Close
New

Medscape is available in 5 Language Editions – Choose your Edition here.

 

Chronic Obstructive Pulmonary Disease (COPD) Medication

  • Author: Zab Mosenifar, MD, FACP, FCCP; Chief Editor: Ryland P Byrd, Jr, MD  more...
 
Updated: Jul 11, 2016
 

Medication Summary

Oral and inhaled medications are used for patients with stable chronic obstructive pulmonary disease (COPD) to reduce dyspnea, improve exercise tolerance, and prevent complications. Most of the medications used in COPD treatment are directed at the following 4 potentially reversible mechanisms of airflow limitation:

  • Bronchial smooth muscle contraction
  • Bronchial mucosal congestion and edema
  • Airway inflammation
  • Increased airway secretions

Bronchodilators act to decrease muscle tone in small and large airways in the lungs, thereby increasing ventilation. The category includes subcutaneous medications, beta-adrenergics, methylxanthines, and anticholinergics.

Additionally, opioids have been shown in multiple studies to relieve dyspnea, particularly near the end of life. Dosage is very patient specific. Currow et al used a low, once-daily dose of sustained-release morphine for chronic refractory dyspnea.[103]

Next

Beta2-Adrenergic Agonists, Short-Acting

Class Summary

Beta2 -agonists activate specific B2 -adrenergic receptors on the surface of smooth muscle cells, which increases intracellular cyclic adenosine monophosphate (cAMP) and smooth muscle relaxation. Beta2 -agonists produce less bronchodilatation in COPD than in asthma. Patients use beta2 -agonists primarily for relief of symptoms of COPD. In patients with mild, intermittent symptoms, short-acting beta2 -agonists is recommended for symptomatic relief.

Albuterol (Proventil HFA, Ventolin HFA, ProAir HFA)

 

Albuterol is a short acting beta-agonist used for bronchospasm refractory to epinephrine. It relaxes bronchial smooth muscle by action on beta2-receptors with little effect on cardiac muscle contractility. Most patients (even those who have no measurable increase in expiratory flow) benefit from treatment. Inhaled beta agonists are prescribed initially as needed.

Metaproterenol

 

Metaproterenol relaxes bronchial smooth muscle by action on beta2-receptors with little effect on cardiac muscle contractility. Most patients (even those who have no measurable increase in expiratory flow) benefit from treatment. Inhaled beta agonists initially are prescribed as needed. Frequency may be increased.

Levalbuterol (Xopenex, Xopenex HFA)

 

Levalbuterol is a selective beta2-agonist agent used for the treatment or prevention of bronchospasm. Albuterol is a racemic mixture, while levalbuterol contains only the active R- enantiomer of albuterol. The S-enantiomer does not bind to beta2-receptors, but it may be responsible for some adverse effects of racemic albuterol, including bronchial hyperreactivity and reduced pulmonary function during prolonged use.

Previous
Next

Beta2-Adrenergic Agonists, Long-Acting

Class Summary

Beta2 -agonist bronchodilators activate specific beta2 -adrenergic receptors on the surface of smooth muscle cells, which increases intracellular cyclic adenosine monophosphate (cAMP) and smooth muscle relaxation. In patients with more persistent symptoms, a long-acting beta agonist should be used. Long-acting beta agonists have been shown to increase exercise endurance, prevent nocturnal dyspnea, and improve quality of life. Long-acting beta-agonists include salmeterol, formoterol, arformoterol, and indacaterol. They all require twice-daily dosing, except for indacaterol and olodaterol, which are administered once daily.

Salmeterol (Serevent Diskus)

 

By relaxing the smooth muscles of the bronchioles in conditions associated with bronchitis, emphysema, asthma, or bronchiectasis, salmeterol can relieve bronchospasms. The effect also may facilitate expectoration. It is shown to improve symptoms and morning peak flows. When administered at high or more frequent doses than recommended, incidence of adverse effects is higher. Bronchodilating effect lasts more than 12 hours. It is used on a fixed schedule in addition to regular use of anticholinergic agents.

Formoterol (Perforomist)

 

Formoterol relaxes the smooth muscles of the bronchioles and relieves bronchospasms. This effect also may facilitate expectoration. It is shown to improve symptoms and morning peak flows. When administered at high or more frequent doses than recommended, incidence of adverse effects is higher. Bronchodilating effect lasts more than 12 hours. It is used in addition to anticholinergic agents.

Arformoterol (Brovana)

 

Arformoterol is a selective, long-acting beta-2 adrenergic receptor agonist that has 2-fold greater potency than racemic formoterol. Pharmacologic effects of arformoterol are from the stimulation of intracellular adenyl cyclase, the enzyme that catalyzes the conversion of adenosine triphosphate to cyclic-3',5'-adenosine monophosphate (cAMP). Increases in intracellular cyclic AMP levels in turn cause relaxation of bronchial smooth muscles.

Indacaterol, inhaled (Arcapta Neohaler)

 

Long-acting beta2-agonist (LABA) indicated for long-term, once-daily maintenance bronchodilator treatment of airflow obstruction in patients with chronic obstructive pulmonary disease (COPD), including chronic bronchitis and/or emphysema. LABAs act locally in the lungs as bronchodilators. Stimulates intracellular adenyl cyclase, causing conversion of ATP to cyclic AMP; increased cyclic AMP levels cause relaxation of bronchial smooth muscle. Not for use as initial therapy in patients with acute deteriorating COPD.

Olodaterol inhaled (Striverdi Respimat)

 

Olodaterol is a once-daily LABA inhaler indicated for maintenance bronchodilator treatment in patients with COPD, including chronic bronchitis and/or emphysema in patients who are experiencing airflow obstruction. LABAs activate specific β2-adrenergic receptors on the surface of smooth muscle cells, which increases intracellular cAMP and smooth muscle relaxation.

Previous
Next

Anticholinergics, Respiratory

Class Summary

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

Ipratropium (Atrovent HFA)

 

Short-acting anticholinergics, such as ipratropium bromide (Atrovent), have been shown to have equivalent or superior activity in patients with stable COPD when compared with a beta2 agonist. When combined with a beta2 agonist, a synergistic effect on bronchodilatation occurs. Typically, 2-4 puffs of ipratropium bromide are administered every 6-8 hours. This medication has a slower onset and a longer duration than a beta2 agonist and is less suitable for use on an as-needed basis.

Tiotropium (Spiriva)

 

Tiotropium, a bronchodilator similar to ipratropium, is a once-daily, long-acting anticholinergic medication that has been shown to have significant clinical benefit. A quaternary ammonium compound, it elicits anticholinergic/antimuscarinic effects, with inhibitory effects on M3 receptors on airway smooth muscles, leading to bronchodilation. Tiotropium is the only long-acting muscarinic agent available at this time and has become a first-line therapy in patients with persistent symptoms. Tiotropium is more effective than salmeterol in preventing exacerbations.[63]

Aclidinium (Tudorza Pressair)

 

Aclidinium is a twice-daily, long-acting selective muscarinic (M3) antagonist (anticholinergic) indicated for long-term maintenance of COPD including bronchitis and emphysema. It is available as breath-activated, dry powder metered-dose inhaler.

Umeclidinium bromide (Incruse Ellipta)

 

Umeclidinium bromide is a long-acting muscarinic antagonist (LAMA) inhalation powder, often referred to as an anticholinergic. It blocks action of acetylcholine at muscarinic receptors (M1 to M5) in the bronchial airways (M3) by preventing an increase in intracellular calcium concentration, leading to relaxation of airway smooth muscle, improved lung function, and decreased mucus secretion. Umeclidinium dissociates slowly from M3 muscarinic receptors extending its duration of action. It is indicated for the long-term, once-daily, maintenance treatment of airflow obstruction in patients with COPD), including chronic bronchitis and/or emphysema.

Glycopyrrolate inhaled (Seebri Neohaler)

 

Contains glycopyrronium, which is a long-acting muscarinic antagonist (LAMA) that produces bronchodilation by inhibiting acetylcholine’s effect on muscarinic receptor in the airway smooth muscle. It is indicated for long-term maintenance treatment of airflow obstruction in patients with COPD, including chronic bronchitis and/or emphysema.

Previous
Next

Xanthine Derivative

Class Summary

Xanthine derivatives such as theophylline relax the smooth muscles of the bronchi and pulmonary blood vessels. Inhibition of phosphodiesterase by these agents causes an increase in cyclic adenosine monophosphate (cAMP), causing the relaxation of bronchial smooth muscles.

Theophylline (Elixophyllin, Theo-24, Theochron)

 

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

Aminophylline

 

Methylxanthine; directly relaxes smooth muscles of respiratory tract. It is reserved for patients with hard-to-control COPD or for individuals who are not able to use inhaled agents effectively.

Previous
Next

Phosphodiesterase-4 Inhibitors

Class Summary

Selective phosphodiesterase-4 (PDE-4) inhibitors reduce exacerbations, improve dyspnea, and increase lung function in patients with severe COPD.

Roflumilast (Daliresp)

 

Roflumilast is a selective phosphodiesterase-4 (PDE-4) inhibitor. The specific mechanism of action is not well defined but is thought to be related to the effects of increased intracellular cyclic AMP in lung cells. It is indicated to decrease the frequency of exacerbations or the worsening of symptoms from severe COPD.

Previous
Next

Corticosteroids, Inhalant

Class Summary

In acute exacerbations, steroids improve symptoms and lung function. Inhaled corticosteroids provide a more direct route of administration to the airways and, similar to other inhaled agents, are only minimally absorbed. Inhaled steroids have fewer adverse effects than do oral agents, although they improve expiratory flows less effectively, even at high doses. These agents may be beneficial in slowing the rate of progression in a subset of patients with COPD who have rapid decline.

Fluticasone inhaled (Flovent)

 

Fluticasone inhibits bronchoconstriction producing direct smooth muscle relaxation. It may decrease the number and activity of inflammatory cells, in turn decreasing airway hyperresponsiveness. Effectiveness in COPD is not established. Inhaled corticosteroids have a lesser role in the management of chronic bronchitis. Several studies demonstrate no benefit, although approximately half of patients who respond to oral steroids may benefit from inhaled agents.

Budesonide inhaled (Pulmicort, Pulmicort Flexhaler)

 

Budesonide inhibits bronchoconstriction, producing direct smooth muscle relaxation. It may decrease the number and activity of inflammatory cells, in turn decreasing airway hyperresponsiveness. It has extremely potent vasoconstrictive and anti-inflammatory activity, and it alters the level of inflammation in airways by inhibiting multiple types of inflammatory cells and decreasing production of cytokines and other mediators. It also decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Effectiveness is not established in COPD.

Previous
Next

Corticosteroids, Oral

Class Summary

The use of oral steroids in the treatment of acute exacerbations is widely accepted and recommended, given their high efficacy. Note that oral steroids are not as effective in treating COPD exacerbations as they are in treating bronchial asthma exacerbations.

Prednisone (Rayos)

 

Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

Methylprednisolone (Solu-Medrol, Medrol, A-Methapred)

 

Methylprednisolone is usually given in IV form for initiation of corticosteroid therapy, although the oral form is theoretically equally efficacious. The 2 forms are equal in potency, time of onset, and adverse effects. Inhaled corticosteroids are probably equally efficacious and have fewer adverse effects.

Previous
Next

Beta-Adrenergic Agonist and Anticholinergic Agent Combinations

Class Summary

These agents combine the benefits of a beta-adrenergic agonist with the prolonged action of an anticholinergic agent.

Albuterol/ipratropium (Combivent Respimat)

 

Ipratropium is chemically related to atropine, and it has antisecretory properties. Albuterol is a beta agonist for bronchospasm refractory to epinephrine. It relaxes bronchial smooth muscle by action on beta2 receptors with little effect on cardiac muscle contractility.

Metered-dose inhalers that contain chlorofluorocarbons (CFCs) are currently being phased out in the US; alternate inhalers without CFCs are available (eg, Combivent Respimat). This combination is also available as a nebulized solution.

Umeclidinium bromide/vilanterol inhaled (Anoro Ellipta)

 

Umeclidinium bromide and vilanterol is a long-acting muscarinic antagonist (LAMA) and long-acting beta2-agonist (LABA) inhalation powder. It is the first once-daily dual bronchodilator approved. It is indicated for long-term maintenance treatment of airflow obstruction in patients with COPD, including chronic bronchitis and/or emphysema.

Tiotropium/olodaterol inhaled (Stiolto Respimat)

 

Tiotropium/olodaterol inhaled (Stiolto Respimat) is a combination product containing olodaterol, a long-acting beta2-adrenergic agonist (LABA) plus tiotropium, a long-acting antimuscarinic agent. It is indicated for long-term, once-daily maintenance treatment of airflow obstruction in patients with COPD, including chronic bronchitis and/or emphysema.

Indacaterol, inhaled/glycopyrrolate inhaled (Utibron Neohaler)

 

Contains glycopyrronium, which is a long-acting muscarinic antagonist (LAMA) that produces bronchodilation by inhibiting acetylcholine’s effect on muscarinic receptor in the airway smooth muscle. Also contains indacaterol, a long-acting beta2-agonist (LABA) that stimulates intracellular adenyl cyclase, causing conversion of ATP to cyclic AMP, and thereby relaxes bronchial smooth muscle. It is indicated for long-term maintenance treatment of airflow obstruction in patients with COPD, including chronic bronchitis and/or emphysema.

Glycopyrrolate inhaled/formoterol (Bevespi Aerosphere)

 

This agent is a combination inhaler with glycopyrrolate, a long-acting muscarinic antagonist (LAMA), often referred to as an anticholinergic, and a long-acting beta2-agonist (LABA) with a rapid onset of action. Pharmacologic effect results in bronchodilation and relaxation of bronchial smooth muscle. It is indicated for the long-term, maintenance treatment of airflow obstruction with COPD, including chronic bronchitis and/or emphysema.

Previous
Next

Beta2-Adrenergic Agonist and Corticosteroid Combinations

Class Summary

Combination therapy is recommended when COPD patients are uncontrolled with bronchodilator monotherapy. Agents that use a long-acting beta agonist and an inhaled corticosteroid are commonly used in asthma and COPD and show increased clinical benefits.

Budesonide/formoterol (Symbicort)

 

Formoterol relieves bronchospasms by relaxing the smooth muscles of the bronchioles in conditions associated with asthma. Budesonide is an inhaled corticosteroid that alters the level of inflammation in airways by inhibiting multiple types of inflammatory cells and decreasing production of cytokines and other mediators involved in the asthmatic response.

Fluticasone and salmeterol (Advair Diskus)

 

Fluticasone inhibits bronchoconstriction mechanisms, producing direct smooth muscle relaxation. It may decrease number and activity of inflammatory cells, in turn decreasing airway hyperresponsiveness. It also has vasoconstrictive activity. Salmeterol relaxes the smooth muscles of the bronchioles in conditions associated with bronchitis, emphysema, asthma, or bronchiectasis and can relieve bronchospasms. Its effect may also facilitate expectoration.

Vilanterol/fluticasone inhaled (Breo Ellipta)

 

LABA and corticosteroid combination inhaler indicated for long-term, once-daily, maintenance treatment of airflow obstruction with COPD, including chronic bronchitis and/or emphysema. It is also approved to reduce COPD exacerbations. The product contains fluticasone fumarate, which has shown in vitro to exhibit a binding affinity for the human glucocorticoid receptor that is approximately 29.9 times that of dexamethasone and 1.7 times that of fluticasone propionate.

Previous
Next

Antibiotics

Class Summary

In patients with COPD, chronic infection or colonization of the lower airways is common from S pneumoniae, H influenzae, and M catarrhalis. In patients with chronic severe airway obstruction, P aeruginosa infection may also be prevalent. The use of antibiotics for the treatment of acute exacerbations is well supported.

Amoxicillin (Moxatag)

 

Amoxicillin interferes with synthesis of cell wall mucopeptides during active multiplication, resulting in bactericidal activity against susceptible bacteria.

Doxycycline (Doryx, Monodox, Doxy 100, Adoxa)

 

Doxycycline is a broad-spectrum, synthetically derived bacteriostatic antibiotic in the tetracycline class. It is almost completely absorbed, it concentrates in bile, and it is excreted in urine and feces as a biologically active metabolite in high concentrations. It inhibits protein synthesis and, thus, bacterial growth by binding to 30S and possibly 50S ribosomal subunits of susceptible bacteria. It may block dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest.

Trimethoprim/sulfamethoxazole (Bactrim, Bactrim DS, Septra DS)

 

Sulfamethoxazole and trimethoprim inhibit bacterial synthesis of dihydrofolic acid by competing with para-aminobenzoic acid, resulting in inhibition of bacterial growth. Antibacterial activity of TMP-SMZ includes common urinary tract pathogens, except Pseudomonas aeruginosa. Like tetracycline, it has in vitro activity against Bartonella pertussis. It is not useful in mycoplasmal infections.

Cefuroxime (Zinacef, Ceftin)

 

Cefuroxime is a second-generation cephalosporin and maintains gram-positive activity of first-generation cephalosporins; it adds activity against P mirabilis, H influenzae, E coli, K pneumoniae, and M catarrhalis. It binds to penicillin-binding proteins and inhibits the final transpeptidation step of peptidoglycan synthesis, resulting in cell wall death. The condition of the patient, the severity of infection, and the susceptibility of the microorganism determine proper dose and route of administration. It also resists degradation by beta-lactamase.

Azithromycin (Zithromax, Zmax)

 

Azithromycin acts by binding to 50S ribosomal subunit of susceptible microorganisms and blocks dissociation of peptidyl t-RNA from ribosomes, causing RNA-dependent protein synthesis to arrest. It is used to treat acute bacterial exacerbations of chronic obstructive pulmonary disease caused by S pneumoniae, H influenzae, and M catarrhalis. They cover most potential etiologic agents, including Mycoplasma. The newer macrolides offer decreased GI upset as well as potential for improved compliance through reduced dosing frequency. They also afford improved action against H influenzae.

Clarithromycin (Biaxin)

 

Clarithromycin is a semisynthetic macrolide antibiotic that reversibly binds to the P site of the 50S ribosomal subunit of susceptible organisms and may inhibit RNA-dependent protein synthesis by stimulating dissociation of peptidyl t-RNA from ribosomes, causing bacterial growth inhibition.

Previous
Next

Smoking Cessation Therapies

Class Summary

Smoking cessation continues to be the most important therapeutic intervention for COPD. Supervised use of pharmacologic agents is an important adjunct to self-help and group smoking cessation programs. Nicotine replacement therapies after smoking cessation reduce withdrawal symptoms.

Nicotine transdermal system (Nicoderm CQ)

 

Transdermal nicotine patches are readily available for replacement therapy. Long-term success rates are 22-42%, compared with 2-25% for placebo. These agents are well tolerated, and the adverse effects are limited to local skin reactions. Nicotine replacement therapy patches are sold under the trade names NicoDerm, Nicotrol, and Habitrol. Each of these products is dosed with a scheduled graduated decrease in nicotine over 6-10 weeks.

Nicotine gum (Nicorette Gum)

 

Nicotine polacrilex is a chewing gum and has better quit rates than does counseling alone. Nicotine-replacement-therapy chewing pieces are marketed in 2 strengths (2 mg, 4 mg). An individual who smokes 1 pack per day should use 4-mg pieces. The 2-mg pieces are to be used by individuals who smoke less than 1 pack per day. Instruct patients to chew hourly and also to chew when needed for their initial cravings for 2 weeks. Gradually reduce the amount chewed over the next 3 months.

Bupropion (Zyban)

 

The use of the antidepressant bupropion (Zyban) is also effective for smoking cessation. This non-nicotine aid to smoking cessation enhances central nervous system nonadrenergic function. Bupropion may also be effective in patients who have not been able to quit smoking with nicotine replacement therapy. It is used in conjunction with a support group and/or behavioral counseling. It inhibits neuronal dopamine reuptake in addition to being a weak blocker of serotonin and norepinephrine reuptake.

Varenicline (Chantix)

 

Varenicline is a partial agonist selective for alpha4, beta2 nicotinic acetylcholine receptors. Its action is thought to result from activity at a nicotinic receptor subtype, where its binding produces agonist activity while simultaneously preventing nicotine binding. Agonistic activity is significantly lower than nicotine.

Previous
 
Contributor Information and Disclosures
Author

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

Disclosure: Nothing to disclose.

Coauthor(s)

Nader Kamangar, MD, FACP, FCCP, FCCM Professor of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Division of Pulmonary and Critical Care Medicine, Vice-Chair, Department of Medicine, Olive View-UCLA Medical Center

Nader Kamangar, MD, FACP, FCCP, FCCM is a member of the following medical societies: Academy of Persian Physicians, American Academy of Sleep Medicine, American Association for Bronchology and Interventional Pulmonology, American College of Chest Physicians, American College of Critical Care Medicine, American College of Physicians, American Lung Association, American Medical Association, American Thoracic Society, Association of Pulmonary and Critical Care Medicine Program Directors, Association of Specialty Professors, California Sleep Society, California Thoracic Society, Clerkship Directors in Internal Medicine, Society of Critical Care Medicine, Trudeau Society of Los Angeles, World Association for Bronchology and Interventional Pulmonology

Disclosure: Nothing to disclose.

Nidhi S Nikhanj, MD Fellow, Department of Pulmonary and Critical Care Medicine, Cedars-Sinai Medical Center, Los Angeles

Nidhi S Nikhanj, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

Annie Harrington, MD Fellow in Pulmonary and Critical Care Medicine, Cedars-Sinai Medical Center

Annie Harrington, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Chief Editor

Ryland P Byrd, Jr, MD Professor of Medicine, Division of Pulmonary Disease and Critical Care Medicine, James H Quillen College of Medicine, East Tennessee State University

Ryland P Byrd, Jr, MD is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Acknowledgements

Ryland P Byrd Jr, MD Professor, Department of Internal Medicine, Division of Pulmonary Medicine and Critical Care Medicine, Program Director of Pulmonary Diseases and Critical Care Medicine Fellowship, East Tennessee State University, James H Quillen College of Medicine; Medical Director of Respiratory Therapy, James H Quillen Veterans Affairs Medical Center

Ryland P Byrd Jr, MD is a member of the following medical societies: American College of Chest Physicians and American Thoracic Society

Disclosure: Nothing to disclose.

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, and World Medical Association

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

References
  1. Brooks M. FDA Clears Olodaterol (Striverdi Respimat) for COPD. Medscape Medical News. Available at http://www.medscape.com/viewarticle/829248. Accessed: August 4, 2014.

  2. Maclay JD, Rabinovich RA, MacNee W. Update in chronic obstructive pulmonary disease 2008. Am J Respir Crit Care Med. 2009 Apr 1. 179(7):533-41. [Medline].

  3. Casanova C, Cote C, Marin JM, Pinto-Plata V, de Torres JP, Aguirre-Jaime A, et al. Distance and oxygen desaturation during the 6-min walk test as predictors of long-term mortality in patients with COPD. Chest. 2008 Oct. 134(4):746-52. [Medline].

  4. [Guideline] Global strategy for diagnosis, management, and prevention of COPD: 2016. Global Initiative for Chronic Obstructive Lung Disease. Available at http://goldcopd.org/gold-reports/ . Accessed: May 7, 2016.

  5. Feghali-Bostwick CA, Gadgil AS, Otterbein LE, Pilewski JM, Stoner MW, Csizmadia E. Autoantibodies in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. Jan 15 2008. 177(2):156-63.

  6. Houben JM, Mercken EM, Ketelslegers HB, Bast A, Wouters EF, Hageman GJ. Telomere shortening in chronic obstructive pulmonary disease. Respir Med. 2009 Feb. 103(2):230-6. [Medline].

  7. Morissette MC, Vachon-Beaudoin G, Parent J, Chakir J, Milot J. Increased p53 level, Bax/Bcl-x(L) ratio, and TRAIL receptor expression in human emphysema. Am J Respir Crit Care Med. 2008 Aug 1. 178(3):240-7. [Medline].

  8. Hodge S, Hodge G, Jersmann H, Matthews G, Ahern J, Holmes M, et al. Azithromycin improves macrophage phagocytic function and expression of mannose receptor in chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2008 Jul 15. 178(2):139-48. [Medline].

  9. Casanova C, de Torres JP, Navarro J, Aguirre-Jaime A, Toledo P, Cordoba E, et al. Microalbuminuria and hypoxemia in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2010 Oct 15. 182(8):1004-10. [Medline].

  10. Ofir D, Laveneziana P, Webb KA, Lam YM, O'Donnell DE. Mechanisms of dyspnea during cycle exercise in symptomatic patients with GOLD stage I chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2008 Mar 15. 177(6):622-9. [Medline].

  11. Belman MJ, Botnick WC, Shin JW. Inhaled bronchodilators reduce dynamic hyperinflation during exercise in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1996 Mar. 153(3):967-75. [Medline].

  12. O'Donnell DE, Lam M, Webb KA. Spirometric correlates of improvement in exercise performance after anticholinergic therapy in chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 1999 Aug. 160(2):542-9. [Medline].

  13. Marin JM, Carrizo SJ, Gascon M, Sanchez A, Gallego B, Celli BR. Inspiratory capacity, dynamic hyperinflation, breathlessness, and exercise performance during the 6-minute-walk test in chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2001 May. 163(6):1395-9. [Medline].

  14. O'Donnell DE, Fluge T, Gerken F, Hamilton A, Webb K, Aguilaniu B. Effects of tiotropium on lung hyperinflation, dyspnoea and exercise tolerance in COPD. Eur Respir J. 2004 Jun. 23(6):832-40. [Medline].

  15. Martinez FJ, de Oca MM, Whyte RI, Stetz J, Gay SE, Celli BR. Lung-volume reduction improves dyspnea, dynamic hyperinflation, and respiratory muscle function. Am J Respir Crit Care Med. 1997 Jun. 155(6):1984-90. [Medline].

  16. Celli BR. Update on the management of COPD. Chest. 2008 Jun. 133(6):1451-62. [Medline].

  17. Casanova C, Cote C, de Torres JP, Aguirre-Jaime A, Marin JM, Pinto-Plata V. Inspiratory-to-total lung capacity ratio predicts mortality in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2005 Mar 15. 171(6):591-7. [Medline].

  18. Nagelmann A, Tonnov A, Laks T, Sepper R, Prikk K. Lung Dysfunction of Chronic Smokers with No Signs of COPD. COPD. 2011 Apr 22. [Medline].

  19. Lamprecht B, McBurnie MA, Vollmer WM, Gudmundsson G, Welte T, Nizankowska-Mogilnicka E, et al. COPD in Never Smokers: Results From the Population-Based Burden of Obstructive Lung Disease Study. Chest. 2011 Apr. 139(4):752-763. [Medline].

  20. Andersen ZJ, Hvidberg M, Jensen SS, Ketzel M, Loft S, Sorensen M, et al. Chronic obstructive pulmonary disease and long-term exposure to traffic-related air pollution: a cohort study. Am J Respir Crit Care Med. 2011 Feb 15. 183(4):455-61. [Medline].

  21. Crothers K, Butt AA, Gibert CL, Rodriguez-Barradas MC, Crystal S, Justice AC. Increased COPD among HIV-positive compared to HIV-negative veterans. Chest. 2006 Nov. 130(5):1326-33. [Medline].

  22. Adams PF, Barnes PM, Vickerie JL. Summary health statistics for the U.S. population: National Health Interview Survey, 2007. Vital Health Stat 10. 2008 Nov. 1-104. [Medline].

  23. Buist AS, McBurnie MA, Vollmer WM, Gillespie S, Burney P, Mannino DM, et al. International variation in the prevalence of COPD (the BOLD Study): a population-based prevalence study. Lancet. 2007 Sep 1. 370(9589):741-50. [Medline].

  24. Halbert RJ, Natoli JL, Gano A, Badamgarav E, Buist AS, Mannino DM. Global burden of COPD: systematic review and meta-analysis. Eur Respir J. 2006 Sep. 28(3):523-32. [Medline].

  25. Foreman MG, Zhang L, Murphy J, et al. Early-Onset COPD is Associated with Female Gender, Maternal Factors, and African American Race in the COPDGene Study. Am J Respir Crit Care Med. 2011 May 11. [Medline].

  26. Mintz ML, Yawn BP, Mannino DM, et al. Prevalence of airway obstruction assessed by lung function questionnaire. Mayo Clin Proc. 2011 May. 86(5):375-81. [Medline]. [Full Text].

  27. Spitzer C, Koch B, Grabe HJ, et al. Association of airflow limitation with trauma exposure and post-traumatic stress disorder. Eur Respir J. 2011 May. 37(5):1068-75. [Medline].

  28. Celli BR, Cote CG, Marin JM, Casanova C, Montes de Oca M, Mendez RA, et al. The body-mass index, airflow obstruction, dyspnea, and exercise capacity index in chronic obstructive pulmonary disease. N Engl J Med. 2004 Mar 4. 350(10):1005-12. [Medline].

  29. Waschki B, Kirsten A, Holz O, et al. Physical activity is the strongest predictor of all-cause mortality in patients with COPD: a prospective cohort study. Chest. 2011 Aug. 140(2):331-42. [Medline].

  30. Abrams TE, Vaughan-Sarrazin M, Fan VS, Kaboli PJ. Geographic isolation and the risk for chronic obstructive pulmonary disease-related mortality: a cohort study. Ann Intern Med. 2011 Jul 19. 155(2):80-6. [Medline].

  31. Sundh J, Stallberg B, Lisspers K, Montgomery SM, Janson C. Co-Morbidity, Body Mass Index and Quality of Life in COPD Using the Clinical COPD Questionnaire. COPD. 2011 Apr 22. [Medline].

  32. McNamara D. Bronchiectasis Linked to Higher Mortality in COPD Patients. Medscape Medical News. February 8, 2013. [Full Text].

  33. Martinez-Garcia MA, de la Rosa D, Soler-Cataluna JJ, Donat-Sanz Y, Catalan Serra P, Agramunt Lerma M, et al. Prognostic Value of Bronchiectasis in Patients with Moderate-to-Severe Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med. 2013 Feb 7. [Medline].

  34. [Guideline] Qaseem A, Wilt TJ, Weinberger SE, et al. Diagnosis and Management of Stable Chronic Obstructive Pulmonary Disease: A Clinical Practice Guideline Update from the American College of Physicians, American College of Chest Physicians, American Thoracic Society, and European Respiratory Society. Ann Intern Med. 2011 Aug 2. 155(3):179-191. [Medline].

  35. Hurst JR, Vestbo J, Anzueto A, Locantore N, Mullerova H, Tal-Singer R, et al. Susceptibility to exacerbation in chronic obstructive pulmonary disease. N Engl J Med. 2010 Sep 16. 363(12):1128-38. [Medline].

  36. Casanova C, Cote C, Marin JM, Pinto-Plata V, de Torres JP, Aguirre-Jaime A, et al. Distance and oxygen desaturation during the 6-min walk test as predictors of long-term mortality in patients with COPD. Chest. 2008 Oct. 134(4):746-52. [Medline].

  37. Singh B, Parsaik AK, Mielke MM, et al. Chronic obstructive pulmonary disease and association with mild cognitive impairment: the Mayo Clinic study of aging. Mayo Clin Proc. 2013 Nov. 88(11):1222-30. [Medline]. [Full Text].

  38. Barclay L. COPD linked to cognitive impairment and memory loss. Medscape Medical News. December 12, 2013. [Full Text].

  39. Prosen G, Klemen P, Strnad M, Grmec S. Combination of lung ultrasound (a comet-tail sign) and N-terminal pro-brain natriuretic peptide in differentiating acute heart failure from chronic obstructive pulmonary disease and asthma as cause of acute dyspnea in prehospital emergency setting. Crit Care. 2011. 15(2):R114. [Medline].

  40. Sin DD, Miller BE, Duvoix A, et al. Serum PARC/CCL-18 Concentrations and Health Outcomes in Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med. 2011 May 1. 183(9):1187-1192. [Medline].

  41. Osterweil N. COPD: Clinicians Miss Myriad Chances to Spot It Early. Medscape Medical News. Available at http://www.medscape.com/viewarticle/820597. Accessed: February 18, 2014.

  42. Miller MR, Quanjer PH, Swanney MP, Ruppel G, Enright PL. Interpreting lung function data using 80% predicted and fixed thresholds misclassifies more than 20% of patients. Chest. 2011 Jan. 139(1):52-9. [Medline].

  43. Rice KL, Dewan N, Bloomfield HE, Grill J, Schult TM, Nelson DB, et al. Disease management program for chronic obstructive pulmonary disease: a randomized controlled trial. Am J Respir Crit Care Med. 2010 Oct 1. 182(7):890-6. [Medline].

  44. Dewan NA, Rice KL, Caldwell M, Hilleman DE. Economic Evaluation of a Disease Management Program for Chronic Obstructive Pulmonary Disease. COPD. 2011 Apr 22. [Medline].

  45. Stephenson A, Seitz D, Bell CM, et al. Inhaled anticholinergic drug therapy and the risk of acute urinary retention in chronic obstructive pulmonary disease: a population-based study. Arch Intern Med. 2011 May 23. 171(10):914-20. [Medline].

  46. Gershon A, Croxford R, Calzavara A, To T, Stanbrook MB, Upshur R, et al. Cardiovascular Safety of Inhaled Long-Acting Bronchodilators in Individuals With Chronic Obstructive Pulmonary Disease. JAMA Intern Med. 2013 May 20. 1-9. [Medline].

  47. Wood S. Inhaled Long-Acting Bronchodilators in COPD Flagged Again for CV Hazard. Medscape Medical News. Available at http://www.medscape.com/viewarticle/804441. Accessed: June 4, 2013.

  48. Canavan N. Dual-Action Bronchodilator Eases COPD Exacerbations. Medscape [serial online]. Available at http://www.medscape.com/viewarticle/810739. Accessed: September 16, 2013.

  49. Decramer ML, Chapman KR, Dahl R, et al. Once-daily indacaterol versus tiotropium for patients with severe chronic obstructive pulmonary disease (INVIGORATE): a randomised, blinded, parallel-group study. The Lancet Respiratory Medicine. Available at http://www.thelancet.com/journals/lanres/article/PIIS2213-2600(13)70158-9/abstract. Accessed: October 7, 2013.

  50. Macfarlane L. Indacaterol and Tiotropium Similar in Effect and Safety. Medscape [serial online]. Available at http://www.medscape.com/viewarticle/811871. Accessed: October 7, 2013.

  51. Mahler DA, Kerwin E, Ayers T, FowlerTaylor A, Maitra S, Thach C, et al. FLIGHT1 and FLIGHT2: Efficacy and Safety of QVA149 (Indacaterol/Glycopyrrolate) versus Its Monocomponents and Placebo in Patients with Chronic Obstructive Pulmonary Disease. Am J Respir Crit Care Med. 2015 Nov 1. 192 (9):1068-79. [Medline].

  52. Rabe K, Martinez F, Rodriguez-Roisin R, Fabbri LM, Ferguson GT, Jones P, et al. PT003, a novel co-suspension MDI glycopyrronium/formoterol fixed-dose combination is superior to monocomponents in patients with COPD. Eur Respir J. 2015 Sep 01. 46(suppl 59):[Full Text].

  53. US Food and Drug Administration. FDA approves Anoro Ellipta to treat chronic obstructive pulmonary disease [press release]. December 18, 2013. Available at http://www.fda.gov/newsevents/newsroom/pressannouncements/ucm379057.htm. Accessed: December 30, 2013.

  54. Brown T. FDA approves umeclidinium and vilanterol combo for COPD. Medscape Medical News. December 18, 2013. [Full Text].

  55. Donohue JF, Maleki-Yazdi MR, Kilbride S, Mehta R, Kalberg C, Church A. Efficacy and safety of once-daily umeclidinium/vilanterol 62.5/25 mcg in COPD. Respir Med. 2013 Oct. 107(10):1538-46. [Medline].

  56. Koch A, Pizzichini E, Hamilton A, Hart L, Korducki L, De Salvo MC. Lung function efficacy and symptomatic benefit of olodaterol once daily delivered via Respimat versus placebo and formoterol twice daily in patients with GOLD 2-4 COPD: results from two replicate 48-week studies. Int J Chron Obstruct Pulmon Dis. 2014. 9:697-714. [Medline].

  57. Ferguson GT, Feldman GJ, Hofbauer P, Hamilton A, Allen L, Korducki L, et al. Efficacy and safety of olodaterol once daily delivered via Respimat in patients with GOLD 2-4 COPD: results from two replicate 48-week studies. Int J Chron Obstruct Pulmon Dis. 2014. 9:629-45. [Medline]. [Full Text].

  58. Casaburi R, Mahler DA, Jones PW, Wanner A, San PG, ZuWallack RL, et al. A long-term evaluation of once-daily inhaled tiotropium in chronic obstructive pulmonary disease. Eur Respir J. 2002 Feb. 19(2):217-24. [Medline].

  59. Donohue JF, van Noord JA, Bateman ED, Langley SJ, Lee A, Witek TJ Jr, et al. A 6-month, placebo-controlled study comparing lung function and health status changes in COPD patients treated with tiotropium or salmeterol. Chest. 2002 Jul. 122(1):47-55. [Medline].

  60. Vincken W, van Noord JA, Greefhorst AP, Bantje TA, Kesten S, Korducki L, et al. Improved health outcomes in patients with COPD during 1 yr's treatment with tiotropium. Eur Respir J. 2002 Feb. 19(2):209-16. [Medline].

  61. Tashkin DP, Celli B, Senn S, Burkhart D, Kesten S, Menjoge S, et al. A 4-year trial of tiotropium in chronic obstructive pulmonary disease. N Engl J Med. 2008 Oct 9. 359(15):1543-54. [Medline].

  62. Brusasco V, Hodder R, Miravitlles M, Korducki L, Towse L, Kesten S. Health outcomes following treatment for six months with once daily tiotropium compared with twice daily salmeterol in patients with COPD. Thorax. 2003 May. 58(5):399-404. [Medline]. [Full Text].

  63. Vogelmeier C, Hederer B, Glaab T, Schmidt H, Rutten-van Molken MP, Beeh KM, et al. Tiotropium versus salmeterol for the prevention of exacerbations of COPD. N Engl J Med. 2011 Mar 24. 364(12):1093-103. [Medline].

  64. Singh S, Loke YK, Enright PL, Furberg CD. Mortality associated with tiotropium mist inhaler in patients with chronic obstructive pulmonary disease: systematic review and meta-analysis of randomised controlled trials. BMJ. 2011 Jun 14. 342:d3215. [Medline]. [Full Text].

  65. Jones PW, Rennard SI, Agusti A, Chanez P, Magnussen H, Fabbri L, et al. Efficacy and safety of once-daily aclidinium in chronic obstructive pulmonary disease. Respir Res. 2011 Apr 26. 12:55. [Medline]. [Full Text].

  66. Hand L. FDA OKs Umeclidinium (Incruse Ellipta) for COPD. Medscape [serial online]. Available at http://www.medscape.com/viewarticle/824419. Accessed: May 4, 2014.

  67. Anoro Ellipta (umeclidinium and vilanterol inhalation powder) [package insert]. Research Triangle Park, NC: GlaxoSmithKline. 2013. Available at [Full Text].

  68. Calverley PM, Rabe KF, Goehring UM, Kristiansen S, Fabbri LM, Martinez FJ. Roflumilast in symptomatic chronic obstructive pulmonary disease: two randomised clinical trials. Lancet. 2009 Aug 29. 374(9691):685-94. [Medline].

  69. Gifford AH, Mahler DA, Waterman LA, et al. Neuromodulatory Effect of Endogenous Opioids on the Intensity and Unpleasantness of Breathlessness during Resistive Load Breathing in COPD. COPD. 2011 Apr 22. [Medline].

  70. Short PM, Lipworth SI, Elder DH, Schembri S, Lipworth BJ. Effect of beta blockers in treatment of chronic obstructive pulmonary disease: a retrospective cohort study. BMJ. 2011 May 10. 342:d2549. [Medline]. [Full Text].

  71. Mottillo S, Filion KB, Belisle P, Joseph L, Gervais A, O'Loughlin J. Behavioural interventions for smoking cessation: a meta-analysis of randomized controlled trials. Eur Heart J. 2009 Mar. 30(6):718-30. [Medline].

  72. Wood-Baker RR, Gibson PG, Hannay M, Walters EH, Walters JA. Systemic corticosteroids for acute exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2005. (1):CD001288. [Medline].

  73. Walters JA, Walters EH, Wood-Baker R. Oral corticosteroids for stable chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2005 Jul 20. CD005374. [Medline].

  74. Spencer S, Calverley PM, Burge PS, Jones PW. Impact of preventing exacerbations on deterioration of health status in COPD. Eur Respir J. 2004 May. 23(5):698-702. [Medline].

  75. Calverley PM, Anderson JA, Celli B, Ferguson GT, Jenkins C, Jones PW, et al. Salmeterol and fluticasone propionate and survival in chronic obstructive pulmonary disease. N Engl J Med. 2007 Feb 22. 356(8):775-89. [Medline].

  76. Sin DD, Tashkin D, Zhang X, Radner F, Sjobring U, Thoren A. Budesonide and the risk of pneumonia: a meta-analysis of individual patient data. Lancet. 2009 Aug 29. 374(9691):712-9. [Medline].

  77. Chen D, Restrepo MI, Fine MJ, et al. Observational study of inhaled corticosteroids on outcomes for COPD patients with pneumonia. Am J Respir Crit Care Med. 2011 Aug 1. 184(3):312-6. [Medline].

  78. Seemungal TA, Wilkinson TM, Hurst JR, Perera WR, Sapsford RJ, Wedzicha JA. Long-term erythromycin therapy is associated with decreased chronic obstructive pulmonary disease exacerbations. Am J Respir Crit Care Med. 2008 Dec 1. 178(11):1139-47. [Medline].

  79. Albert RK, Connett J, Bailey WC, et al. Azithromycin for prevention of exacerbations of COPD. N Engl J Med. 2011 Aug 25. 365(8):689-98. [Medline].

  80. Daniels JM, Snijders D, de Graaff CS, Vlaspolder F, Jansen HM, Boersma WG. Antibiotics in addition to systemic corticosteroids for acute exacerbations of chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2010 Jan 15. 181(2):150-7. [Medline].

  81. Sasaki T, Nakayama K, Yasuda H, Yoshida M, Asamura T, Ohrui T, et al. A randomized, single-blind study of lansoprazole for the prevention of exacerbations of chronic obstructive pulmonary disease in older patients. J Am Geriatr Soc. 2009 Aug. 57(8):1453-7. [Medline].

  82. Duiverman ML, Wempe JB, Bladder G, Jansen DF, Kerstjens HA, Zijlstra JG. Nocturnal non-invasive ventilation in addition to rehabilitation in hypercapnic patients with COPD. Thorax. 2008 Dec. 63(12):1052-7. [Medline].

  83. Crockett AJ, Moss JR, Cranston JM, Alpers JH. Domicilary oxygen for chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2000. (2):CD001744. [Medline].

  84. Ringbaek TJ. Continuous oxygen therapy for hypoxic pulmonary disease: guidelines, compliance and effects. Treat Respir Med. 2005. 4(6):397-408. [Medline].

  85. Sandland CJ, Morgan MD, Singh SJ. Patterns of domestic activity and ambulatory oxygen usage in COPD. Chest. 2008 Oct. 134(4):753-60. [Medline].

  86. Lightowler JV, Wedzicha JA, Elliott MW, Ram FS. 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 Jan 25. 326(7382):185. [Medline]. [Full Text].

  87. Carrera M, Marin JM, Anton A, Chiner E, Alonso ML, Masa JF, et al. A controlled trial of noninvasive ventilation for chronic obstructive pulmonary disease exacerbations. J Crit Care. 2009 Sep. 24(3):473.e7-14. [Medline].

  88. Keenan SP, Kernerman PD, Cook DJ, Martin CM, McCormack D, Sibbald WJ. Effect of noninvasive positive pressure ventilation on mortality in patients admitted with acute respiratory failure: a meta-analysis. Crit Care Med. 1997 Oct. 25(10):1685-92. [Medline].

  89. Confalonieri M, Garuti G, Cattaruzza MS, Osborn JF, Antonelli M, Conti G. A chart of failure risk for noninvasive ventilation in patients with COPD exacerbation. Eur Respir J. 2005 Feb. 25(2):348-55. [Medline].

  90. Hubbard RC, Crystal RG. Augmentation therapy of alpha 1-antitrypsin deficiency. Eur Respir J Suppl. 1990 Mar. 9:44s-52s. [Medline].

  91. Hurst JR, Donaldson GC, Quint JK, Goldring JJ, Baghai-Ravary R, Wedzicha JA. Temporal clustering of exacerbations in chronic obstructive pulmonary disease. Am J Respir Crit Care Med. 2009 Mar 1. 179(5):369-74. [Medline].

  92. Fishman A, Martinez F, Naunheim K, Piantadosi S, Wise R, Ries A, et al. A randomized trial comparing lung-volume-reduction surgery with medical therapy for severe emphysema. N Engl J Med. 2003 May 22. 348(21):2059-73. [Medline].

  93. Titman A, Rogers CA, Bonser RS, Banner NR, Sharples LD. Disease-specific survival benefit of lung transplantation in adults: a national cohort study. Am J Transplant. 2009 Jul. 9(7):1640-9. [Medline].

  94. Burton CM, Milman N, Carlsen J, Arendrup H, Eliasen K, Andersen CB, et al. The Copenhagen National Lung Transplant Group: survival after single lung, double lung, and heart-lung transplantation. J Heart Lung Transplant. 2005 Nov. 24(11):1834-43. [Medline].

  95. Cote CG, Celli BR. Pulmonary rehabilitation and the BODE index in COPD. Eur Respir J. 2005 Oct. 26(4):630-6. [Medline].

  96. Dodd JW, Hogg L, Nolan J, et al. The COPD assessment test (CAT): response to pulmonary rehabilitation. A multicentre, prospective study. Thorax. 2011 May. 66(5):425-9. [Medline].

  97. [Guideline] Guirguis-Blake JM, Senger CA, Webber EM, Mularski RA, Whitlock EP. Screening for Chronic Obstructive Pulmonary Disease: Evidence Report and Systematic Review for the US Preventive Services Task Force. JAMA. 2016 Apr 5. 315 (13):1378-93. [Medline].

  98. [Guideline] US Preventive Services Task Force. Counseling and interventions to prevent tobacco use and tobacco-caused disease in adults and pregnant women: US Preventive Services Task Force Reaffirmation Recommendation Statement. Ann Int Med. Apr 21 2009. 150(8):551-555. [Full Text].

  99. [Guideline] Management of Chronic Obstructive Pulmonary Disease Working Group. VA/DoD clinical practice guideline for the management of chronic obstructive pulmonary disease. Washington (DC): Department of Veterans Affairs, Department of Defense. Available at http://www.healthquality.va.gov/guidelines/cd/copd/. December 2014; Accessed: May 7, 2016.

  100. [Guideline] Keenan SP, Sinuff T, Burns KE, Muscedere J, Kutsogiannis J, Mehta S, et al. Clinical practice guidelines for the use of noninvasive positive-pressure ventilation and noninvasive continuous positive airway pressure in the acute care setting. CMAJ. 2011 Feb 22. 183(3):E195-214. [Medline]. [Full Text].

  101. [Guideline] Criner GJ, Bourbeau J, Diekemper RL, et al. Prevention of acute exacerbations of COPD: American College of Chest Physicians and Canadian Thoracic Society Guideline. Chest. 2015 Apr. 147 (4):894-942. [Medline].

  102. [Guideline] Institute for Clinical Systems Improvement. Diagnosis and Management of Chronic Obstructive Pulmonary Disease (COPD). 10th Edition. January 2016. Available at https://www.icsi.org/guidelines__more/catalog_guidelines_and_more/catalog_guidelines/catalog_respiratory_guidelines/copd/ . Accessed: May 6, 2016.

  103. Currow DC, McDonald C, Oaten S, Kenny B, Allcroft P, Frith P, et al. Once-daily opioids for chronic dyspnea: a dose increment and pharmacovigilance study. J Pain Symptom Manage. 2011 Sep. 42(3):388-99. [Medline].

 
Previous
Next
 
Venn diagram of chronic obstructive pulmonary disease (COPD). Chronic obstructive lung disease is a disorder in which subsets of patients may have dominant features of chronic bronchitis, emphysema, or asthma. The result is airflow obstruction that is not fully reversible.
Histopathology of chronic bronchitis showing hyperplasia of mucous glands and infiltration of the airway wall with inflammatory cells.
Histopathology of chronic bronchitis showing hyperplasia of mucous glands and infiltration of the airway wall with inflammatory cells (high-powered view).
Gross pathology of advanced emphysema. Large bullae are present on the surface of the lung.
Gross pathology of a patient with emphysema showing bullae on the surface.
At high magnification, loss of alveolar walls and dilatation of airspaces in emphysema can be seen.
Posteroanterior (PA) and lateral chest radiograph in a patient with severe chronic obstructive pulmonary disease (COPD). Hyperinflation, depressed diaphragm, increased retrosternal space, and hypovascularity of lung parenchyma are demonstrated.
A lung with emphysema shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragm on lateral chest radiograph.
A lung with emphysema shows increased anteroposterior (AP) diameter, increased retrosternal airspace, and flattened diaphragm on posteroanterior chest radiograph.
Severe bullous disease as seen on a computed tomography (CT) scan in a patient with chronic obstructive pulmonary disease (COPD).
Pressure volume curve comparing lungs with emphysema, lungs with restrictive disease, and normal lungs.
Flow volume curve of a patient with emphysema shows marked decrease in expiratory flow, hyperinflation, and air trapping (patient B) compared with a patient with restrictive lung disease, who has reduced lung volumes and preserved flow (patient A).
Forced expiratory volume in 1 second (FEV1) can be used to evaluate the prognosis in patients with emphysema. The benefit of smoking cessation is shown here because the deterioration in lung function parallels that of a nonsmoker, even in late stages of the disease. Redrawn from Fletcher C, Peato R. The natural history of chronic airflow obstruction. Br Med J 1977; 1: 1645-1648.
Oxygen therapy via nasal cannula.
Home supplemental oxygen.
Bilevel positive airway pressure (BiPAP).
Pulmonary rehabilitation.
Chronic obstructive pulmonary disease (COPD). Pulmonary rehabilitation.
Chest radiograph of an emphysematous patient shows hyperinflated lungs with reduced vascular markings. Pulmonary hila are prominent, suggesting some degree of pulmonary hypertension (Correa da Silva, 2001).
Schematic representation of another sign of emphysema on the lateral chest radiograph. When the retrosternal space (defined as the space between the posterior border of the sternum and the anterior wall of the mediastinum) is larger than 2.5 cm, it is highly suggestive of overinflated lungs. This radiograph is from a patient with pectus carinatum, an important differential diagnosis to consider when this space is measured (Correa da Silva, 2001).
Close-up image shows emphysematous bullae in the left upper lobe. Note the subpleural, thin-walled, cystlike appearance (Correa da Silva, 2001).
A, Frontal posteroanterior (PA) chest radiograph shows no abnormality of the pulmonary vasculature, with normal intercostal spaces and a diaphragmatic dome between the 6th and 7th anterior ribs on both sides. B, Image in a patient with emphysema demonstrating reduced pulmonary vasculature resulting in hyperlucent lungs. The intercostal spaces are mildly enlarged, and the diaphragmatic domes are straightened and below the extremity of the seventh rib (Correa da Silva, 2001).
A, Lateral radiograph of the chest shows normal pulmonary vasculature, a retrosternal space within normal limits (< 2.5 cm), and a normal angle between the diaphragm and the anterior thoracic wall. B, Lateral view of the chest shows increased pulmonary transparency, increased retrosternal space (>2.5 cm), and an angle between the thoracic wall and the diaphragm >90 degrees. Straightening of the diaphragm can be more evident in this projection than on others (Correa da Silva, 2001).
High-resolution CT (HRCT) in a patient after viral bronchiolitis obliterans demonstrates areas of airtrapping, which is predominant in the inferior lobes and associated with bronchiectasis in the left lower lobe. Note that the decreased attenuation caused by the airtrapping can simulate emphysema (Correa da Silva, 2001).
Pediatric high-resolution CT (HRCT) shows a hyperinflated right lung with large pulmonary bullae due to congenital lobar emphysema (Correa da Silva, 2001).
High-resolution CT (HRCT) demonstrates areas of centriacinar emphysema. Note the low attenuation areas without walls due to destruction of the alveoli septae centrally in the acini. Red element shows the size of a normal acinus (Correa da Silva, 2001).
High-resolution CT (HRCT) shows large bullae in both inferior lobes due to uniform enlargement and destruction of the alveoli walls causing distortion of the pulmonary architecture (Correa da Silva, 2001).
Panacinar emphysema of the left lung in a patient with a right lung transplant. Note the red element showing the size of a normal acinus and its discrepancy with the destroyed and enlarged airspaces of the left lower lobe (Correa da Silva, 2001).
High-resolution CT (HRCT) shows subpleural bullae consistent with paraseptal emphysema. Red mark shows the size of a normal acinus (Correa da Silva, 2001).
High-resolution CT (HRCT) shows enlarged air-spaces or bullae adjoining pulmonary scars, consistent with paracicatricial emphysema. Red mark shows the size of a normal acinus (Correa da Silva, 2001).
CT densitovolumetry of a nonsmoker, healthy young patient shows normal lungs. Less than 0.35% of lungs have attenuations below -950 HU (Correa da Silva, 2001).
Expiratory CT densitovolumetry shows no areas of airtrapping (Correa da Silva, 2001).
CT densitovolumetry in a patient with lung cancer. Three-dimensional (3D) image shows that the cancer is in the portion of the right lung that was less affected by emphysema in a patient with poor pulmonary function (Correa da Silva, 2001).
CT densitovolumetry shows the attenuation mask. Green areas are those with attenuation below the selected threshold (here, -950 HU to evaluate emphysema), and pink areas are those with attenuations above the threshold. Area outside the patient is highlighted in green because of air (Correa da Silva, 2001).
CT densitovolumetry demonstrates irregular distribution of the emphysema, with substantial predominance in the left lung (Correa da Silva, 2001).
 
 
 
All material on this website is protected by copyright, Copyright © 1994-2016 by WebMD LLC. This website also contains material copyrighted by 3rd parties.