Emphysema: A Clinical Review

Release Date: July 1, 2012

Expiration Date: July 31, 2014


Joshua Shipley, PharmD, BCPS, CGP
Clinical Staff Pharmacist, Emergency Department
St. John’s Hospital
Springfield, Illinois


Dr. Shipley has no actual or potential conflict of interest in relation to this activity.

Postgraduate Healthcare Education, LLC does not view the existence of relationships as an implication of bias or that the value of the material is decreased. The content of the activity was planned to be balanced, objective, and scientifically rigorous. Occasionally, authors may express opinions that represent their own viewpoint. Conclusions drawn by participants should be derived from objective analysis of scientific data.


Pharmacy acpe
Postgraduate Healthcare Education, LLC is accredited by the Accreditation Council for Pharmacy Education as a provider of continuing pharmacy education.
UAN: 0430-0000-12-015-H01-P
Credits: 2.0 hours (0.20 ceu)
Type of Activity: Knowledge


Payment of $6.50 required for exam to be graded.


This accredited activity is targeted to pharmacists. Estimated time to complete this activity is 120 minutes.

Exam processing and other inquiries to:
CE Customer Service: (800) 825-4696 or cecustomerservice@jobson.com


Participants have an implied responsibility to use the newly acquired information to enhance patient outcomes and their own professional development. The information presented in this activity is not meant to serve as a guideline for patient management. Any procedures, medications, or other courses of diagnosis or treatment discussed or suggested in this activity should not be used by clinicians without evaluation of their patients' conditions and possible contraindications or dangers in use, review of any applicable manufacturer's product information, and comparison with recommendations of other authorities.


To review the general etiology, symptoms, diagnosis, and treatment of patients with emphysema.


After completing this activity, the participant should be able to:

  1. Describe risk factors associated with emphysema.
  2. Identify symptoms and clinical findings associated with emphysema.
  3. Explain the disease development and progression of emphysema.
  4. Discuss nonpharmacologic and pharmacologic treatment options utilized in patients with emphysema.

In 1698, the physician John Floyer first described emphysema as foreign expanded "air bladders" interspersed within normal lung tissue. Interestingly, due to the then-public aversion to human autopsy, his finding was undertaken on equine specimens. Yet his 300-year old description of these abnormal tissues, updated in current clinical terminology, is the hallmark diagnostic finding in emphysema today.1 Emphysema is part of a group of conditions termed chronic obstructive pulmonary disease (COPD), which generally also includes chronic bronchitis.2 The diagnosis of emphysema is often intertwined with some presentation of bronchitis, which historically may have convoluted the diagnostic process. As such, current guidelines do not differentiate between emphysema and chronic bronchitis, but collectively address treatment under the heading of COPD.

Etiology, Pathophysiology, and Assessment

Per the CDC, the prevalence of emphysema alone in the United States was approximately 4.3 million people (~1.9%) in 2010, accounting for an estimated 11,000 deaths annually.3 The primary risk factor for the development of emphysema is cigarette smoking, which accounts for approximately 90% of all emphysema cases. Other risk factors include alpha1-antitrypsin deficiency, air pollution, occupational chemicals or dust, and impaired lung growth.2 To provide data regarding the relationship between smoking and emphysema, a systematic review and meta-analysis of over 200 studies on COPD showed the relative risk of smoking and the emphysema subset to be 4.87 (2.83-8.41) for current smokers and 3.52 (2.51-4.94) for ex-smokers, indicating an approximate 5-fold and 3-fold increased risk of developing emphysema, respectively.4

In the U.S. in 2009, the prevalence of smoking varied from state to state, with Utah at 9.8% and Kentucky at 25.6%, with an overall national average of about 1 in 5 people.5 Fortunately, given the large prevalence of smokers, only approximately 15% of all smokers end up actually developing COPD at some point in their lives, with emphysema constituting about 3% of that.5 There is also a hereditary form of emphysema, termed alpha1-antitrypsin deficiency, which accounts for <1% of diagnosed emphysema.6 Beyond the U.S. and smoking, an important risk factor for developing emphysema is the use of biomass fuel such as plant or agricultural waste. In particular, women in nonindustrialized nations that utilize biomass fuels for daily living are susceptible to disproportionately increased incidence of exposure to inhaled irritants, and likewise show an increased prevalence of emphysema.2

Emphysema is a progressive, irreversible, and destructive disease of the alveolar and parenchymal lung tissues in which the capacity and efficiency of the lungs to utilize oxygen are diminished. Emphysema is defined as abnormal permanent enlargement of the air spaces distal to the terminal bronchioles, accompanied by destruction of their walls without obvious fibrosis.2 The condition is characterized by chronic inflammation that causes irreversible destructive changes leading to increased airway limitation. The inflammation is most often caused by noxious particles via gas inhalation. There are also damaging chemical mediators involved including tumor necrosis factor-α, interleukin-8, leukotriene B4, oxidants, and proteases.7 To counter some of these destructive chemicals, there is a widely distributed protective antiprotease termed alpha1-antitrypsin, which normally balances the destructive proteases. But a deficiency in alpha1-antitrypsin can lead to premature lung tissue destruction and emphysema, typically at a younger age than emphysema related to inhaled irritants. The alpha1-antitrypsin-deficient form of emphysema is hereditary.7

In the majority of emphysema cases that are in part due to smoke inhalation, the final cellular destruction takes place over long periods of time. There is a constant cycle of irritation, cellular isolation, and then regeneration that weakens the lung tissue itself as well as the body's defense mechanisms to the inflammation. This inflammation can lead to the narrowing of distal airways, which will result in a decrease in forced expiratory volume (FEV), or a decrease in the total gaseous capacity of the lungs, termed forced vital capacity (FVC).2 Constant inflammation can also lead to destruction of the lung parenchyma, alveoli, or terminal bronchioles. This will add to the limitation of airflow and decrease the overall capacity of oxygen transfer. The alveolar clusters responsible for the blood-gas exchange suffer a dramatic loss of surface area and ability to function when damaged.6

Normally a branch of alveoli might resemble a bunch of grapes. Each grape is connected via a small stem and has its own complete surface area attributed to itself. Alveoli are similar in shape and surface area design in that many little spheres connected to each other tightly via small bronchioles constitute a large surface area for gas exchange. When these alveoli and lung parenchyma are damaged or destroyed, the individual spheres break down and give way to connective tissue and form larger cavities with reduced or lost functionality. Due to the creation of larger cavities that replaced the normal lung parenchyma, patients with emphysema have a larger but less efficient total lung volume. The damaged areas and connective tissue changes also frequently reduce or obstruct the airflow to these areas. These larger damaged cavities are the hallmark of emphysema. The number and severity of damaged terminal bronchioles and alveolar clusters essentially determine the loss of function and severity of emphysema.

The diagnosis of emphysema is made based on a combination of factors, including a patient history of smoking or occupational irritant exposure, chest x-ray, cough or dyspnea, alpha1-antitrypsin testing, arterial blood gas readings, and spirometry testing.2,3 Patients may endure years of symptoms presenting as mild nuisances until the disease progresses to the point of true breathing difficulty and is formally assessed.

Guidelines for treatment of emphysema are within the Global Initiative for Chronic Obstructive Lung Disease (GOLD) report.2 Spirometry is the standard for assessing airflow limitation in all forms of COPD, including emphysema. A ratio of less than 70% of forced expiratory volume in 1 second (FEV1) divided by the total FVC is diagnostic of airway obstruction. Along with an FEV1/FVC of <70%, COPD is further classified by decline in FEV1 into mild, moderate, severe, and very severe.2 Spirometry alone is inadequate for an accurate diagnosis; however, a complete patient assessment of comorbid symptoms and complications will provide a better picture of status. Patients with mild forms of emphysema may present normally on physical examination. Patients with more severe disease may present with a decreased body mass index, appear barrel-chested due to lung hyperinflation, show signs of cyanosis in distal extremities, or breathe with shallow, quick breaths.8

It is important to remember that in patients with emphysema there are most likely comorbid conditions that influence the total care of these patients, such as decreased immune response or cardiac-related ailments. Furthermore, emphysema is rarely a lone lung condition, and often incorporates parts of other airway diseases, such as bronchial hyperresponsiveness as in asthma or chronic inflammatory processes as in bronchitis, which convolute the treatment process.

Pharmacologic Therapy

Emphysema is an irreversible disease, so the main treatment goal is to minimize disease progression. Pharmacologic and nonpharmacologic treatment focuses on decreasing symptoms and frequencies of exacerbations. Other objectives are to increase exercise tolerance and to reduce morbidity and mortality.2,9 Patients with emphysema should receive information about their disease, as well as therapy options and potential future strategies to combat the decline of lung function. However, primary importance should also be placed on reduction or removal of risk factors.

Smoking Cessation: Exposure to tobacco smoke is the major risk factor for developing emphysema. Many patients have smoked for years and continue to do so despite their understanding of the detriments of smoking and prospect of declining health. Nevertheless, it is incumbent on all health care practitioners, including pharmacists in primary patient care areas, to address smoking cessation and provide information about it to known smokers.10 It is important to assess the patient's willingness to quit smoking and a history of attempts before continuing on in treatment. Guidelines from the U.S. Public Health Service outline the "5 A's" process for smoking cessation11:

  1. Ask patients about smoking to identify all candidates.
  2. Advise all tobacco users to quit.
  3. Assess the desire of the patient to quit.
  4. Assist in motivation and treatment.
  5. Arrange for follow-up and further smoking cessation monitoring.

Pharmacotherapy at least doubles the effectiveness of smoking cessation attempts and should be offered to all patients with emphysema unless contraindicated.12 First-line pharmacotherapy includes varenicline, bupropion, and nicotine replacement options (TABLE 1).6,12 Second-line therapy may include clonidine and nortriptyline, but there are fewer data supporting their effectiveness and they may produce increased side effects. However, if first-line treatment has failed or second-line therapies coincide favorably with comorbid conditions, they may be viable alternatives. In addition, utilizing behavioral approaches that decrease influences or triggers to smoking and having a social support system for positive reinforcement are valuable additions to a successful smoking cessation program. The patient's family and peer involvement as well as health care follow-up sessions are also important factors in achieving and maintaining success.

Bronchodilators, Corticosteroids, and PDE Inhibitors: Bronchodilators are the mainstay of therapy in the treatment of emphysema, under the guidelines for COPD. The classes of bronchodilators available are beta2-agonists, anticholinergics, and methylxanthines (TABLE 2).2,13 Bronchodilators work by relaxing airway smooth muscle, contributing to increased exercise tolerance or airflow and decreased dyspnea. Based on the latest evidence, long-acting inhaled bronchodilators are preferred over oral or short-acting forms, and methylxanthines are not recommended unless long- or short-acting beta2-agonists and anticholin-ergics are not available.2 First-line treatment options are based on severity of airway inhibition, graded on the GOLD classification scale (TABLE 3), along with patient response. In general, GOLD 1 patients may have an as-needed short-acting beta2-agonist (SABA) or short-acting anticholinergic. GOLD 2 patients should be on a scheduled long-acting beta2-agonist (LABA) or long-acting anticholinergic. Patients who would be classified as GOLD 3 and GOLD 4 should be on inhaled corticosteroids plus a LABA or a long-acting anticholinergic. Combining bronchodilators from different classes can also improve response without increasing the side effects of a higher-dose single agent alone.2,6

The dosing structure and safety of single long-term inhaled corticosteroid use in emphysema treatment is controversial and not currently recommended. Even so, systematic treatment of patients with FEV1 below 50% to 60% predicted with inhaled corticosteroids has been shown, for a minority of patients, to improve lung function, reduce symptoms, improve quality of life, and reduce frequencies of exacerbations.14,15 The rate of decline in FEV1, the major disease status indicator, after inhaled single corticosteroid use compared to placebo resulted in no significant difference in the ISOLDE trial.16 Despite no difference in long-term FEV1 decline, there were significantly fewer exacerbations and a higher health status in the inhaled corticosteroid arm compared to placebo. Studies with similar results have led to using combinations of bronchodilators and corticosteroids together instead of a single inhaled corticosteroid alone.17

In several studies, the combination of inhaled corticosteroids with bronchodilators has shown greater improvement in FEV1, health status, and decreased exacerbations when compared to either an inhaled corticosteroid or a broncho-dilator alone.18,19 There is some concern, however, that increased use of inhaled corticosteroids has been linked to increased rates of pneumonia in COPD patients.19 This risk would be somewhat offset by the benefit of reduced exacerbations and increased FEV1, but no analysis has been undertaken comparing these risks.

In contrast to inhaled corticosteroids, the routine use of long-term oral systemic corticosteroids (e.g., prednisone, methylprednisolone) is not advised. There are some data regarding mild improvements in FEV1 for a select population; however, in view of the long-term side effects of osteoporosis, muscle atrophy, and adrenal suppression as compared with the availability, relative safety, and effectiveness of inhaled therapy, long-term oral corticosteroid use should be avoided.20

Methylxanthines can be utilized in any stage of emphysema, but they are not indicated as first-line therapy.2 Theophylline acts as a nonselective phosphodiesterase inhibitor, among other mechanisms, and is metabolized by CYP450, leading to many drug interactions. Smoking affects the metabolism of theophylline, and clearance of the drug decreases with increasing age. Both of these are a concern in the patient population regarding emphysema. Theophylline also has a narrow therapeutic index, with a window of efficacy that is relatively close to potentially toxic doses, leading to increased side effects and drug management issues.21 Study results have indicated an increased beneficial effect when theophylline is added to combination SABA-anticholinergic therapy, showing that there may be a synergistic component to the combination.22 However, theophylline should not be used as first-line treatment, but is a possible addition to maximized inhaled treatment as further benefit. Nevertheless, with a patient population that is unable to utilize inhalers because of poor motor function or their prohibitive cost, methylxanthines remain an effective alternative or addition to treatment regimens.2

Phosphodiesterase-4 (PDE-4) inhibitors, in contrast to methylxanthines, are more selective in their PDE isoenzyme inhibition. (Roflumilast is the only currently marketed agent in this class.) The isoenzyme PDE-4 is found in a variety of airway proinflammatory cells, and its inhibition is thought to confer beneficial immunomodulatory effects in COPD patients. PDE-4 inhibitors have been shown to improve FEV1 when given to patients already receiving LABAs or tiotropium, as well as to decrease the number of exacerbations in select groups.23 However, PDE-4 inhibitors are currently advocated as an addition to conventional therapy in moderate-to-severe forms of COPD, and present with more frequent adverse effects such as nausea than inhaled therapies, which may be a limiting factor in their use.24 Similar to methylxanthines, PDE-4 inhibitors have not been tested as first-line therapy in the treatment of COPD but may make adequate therapy additions to inhaled therapy in select patients. As their mechanism of action is similar in part, PDE-4 inhibitors are not to be given in combination with methylxanthines.2

Alpha1-Antitrypsin Deficiency: Persons with alpha1-antitrypsin deficiency are a unique subset of emphysema patients. This is a codominant genetic disposition where either one or the other or both genes can lead to various deficient levels of alpha1-antitrypsin production. Circulating alpha1-antitrypsin is the most abundant protease inhibitor in the body. It is primarily produced in the liver, but also by gut epithelial cells and alveolar macrophages.25 It acts, among other things, to inhibit the enzyme neutrophil elastase. Neutrophil elastase is released at sites of inflammation, and if left unchecked can cause damage to body tissues. Lung tissue is particularly susceptible due to its increased exposure to inflammatory processes by inhalation, and the inflammation can be further aggravated by other noxious elements such as smoking. However, alpha1-antitrypsin deficiency can cause emphysema without the presence of any other risk factors. Nor is an alpha1-antitrypsin deficiency limited to emphysema alone; it can be expressed as other diseases (e.g., cirrhosis).26 Overall, emphysema due to an alpha1-antitrypsin deficiency presents earlier in the patient's life, usually in the 20s. This is much earlier than emphysema due to traditional causes such as smoking. Cases are most prevalent in populations aged between 40 and 60 years.3

Treatment for alpha1-antitrypsin-deficient emphysema is similar in the aforementioned options: Remove possible risk factors and follow the treatment guidelines as necessary. Specific treatment for this type of emphysema can also include alpha1-antitrypsin augmentation therapy. The rationale for augmentation is to keep circulating levels of alpha1-antitrypsin within presumed protective limits where benefit may be gained from counterbalancing the destructive actions of neutrophil elastase within the lung. Therapy is expensive, costing an estimated $55,000 per year.27 Owing in part to this prohibitive cost as well as to finding an adequate patient population, solid data regarding the cause and effect of therapy in clinical trials are lacking. However, one small randomized trial did show retention of lung tissue with alpha1-antitrypsin augmentation therapy with no difference in self-reported FEV1 decline, which was statistically nonsignificant.28 Another observational study showed a slower rate of decline in FEV1 and reduced mortality in augmented patients, but the data cannot be assumed as predictive due to their observational nature.29 Screening patients for alpha1-antitrypsin deficiency is also not routinely done. Screening high-risk patients for this deficiency along with augmentation of an appropriately selected group and a decrease in drug costs may break the barrier of cost versus benefit in the future and make alpha1-antitrypsin augmentation therapy more available.

Vaccines: Immunizations play an important role as adjunctive therapy in emphysema patients. Influenza is a common respiratory complication that can lead to increased exacerbations or respiratory failure in patients with emphysema. Immunization against influenza is known to decrease morbidity and mortality, has shown to be highly effective in the prevention of respiratory illness related to influenza, and should be recommended in all patients with emphysema.30 Likewise, the pneu-mococcal vaccine is recommended to be given once in all adult patients aged less than 65 years with chronic lung disease, followed by a revaccination after 5 years unless contraindicated, and then once again after age 65. The pneumococcal vaccine has been shown to reduce the incidence of community-acquired pneumonia in the moderate-to-severe group of emphysema patients.31 Unfortunately, immunization rates of both influenza and pneumococcal vaccines remain inadequate, especially in this high-risk population. Opportunities abound for pharmacists to make a difference regarding immunizations, both in patient education and in championing efforts to practice preventive medicine.

Nonpharmacologic Therapy

Pulmonary Rehabilitation: Pulmonary rehabilitation is an important part of a complete treatment package in patients with emphysema. Pulmonary rehabilitation through routine exercise has been shown in patients with COPD to reduce fatigue and dyspnea, increase exercise tolerance, improve health-related quality of life, reduce anxiety and depression, improve the effects of long-acting bronchodilator therapy, and improve survival.2 Programs for rehabilitation should include trials of high-intensity training (up to 70% of the patient's maximum perceived workload) for at least 20 minutes per day, with activity sufficient to strengthen but not overly stress lung function. Pulmonary rehabilitation programs lasting less than 3 days per week or less than approximately 6 weeks total have proved ineffective compared to longer therapies. Unfortunately, most data involve limited program length, and beneficial effects from these programs do not seem to last after program discontinuation.32

It would be most beneficial and effective for a pulmonary rehabilitation program to become a permanent practice, but even a limited program can confer improvements in exercise tolerance, dyspnea, quality of life, and normal activities of daily living. Other important aspects of pulmonary rehabilitation programs include encouragement of smoking cessation, motivational encouragement for exercise from family and health care personnel, facilitation of disease education including strategies to reduce dyspnea and seek help, minimize exacerbations, and understand the general therapy approach.2

Oxygen Therapy: Oxygen therapy is reserved for more severe cases of emphysema, and long-term therapy should not be considered unless the patient is in stable condition and pharmacotherapy has been optimized. Long-term oxygen therapy (>15 hours per day) is indicated for patients who have a partial pressure of arterial oxygen (PaO2) less than 55 mmHg (normal >80 mmHg) or an arterial oxygen saturation (SaO2) less than 88% (normal >93%) confirmed twice over 3 weeks in a stable resting patient. Oxygen therapy may also be considered when the PaO2 is less than 60 mmHg in patients with concurrent polycythemia (hematocrit >55%), congestive heart failure, or pulmonary hypertension.2 The use of oxygen therapy in eligible hypoxic patients increases survival, improves the quality of life by increasing exercise tolerance, and reduces the length of hospital stays. However, stable patients who do not meet these criteria should not be initiated on long-term oxygen therapy based on the current evidence.33 The typical method of administration is by a nasal cannula at a flow rate of 1 to 3 L/min, and can be delivered using compressed cylinders, liquid reservoirs, or oxygen concentrators that separate out room-air oxygen. Smoking while on oxygen therapy is dangerous and can precipitate burns or fires, and should be avoided at all times.

Surgical Interventions: Several surgical options are available for severe cases of emphysema. They include bullectomy, lung transplantation, and lung volume reduction surgery (LVRS), among other more infrequent forms. Bullectomy is a procedure where bullae greater than 1 cm in size are removed from the lungs. These large bullae may contribute to increased dyspnea and decreased efficiency of operative lung tissue. Removal of the bullae may decrease symptoms but has not been shown to have a mortality benefit.2 Lung transplantation is considered in the most severe cases of emphysema where the FEV1 is <20% predicted with hypoxemia and pulmonary hypertension existing despite appropriate medical management, and the patient's predicted survival is less than 2 years. Transplantation is limited due to lack of donor organs and cost, but when utilized in the proper patients has been shown to improve survival, functional capacity, and quality of life.34

LVRS is a technique that resects parts of the lung, which in turn decreases overall cavity pressure.35 This allows the diaphragm and subsequent lung tissue to work more efficiently, improves the expiratory flow rates, and reduces exacerbations. LVRS has been shown to improve survival compared to medical treatment alone in severe emphysema patients with upper-lobe disease and low postrehabilitation exercise capacity. Similar patients with high postrehabilitation exercise capacity showed no survival difference, but did improve exercise capacity and health-related quality of life. However, in patients with an FEV1 of <20%, LVRS has shown to have a higher mortality rate than medical treatment alone and should be avoided.35

Treatment of Exacerbations

COPD exacerbations are acute events characterized by worsening respiratory symptoms compared to the patient's baseline function that require a change in medication. Exacerbation events contribute significantly to increased morbidity, mortality, costs, rate of lung function decline, and hospitalizations.2 Exacerbations can present from mild to severe, differing in the severity of airflow limitation, current comorbidities, and the patient's baseline functional status. Exacerbations are thought to be precipitated by respiratory tract infections (viral and bacterial) in approximately 50% of cases, with one-third of total cases presenting from an unknown origin.2,6 The diagnosis of an exacerbation relies solely on the patient's complaints of dyspnea, cough or sputum production that is elevated from the baseline, and general clinical presentation. Spirometry is not recommended for assessment of exacerbations due to the difficulty of measurement and lack of immediate applicability. Tools such as pulse oximetry, chest radiographs, electrocardiograms, blood laboratory values, and the presence of purulent sputum may assist in patient assessment.2,6

Treatment goals for the management of exacerbations in emphysema include preventing acute respiratory failure and death, preventing hospitalization or reducing hospital stay, and resolving exacerbation symptoms and returning to baseline. Pharmacologic therapies utilized most often are bronchodilators, corticosteroids, and antibiotics. Short-acting beta2-agonists with or without anticholinergics are most often utilized initially, with equal efficacy shown between nebulized and meter-dosed inhaled treatment.2,6 IV methylxanthines are second-line therapy and should only be considered when inhaled bronchodilator therapy has not succeeded or is not possible.2 Unlike maintenance treatment, systemic corticosteroids play an important part in management of acute exacerbations of COPD. During exacerbations, corticosteroids have been shown to shorten recovery time, increase lung function (FEV1), decrease hypoxemia (increase PaO2), reduce the risk of treatment failure, and reduce hospital stay.36,37 Treatment doses and duration are still somewhat controversial. Generally, oral is preferred over IV therapy, and 30 to 40 mg of prednisolone or equivalent for 10 to 14 days is recommended. Longer therapy increases side effects with no benefit.2

Antibiotic therapy has been shown to decrease sputum purulence, treatment failure, and short-term mortality in select COPD patients. Antibiotics are indicated if three cardinal symptoms are present: an increase in dyspnea, sputum volume, and sputum purulence. Only two symptoms are needed if increased sputum purulence is one of the two.2 Another indication for antibiotic use is when there is a need for invasive or noninvasive mechanical ventilation. Typical antibiotic choices are based on local resistance patterns and typical bacterial pathogens (TABLE 4).6,38 Oral therapy is preferred over IV, and therapy duration should average 5 to 10 days. Sputum or lung effluent cultures should be obtained in patients with frequent severe exacerbations or those that require mechanical ventilation prior to initiating antibiotics.38 Improvements in dyspnea and sputum purulence suggest clinical success.2

Respiratory Support: Oxygen therapy is a key component in treating COPD exacerbations. Oxygen should be administered by venturi masks or nasal cannula if possible to a target oxygen saturation of 88% to 92%.2 Ventilatory support either by noninvasive mechanical ventilation (NIV) or invasive mechanical ventilation may be necessary for severe exacerbations. NIV has been shown to be effective in approximately 85% of cases and is associated with shorter hospital stays and lower rates of intubation, pneumonia, and mortality, and should be tried whenever possible.39 Indications such as respiratory or cardiac arrest, heart rate <50 beats per minute with loss of alertness, ventricular arrhythmias, and other manifestations where patients cannot tolerate NIV may result in the need for invasive mechanical ventilation. Major risks associated with invasive ventilation are a failure to wean to spontaneous ventilation, barotrauma, and ventilator-acquired pneumonia.2

The Pharmacist's Role

Pharmacists are exceptionally positioned to positively affect patients' health and promote efficiency in the health care system. Since emphysema is not curable, pharmacists' efforts must be directed toward disease prevention and medication optimization. There are many opportunities for pharmacists regarding smoking cessation and immunization efforts. Furthermore, along the continuum of emphysema treatment pharmacists are ideally placed to maximize medication streamlining and optimization where necessary, based on literature guidelines and best practices. Often there are comorbid conditions necessitating duplicate therapies or drug additions that complicate the interactions with other treatments. Pharmacists are uniquely equipped to facilitate these transitions in care, and the savings in patients' lives and health care system costs in disease prevention are inestimably large. It will be increasingly prudent for the health care system as a whole to develop viable practice models based on these types of preventive care versus traditional reactive models of health care. Pharmacists are indispensable in their health care position, expertise, and ability to facilitate this revolution.


  1. Sakula A. Sir John Floyer's A Treatise of the Asthma (1698). Thorax. 1984;39:248-254.
  2. Global Initiative for Chronic Obstructive Lung Disease. Global Strategy for the Diagnosis, Management, and Prevention of COPD. Updated December 2011. www.goldcopd.org. Accessed February 1, 2012.
  3. Chronic obstructive pulmonary disease. Includes chronic bronchitis and emphysema. CDC. www.cdc.gov/nchs/ fastats/copd.htm. Accessed February 1, 2012.
  4. Forey BA, Thornton AJ, Lee PN. Systematic review with meta-analysis of the epidemiological evidence relating smoking to COPD, chronic bronchitis and emphysema. BMC Pulm Med. 2011;14:11:36.
  5. CDC. State-specific prevalence of cigarette smoking and smokeless tobacco use among adults—United States, 2009. MMWR Morb Mortal Wkly Rep. 2010;59:1400-1406. www.cdc.gov/mmwr/preview/mmwrhtml/mm5943a2.htm. Accessed February 1, 2012.
  6. Celli BR, MacNee W; ATS/ERS Task Force. Standards for the diagnosis and treatment of patients with COPD: a summary of the ATS/ERS position paper. Eur Respir J. 2004;23:932-946.
  7. Stoller JK, Aboussouan LS. A review of a1-antitrypsin deficiency. Am J Respir Crit Care Med. 2012;185:246-259.
  8. Takahashi M, Fukuoka J, Nitta N, et al. Imaging of pulmonary emphysema: a pictorial review. Int J Chron Obstruct Pulm Dis. 2008;3:193-204.
  9. Donaldson GC, Seemungal TA, Bhowmik A, Wedzicha JA. Relationship between exacerbation frequency and lung function decline in chronic obstructive pulmonary disease. Thorax. 2002;57:847-852.
  10. Coronini-Cronberg S, Heffernan C, Robinson M. Effective smoking cessation interventions for COPD patients: a review of the evidence. JRSM Short Rep. 2011;2:78
  11. Clinical topics in tobacco cessation. Public Health. U.S. Department of Veterans Affairs. www.publichealth.va.gov/ smoking/clinicaltopics.asp#CessationGuidance. Accessed February 1, 2012.
  12. Jorenby DE, Leischow SJ, Nides MA, et al. A controlled trial of sustained-release bupropion, a nicotine patch or both for smoking cessation. N Engl J Med. 1999;340:685-691.
  13. Drug Information Handbook. 20th ed. Hudson, OH: Lexi-Comp, Inc; 2011.
  14. Calverley P, Pauwels R, Vestbo J, et al. Combined salmeterol and fluticasone in the treatment of chronic obstructive pulmonary disease: a randomized controlled trial. Lancet. 2003;361:449-456.
  15. Szafranski W, Cukier A, Ramirez A, et al. Efficacy and safety of budesonide/formoterol in the management of chronic obstructive pulmonary disease. Eur Respir J. 2003;21:74-81.
  16. Burge PS, Calverley PM, Jones PW, et al. Randomised, double-blind, placebo-controlled study of fluticasone propionate in patients with moderate to severe chronic obstructive pulmonary disease: the ISOLDE trial. BMJ. 2000;320:1297-1303.
  17. Pauwels RA, Claes-Goran L, Latinen LA, et al. Long-term treatment with inhaled budesonide in persons with mild chronic obstructive pulmonary disease who continue smoking. N Engl J Med. 1999;340:1948-1953.
  18. Kardos P, Wencker M, Glaab T, et al. Impact of salmeterol/fluticasone propionate versus salmeterol on exacerbations in severe chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2007;175:144-149.
  19. Crim C, Calverley PM, Anderson JA, et al. Pneumonia risk in COPD patients receiving inhaled corticosteroids alone or in combination: TORCH study results. Eur Respir J. 2009;34:641-647.
  20. Callahan CM, Dittus RS, Katz BP. Oral corticosteroid therapy for patients with stable chronic obstructive pulmonary disease: a meta-analysis. Ann Intern Med. 1991;114:216-223.
  21. Zhou Y, Wang X, Zeng X, et al. Positive benefits of theophylline in a randomized, double-blind, parallel-group, placebo-controlled study of low-dose, slow-release theophylline in the treatment of COPD for 1 year. Respirology. 2006;11:603-610.
  22. Ram FS. Use of theophylline in chronic obstructive pulmonary disease: examining the evidence. Curr Opin Pum Med. 2006;12:132-139.
  23. Currie GP, Butler CA, Anderson WJ, et al. Phosphodiesterase 4 inhibitors in chronic obstructive pulmonary disease: a new approach to oral treatment. Br J Clin Pharmacol. 2008;65:803-810.
  24. Fabbri LM, Calverley PM, Izquierdo-Alonso JL, et al. Roflumilast in moderate-to-severe chronic obstructive pulmonary disease treated with long acting bronchodilators: two randomized clinical trials. Lancet. 2009;374:695-703.
  25. Juvelekian GS, Stoller JK. Augmentation therapy for alpha1-antitrypsin deficiency. Drugs. 2004;64:1743-1756.
  26. Stoller JK, Fallat R, Schluchter MD, et al. Augmentation therapy with alpha1-antitrypsin: patterns of use and adverse events. Chest. 2003;123(5):1425-1434.
  27. Gildea TR, Shermock KM, Singer ME, et al. Cost-effectiveness analysis of augmentation therapy for severe alpha 1 antitrypsin deficiency. Am J Respir Crit Care Med. 2003;167:1387-1392.
  28. Dirksen A, Dijkman JH, Madsen F, et al. A randomized clinical trial of alpha 1 antitrypsin augmentation therapy. Am J Respir Crit Care Med. 1999;160:1468-1472.
  29. Alpha-1-Antitrypsin Deficiency Registry Study Group. Survival and FEV1 decline in individuals with severe deficiency of alpha-1-antitrypsin. Am J Respir Crit Care Med. 1998;158:49-59.
  30. Wongsurakiat P, Maranetra KN, Wasi C, et al. Acute respiratory illness in patients with COPD and the effectiveness of influenza vaccination: a randomized controlled study. Chest. 2004;125:2011-2020.
  31. Alfageme I, Vazquez R, Reyes N, et al. Clinical efficacy of anti-pneumococcal vaccination in patients with COPD. Thorax. 2006;61:189-95.
  32. Ries AL, Kaplan RM, Myers R, Prewitt LM. Maintenance after pulmonary rehabilitation in chronic lung disease: a randomized trial. Am J Respir Crit Care Med. 2003;167:880-888.
  33. Moore RP, Berlowitz DJ, Denehy L, et al. A randomized trial of domiciliary, ambulatory oxygen in patients with COPD and dyspnea but without resting hypoxaemia. Thorax. 2011;66:32-37.
  34. Christie JD, Edwards LB, Kucheryavaya AY, et al. The Registry of the International Society for Heart and Lung Transplantation: twenty-seventh official adult lung and heart-lung transplant report-2010. J Heart Lung Transplant. 2010;29:1104-1118.
  35. Naunheim KS, Wood DE, Mohsenifar Z, et al. Long-term follow-up of patients receiving lung-volume-reduction surgery versus medical therapy for severe emphysema by the National Emphysema Treatment Trial Research Group. Ann Thorac Surg. 2006;82:431-443.
  36. de Jong YP, Uil SM, Grotjohan HP, et al. Oral or IV prednisolone in the treatment of COPD exacerbations: a randomized, controlled, double-blind study. Chest. 2007;132:1741-1747.
  37. Aaron SD, Vandemheen KL, Hebert P, et al. Outpatient oral prednisone after emergency treatment of chronic obstructive pulmonary disease. N Engl J Med. 2003;348:2618-2625.
  38. Ram FS, Rodriguez-Roisin R, Granados-Navarrete A, et al. Antibiotics for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2006(2):CD004403.
  39. Lightowler JV, Wedzicha JA, Elliott MW, et al. Non-invasive positive pressure ventilation to treat respiratory failure resulting from exacerbations of chronic obstructive pulmonary disease: Cochrane systematic review and meta-analysis. BMJ. 2003;326:185.

Back to Top

  Take Test  |  View Questions