Thursday, August 14, 2008



Nicholas Anthonisen > Goldman: Cecil Medicine, 23rd ed. Saunders. 2007.


Chronic obstructive pulmonary disease (COPD) is the term used to describe slowly progressive airways obstruction, usually associated with smoking, that is not reversible and is not due to another specific cause. Patients with COPD have varying degrees of three pathologic processes, each associated with smoking: chronic bronchitis, small airways obstruction, and emphysema. Whereas chronic bronchitis can be defined clinically, small airways obstruction and emphysema cannot be reliably diagnosed during life. COPD results in airways obstruction, which is easily measured, and current therapy is largely aimed at reducing obstruction. Physicians, therefore, can commonly focus on the COPD syndrome and not its specific pathologic causes.

Although patients with COPD may improve with treatment, especially when an acute infection or exposure precipitates decompensation, COPD by definition implies some degree of fixed, irreversible disease. By comparison, patients with pure asthma have intermittent airway obstruction that may revert to normal after treatment and in between exacerbations.


COPD is common, affecting about 16 million Americans. It is the fourth most common cause of death in the United States, and mortality from COPD is increasing. The economic burden of COPD is enormous, although it is extremely difficult to assess accurately and inclusively.

The prevalence of COPD reflects societal smoking habits, increasing steadily in men in the United States until the early 1990s and then leveling off. In women, COPD was previously uncommon, but the prevalence has increased and is still rising owing to increased smoking rates in women. 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

Figure 1 shows a well-validated model of the development of COPD in terms of the most commonly used index of airways obstruction, which is the forced expiratory volume in 1 second, or FEV1. In normal nonsmoking men, FEV1 declines by about 30 mL per year after the age of 30 years, and disability due to dyspnea does not occur. In the “average” smoker, FEV1 declines at a rate that is approximately twice as fast but still slow enough so that disability due to dyspnea is unlikely until late in life. About 15 to 20% of smokers, however, have more rapid declines of up to 100 mL per year, and it is these patients in whom symptomatic COPD develops in middle age. These individuals are in some way “sensitive” to tobacco products and constitute a high-risk group. A variety of additional risk factors have been identified, but all have relatively weak effects, and no currently known combination of factors satisfactorily explains why some smokers fare so much worse than others.

FIGURE 1 Course of lung function decline through adulthood. The vertical axis is forced expiratory volume in 1 second (FEV1); the horizontal axis is age. The course of decline is shown in a normal nonsmoker (N), in an average smoker (S), in a smoker who is sensitive to tobacco smoke (SS), and in an individual who quits smoking (Q, dashed line). Dyspnea first occurs when the FEV1 is less than 2 L (50% of the normal value) and becomes severe when the FEV1 is about 1 L.

Quitting smoking often alters the subsequent loss of lung function to the same rate as in nonsmokers during a few years' time. Thus, smoking cessation early enough in life can prevent the onset of clinical disease in middle age. However, severe COPD may progress even in patients who stop smoking.


Chronic Bronchitis

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. At least one third of smokers aged 35 to 59 years have chronic bronchitis, and its prevalence increases with age.

The anatomic basis of chronic bronchitis is hypertrophy and hyperplasia of the mucus-secreting 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. This expansion of mucus-secreting cells is accompanied by low-grade neutrophilic inflammation and increased airway smooth muscle. Chronic bronchitis is not necessarily associated with airways obstruction, and smokers can develop severe COPD in the absence of bronchitis. However, chronic bronchitis is associated with an increased tendency to develop repetitive episodes of acute bronchitis, which result in morbidity and may contribute to the progression of airways obstruction.

Peripheral Airway Disease

In COPD, the most striking increase in the resistance to airflow occurs in peripheral airways or bronchioles. Smokers have increased bronchiolar smooth muscle, inflammation, and fibrosis that narrow the airway lumens and thicken their walls. The degree of abnormality in these airways is correlated with lung function. The mechanisms involved in these changes are unknown.


Emphysema is defined as the enlargement of air spaces distal to the conducting airways, that is, respiratory bronchioles and alveoli, due to destruction of the walls of these air spaces. There are two important types of emphysema, centrilobular and panacinar. Centrilobular emphysema primarily involves the respiratory bronchioles, often with normal distal alveoli; however, in severe disease, distal alveoli may also be damaged and incorporated into the central air space. Centrilobular emphysema is seen almost exclusively in smokers, in whom it tends to occur in the upper lung lobes. Panacinar emphysema involves the entire distal lung unit, distorting and destroying alveoli and respiratory bronchioles alike; it can occur throughout the lung but may involve chiefly the lower lobes.

Some families develop early-onset, 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. Smoking causes an inflammatory process by which activated neutrophils are recruited into the lung; elastase released by neutrophils digests lung tissue in the absence of AAT. The elastase-antielastase imbalance present in patients with AAT deficiency might also occur in people without the deficiency under the proper conditions, such as oxidation of AAT, but it is not clear that this is the case.

There are a number of abnormal alleles of the gene AAT, the most common and important of which is termed Z. Patients homozygous for the Z allele (ZZ), a rare condition, have very low serum AAT levels and develop severe panacinar emphysema early in life if they smoke. Patients who do not smoke may not develop significant lung disease. Heterozygotes (AZ) are more common, representing about 2 to 3% of North European populations, and have serum levels of AAT that are intermediate between those of normals and homozygotes. Although it is not certain, it is likely that these individuals are predisposed to airways obstruction if they smoke.

Reduction in Maximum Expiratory Flow

Reduced expiratory flow is the hallmark of COPD. Figure 2 shows a maximum expiratory flow-volume curve and a diagrammatic representation of the lungs and airways inside the thorax. In the maximum expiratory flow-volume curve, flow from the lungs is plotted against lung volume during expiration at maximum effort, beginning with the lung expanded to total lung capacity. In the model, expiratory effort is generated by compression of the thorax, causing an increase in pleural and alveolar pressure. During expiration, the pressure that drives flow down the airways is the alveolar pressure. As air flows down the airways, pressure is lost because of frictional resistance and the acceleration of gas particles as the airway narrows.

FIGURE 2 Maximum expiratory flow-volume curve (left) with an explanatory model (right). The left panel shows flow as a function of expired volume during forced expiration at maximum effort, from the total lung capacity (TLC) before expiration to the residual volume (RV) after expiration in a normal individual. Flow rises to a maximum and then declines as lung volume decreases. Flow over much of the declining limb is independent of expiratory effort, provided a threshold effort is achieved. In the model, the thorax is represented by a box and the expiratory muscles by a piston (M). The lung is a balloon inside the box, and the airways are represented as a tube that branches as it goes from outside the lung to the inside. The expiratory muscles compress the thoracic contents and raise pleural pressure (Ppl). Alveolar pressure (PA) in the lung increases by the same amount because it is related to Ppl by the elastic recoil of the lung (Pel). Because of the increase in Ppl and PA, gas flows out of the lung, reaching a peak (peak flow) and declining thereafter. The pressure driving flow is PA, and the flow achieved is related to the resistance of the airways. As lung volume decreases, Pel decreases, so PA decreases in relation to Ppl. Also, as lung volume decreases, resistance increases. Because of the reduced PA and increased resistance, as lung volume decreases, the pressure in a major airway becomes less than Ppl, and the airway is compressed (dashed lines), thereby limiting flow. Further increases in effort (Ppl) simply further compress the airway and do not increase flow. Flow limitation occurs after about 30% of the vital capacity is expired. When this limitation occurs, maximum expiratory flow is dependent on lung elastic recoil (Pel), which determines PA, the resistance of the airways upstream from the flow-limiting segment, and the mechanical properties of the flow-limiting segment.

At the onset of the expiration, flow rises sharply to a maximum (peak flow) related to the properties of the lung and the intensity of effort. Thereafter, flow declines as lung volume decreases. After about 30% of the vital capacity is expired, expiratory flow becomes effort independent, that is, unchanged over a variety of expiratory efforts and pleural pressures, because of flow-related pressure losses down the airway. As a result, pressure in a central airway is less than the pleural pressure, the airway is compressed, and flow attains a maximum value after which further increases in pleural pressure compress the airway further. These so-called flow-limiting segments are initially found only in large central airways, but such segments exist in intrapulmonary airways at low lung volumes. Under the condition of flow limitation, the maximum flow attained depends on the upstream or alveolar pressure, the resistance of the airways, and the properties of the compressed, flow-limiting segment. If the lung's elastic recoil is reduced (e.g., as in emphysema), alveolar pressures are reduced relative to pleural pressure, and so is maximum expiratory flow. Increases in airways resistance (e.g., as in chronic bronchitis) increase pressure losses down the airway and decrease maximum expiratory flow. Finally, abnormally “floppy” segments of airway, a rare phenomenon, undergo premature collapse and cause abnormal limitation of flow.

In normal lungs, flow decreases as lung volume decreases because the lung's elastic recoil decreases and resistance increases. In 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.

Clinical Manifestations

Lung Function

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). Both FEV1 and FVC decline with normal aging, but their ratio, FEV1/FVC, normally exceeds 0.7; lower ratios indicate airways obstruction. 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, the lung volume after a maximum expiration, often is increased even in mild cases of COPD. Functional residual capacity, the lung volume at the end of a normal expiration, is routinely increased in moderate and severe COPD. The diffusing capacity for carbon monoxide, which measures the alveolar uptake of trace amounts of carbon monoxide, is reduced in emphysema because of loss of alveolar surface area. It is the most reliable physiologic method for assessing the presence of emphysema.

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 ventilation-perfusion 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, as illustrated in Figure 3 , which shows flow-volume plots in a patient with COPD during resting breathing and forced expiration after full inspiration. At the same lung volume, expiratory flows during resting breathing are similar to flows during a maximum effort. The only way this patient can increase expiratory flow, and therefore ventilation, is to breathe at higher lung volumes than at rest.

FIGURE 3 Flow-volume relationships during quiet resting breathing (small inner loop) and maximum forced expiration in a patient with severe COPD. The vertical axis is flow in liters per second (V.L/S); the horizontal axis is lung volume, expressed as a percentage of the normal total lung capacity (TLC). The shaded area shows normal maximal inspiration and expiration. The patient has substantial increases in the maximum lung volume (TLC) and the minimum lung volume attained (residual volume). Expiratory flow during maximal expiration is grossly reduced and is similar to the flow used during resting breathing. With exercise, the only way for this patient to increase expiratory flow and thereby increase ventilation is to breathe at higher lung volumes than at rest.

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.



COPD is insidious. Although the diagnosis can be made in any smoker with airways obstruction, most people are first seen only when they experience dyspnea. 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. Dyspnea usually is first experienced during episodes of acute bronchitis. Eventually, dyspnea becomes consistent, and during approximately 10 to 15 years, dyspnea progresses from occurring only with extreme exertion to being present with any effort and finally to 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. The sputum often changes in color from the usual white (mucoid) to yellow or green, sometimes with blood streaking. 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. The causes vary from patient to patient and from time to time, but many are associated with bacterial infection of the airways. 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.

Physical Examination

In mild to moderate COPD, the physical examination is usually normal. In severe disease, signs are often apparent but are not specific. 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 related to hyperinflation include 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, which commonly is termed cor pulmonale. Signs of cor pulmonale include an increased pulmonic second sound, jugular venous distention, hepatic congestion, and ankle edema.


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 <>

Radiologic Studies

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. 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. The chief value of the chest radiograph is to assess other causes of airways obstruction and to look for evidence of lung cancer.

FIGURE 4 Posteroanterior and lateral radiographs of the thorax in a patient with emphysema. The most obvious abnormalities are those associated with increased lung volume. The lungs appear dark because of their increased air relative to tissue. The diaphragms are caudal to their normal position and appear flatter than normal. The heart is oriented more vertically than normal because of caudal displacement of the diaphragm, and the transverse diameter of the rib cage is increased; as a result, the width of the heart relative to the rib cage on the posteroanterior view is decreased. The space between the sternum and heart and great vessels is increased on the lateral view.

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 ( Fig. 5 ).

FIGURE 5 High-resolution axial CT scan of a 1-mm section of the thorax of a patient with emphysema at the level of the tracheal carina. The right lung is on the left. Multiple large bullae—black holes—are evident. Many smaller areas of similar tissue destruction are also present in both lungs. The right upper lobe bronchus is seen entering the lung; its walls are thickened, suggesting chronic inflammation. (Courtesy of Dr. Bruce Maycher.)

Serial Evaluation

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.

Differential Diagnosis

The most difficult disease to differentiate from COPD is asthma, although the distinction can be made on the basis of history alone in most cases. 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, and some smokers with chronic airways obstruction demonstrate substantial reversibility 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.

Several other diseases cause chronic airways obstruction but differ from COPD in important ways. Cystic fibrosis and bronchiectasis occur at an earlier age and are normally accompanied by specific radiologic abnormalities. Eosinophilic granuloma which is associated with cigarette smoking, and lymphangioleiomyomatosis cause airways obstruction, but both present with abnormal chest radiographs and have characteristic abnormalities on CT scan. Bronchiolitis obliterans also causes airways obstruction; however, bronchiolitis obliterans usually occurs in a setting different from that of COPD, and it may be accompanied by more radiographic changes than in COPD.

It is important to differentiate upper or central airways obstruction from COPD. Extrathoracic airways obstruction is accompanied by stridor and compromised inspiratory flow. Intrathoracic tracheal obstruction produces characteristic changes in the maximum expiratory flow-volume curve.

Prevention and Treatment

Stable COPD

Smoking cessation is the only treatment that has been shown to alter the course of COPD.[1] 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 ( Fig. 6 ). There are a number of effective agents with few side effects. 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 β2-agonist; 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 β2-agonists 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. A very long acting (once a day) inhaled anticholinergic drug, tiotropium (18 μg), is available. Long-acting bronchodilators are unquestionably effective and tend to control symptoms better than short-acting agents do. They also may prevent exacerbations.[2] Metered-dose and powdered formulations of these drugs are less expensive than those used in wet nebulizers and are equally effective.

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. Theophylline has a relatively narrow dosage range in which it is effective and nontoxic, and many drugs and conditions influence theophylline metabolism. 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) one-time increase in FEV1. Of greater importance is evidence that inhaled steroids reduce the frequency and severity of exacerbations and reduce mortality in COPD.[3] Patients with severe disease and multiple exacerbations should be given inhaled steroids in relatively high doses, such as 500 to 1000 μg of fluticasone per day. 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.[4]

Many older COPD guidelines recommend trials of high-dose oral steroids in patients who are not doing well. The evidence cited earlier has largely superseded these recommendations, and at present there is not convincing evidence for the use of oral steroids in stable COPD, although many current guidelines recommend trials of oral steroids.

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.

In hypoxemic COPD, home oxygen therapy prolongs life, and home oxygen should be prescribed for 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. There is no good evidence that oxygen therapy benefits COPD patients who do not have continuous hypoxemia. However, some patients who are not hypoxemic during the day exhibit hypoxemia while asleep, and many patients with severe COPD develop significant hypoxemia with exercise. As a result, oxygen therapy may be considered in such patients during sleep or exercise. Oxygen delivery systems vary greatly in terms of mobility and cost, and the choice among systems should be individualized.

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. In patients with emphysema predominantly in the upper lung zones, surgery improves exercise tolerance and also reduces mortality in those with poor initial exercise tolerance. On the other hand, surgery is dangerous in very ill patients, defined as those with FEV1 less than 20% of the predicted normal and either a diffusing capacity below 20% of the predicted normal or homogeneous emphysema distribution.[5]

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.

Exacerbations of COPD

Exacerbations of COPD are associated with transient decreases in lung function, which account for the increased dyspnea. Increased bronchodilator therapy with short-acting agents is rational and recommended. When exacerbations are accompanied by increases in sputum volume or purulence, antibiotic therapy is associated with measurable benefit (Tables 1 and 2 [1] [2]). Sputum smear and culture are not usually helpful, and empirical treatment is the rule. In low-risk patients, inexpensive antibiotics such as amoxicillin and trimethoprim-sulfamethoxazole may be used for 10 days, but bacterial resistance to these agents is common. In high-risk patients, the newer macrolides (e.g., azithromycin, 500 mg on day 1, 250 mg on days 2 to 5) or fluoroquinolones (e.g., levofloxacin, 500 mg/day for 7 to 10 days) may be advisable. In severe exacerbations, systemic steroid therapy has been shown to result in a relatively rapid recovery, [6] 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 may be difficult to distinguish from acute heart failure, and many elderly smokers may have both conditions concurrently. The distinction can be especially difficult in patients with right-sided heart failure, in whom the cause may be cor pulmonale from advanced COPD or worsening right-sided heart failure caused by worsening left-sided heart failure. The chest radiograph and the electrocardiogram are the best tools for differentiation here. A careful physical examination may reveal left-sided murmurs or a left-sided S3 gallop typical of left-sided heart failure. An electrocardiogram is occasionally helpful, whereas a chest radiograph may provide diagnostic information. An echocardiogram can detect left ventricular systolic dysfunction, valvar heart disease, and sometimes diastolic dysfunction causing heart failure. Brain natriuretic peptide levels have been shown to be a reliable way to distinguish an exacerbation of heart failure (elevated levels) from a worsening of COPD or other conditions.7]

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.[8]

FIGURE 6 Flow diagram for the management of stable COPD. FEV1 levels are approximate; the level of symptoms is equally important in determining treatment. As patients become more severely ill, therapies are added; for example, virtually all patients should receive a short-acting “rescue” inhaled bronchodilator.

TABLE 1 --


Mode of Delivery




β-Adrenergic agonist


Metered-dose inhaler

100–200 μg

4 times daily


0.5–2.0 mg

4 times daily



0.1–0.2 mg

4 times daily


Metered-dose inhaler

400 μg

4 times daily

Anticholinergic agent

Ipratropium bromide

Metered-dose inhaler

18–36 μg

4 times daily


0.5 mg

4 times daily




0.9 mg/kg of body weight/hr



Pill (sustained-release preparations)

150–450 mg[†]

Twice daily


Methylprednisolone succinate

Infusion, then pill

125 mg

Every 6 hours for 3 days, then

60 mg

Daily for 4 days

40 mg

Daily for 4 days

20 mg

Daily for 4 days

Prednisone (for outpatients)


30–60 mg

Daily for 5 to 10 days

Limited-spectrum antibiotics



160 mg and 800 mg

Twice daily for 5 to 10 days



250 mg

4 times daily for 5 to 10 days



100 mg

2 tablets first day, then 1 tablet/day for 5 to 10 days

From Stoller JK: Acute exacerbations of chronic obstructive pulmonary disease. N Engl J Med 2002;346:988–994.


Aminophylline is sometimes administered after a loading dose; the dose should be determined on the basis of serum levels of theophylline.

The dose varies among and within patients.


Even though the average patient with COPD suffers relentless progression of the disease, the course may be variable in different individuals. The two most important predictors of the course of COPD are age and severity of airways obstruction as evidenced by FEV1. Other key prognostic factors include weight loss, degree of dyspnea, and exercise capacity.

The need for hospital admission for an exacerbation, especially if intensive care is required, is an ominous prognostic sign in COPD; at least half such patients do not survive a year after admission. In patients with severe COPD, the issue of intensive care and artificial ventilation should be raised to ascertain the patient's attitudes with regard to these interventions and end-of-life care, and the results of these discussions must be documented


Anonymous said...

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Anonymous said...

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The dear man with COPD that I'd taken care of for the past 7 years decided, after 11 days, that he wanted removed from life support in the ICU 13 days ago. He peacefully expired from carbon dioxide narcosis 28.5 hours later. said...


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