost productivity.[9]

Factors That Affect Survival

Factors that predict survival in COPD patients include age, severity of airflow obstruction (as measured by FEV1), degree of dyspnea, severity of hypoxemia, presence of hypercapnia, low body mass index (BMI), and weight loss.[10-14] The synergistic effects of these variables are factored into the BODE index (ie, BMI, airway obstruction, dyspnea, and exercise capacity), which correlates better with mortality than FEV1 alone.[15]

Cigarette smoking is the underlying cause of COPD in the vast majority of patients, and smoking cessation improves outcome even in patients who have smoked heavily for decades (Figure 2).[16] Patients who have moderate COPD (FEV1 of 40% to 54% predicted) have a 1-year survival rate of 98% and a 10-year survival rate of 45% as compared with a matched population.[17]

Patients who have severe COPD (FEV1 < 40% of predicted) have survival rates of 90% at 1 year and 25% at 10 years.[17] Death is often caused by an exacerbation complicated by respiratory failure, pneumonia, pulmonary embolism, cardiac arrhythmia, or pneumothorax. For patients who have COPD exacerbations that require mechanical ventilation, in-hospital mortality is 12%. Factors associated with a worse prognosis are extubation failure and need for mechanical ventilation exceeding 72 hours[18] and have 1- and 3-year survival rates of 51% and 36%, respectively.[19] Being admitted to the hospital for a COPD exacerbation is associated with a 1-year mortality rate of 21%.[20]

Pulmonary function follows a predictable pattern over a person's lifespan: FEV1 values increase steadily during childhood and adolescence, plateau in early adulthood, and then gradually decline with advancing age. Familial and environmental factors, as well as their interactions, may accelerate the decline and result in COPD.

Cigarette Smoking

Cigarette smoking is the cause of COPD in 80% to 90% of patients.[21] However, other factors can enhance the risk for COPD in a specific patient. Approximately 25% of cigarette smokers are diagnosed with COPD.[21] Why some smokers do not develop COPD is unknown but probably can be attributed to constitutional differences. Smokers have higher death rates for COPD, more rapid decline in lung function, and more respiratory symptoms than nonsmokers.[21] More than 50% of middle-aged men who smoke more than a pack a day have a chronic productive cough. In autopsy studies, 19% of those who smoke more than a pack a day had emphysema. These statistics underscore the significant effect of smoking on the development of COPD.

Hyperreactive Airway

In smokers, a hyperreactive airway (ie, increased bronchoconstriction in response to nonspecific stimuli) has been hypothesized to be a cofactor in the development of COPD.[22] However, patients who smoke may also develop hyperreactivity secondary to airway inflammation.

Nonsmokers who have asthma may develop chronic airflow obstruction that is indistinguishable from COPD[23]; however, these patients should not be diagnosed as having COPD.

Occupational Factors

Prolonged exposure to various types of dust, such as those found in coal mining, gold mining, textile manufacturing, and cement and steel industries, are associated with industrial or occupational bronchitis.[24] Long-term studies of nonsmokers in these settings have detected the development of airflow obstruction. However, in most studies of occupational lung disease, the effects of smoking greatly outweigh the effects of occupational exposures.

Alpha1-Antitrypsin Deficiency

Alpha1-antitrypsin deficiency is a genetic disorder associated with early development of emphysema.[25] Alpha1-antitrypsin, also called alpha1-protease inhibitor, is a serum protein that inhibits production of neutrophil elastase, an enzyme that, if left to proliferate in the lung, causes emphysema. Deficiency of this protein accounts for 1% to 2% of the cases of COPD in the United States.

Other Factors

Other factors believed to influence the development of COPD include genetic predisposition,[26] ambient air pollution,[27] passive smoking, low BMI,[28] socioeconomic status (eg, COPD incidence is higher in blue-collar workers), HIV,[29] hepatitis C virus infection,[30] chronic bacterial infection,[31] and low dietary antioxidants.[32]

Pathogenesis

Emphysema

Early development of emphysema in patients with alpha1-antitrypsin deficiency suggests that the protease-antiprotease system in the lung is central to the pathogenesis of this disorder.[33-35]

When the lungs of young smokers are examined, abnormal accumulations of pigmented macrophages are found in the respiratory bronchioles. This is significant because the respiratory bronchioles are the site not only of the initial airflow obstruction in early COPD but also of the pathologic changes seen in centriacinar emphysema -- the type seen in cigarette smokers. It is hypothesized that these macrophages secrete chemotactic factors (ie, leukotriene B4 and IL-8) that attract neutrophils and other inflammatory cells to the respiratory bronchioles and alveoli. Neutrophils are potent sources of oxidants and proteolytic enzymes, such as elastase. Normally, the secreted elastase is inhibited by alpha1-antitrypsin, which is present in significant concentrations in the alveolar lining fluid. However, oxidants in cigarette smoke, as well as oxygen-free radicals secreted from macrophages and neutrophils, oxidize and inactivate the alpha1-antitrypsin.[34] This allows the elastase and other proteolytic enzymes to degrade the lung elastin and other extracellular matrix components, which, in turn, destroys the respiratory bronchiole and alveolar walls. Cigarette smoke may also inhibit repair of damaged elastin.

Emphysema reduces the surface area needed for carbon monoxide diffusion, which results in abnormal gas exchange and reduction in elastic recoil. Elastic recoil pressure is needed to drive expiration, and reduction results in a decreased expiratory airflow and produces hyperinflation. The enzyme-induced destruction of the tethering structures that hold open small airways during expiration restricts airflow and further contributes to the decreased expiratory airflow that is seen in emphysema.

Chronic Bronchitis

Pathologically, the airways of patients with chronic bronchitis show an increased volume of tissue in the wall and an accumulation of inflammatory mucus in the lumen. Inflammation in the airway walls and mucous glands is characterized by infiltration of macrophages, neutrophils, and CD8+ T cells.[36] Chronic infection may play a synergistic role by magnifying these inflammatory changes.[31] Excessive oxidants vs antioxidants and proteases vs antiproteases is hypothesized to cause the mucous hypersecretion and injury to both the epithelial cells and extracellular matrix that is characteristic of chronic bronchitis.

Pathophysiology

Airway Obstruction

In the COPD patient, routine pulmonary function tests depict the characteristic pattern of volume-dependent airway obstruction. Spirometry typically reveals a reduction in the FEV1/FVC ratio and an even greater relative decline in FEV, which may decrease between 25% and 75% of vital capacity (Table 1). As airflow obstruction worsens, a normal volume of gas can no longer be exhaled in the time available, and vital capacity declines. Measurement of lung volume consistently reveals an increased residual volume (RV) and a normal-to-increased functional residual capacity (FRC). The RV may be 2 to 4 times higher than normal, because as the expiratory airflow slows, gas becomes trapped in airways that close prematurely. The FRC may become increased by 2 mechanisms: dynamic hyperinflation and activation of inspiratory muscles during exhalation. Hyperinflation flattens the diaphragm, which increases the work of breathing, diminishes the capacity for exercise, and increases dyspnea. Hyperinflation becomes worse with exercise, causing dynamic hyperinflation, which adds to the load of inspiratory muscles.

As a result of these processes, tidal breathing may take place at lung volumes as high as 1 to 2 L above normal levels. In the patient who has significant airflow obstruction, an increased FRC provides the benefits of an enlarged airway diameter -- which provides greater radial support and thus less airway resistance -- and an increased driving pressure (ie, elastic recoil) required for exhalation. The cost to the patient of an increased FRC is the greater work of breathing incurred at the higher lung volume.

Abnormalities in Gas Exchange

It has long been recognized that the pattern of gas exchange abnormalities in COPD may differ greatly among patients with airflow obstruction of identical severity. Early in the course of disease, when expiratory flow is only slightly reduced, mild hypoxemia may be the only blood gas abnormality. However, in advanced stages of COPD, 2 distinct patterns emerge (Table 2).

Table 2. Clinical Findings in Emphysema and Chronic Bronchitis

	Emphysema (Pink Puffer)	Chronic Bronchitis (Blue Bloater)
Dominant symptom	Dyspnea	Productive cough
Signs	Thin build; hyperinflated, quiet chest	Stocky build, wheezy, right heart failure
Chest radiograph	Normal or hyperinflation, decreased markings, bullae	Normal or only increased markings
Arterial blood gas
PaO2	Slightly reduced	Markedly reduced
PaCO2	Normal	Increased
Spirometry	Decreased FEV1	Decreased FEV1
Total lung capacity	Increased	Normal or slightly increased
DLCO	Decreased	Normal
Pulse oximetry:
Rest	Normal	Decreased
Exercise	Severe desaturation	May improve
Hematrocit	Normal	Increased

DLCO = diffusing capacity of the lung for carbon monoxide; FEV1 = forced expiratory volume in 1 second; Pao2 = partial pressure of arterial oxygen; PaCO2 = partial pressure of arterial carbon dioxide

Two clinical patterns. Patients with the type A pattern have dyspnea and only mild-to-moderate hypoxemia (partial pressure of arterial oxygen[PaO2] is usually > 65 mm Hg). In addition, these patients maintain normal or even slightly reduced partial pressure of arterial carbon dioxide (PaCO2). These patients are sometimes referred to as pink puffers -- they tend to be thin, to experience hyperinflation at total lung capacity, and to be free of signs of right heart failure. The pink puffer usually has emphysema.

Patients with the type B pattern are characterized by marked hypoxemia and peripheral edema resulting from right heart failure. These patients, sometimes called blue bloaters, typically exhibit cough and sputum production. They have frequent respiratory tract infections, experience chronic carbon dioxide retention (PaCO2 > 45 mm Hg), and have recurrent episodes of cor pulmonale. Type B patients may have pathologic evidence of severe emphysema, as well as inflammation of large and small airways and possible defects in ventilatory control. These patients usually meet the criteria for chronic bronchitis.

Many patients have features of both clinical types, giving rise to either mixed or intermediate clinical presentations.

Differing effects on the cardiovascular system. The 2 clinical types also have very different consequences for the cardiovascular system. In the type B patient, both alveolar hypoxia and acidosis (secondary to chronic hypercapnia) stimulate pulmonary arterial vasoconstriction, and hypoxemia stimulates erythrocytosis. Increased pulmonary vascular resistance, increased pulmonary blood volume, and possibly increased blood viscosity from secondary erythrocytosis all contribute to pulmonary arterial hypertension.[37] In response to long-term pulmonary hypertension, cor pulmonale generally develops: The right ventricle becomes hypertrophic, and increases in cardiac output are achieved by abnormally high filling pressure in the right ventricle. Additional hemodynamic loads may cause the right ventricle to fail, with the consequent development of systemic venous hypertension, which is manifested by jugular venous distention, peripheral edema, passive hepatic congestion, and sometimes ascites. It should be noted that, in the absence of left heart failure, pleural effusion is not a manifestation of cor pulmonale. In type B patients, echocardiographic evaluation of right heart function and estimation of pulmonary artery systolic pressure are useful in quantifying the degree of pulmonary hypertension.[37]

The emphysematous lung destruction characteristic of type A patients leads to a restricted vascular bed because of the loss of pulmonary capillaries from the destroyed alveolar walls. This condition is reflected in the reduced diffusing capacity of the lung for carbon monoxide (DLCO) observed in type A (but not type B) patients.[38] However, because PaO2 levels are only mildly depressed in type A patients, pulmonary vasoconstriction is minimal and secondary erythrocytosis does not develop. Cardiac output may be slightly reduced. As a result, pulmonary hypertension in type A patients is milder than that in type B patients, and cor pulmonale develops infrequently, usually only in the terminal phase of the illness.

Differing degrees of oxygen saturation on exertion. Differences in gas exchange during exercise also distinguish the 2 clinical types. Type A patients develop oxygen desaturation during exercise, whereas type B patients may exhibit increases in oxygen saturation during exercise.

Differential Diagnosis

The differential diagnosis of an older cigarette smoker presenting with chronic dyspnea or cough and sputum production is wide.

Dyspnea in these patients can be caused by ischemic heart disease; congestive heart failure; valvular heart disease; anemia; and other types of lung disease, such as interstitial lung disease, lung cancer, asthma, pleural effusion, pulmonary embolism, and pulmonary hypertension.

Cough and sputum in the patients can be the result of postnasal drip, asthma, gastroesophageal reflux, lung cancer, and such chronic pulmonary infections as atypical mycobacterial infection and bronchiectasis.

Patients who are known to have COPD and who present emergently because of increased dyspnea or an alteration of their normal cough and sputum may be experiencing an exacerbation of COPD. However, they must also be evaluated for ischemic heart disease, congestive heart failure, pneumonia, pneumothorax, pulmonary embolism, and lung cancer.

Diagnosis

Common presenting symptoms of COPD are productive cough or shortness of breath occurring; typically, the patient will be 50 years or older and will have smoked at least a pack of cigarettes a day for 20 years.

Patient History

The presentation of COPD varies, depending on whether the patient has dominant emphysema or chronic bronchitis, and most patients have some degree of overlap (Table 2). The patient with emphysema presents with dyspnea on exertion -- a condition that has been slowly increasing for years and that is fairly constant from day to day. In contrast, the patient with chronic bronchitis usually presents with a cough that often occurs in the morning and that produces mucoid phlegm. The volume of phlegm is usually less than 2 tablespoons. If the volume of phlegm is more than 2 tablespoons, bronchiectasis should be suspected.

Both types of patients are subject to exacerbations, which are usually associated with increased cough with purulent sputum, and increased dyspnea. Hemoptysis can occur during these episodes. Patients who have chronic bronchitis develop peripheral edema much earlier in their illness than those who have emphysema.

Physical Examination

Early in the evolution of both types of COPD, the physical examination may be normal. Later in the disease, the patient who has emphysema tends to be thin, with a quiet, hyperinflated chest (pink puffers). In contrast, the patient who has chronic bronchitis tends to be stocky to obese and plethoric as a result of erythrocytosis. In addition, the chronic bronchitis patient usually presents with a noisy, wheezy chest and signs of right heart failure, such as neck vein distention and edema (blue bloaters) (Table 2). As the disease progresses, both patients prefer to sit upright with arms extended and weight supported on the palms. On expiration, patients may tend to purse the lips; on inspiration, a paradoxical indrawing of the lower intercostal interspaces may be noted. Cyanosis may be present, often associated with an enlarged, tender liver. Asterixis is sometimes seen in association with severe hypercapnia.

Systemic effects of COPD are also seen.[39] Possibly as a consequence of systemic inflammation, it is not uncommon to find COPD associated with nutritional abnormalities and weight loss, skeletal muscle dysfunction (contributing to exercise limitations), coronary artery disease, low serum testosterone levels (in males), and osteoporosis.

Diagnostic Studies

Spirometry is a useful test in screening for COPD and should be performed in all smokers with respiratory symptoms and in all smokers older than 45 years.[40] Diagnosis of COPD by the history and physical examination alone is sometimes incorrect. For this reason, laboratory studies should be performed to confirm the diagnosis, determine a likely prognosis, and detect potential complications (eg, pneumothorax) and comorbid conditions (eg, lung cancer).[41]

COPD is usually diagnosed on the basis of pulmonary function testing, although radiographic studies and other tests are sometimes helpful. There are significant differences in the findings of pulmonary function testing in patients who primarily have emphysema as compared with those who have chronic bronchitis (Table 2).

Pulmonary function tests. In COPD patients, pulmonary function tests are used to confirm the obstructive abnormality, quantify the severity of the defect, assess the reversibility of the airflow obstruction in response to therapy,[42] and monitor the course of the disease. Spirometry is the test of choice for determining the presence of airflow obstruction. A low FEV1/FVC ratio and a decreased expiratory flow rate confirm airway obstruction, but the best way to measure the severity of the obstruction is the FEV1. Other useful tests include lung volumes, diffusing capacity, arterial blood gases, and rest and exercise pulse oximetry.

Spirometry. Spirometry is the most useful test for screening airflow obstruction of any type.[40] The results are presented as the absolute value and the percentage predicted on the basis of the patient's gender, age, and height. The earliest abnormality may be a reduction in the forced expiratory flow (FEF) during the mid-portion of the expiratory maneuver (FEF25% -75%). The next abnormality to develop may be a reduced FEV1 and FEV1/ FVC ratio. It is the reduction in this ratio that identifies the abnormality as an obstructive defect. As the disease worsens, FVC is also reduced. Repeated spirometry after inhalation of a beta-agonist, an anticholinergic, or a combination of both bronchodilator agents can detect reversible airflow obstruction, although the degree of reversibility can vary from day to day.[42] The severity of COPD can be determined from the FEV1/FVC ratio; the FEV1 compared with the predicted value for a person of that gender, age, and height; and the clinical findings (Table 1).[1]

Lung volume. Measurement of lung volume detects increases in the RV and FRC, and these measurements can indicate hyperinflation. Total lung capacity is usually increased in emphysema and tends to be normal in chronic bronchitis.

Diffusion capacity. The diffusion capacity for carbon monoxide is useful as an indicator of the presence of emphysema. One of the physiologic consequences of emphysema is loss of alveolar-capillary surface area, and this loss is detected by a reduction in the lung's diffusion capacity.

Arterial blood gases. Arterial blood gases should be measured in all patients with advanced COPD. Emphysema patients will maintain a resting PaO2 only mildly to moderately decreased and will have a normal PaCO2 until they are in end-stage COPD. In contrast, chronic bronchitis patients develop severe hypoxemia and daytime hypercapnia much earlier in the illness, necessitating careful titration of supplemental oxygen.

Pulse oximetry. Pulse oximetry performed when the patient is at rest and during exercise is recommended for all patients with severe COPD. Most patients with severe emphysema (diffusion capacity < 55% of normal) have significant oxygen desaturation during exercise and require oxygen supplementation during exercise to maintain oxygen saturation at a level greater than 88%.

Chest Radiography

The chest radiograph may be normal, even in severe cases (Table 2). Radiographic findings that suggest the presence of emphysema include arterial deficiency in the peripheral lung, hyperinflation of the lung, and visible bullae.

In chronic bronchitis, the chest radiograph is usually normal (Table 2), but abnormal findings may include thickening of the bronchial wall of a perihilar bronchus as viewed end-on, as well as increased bronchovascular lung markings, which account for the so-called "dirty chest" of chronic bronchitis. Chest radiography is also useful to exclude other lung diseases, suggest the presence of associated congestive heart failure, and detect lung masses or pulmonary nodules.

Computed Tomography of the Chest

Computed tomography (CT) is much more sensitive than chest radiography for the diagnosis of emphysema; however, CT should be done only when the diagnosis is uncertain.[43] Patients who have a normal chest radiograph and normal lung function or only an isolated decrease in diffusing capacity can have extensive emphysema, as detected by high-resolution CT.

Other Tests

The hematocrit is often elevated in patients who have a PaO2 less than 55 mm Hg or in patients who have nocturnal desaturation. Elevated hematocrit is most common in chronic bronchitis patients.

Sputum examination is indicated only in the setting of suspected infection, and even then only when the results will alter therapy.[44]

Measurement of the alpha1-antitrypsin level is indicated when a patient presents with COPD before age 50 years, has a predominance of basilar emphysema on a chest radiograph, or has a family history of COPD before age 50 years.[24]

Many COPD patients have nocturnal worsening of oxygen desaturation, sometimes associated with obstructive sleep apnea.[45] Nocturnal monitoring of pulse oximetry allows detection of the desaturation and titration of nocturnal oxygen therapy. Formal polysomnography (sleep study) should be performed in patients with a history of snoring and excessive daytime somnolence.[45]

Echocardiography is useful to detect complicating pulmonary hypertension in patients with severe COPD, although right heart catheterization may be necessary for confirmation and measurement of the extent of elevation of pulmonary artery pressure.[36]

Bone density should be measured because of the common finding of osteoporosis in COPD patients and the frequent need for steroid therapy.[46]

Case Resolution and Key Points

Case Resolution

The physical examination and chest radiograph of the patient discussed above were both normal, and spirometry was the next logical step in the diagnostic workup. Office spirometry was performed, and the results were FVC 85% of predicted, FEV1 50% of predicted, and FEV1/FVC ratio 59%. The spirometry findings indicate that the diagnosis is moderate COPD, which is probably caused predominately by emphysema.

Key Points

• The most recent guidelines issued by the American Thoracic Society (ATS) and the European Respiratory Society (ERS) define COPD as follows: Chronic obstructive pulmonary disease (COPD) is a preventable and treatable disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles and gases, primarily caused by cigarette smoking. Although COPD affects the lungs, it also produces significant systemic consequences.
• COPD is the fourth leading cause of death in the United States, and the death rate is rising, whereas the death rates from other leading causes are declining.
• Almost all cases of COPD in the United States are caused by cigarette smoking.
• COPD results from the inflammation and alterations of airway and lung parenchymal structure caused by cigarette smoke.
• COPD is diagnosed on the basis of a history of cigarette smoking and a finding of airflow obstruction on spirometry.