eMedicine Specialties > Pulmonology > Obstructive Airways Diseases

Emphysema: Follow-up

Author: Berj George Demirjian, MD, Fellow, Division of Pulmonary/Critical Care Medicine, Cedars-Sinai Medical Center
Coauthor(s): Nader Kamangar, MD, FACP, FCCP, FAASM, Associate Professor of Clinical Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Multi-campus Pulmonary and Critical Care Fellowship Program, University of California, Los Angeles, David Geffen School of Medicine; Medical Director, Hospitalist/Intensivist Program, Olive View-UCLA Medical Center; Associate Program Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA Medical Center/West Los Angeles Veterans Affairs Medical Center
Contributor Information and Disclosures

Updated: Oct 26, 2009

Follow-up

Further Inpatient Care

Acute exacerbation of COPD

Acute exacerbations of chronic obstructive pulmonary disease (AECOPDs) is defined as worsening of cough, increase in phlegm production, change in phlegm quality, and increase in dyspnea. AECOPDs are common in the course of the disease. Previously thought to occur at random, careful analysis by Hurst et al has shown AECOPDs occur in clusters.25 The study showed patients with an AECOPD were at an increased risk of another attack in the 8 weeks following their initial episode. Close follow up during this “brittle” period may lead to earlier treatment and better clinical outcomes.

AECOPDs are a major reason for hospital admission in the United States, although mild episodes may be treated in an outpatient setting. Indications for admission include failure of outpatient treatment, marked increase in dyspnea, altered mental status, and increase in hypoxemia or hypercapnia. Care must be taken to evaluate for other conditions that may mimic AECOPD.

AECOPD can result in hypoxemia and hypercapnia. Mild episodes may be managed with supplemental oxygen to keep PaO2 of 60 mm Hg. If the episode is severe, the patient may require ventilatory support in the form of either noninvasive positive-pressure ventilation (NIPPV) or invasive positive-pressure ventilation. The use of NIPPV is now well studied and supported in patients who have no contraindication to its use. A Cochrane review showed NIPPV reduces mortality, avoids endotracheal intubation, and decreased treatment failure.26

Pharmacological treatment of COPD includes bronchodilators, antibiotics, and steroids. Short-acting bronchodilators are the mainstay of therapy. Combinations of a beta2-agonist and anticholinergic agent are commonly used together, although the benefit of both over either is marginal. Oral or parenteral steroids are indicated in the treatment of AECOPD and have been shown to shorten recovery time and improve outcome. Importantly, taper the steroid course over 7-14 days because prolonged courses offer no additional benefit and increase adverse effects. Antibiotics have been shown to provide benefit in patients who present with dyspnea, increased purulence, and increased volume of sputum. The choice of antibiotics should be based on suspected etiology, patient history, and prevalent resistance patterns.

Further Outpatient Care

Pulmonary rehabilitation

Many patients with COPD are unable to enjoy life to the fullest because of shortness of breath, physical limitations, and inactivity. Pulmonary rehabilitation encompasses an array of therapeutic modalities designed to improve patients' quality of life by decreasing airflow limitation, preventing secondary medical complications, and alleviating respiratory symptoms.

Successful implementation of a pulmonary rehabilitation program usually requires a team approach, with individual components provided by healthcare professionals who have experience in managing COPD. These individuals include physicians, nurses, dietitians, respiratory therapists, exercise physiologists, physical therapists, occupational therapists, recreational therapists, cardiorespiratory technicians, pharmacists, and psychosocial professionals. This multidisciplinary approach emphasizes the following:

  • Patient and family education
  • Smoking cessation
  • Medical management (including oxygen and immunization)
  • Respiratory and chest physiotherapy
  • Physical therapy with bronchopulmonary hygiene, exercise, and vocational rehabilitation
  • Psychosocial support
Pulmonary rehabilitation programs usually are conducted in an inpatient or outpatient setting. A rehabilitation program may include a number of components and should be tailored to the needs of the individual patient. All patients who complete the program should be provided guidelines for home continuation of the program. Exercise training is a mandatory component of pulmonary rehabilitation. Patients with COPD should perform aerobic lower extremity endurance exercises regularly to enhance performance of daily activities and reduce dyspnea. Upper extremity exercise training improves dyspnea and allows increased activities of daily living requiring the use of the upper extremities. Breathing retraining techniques (eg, diaphragmatic and pursed-lip breathing) may improve the ventilatory pattern and may prevent dynamic airway compression.

Following pulmonary rehabilitation, improvements have been demonstrated in objective measures of quality of life, well-being, and health status, including reduction in respiratory symptoms, increases in exercise tolerance and functional activities, less anxiety and depression, and increased feelings of control and self-esteem. Pulmonary rehabilitation also results in substantial savings in healthcare costs by reducing hospital and medical resource use. 
 
Also see Pulmonary Rehabilitation and the clinical guideline summary, Pulmonary Rehabilitation: Joint ACCP/AACVPR Evidence-Based Clinical Practice Guidelines.27

Prognosis

The forced expiratory volume in 1 second (FEV1) has been historically used to predict outcome in COPD. Recent appreciation for other factors that determine outcome has resulted in creation of the BODE index (ie, body mass index, obstruction [FEV1], dyspnea [ie, Medical Research Council Dyspnea Scale, MMRC], and exercise capacity [ie, 6MWD]).28 This index was developed to assess an individual’s risk of death or hospitalization. All 4 factors are used to determine the score.

BODE index 

  • Body mass index
    • Greater than 21 = 0 points
    • Less than 21 = 1 point
  • FEV1 (postbronchodilator percent predicted)
    • Greater than 65% = 0 points
    • 50-64% = 1 point
    • 36-49% = 2 points
    • Less than 35% = 3 points
  • MMRC dyspnea scale
    • MMRC 0 = Dyspneic on strenuous exercise (0 points)
    • MMRC 1 = Dyspneic on walking a slight hill (0 points)
    • MMRC 2 = Dyspneic on walking level ground; must stop occasionally due to breathlessness (1 point)
    • MMRC 3 = Dyspneic after walking 100 yards or a few minutes (2 points)
    • MMRC 4 = Cannot leave house; dyspneic doing activities of daily living (3 points)
  • Six-minute walking distance
    • Greater than 350 meters = 0 points
    • 250-349 meters = 1 point
    • 150-249 meters = 2 points
    • Less than 149 meters = 3 points
  • Approximate 4-year survival
    • 0-2 points = 80%
    • 3-4 points = 67%
    • 5-6 points = 57%
    • 7-10 points = 18%

Patient Education

Miscellaneous

Medicolegal Pitfalls

  • The natural history of alpha1-antitrypsin (AAT) deficiency is unknown. The effect of replacement therapy has not been determined in randomized controlled trials. Although some investigators have argued that the duration and associated costs of controlled studies make such clinical trials impractical, the cost of AAT replacement is enormous, and the lack of consistent data regarding the course of untreated disease results in considerable skepticism about its efficacy. Whether widespread population screening should be undertaken also is unclear.
  • Differentiating COPD from asthma has been difficult because of overlap in pathophysiology, clinical presentation, pulmonary function testing, and treatment; approaches to treatment and prognosis differ.
  • The cost effectiveness of various interventions (eg, pulmonary rehabilitation, lung reduction surgery, lung transplantation) needs to be established.
  • The role of noninvasive ventilation to provide intermittent respiratory muscle rest needs be further defined.

Special Concerns

Air travel  

Many commercial airplanes fly at altitudes os 30,000-40,000 feet, but the cabin is pressurized to an altitude of 5,000-8,000 feet. At these altitudes, atmospheric partial pressure of oxygen (PO2) is 132-109 mm Hg, compared with 159 mm Hg at sea level. Acute reduction in PO2 stimulates peripheral chemoreceptors, which results in hyperventilation. The following is a prediction equation used to estimate PaO2 at 8000 feet (2440 m): 

PaO2 = 22.8 - 2.74x + 0.68y
x = Altitude
y = Arterial PO2 at sea level

A predicted PaO2 of 50 mm Hg or less at an altitude of 8,000 feet is an indication for supplemental oxygen. This can be arranged prior to the flight through the airline directly or through the airline agent but requires extra expense.

Sleep and COPD

Patients with COPD may develop substantial decreases in nocturnal PaO2 during all phases of sleep but particularly during rapid eye movement sleep. These episodes are associated with rises in pulmonary arterial pressures and disturbance in sleep architecture initially, but patients may develop pulmonary arterial hypertension and cor pulmonale if the hypoxemia remains untreated. Therefore, patients who have a daytime PaO2 greater than 60 mm Hg but demonstrate substantial nocturnal hypoxemia should be prescribed oxygen supplementation for use during sleep.

 
Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Sat Sharma, MD, FRCPC, to the development and writing of this article.



More on Emphysema

Overview: Emphysema
Differential Diagnoses & Workup: Emphysema
Treatment & Medication: Emphysema
Follow-up: Emphysema
Multimedia: Emphysema
References
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References

  1. Global Initiative for Chronic Obstructive Pulmonary Disease. Caverley P, Augusti A, Anzueto, et al, eds. Global Strategy for the Diagnosis, Management, and Prevention of Chronic Obstructive Pulmonary Disease. Medical Communications Resources; 2008.

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

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

  4. Menezes AM, Perez-Padilla R, Jardim JR, et al. Chronic obstructive pulmonary disease in five Latin American cities (the PLATINO study): a prevalence study. Lancet. Nov 26 2005;366(9500):1875-81. [Medline].

  5. Centers for Disease Control and Prevention. Deaths from chronic obstructive pulmonary disease--United States, 2000-2005. MMWR Morb Mortal Wkly Rep. Nov 14 2008;57(45):1229-32. [Medline].

  6. Silverman EK, Weiss ST, Drazen JM, et al. Gender-related differences in severe, early-onset chronic obstructive pulmonary disease. Am J Respir Crit Care Med. Dec 2000;162(6):2152-8. [Medline].

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

  8. [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].

  9. COMBIVENT Inhalation Aerosol Study Group. In chronic obstructive pulmonary disease, a combination of ipratropium and albuterol is more effective than either agent alone. An 85-day multicenter trial. COMBIVENT Inhalation Aerosol Study Group. Chest. May 1994;105(5):1411-9. [Medline].

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

  11. O'Donnell DE, Flüge T, Gerken F, et al. Effects of tiotropium on lung hyperinflation, dyspnoea and exercise tolerance in COPD. Eur Respir J. Jun 2004;23(6):832-40. [Medline].

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

  13. 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. May 2003;58(5):399-404. [Medline].

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

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

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

  17. 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. Jan 25 2005;CD001288. [Medline].

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

  19. [Best Evidence] Sin DD, Tashkin D, Zhang X, et al. Budesonide and the risk of pneumonia: a meta-analysis of individual patient data. Lancet. Aug 29 2009;374(9691):712-9. [Medline].

  20. Petty TL. The National Mucolytic Study. Results of a randomized, double-blind, placebo-controlled study of iodinated glycerol in chronic obstructive bronchitis. Chest. Jan 1990;97(1):75-83. [Medline].

  21. [Best Evidence] Sasaki T, Nakayama K, Yasuda H, 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. Aug 2009;57(8):1453-7. [Medline].

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

  23. 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. Aug 2006;82(2):431-43. [Medline].

  24. [Guideline] Orens JB, Estenne M, Arcasoy S, et al. International guidelines for the selection of lung transplant candidates: 2006 update--a consensus report from the Pulmonary Scientific Council of the International Society for Heart and Lung Transplantation. J Heart Lung Transplant. Jul 2006;25(7):745-55. [Medline].

  25. 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. Mar 1 2009;179(5):369-74. [Medline].

  26. 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. Jan 25 2003;326(7382):185. [Medline].

  27. Ries AL, Bauldoff GS, Carlin BW, et al. Pulmonary Rehabilitation: Joint ACCP/AACVPR Evidence-Based Clinical Practice Guidelines. Chest. May 2007;131(5 Suppl):4S-42S. [Medline].

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

  29. Anthonisen NR. Prognosis in chronic obstructive pulmonary disease: results from multicenter clinical trials. Am Rev Respir Dis. Sep 1989;140(3 Pt 2):S95-9. [Medline].

  30. Anthonisen NR, Connett JE, Kiley JP, et al. Effects of smoking intervention and the use of an inhaled anticholinergic bronchodilator on the rate of decline of FEV1. The Lung Health Study. JAMA. Nov 16 1994;272(19):1497-505. [Medline].

  31. Brenes GA. Anxiety and chronic obstructive pulmonary disease: prevalence, impact, and treatment. Psychosom Med. Nov-Dec 2003;65(6):963-70. [Medline].

  32. Burrows B, Bloom JW, Traver GA, Cline MG. The course and prognosis of different forms of chronic airways obstruction in a sample from the general population. N Engl J Med. Nov 19 1987;317(21):1309-14. [Medline].

  33. Chapman KR. Therapeutic algorithm for chronic obstructive pulmonary disease. Am J Med. Oct 21 1991;91(4A):17S-23S. [Medline].

  34. Davis RM, Novotny TE. The epidemiology of cigarette smoking and its impact on chronic obstructive pulmonary disease. Am Rev Respir Dis. Sep 1989;140(3 Pt 2):S82-4. [Medline].

  35. Dunn WF, Nelson SB, Hubmayr RD. Oxygen-induced hypercarbia in obstructive pulmonary disease. Am Rev Respir Dis. Sep 1991;144(3 Pt 1):526-30. [Medline].

  36. Fabbri LM, Luppi F, Beghé B, Rabe KF. Update in chronic obstructive pulmonary disease 2005. Am J Respir Crit Care Med. May 15 2006;173(10):1056-65. [Medline].

  37. Ferguson GT, Cherniack RM. Management of chronic obstructive pulmonary disease. N Engl J Med. Apr 8 1993;328(14):1017-22. [Medline].

  38. Fletcher C, Peto R. The natural history of chronic airflow obstruction. Br Med J. Jun 25 1977;1(6077):1645-8. [Medline].

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

  40. Karpel JP, Kotch A, Zinny M, Pesin J, Alleyne W. A comparison of inhaled ipratropium, oral theophylline plus inhaled beta-agonist, and the combination of all three in patients with COPD. Chest. Apr 1994;105(4):1089-94. [Medline].

  41. Lopez-Majano V, Dutton RE. Regulation of respiration during oxygen breathing in chronic obstructive lung disease. Am Rev Respir Dis. Aug 1973;108(2):232-40. [Medline].

  42. Mannino DM, Watt G, Hole D, Gillis C, Hart C, McConnachie A. The natural history of chronic obstructive pulmonary disease. Eur Respir J. Mar 2006;27(3):627-43. [Medline].

  43. McKay SE, Howie CA, Thomson AH, Whiting B, Addis GJ. Value of theophylline treatment in patients handicapped by chronic obstructive lung disease. Thorax. Mar 1993;48(3):227-32. [Medline].

  44. Medical Research Council Working Party. Long term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema. Report of the Medical Research Council Working Party. Lancet. Mar 28 1981;1(8222):681-6. [Medline].

  45. Nocturnal Oxygen Therapy Trial Group. Continuous or nocturnal oxygen therapy in hypoxemic chronic obstructive lung disease: a clinical trial. Nocturnal Oxygen Therapy Trial Group. Ann Intern Med. Sep 1980;93(3):391-8. [Medline].

  46. O'Donnell DE, Parker CM. COPD exacerbations . 3: Pathophysiology. Thorax. Apr 2006;61(4):354-61.

  47. O'Donnell DE, Sanii R, Anthonisen NR, Younes M. Effect of dynamic airway compression on breathing pattern and respiratory sensation in severe chronic obstructive pulmonary disease. Am Rev Respir Dis. Apr 1987;135(4):912-8. [Medline].

  48. O'Donnell R, Breen D, Wilson S, Djukanovic R. Inflammatory cells in the airways in COPD. Thorax. May 2006;61(5):448-54. [Medline].

  49. Papi A, Luppi F, Franco F, Fabbri LM. Pathophysiology of exacerbations of chronic obstructive pulmonary disease. Proc Am Thorac Soc. May 2006;3(3):245-51. [Medline].

  50. Peto R, Speizer FE, Cochrane AL, et al. The relevance in adults of air-flow obstruction, but not of mucus hypersecretion, to mortality from chronic lung disease. Results from 20 years of prospective observation. Am Rev Respir Dis. Sep 1983;128(3):491-500. [Medline].

  51. Petty TL, Finigan MM. Clinical evaluation of prolonged ambulatory oxygen therapy in chronic airway obstruction. Am J Med. Aug 1968;45(2):242-52. [Medline].

  52. Postma DS, Sluiter HJ. Prognosis of chronic obstructive pulmonary disease: the Dutch experience. Am Rev Respir Dis. Sep 1989;140(3 Pt 2):S100-5. [Medline].

  53. Prigmore S. End-of-life decisions and respiratory disease. Nurs Times. Feb 14-20 2006;102(7):56, 59, 61. [Medline].

  54. Ram FS, Rodriguez-Roisin R, Granados-Navarrete A. Antibiotics for exacerbations of chronic obstructive pulmonary disease. Cochrane Database Syst Rev. 2006;CD004403.

  55. Rutten FH, Cramer MJ, Lammers JW, Grobbee DE, Hoes AW. Heart failure and chronic obstructive pulmonary disease: An ignored combination?. Eur J Heart Fail. Nov 2006;8(7):706-11. [Medline].

  56. Sanders C. The radiographic diagnosis of emphysema. Radiol Clin North Am. Sep 1991;29(5):1019-30. [Medline].

  57. Schachter EN. Cilomilast. Drugs Today (Barc). Apr 2006;42(4):237-47.

  58. Sutherland ER, Martin RJ. Airway inflammation in chronic obstructive pulmonary disease: comparisons with asthma. J Allergy Clin Immunol. Nov 2003;112(5):819-27; quiz 828. [Medline].

  59. Thurlbeck WM. Overview of the pathology of pulmonary emphysema in the human. Clin Chest Med. Sep 1983;4(3):337-50. [Medline].

  60. Thurlbeck WM. Pathophysiology of chronic obstructive pulmonary disease. Clin Chest Med. Sep 1990;11(3):389-403. [Medline].

  61. Tsoumakidou M, Siafakas NM. Novel insights into the aetiology and pathophysiology of increased airway inflammation during COPD exacerbations. Respir Res. May 22 2006;7(1):80.

  62. Vestbo J. Clinical assessment, staging, and epidemiology of chronic obstructive pulmonary disease exacerbations. Proc Am Thorac Soc. May 2006;3(3):252-6. [Medline].

  63. Weitzenblum E, Sautegeau A, Ehrhart M, Mammosser M, Pelletier A. Long-term oxygen therapy can reverse the progression of pulmonary hypertension in patients with chronic obstructive pulmonary disease. Am Rev Respir Dis. Apr 1985;131(4):493-8. [Medline].

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Further Reading

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Keywords

emphysema, chronic obstructive pulmonary disease, COPD, chronic obstructive lung disease, chronic lung, chronic bronchitis, airflow obstruction, centriacinar emphysema, centrilobular emphysema, panacinar emphysema, paraseptal emphysema, distal acinar emphysema, alpha1-antitrypsin deficiency, AAT

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Contributor Information and Disclosures

Author

Berj George Demirjian, MD, Fellow, Division of Pulmonary/Critical Care Medicine, Cedars-Sinai Medical Center
Berj George Demirjian, MD is a member of the following medical societies: American College of Chest Physicians, American Medical Association, California Medical Association, California Thoracic Society, and Phi Beta Kappa
Disclosure: Nothing to disclose.

Coauthor(s)

Nader Kamangar, MD, FACP, FCCP, FAASM, Associate Professor of Clinical Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Multi-campus Pulmonary and Critical Care Fellowship Program, University of California, Los Angeles, David Geffen School of Medicine; Medical Director, Hospitalist/Intensivist Program, Olive View-UCLA Medical Center; Associate Program Director, Combined Pulmonary and Critical Care Fellowship Program, Cedars-Sinai/Olive View-UCLA Medical Center/West Los Angeles Veterans Affairs Medical Center
Nader Kamangar, MD, FACP, FCCP, FAASM is a member of the following medical societies: American Academy of Sleep Medicine, American Association of Bronchology, American College of Chest Physicians, American College of Physicians, American Lung Association, American Medical Association, American Thoracic Society, California Thoracic Society, and Society of Critical Care Medicine
Disclosure: Nothing to disclose.

Medical Editor

Helen M Hollingsworth, MD, Director, Adult Asthma and Allergy Services, Associate Professor, Department of Internal Medicine, Division of Pulmonary and Critical Care, Boston Medical Center
Helen M Hollingsworth, MD is a member of the following medical societies: American Academy of Allergy Asthma and Immunology, American College of Chest Physicians, American Thoracic Society, and Massachusetts Medical Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

CME Editor

Timothy D Rice, MD, Associate Professor, Departments of Internal Medicine and Pediatrics and Adolescent Medicine, Saint Louis University School of Medicine
Timothy D Rice, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Physicians
Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, Director, Division of Pulmonary and Critical Care Medicine, Director, Women's Guild Pulmonary Disease Institute, Executive Vice Chair, Department of Medicine, Cedars Sinai Medical Center; Professor of Medicine, David Geffen School of Medicine at UCLA
Zab Mosenifar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, and American Thoracic Society
Disclosure: Nothing to disclose.

 
 
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