• Chronic bronchitis is defined clinically as the presence of a chronic productive cough for 3 months during each of 2 consecutive years

(other causes of cough being excluded). • Emphysema, on the other hand, is defined pathologically as an abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis.

• Airflow limitation in emphysema is due to loss of elastic recoil, whereas chronic bronchitis leads to narrowing of airway caliber and increase in airway resistance. Although some patients predominantly display signs of one of these diseases or the other, most fall somewhere in the middle of the spectrum between the 2 conditions.

Pathophysiology
• Pathologic changes in COPD occur in the large (central) airways, the small (peripheral) bronchioles, and the lung parenchyma. Most cases of COPD are the result of exposure to noxious stimuli, most often cigarette smoke. The normal inflammatory response is amplified in persons prone to COPD development. The pathogenic mechanisms are not clear but are most likely diverse. Increased numbers of activated polymorphonuclear leukocytes and macrophages release elastases in a manner that cannot be counteracted effectively by antiproteases, resulting in lung destruction.

Pathophysiology • Chronic bronchitis • Mucous gland hyperplasia is the histologic hallmark of chronic bronchitis. focal squamous metaplasia. Airway structural changes include atrophy. ciliary abnormalities. inflammation. variable amounts of airway smooth muscle hyperplasia. and bronchial wall thickening .

. goblet cell metaplasia. The respiratory bronchioles display a mononuclear inflammatory process. Inflammation and secretions provide the obstructive component of chronic bronchitis. cause airflow limitation by allowing airway walls to deform and narrow the airway lumen. and neutrophilic infiltrates accumulate in the submucosa. Neutrophilia develops in the airway lumen.• Damage to the endothelium impairs the mucociliary response that clears bacteria and mucus. smooth muscle hyperplasia. combined with loss of supporting alveolar attachments. lumen occlusion by mucus plugging. These changes. and distortion due to fibrosis.

The body responds by decreasing ventilation and increasing cardiac output. these patients have signs of right heart failure and are known as "blue bloaters. leading to pulmonary artery vasoconstriction and cor pulmonale. . With the ensuing hypoxemia. This V/Q mismatch results in rapid circulation in a poorly ventilated lung. and increased CO2 retention. chronic bronchitis is associated with a relatively undamaged pulmonary capillary bed.• In contrast to emphysema. leading to hypoxemia and polycythemia. hypercapnia and respiratory acidosis develop. Eventually. polycythemia.

or paraseptal . loss of the alveolar supporting structure leads to airway narrowing. loss of alveoli leads to airflow limitation by 2 mechanisms. which leads to airflow limitation. • Emphysema has 3 morphologic patterns: • Centriacinar • Panacinar • Distal acinar. loss of the alveolar walls results in a decrease in elastic recoil. which further limits airflow.Pathophysiology • Emphysema • Emphysema is a pathologic diagnosis defined by permanent enlargement of airspaces distal to the terminal bronchioles. This leads to a dramatic decline in the alveolar surface area available for gas exchange. Furthermore. Second. First.

. This form of emphysema is associated with cigarette smoking and is typically most severe in the upper lobes.• Centriacinar emphysema is characterized by focal destruction limited to the respiratory bronchioles and the central portions of the acini.

• Panacinar emphysema involves the entire alveolus distal to the terminal bronchiole. The panacinar type is typically most severe in the lower lung zones and generally develops in patients with homozygous alpha1-antitrypsin (AAT) deficiency .

is the least common form and involves distal airway structures. or paraseptal emphysema. This form of emphysema is localized to fibrous septa or to the pleura and leads to formation of bullae. and sacs. The apical bullae may cause pneumothorax .• Distal acinar emphysema. alveolar ducts.

" . these patients develop muscle wasting and weight loss and are identified as "pink puffers. Because of low cardiac output.Pathophysiology • The gradual destruction of alveolar septae and of the pulmonary capillary bed in emphysema leads to a decreased ability to oxygenate blood. in contrast to the situation in chronic bronchitis. The body compensates with lowered cardiac output and hyperventilation. Eventually. This V/Q mismatch results in relatively limited blood flow through a fairly well oxygenated lung with normal blood gases and pressures in the lung. the rest of the body suffers from tissue hypoxia and pulmonary cachexia.

Pathophysiology • Emphysematous destruction and small airway inflammation • Emphysematous destruction and small airway inflammation often are found in combination in individual patients. is the dominant mechanism of airflow limitation. When emphysema is moderate or severe. Although airflow obstruction in emphysema is often irreversible. loss of elastic recoil. rather than bronchiolar disease. leading to the spectrum that is known as COPD. bronchiolar abnormalities are most responsible for the majority of the deficit in lung function. Airflow limitation is not the only pathophysiologic mechanism by which symptoms occur. when emphysema is mild. bronchoconstriction due to inflammation accounts for some reversibility. By contrast. .

the improvement in exercise capacity brought about by several treatment modalities. and maneuvers learned in pulmonary rehabilitation. In fact. oxygen therapy. including bronchodilators. particularly dynamic hyperinflation.Pathophysiology • Dynamic hyperinflation • Lung volumes. lung volume reduction surgery (LVRS). hyperinflation (defined as the ratio of inspiratory capacity to total lung capacity [IC/TLC]) has been shown to predict survival better than forced expiratory volume in 1 second (FEV1) . have also been shown to play a crucial role in the development of dyspnea perceived during exercise. Additionally. is more likely due to delaying dynamic hyperinflation rather than improving the degree of airflow obstruction.

Age of initiation of smoking. and causes a measurable reduction in pulmonary function. Clinically significant COPD develops in 15% of cigarette smokers. or environmental tobacco smoke. Secondhand smoke. tobacco smoking accounts for as much as 90% of COPD risk. total pack-years.Etiology • • • Cigarette smoking The primary cause of COPD is exposure to tobacco smoke. • • • . increases the risk of respiratory infections. A study by Nagelmann et al concluded that lung function deviation and lung structural changes are present in people who smoke cigarettes before the clinical signs of airway obstruction reveal them. although this number is believed to be an underestimate. augments asthma symptoms. but the rate of decline in COPD patients is generally 60 ml/y or greater. and current smoking status predict COPD mortality. Overall. which lead to tissue destruction. People who smoke have an increased annual decline in FEV1: the physiologic normal decline in FEV1 is estimated to be 20-30 ml/y. Cigarette smoking induces macrophages to release neutrophil chemotactic factors and elastases.

. the use of biomass fuels with indoor cooking and heating is likely to be a major contributor to the worldwide prevalence of COPD. In developing countries.• Environmental factors • COPD does occur in individuals who have never smoked. the effect is small when compared with that of cigarette smoking. Although the role of air pollution in the etiology of COPD is unclear. Long-term exposure to traffic-related air pollution may be a factor in COPD in patients with diabetes and asthma.

Nonspecific airway hyperreactivity is inversely related to FEV1 and may predict a decline in lung function. . This may contribute to airway remodeling.• Airway hyperresponsiveness • Airway hyperresponsiveness stipulates that patients who have nonspecific airway hyperreactivity and who smoke are at increased risk of developing COPD with an accelerated decline in lung function. bronchial hyperreactivity may result from airway inflammation observed with the development of smoking-related chronic bronchitis. • The possible role of airway hyperresponsiveness as a risk factor for the development of COPD in people who smoke is unclear. Moreover. as is seen in persons with COPD. leading to a more fixed obstruction.

The main purpose of this protein is to neutralize neutrophil elastase in the lung interstitium and to protect the lung parenchyma from elastolytic breakdown.• Alpha1-antitrypsin deficiency • Alpha1-antitrypsin (AAT) is a serine protease inhibitor family that is synthesized in the liver and is secreted into the bloodstream. Severe AAT deficiency leads to premature emphysema at an average age of 53 years for nonsmokers and 40 years for smokers. Severe AAT deficiency predisposes to unopposed elastolysis with the clinical sequela of an early onset of panacinar emphysema • AAT deficiency is the only known genetic risk factor for developing COPD and accounts for less than 1% of all cases in the United States. .

• Intravenous drug use • Emphysema occurs in approximately 2% of persons who use intravenous (IV) drugs. This is attributed to pulmonary vascular damage that results from the insoluble filler (eg, cornstarch, cotton fibers, cellulose, talc) contained in methadone or methylphenidate. • The bullous cysts found in association with IV use of cocaine or heroin occur predominantly in the upper lobes. In contrast, methadone and methylphenidate injections are associated with basilar and panacinar emphysema.

• Immunodeficiency syndromes • Human immunodeficiency virus (HIV) infection has been found to be an independent risk factor for COPD, even after controlling for confounding variables such as smoking, IV drug use, race, and age.[19] • Apical and cortical bullous lung damage occurs in patients who have autoimmune deficiency syndrome and Pneumocystis carinii infection.

• Connective tissue disorders • Marfan syndrome is an autosomal dominant inherited disease of type I collagen characterized by abnormal length of the extremities, subluxation of the lenses, and cardiovascular abnormality. Pulmonary abnormalities, including emphysema, have been described in approximately 10% of patients. • Ehlers-Danlos syndrome refers to a group of inherited connective tissue disorders with manifestations that include hyperextensibility of the skin and joints, easy bruisability, and pseudotumors; it has also been associated with a higher prevalence of COPD.

the exact prevalence of COPD in the United States is believed to be underestimated.Epidemiology • The National Health Interview Survey reports the prevalence of emphysema at 18 cases per 1000 persons and chronic bronchitis at 34 cases per 1000 persons.However. because most patients do not present for medical care until the disease is in a late stage. This is largely due to the fact that it is an underdiagnosed (and undertreated) disease.1% in the United States. While the rate of emphysema has stayed largely unchanged since 2000. Another study estimates a prevalence of 10. . the rate of chronic bronchitis has decreased.

5%. Men were found to have a pooled prevalence of 11. The numbers vary in different regions of the world.8% and women 8. .7% of women. Cape Town.2% of men and 16.1%.• The exact prevalence of COPD worldwide is largely unknown. has the highest prevalence. but estimates have varied from 7-19%. The Burden of Obstructive Lung Disease (BOLD) study found a global prevalence of 10. South Africa. affecting 22.

the prevalence in women is believed to be increasing. on the other hand. .• Germany. has the lowest prevalence. of 8.6% for men and 3. The differences can be explained in part by site and sex differences in the prevalence of smoking. Additionally.7% for women.

. With retroactive questioning. Patients often modify their lifestyle to minimize dyspnea and ignore cough and sputum production. Patients often ignore the symptoms because they start gradually and progress over the course of years.History • Most patients with COPD seek medical attention late in the course of their disease. a multiyear history can be elicited.

sputum production.• Patients typically present with a combination of signs and symptoms of chronic bronchitis and emphysema. and alteration in mental status. These include cough. worsening dyspnea. progressive exercise intolerance. .

. the FEV1 is the most common variable used to grade the severity of COPD.Symptoms include the following: • Productive cough or acute chest illness is common. the patient is usually breathless upon minimal exertion. The cough usually is worse in the mornings and produces a small amount of colorless sputum • Breathlessness:the most significant symptom. In fact. By the time the FEV1 has fallen to 50% of predicted. although it is not the best predictor of mortality. but it usually does not occur until the sixth decade of life (although it may occur much earlier).

Depression is not uncommon in subjects with COPD . cor pulmonale. osteoporosis. Systemic manifestations : COPD is now known to be a disease with systemic manifestations. pulmonary hypertension.• Wheezing:Wheezing may occur in some patients. anemia. particularly during exertion and exacerbations. depression. Many patients with COPD may have decreased fat-free mass. impaired systemic muscle function. and even left-sided heart failure. and the quantification of these manifestations has proved to be a better predictor of mortality than lung function alone.

frequent and recurrent pulmonary infections.• Some important clinical and historical differences may help distinguish between the types of COPD. Classic findings for patients with chronic bronchitis include productive cough with gradual progression to intermittent dyspnea. Classic findings for patients with emphysema include a long history of progressive dyspnea with late onset of nonproductive cough. and progressive cardiac/respiratory failure with edema and weight gain. occasional mucopurulent relapses. and eventual cachexia and respiratory failure. .

Physical Examination • The sensitivity of a physical examination in detecting mild to moderate COPD is relatively poor. physical signs are quite specific and sensitive for severe disease. however. Patients with severe disease experience tachypnea and respiratory distress with simple activities. .

In advanced disease.• The respiratory rate increases in proportion to disease severity. Use of accessory respiratory muscles and paradoxical indrawing of lower intercostal spaces is evident (known as the Hoover sign). . elevated jugular venous pulse (JVP). cyanosis. and peripheral edema can be observed.

.Thoracic examination reveals the following: • Hyperinflation (barrel chest) • Wheezing – Frequently heard on forced and unforced expiration • Diffusely decreased breath sounds • Hyperresonance on percussion • Prolonged expiration In addition. coarse crackles beginning with inspiration may be heard.

patients may adopt the tripod sitting position The chest may be hyperresonant. and wheezing may be heard Heart sounds are very distant Overall appearance is more like classic COPD exacerbation Chronic bronchitis characteristics include the following: Patients may be obese Frequent cough and expectoration are typical Use of accessory muscles of respiration is common Coarse rhonchi and wheezing may be heard on auscultation Patients may have signs of right heart failure (ie. such as edema and cyanosis .Certain characteristics allow differentiation between disease that is predominantly chronic bronchitis and that which is predominantly emphysema. cor pulmonale). Emphysema characteristics include the following: Patients may be very thin with a barrel chest Patients typically have little or no cough or expectoration Breathing may be assisted by pursed lips and use of accessory respiratory muscles.

and typical findings on chest radiographs can lead to the diagnosis of CHF.Differential Diagnoses • Congestive heart failure (CHF) may produce wheezing and often may be difficult to differentiate from emphysema. . A history of orthopnea and paroxysmal nocturnal dyspnea. fine basal crackles on chest auscultation.

but the important distinction is a significant bronchodilator response and normal diffusion (ie. coarse crackles and clubbing upon physical examination. • Chronic asthma: The delayed onset of severe asthma may be difficult to distinguish from COPD in older patients. and abnormal findings on chest radiographs and CT scans. • Bronchiolitis obliterans: is observed in younger persons who do not smoke and in persons with collagen-vascular diseases. diffusing capacity of lung for carbon monoxide [DLCO]) on pulmonary function tests. A CT scan characteristically shows areas of mosaic attenuation without evidence of generalized emphysema.• Bronchiectasis: Patients with bronchiectasis have chronic production of copious purulent sputum. .

including laboratory studies and imaging. . when the ratio of forced expiratory volume in 1 second over forced vital capacity (FEV1/FVC) is less than 70% of that predicted for a matched control. it is diagnostic for a significant obstructive defect. are particularly important during acute exacerbations of disease. This may result from a loss of elastic recoil due to lung tissue destruction or from an increase in the resistance of the conducting airways. Other studies. The formal diagnosis of COPD is made with spirometry.Investigations • The defining feature of COPD is irreversible airflow limitation during forced expiration.

Generally. • Patients with mild COPD have mild to moderate hypoxemia without hypercapnia. Lung mechanics and gas exchange worsen during acute exacerbations. hypoxemia worsens and hypercapnia may develop. • In general.Arterial Blood Gas Analysis • provides the best clues as to acuteness and severity of disease exacerbation. As the disease progresses. consider any pH below 7. thus. renal compensation occurs even in chronic CO2 retainers (ie. pH usually is near normal. .3 to be a sign of acute respiratory compromise. bronchitics). with the latter commonly being observed as the FEV1 falls below 1 L/s or 30% of the predicted value.

In the absence of blood gas measurements. because diuretics. • Beta-adrenergic agonists also increase renal excretion of serum calcium and magnesium. In addition. • Chronic respiratory acidosis leads to compensatory metabolic alkalosis. . beta-adrenergic agonists. which may be important in the presence of hypokalemia. bicarbonate levels are useful for following disease progression. serum potassium should be monitored carefully.Serum Chemistries • Patients with COPD tend to retain sodium. and theophylline act to lower potassium levels.

. in the range of 3-7 mmol/L).Alpha1-Antitrypsin • Measure alpha1-antitrypsin (AAT) in all patients younger than 40 years or in those with a family history of emphysema at an early age. The diagnosis of severe AAT deficiency is confirmed when the serum level falls below the protective threshold value of 11 mmol/L (ie.

The pathogens cultured most frequently during exacerbations are Streptococcus pneumoniae andHaemophilus influenzae. and Pseudomonas aeruginosa can be seen in patients with severe obstruction. With an exacerbation. the sputum is mucoid and macrophages are the predominant cells. . • A mixture of organisms often is visible with Gram stain.Sputum Evaluation • In persons with stable chronic bronchitis.Moraxella catarrhalis is also a common organism. an increase in the quantity of sputum production is often a sign of an acute exacerbation. sputum becomes purulent because of the presence of neutrophils. Although the quality of sputum can vary between patients in chronic stable disease.

Rapidly tapering vascular shadows accompanied by hyperlucency of the lungs are other signs of emphysema. including flattening of the diaphragm and a long. the hilar vascular shadows are prominent. narrow heart shadow.Chest Radiography • of patients with emphysema reveal signs of hyperinflation. • With complicating pulmonary hypertension. • Chronic bronchitis is associated with increased bronchovascular markings and cardiomegaly. . with possible right ventricular enlargement.

Computed Tomography • CT scanning is more sensitive than standard chest radiography and is highly specific for diagnosing emphysema (outlined bullae are not always visible on a radiograph). • CT scanning may provide an adjunct means of diagnosing various forms of COPD (ie. lower lobe disease may suggest AAT deficiency) and may help the clinician to determine whether surgical intervention would benefit the patient .

This may result in eventual rightsided heart failure (cor pulmonale).Echocardiography • Many patients with long-standing COPD develop secondary pulmonary hypertension from chronic hypoxemia and vascular remodeling. even with severe COPD. . However. the degree of pulmonary hypertension is usually only mild to moderate. Findings of severe pulmonary hypertension on echocardiogram or cardiac catheterization warrant further workup.

and they are helpful in following its progress. • In addition to the spirometry findings that define the disease. the absence of bronchodilator response does not justify withholding therapy. • As many as 30% of patients have an increase in FEV1 of 15% or more after inhalation of a bronchodilator. FEV1 is the most commonly used index of airflow obstruction.Pulmonary Function Tests • Pulmonary function tests are essential for the diagnosis and assessment of the severity of disease. . and residual volume. lung volume measurements often show an increase in total lung capacity. Dynamic hyperinflation during exercise is now thought be a greater contributor to the sensation of dyspnea than airflow obstruction alone (as measured by FEV1). functional residual capacity. The vital capacity often decreases. However.

GOLD CLASSIFICATION .

people with COPD take longer to blow air out. the lower their FEV1. The worse a person's airflow limitation is. FEV1 tends to decline. also measured in liters.• The GOLD staging system classifies people with COPD based on their degree of airflow limitation (obstruction). As COPD progresses. GOLD COPD staging uses four categories of severity for COPD. FEV1 is at least 70% of FVC. The airflow limitation is measured during pulmonary function tests (PFTs). The total exhaled breath is called the forced vital capacity (FVC). based on the value of FEV1: . and are used to diagnose COPD and its severity: • The volume in a one-second forced exhalation is called the forced expiratory volume in one second (FEV1). Pulmonary function tests measure this and other values. • In GOLD COPD. classifications are then used to describe the severity of the obstruction or airflow limitation. people with normal lungs can exhale most of the air in their lungs in one second. • When blowing out forcefully. In people with normal lung function. An FEV1 less than 70% of FVC can make the diagnosis of COPD in someone with compatible symptoms and history. • Because of lung damage. measured in liters. This impairment is called obstruction or airflow limitation.

70FEV1 50-79% normal Stage III-Severe COPD • FEV1/FVC<0.70FEV1 30-49% normal Stage IV-Very Severe COPD • FEV1/FVC<0. or <50% normal with chronic respiratory failure presen .Stage I-Mild COPD • FEV1/FVC<0.70FEV1≥ 80% normal Stage II-Moderate COPD • FEV1/FVC<0.70FEV1 <30% normal.

it is important to educate the patient about the disease and to encourage his or her active participation in therapy. Currently. no treatments aside from lung transplantation have been shown to significantly improve lung function or decrease mortality.Treatment • The goal of COPD management is to improve a patient’s functional status and quality of life by preserving optimal lung function. and preventing the recurrence of exacerbations. Once the diagnosis of COPD is established. improving symptoms. .

cardiopulmonary rehabilitation. short-acting bronchodilator as needed. consider surgical options such as LVRS and lung transplantation .Approaches to management include recommendations such as those provided by GOLD: • Stage I (mild obstruction): reduction of risk factors (influenza vaccine). long-acting bronchodilator(s). short-acting bronchodilator as needed. cardiopulmonary rehabilitation. long-acting bronchodilator(s). inhaled glucocorticoids if repeated exacerbation. inhaled glucocorticoids if repeated exacerbations • Stage IV (very severe obstruction or moderate obstruction with evidence of chronic respiratory failure): reduction of risk factors (influenza vaccine). cardiopulmonary rehabilitation • Stage III (severe obstruction): reduction of risk factors (influenza vaccine). short-acting bronchodilator as needed. short-acting bronchodilator as needed • Stage II (moderate obstruction): reduction of risk factors (influenza vaccine). long-term oxygen therapy (if criteria met). long-acting bronchodilator(s).

Most of the medications used are directed at the following 4 potentially reversible causes of airflow limitation in a disease state that has largely fixed obstruction: • Bronchial smooth muscle contraction • Bronchial mucosal congestion and edema • Airway inflammation • Increased airway secretions .• Oral and inhaled medications are used for patients with stable disease to reduce dyspnea and improve exercise tolerance.

• Bronchodilation • Bronchodilators are the backbone of any COPD treatment regimen. thereby decreasing airflow resistance. Lack of response in pulmonary function testing should not preclude their use. . These drugs provide symptomatic relief but do not alter disease progression or decrease mortality. This increases airflow and decreases dynamic hyperinflation. They work by dilating airways.

Beta2 agonists and anticholinergics • The initial choice of agent remains in debate. beta2 agonists were considered first line and anticholinergics were added as adjuncts. studies have shown combination therapy results in greater bronchodilator response and provides greater relief. Historically. . long-acting bronchodilators are more beneficial than short-acting ones. Generally. The adverse effect profile may help guide therapy. Not surprisingly. Monotherapy with either agent and combination therapy with both are acceptable options.

Although rare.Beta2-agonist bronchodilators • Even patients who have no measurable increase in post-bronchodilator expiratory airflow may benefit from treatment with beta2 agonists. . The inhaled route is preferred because it minimizes adverse systemic effects. The adverse effects are predictable and include tachycardia and tremors. beta2 agonists may also precipitate a cardiac arrhythmia.

resulting in bronchodilation.• Anticholinergic drugs compete with acetylcholine for postganglionic muscarinic receptors. They block vagally mediated reflex arcs that cause bronchoconstriction. thereby inhibiting cholinergically mediated bronchomotor tone. metallic taste. These agents are poorly absorbed systemically and are relatively safe. dry eyes. Clinical benefit is gained through a decrease in exercise-induced dynamic hyperinflation. Reported adverse effects include dry mouth. and prostatic symptoms .

.• Inhaled delivery of medications is preferred over the oral route to help minimize potential adverse effects. use of a spacer or nebulizer may be beneficial in these patients. Some patients may have difficulty achieving effective delivery of the medication using a metered-dose inhaler.

• Phosphodiesterase inhibitors • Phosphodiesterase inhibitors result in bronchodilation. The previously recommended target range of 15-20 mg/dL has now been reduced to 8-13 mg/dL. they may improve diaphragm muscle contractility and stimulate the respiratory center. tremors. Serum levels of theophylline need to be monitored because of the potential for toxicity. and seizures. a process affected by age. • Theophylline is metabolized primarily via the hepatic cytochrome P450 system. Theophylline has a narrow therapeutic window with significant adverse effects. Additionally. cardiac status. and liver abnormalities. . including anxiety. cardiac arrhythmia (particularly multifocal atrial tachycardia). It is reserved for patients with hard-tocontrol COPD or for individuals who are not able to use inhaled agents effectively. • Theophylline is a nonspecific phosphodiesterase inhibitor and is now limited to use as an adjunctive agent. nausea. insomnia.

these results need to be confirmed in larger trials. Nausea. A dose of 15 mg twice daily has been found to be clinically effective. presumably of central origin. selective phosphodiesterase-4 inhibitors. is the principal adverse reaction.5 hours.• Cilomilast (Ariflo) and roflumilast are secondgeneration. Cilomilast is completely absorbed following oral administration and has a half-life of approximately 6. Preliminary clinical studies suggest a favorable clinical effect in COPD. . They cause a reduction of the inflammatory process (macrophages and CD8+ lymphocytes) in patients with COPD.

and will likely require multiple attempts to maintain success. the success rates for cessation programs are low because of the addictive power of nicotine. The process of smoking cessation typically requires multiple interventional approaches. forceful promotional campaigns by the tobacco industry. poor education. A smoking cessation plan is an essential part of a comprehensive management plan. Most patients with COPD have a history of smoking or are currently smoking tobacco products.Smoking Cessation • Smoking cessation continues to be the most important therapeutic intervention for COPD. and psychological problems. These rates can also be negatively impacted by such factors as conditioned responses to smoking-associated stimuli. . including both pharmacologic and non-pharmacologic modalities. • However. including depression.

given their high efficacy. Systemic and inhaled corticosteroids attempt to temper this inflammation and positively alter the course of disease.Management of Inflammation • Inflammation plays a significant role in the pathogenesis of COPD. . • The use of systemic steroids in the treatment of acute exacerbations is widely accepted and recommended. A meta-analysis concluded that oral and parenteral corticosteroids significantly reduced treatment failure and the need for additional medical treatment and that they increased the rate of improvement in lung function and dyspnea over the first 72 hours.Note that systemic steroids are not as effective in treating COPD exacerbations as they are in treating bronchial asthma exacerbations.

glucose intolerance. which include hypertension. . given their adverse effects.• On the other hand. and cataracts. the use of oral steroids in persons with chronic stable COPD is widely discouraged. fractures. osteoporosis.

are only minimally absorbed. although they have been shown to decrease the frequency of exacerbations and improve quality of life for symptomatic patients with an FEV1 of less than 50%. Despite the theoretical benefit. the current consensus is that inhaled corticosteroids do not decrease the decline in FEV1. similar to other inhaled agents. Consequently. the systemic adverse effects of these medications at standard doses are negligible.• Inhaled corticosteroids provide a more direct route of administration to the airways and.[56] The 2011 ICSI guidelines conclude that inhaled steroids are appropriate in patients with recurrent exacerbations of COPD . aside from the development of thrush.

inhaled corticosteroids should be used only in conjunction with a long-acting beta agonist.[57] These data suggest that in patients with COPD.• Inhaled corticosteroids are not recommended as monotherapy and should be added to a regimen that already includes a long-acting bronchodilator. The Towards a Revolution in COPD Health (TORCH) trial showed that a combination of an inhaled corticosteroid and a long-acting beta agonist was more beneficial than inhaled corticosteroids alone. .

and thus IV steroids should be reserved only for those patients unable to tolerate oral intake. . recent research suggests that there is likely no benefit of IV over oral steroid formulations in acute exacerbations.• Intravenous steroids are often used in high doses for acute exacerbations in the inpatient setting.

.Management of Infection • In patients with COPD. H influenzae. chronic infection or colonization of the lower airways is common from S pneumoniae. In patients with chronic severe airway obstruction. sputum production. P aeruginosa infection may also be prevalent.[20] Patients who benefited most from antibiotic therapy were those with exacerbations that were characterized by at least 2 of the following: increases in dyspnea. No evidence supports the continuous or prophylactic use of antibiotics to prevent exacerbations. and sputum purulence (The Winnipeg criteria). and M catarrhalis. The use of antibiotics for the treatment of acute exacerbations is well supported.

. leukocytosis. The antibiotic choice must be comprehensive and should cover all likely pathogens in the context of the clinical setting and local resistance patterns. or an infiltrate on chest radiograph. such as fever.• Empiric antimicrobial therapy is recommended in patients with an acute exacerbation (as evidenced by an increase in baseline dyspnea and/or a change in the quantity or quality of cough) and evidence of an infectious process.

Management of Sputum Viscosity and Secretion Clearance • Mucolytic agents reduce sputum viscosity and improve secretion clearance. the efficacy of mucolytic agents in the treatment of COPD remains controversial. Although they have been shown to decrease cough and chest discomfort. and they have also been shown to elicit bronchospasm. • The oral agent N -acetylcysteine has antioxidant and mucokinetic properties and is used to treat patients with COPD. they have not been shown to improve dyspnea or lung function. . When used as an inhalational therapy. N acetylcysteine should be administered along with a bronchodilator such as albuterol in order to counteract potential induction of bronchospasm. However.

Lung and Blood Institute’s Nocturnal Oxygen Therapy Trial (NOTT). the British Medical Research Council (MRC) study and the US National Heart. Oxygen administration reduces mortality rates in patients with advanced COPD because of the favorable effects on pulmonary hemodynamics. • Long-term oxygen therapy improves survival 2-fold or more in hypoxemic patients with COPD. according to 2 landmark trials. Oxygen was used for 15-19 hours per day . Hypoxemia is defined as PaO2 (partial pressure of oxygen in arterial blood) of less than 55 mm Hg or oxygen saturation of less than 90%.Oxygen Therapy and Hypoxemia • COPD is commonly associated with progressive hypoxemia.

• Many patients with COPD who are not hypoxemic at rest worsen during exertion. and improve exercise tolerance. or cor pulmonale. Home supplemental oxygen commonly is prescribed for these patients. a PaO2 of less than 59 mm Hg with evidence of polycythemia. reduce dyspnea. Oxygen supplementation during exercise can prevent increases in pulmonary artery pressure. because some patients may not require long-term oxygen. . Reevaluate these patients 1-3 months after initiating therapy. specialists recommend long-term oxygen therapy for patients with a PaO2 of less than 55 mm Hg.• Therefore.

• The continuous-flow nasal cannula is the standard means of oxygen delivery for the stable hypoxemic patient. Nasal oxygen delivery also is beneficial for most mouth-breathing patients. and generally well tolerated. It is simple. Each liter of oxygen flow adds 3-4% to the fraction of inspired oxygen (FiO2). reliable. Humidification generally is not necessary when the patient receives oxygen by nasal cannula at flows of less than 5 L/min .

Indications for admission include failure of outpatient treatment.Treatment for acute exacerbation of COPD • Acute exacerbation (AE) COPDs are a major reason for hospital admission in the United States. Care must be taken to evaluate for other conditions that may mimic AECOPD. and inability to tolerate oral medications such as antibiotics or steroids. although mild episodes may be treated in an outpatient setting. increase in hypoxemia or hypercapnia. . altered mental status. marked increase in dyspnea.

parameter—is defined as worsening of cough. may be the only action that prevents frank respiratory failure. • AECOPDs are very common. Care must also be taken to evaluate for other conditions that may mimic acute exacerbations of COPD. along with aggressive and prompt intervention. evaluate for other conditions that may mimic acute exacerbations of COPD. affecting about 20% of patients with moderate to severe COPD.• Patients with COPD are susceptible to many insults that can lead rapidly to an acute deterioration superimposed on chronic disease. AECOPD—an important. and increase in dyspnea. change in sputum quality. Quick and accurate recognition of these patients. . increase in sputum production. but occasionally overlooked.

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