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COPD: Overview and survey of NP knowledge

Blair, Kathryn A. PhD, FNP-BC, FAANP; Evelo, Andrew J MA

doi: 10.1097/01.NPR.0000429892.18502.79

Chronic obstructive pulmonary disease (COPD) is quickly becoming one of the leading causes of morbidity and mortality. The purpose of this article is to review the clinical presentation, spirometry, and pharmacologic management of COPD, as well as the results of a survey examining nurse practitioners' (NPs) knowledge about COPD and its management.

Kathryn A. Blair is a Professor, NP Option Coordinator at University Colorado-Colorado Springs, Beth El College of Nursing and Health Sciences, Colorado Springs, Colo. Andrew J. Evelo is a Graduate Student at John Jay College and Graduate Center, City University New York, New York, NY.

The authors and planners have disclosed that they have no financial relationships related to this article.

Current predictions suggest that chronic obstructive pulmonary disease (COPD) will become the third leading cause of death by 2020,1,2 and yet, 50% of patients with COPD remain undiagnosed.3 Although there is no cure for COPD, primary care providers play an important role in slowing its progression through early diagnosis and management.

Identification of risk factors and recognition of clinical presentation are not sufficient to diagnose COPD. A recent study suggests that symptoms of airway obstruction (coughing, wheezing, sputum, and shortness of breath) were not predictive of COPD.3 However, a simple diagnostic test, postbronchodilator spirometry, which can be performed in the primary care setting, is useful to confirm the diagnosis of obstructive airway disease.

Disease management for COPD will impact the rate of decline in lung function by reducing the frequency of exacerbations. Although primary prevention is the principal goal, secondary and tertiary prevention are equally important. Key factors in the management should be a reduction of risks, such as smoking cessation, reducing exposure to occupational or environmental pollution, controlling asthma, recognition of vulnerable populations (women and teens), and utilization of the recommended pharmacologic therapies.

The purpose of this article is to present an overview of the clinical presentation, spirometry as a diagnostic tool, and pharmacologic agents used in the management of COPD. Additionally, the results of a recent survey examining nurse practitioners' (NPs) knowledge about COPD clinical manifestations, spirometry as the diagnostic tool, and understanding of primary pharmacologic management will be presented. Finally, the differences between family, adult, and population-specific NPs' (pediatric, gerontology, and women's health) knowledge will be highlighted.



COPD is a progressive decline in lung function that is a result of genetics (alpha-1 antitrypsin deficiency), normal aging, reduced lung growth (prematurity), or accelerated decline caused by factors, such as smoking.4-7 While COPD begins with primary involvement of the respiratory system manifested by chronic bronchitis and/or emphysema, over time, it becomes a multisystem disease. COPD often coexists with other diseases, such as ischemic heart disease, heart failure, and lung cancer.8 As this disease progresses, a loss of body fat, muscle, and bone mass occurs.9,10 Some authors propose that the chronic inflammatory process associated with COPD may result in the potential for endocrine dysfunction in the thyroid and adrenal glands, pancreatic disorders, and gonadal malfunction.11 Although most COPD patients will die from the disease, approximately a third will die of comorbidities.12

Gender variability and bias have been noted in the physiological responses and care of women with COPD. Primary care providers are more likely to diagnose COPD in men than women, even when both present with similar risk factors and symptoms.9 Women with COPD tend to have greater airway hyperresponsiveness, experience more dyspnea, and more exacerbations than men.5,13,14 Women with COPD are not only more symptomatic than men but have a higher mortality and higher rates for cardiovascular disease and lung cancer.12

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Clinical presentation

In order to successfully manage COPD, the clinician must use the history and context to interpret the signs and symptoms. For example, asthma and COPD have very similar expressions, such as dyspnea, cough, and wheezing. Asthma is usually associated with a history of atopy, while COPD is linked with smoking or other risk factors (see Risk factors).

The clinical presentation of COPD may vary depending on the severity of the disease; however, the key characteristics are persistent cough, sputum production, dyspnea with activity, history of recurrent lower respiratory tract infections, and airflow limitation, only partially reversible after a bronchodilator.18-20 The patient with moderate-to-severe disease can experience additional manifestations, such as nocturnal dyspnea, chest tightness, and peripheral edema, which may mirror cardiovascular disease.19 More often than not, many symptoms and signs are not specific for COPD and may be attributed to other diseases (see Clinical manifestations).

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As stated earlier, the history and clinical manifestations are inadequate to diagnose COPD. The importance of spirometry in the diagnosis and tracking the progression of COPD cannot be understated; however, it is underutilized in the primary care setting where early diagnosis can reduce the exacerbations2,12,21-23 and alter the course of the disease. The most common barriers cited for the underutilization of spirometry in the primary care setting are as follows: time to perform the test, lack of trained staff, lack of equipment, and primary care providers' fear of misinterpretation of the results.21-24 Research supports that primary care providers are capable of the correct interpretation of spirometry.25-27 Another study highlights that family practice providers were less likely to perform spirometry than pediatricians or internal medicine providers.28

To discuss the procedure of spirometry is beyond the scope of this article. However, a simple description includes having patients take a deep inhalation through a mouthpiece, forcefully blow or “blast” out all air, keep blowing for 6 seconds, then take a deep inhalation with the mouth still on the mouthpiece. There are several detailed resources from the manufacturers of the equipment and online for the specific mechanics of performing spirometry.

The novice needs to understand a few salient issues for accurate interpretation of spirometry results. The key spirometric elements for diagnosing COPD are FEV1 (forced expired volume in one second), FVC (forced vital capacity), and FEV1/FVC (forced expiratory ratio). Normal FEV1/FVC is between 0.7 and 0.8 with norms for the older adult being 0.65 to 0.7.29 Predicted values are based on gender, height, age, and ethnicity. Additionally, the provider must also recognize that COPD may have partial reversibility8,28; therefore, spirometry must be performed post bronchodilator (see Classification of severity of airflow limitation in COPD [post bronchodilator FEV1]). The characteristic COPD graph produced by spirometry demonstrates a reduction of expelled air resulting in reduced FEV1/FVC ratio (see Normal, obstructive, and restrictive spirometry curves).

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The primary pharmacologic treatment for COPD is based on severity of the disease and response to therapy (see Primary management of COPD). Most studies demonstrate that inhaled beta2-agonists (short- and long-acting) with or without inhaled corticosteroids and inhaled anticholinergic (short- and long-acting) agents are the mainstay of COPD management.20-28,30-33 A variety of other pharmacologic agents and therapeutic modalities have been used for the successful management of COPD (see Other treatment strategies).

Mucolytic agents are used; however, the evidence is mixed in terms of overall benefit. Although theophylline (a methylxanthine) can reduce exacerbations, there is little impact on lung function.34 Additional pharmacologic therapies include the use of antibiotics and oral corticosteroids for exacerbations.

Several novel drugs have been recently introduced on the market. Studies of phosphodiesterase-4 inhibitors have been mixed. However, one oral drug, roflumilast, has been shown to improve lung function as well as decrease the frequency of exacerbations in patients with moderate and severe diseases.35-37 In 2012, the FDA approved an inhaled long-acting muscarinic antagonist, aclidinium bromide. Study findings for aclidinium bromide demonstrated improved airflow obstruction, increased exercise tolerance, and improved lung hyperinflation.38 In a 12-week study, an ultra-long-acting bronchodilator (indacaterol) was superior to salmeterol (a twice daily bronchodilator) in decreasing breathlessness and reducing the use of rescue medication.39,40 A recent clinical trial of a 5-lipoxygenase inhibitor, MK-0633, improved symptom complaints, but overall, did not demonstrate any improvement in lung function as measured by the FEV1.41

Many patients will ask about alternative treatments for COPD. Herbal-based expectorants with extracts from Hedera helix (ivy) or Thymus vulgaris (thyme) have been shown to have some efficacy.42 Ginseng has shown some improvement in all parameters of lung function; however, because of its antiplatelet effect, caution regarding long-term use is advised.42,43 Acupuncture may be effective for increasing exercise tolerance and reducing symptoms of dyspnea.42

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Survey results methods

A survey was sent to 2,916 registered NPs obtained from Colorado State Board of Nursing. (The risk factors portion of this survey was reported in an earlier article [in press] “Risk factors for COPD: what do NPs know?”.)44

Only 239 surveys were returned, resulting in an 8% response rate. The survey consisted of demographic information (age, gender, years in practice, certification, etc.) and questions about smoking, symptoms, early diagnostic test, and primary pharmacologic management of COPD. Every section had an “other” option enabling the respondent to add supplemental information. Areas of certification of the respondents were family, 45%; adult, 15%; women's health, 12%; pediatric, 7%; gerontology, 3%; and other, 10%.

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Results item response rates

A list of correct item response rates for all NPs was calculated (see Percentage of correct responses of NPs by certification). The three major symptoms associated with COPD (chronic cough 97%, dyspnea with exertion 97%, and sputum production 90%) were identified by the majority of NPs. The other symptoms, such as peripheral edema, chest tightness, and nocturnal awakening, were recognized less frequently. Ten percent of the respondents listed other symptoms, such as weight loss, fatigue, pallor, cyanosis, barrel chest, frequent infections, and nail clubbing.

The primary diagnostic tool for COPD is spirometry post bronchodilator. Forty-five percent of all respondents indicated spirometry with bronchodilator reversibility. Several NPs indicated chest X-rays, pulmonary function tests, arterial blood gases, pulse oximetry, sleep studies, computed tomography scan, and labs, such as complete blood count, chemistry profile, brain natriuretic peptide, and alpha-1 antitrypsin as primary diagnostic tools.

Finally, the majority of NPs indicated that they favored the use of inhaled pharmacologic treatments as their primary management of COPD compared to alternatives. Other management strategies identified were oxygen, antibiotics, smoking cessation, nutritional support, and pulmonary rehabilitation.

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Correct item identification by area

The authors hypothesized that NPs would differ in their ability to identify COPD symptoms, early diagnostic procedures, and primary treatment methods based on their area of certification. Specifically, adult and family NPs would have more knowledge of COPD than population-specific NPs (a group created by combining NPs certified in pediatric, women's health, and gerontology; n = 53). This hypothesis was based on the assumption that population-specific NPs would have more specialized knowledge of COPD, as it pertains to their target population, while adult and family NPs would have a broader knowledge of COPD because of the diversity of their patient population.

The same type of statistical test could not be used to test this hypothesis for all three questions (symptoms, diagnostic procedures, and treatment methods) because the dependent variable, or what should be considered a correctly identified item, changes depending on the question. For instance, all items listed under “symptoms” are actual symptoms of COPD and should have been identified by NPs. However, for “early diagnostic procedures,” only spirometry and bronchodilator reversibility should have been identified, and under “primary treatment” only inhaled anticholinergics, inhaled beta2-agonists, and inhaled glucocorticosteroids should have been identified. For symptoms, a one-way analysis of variance (ANOVA) was used while a mixed ANOVA was used for diagnostic procedures and treatments. Test statistics (F values), probability values (p values), and both eta-squared (η2) and partial eta-squared (η2 p) effect sizes are presented for each test when appropriate.

In a one-way ANOVA to test for differences in symptom identification, the independent variable was area of certification. A dependent variable was created by simply calculating the percentage of symptoms identified by each respondent. The scores ranged from 0% to 100% with a mean of 83% (with higher score indicating more symptoms identified). Results from the ANOVA indicated that there were no differences between NP groups in percentage of symptoms identified, F (2,194) = 0.89, p = 0.42, η2 = .01. Contrary to our hypothesis, adult (86%), family (83%), and population-specific NPs (80%) identified about that same amount of COPD symptoms regardless of the area of certification.

To test the hypothesis that adult and family NPs would have a broader knowledge about early diagnostic procedures and primary treatment for COPD, a mixed ANOVA was performed. Each diagnostic procedure and treatment was treated as a repeated measures independent variable and the NP area of certification as a between subjects variable. The dependent variable was the amount of responses. Possible interactions were tested, and pairwise comparisons were utilized to test the hypotheses. If family and adult NPs display more knowledge about early diagnostic procedures and primary treatment than population-specific NPs, they should then identify an item more than population-specific NPs only when that item is correct. For instance, when identifying early diagnostic procedures, family and adult NPs should more often identify spirometry and bronchodilator reversibility than population-specific NPs. Additionally, family and adult NPs should correctly identify postbronchodilator and spirometry more frequently than population specific NPs and identify arterial blood gases, chest X-ray, and pulmonary functions tests no differently—or even less often—than population-specific NPs.

The test on diagnostic procedures was a 3 (area of certification: adult, family, population specific) × 5 (diagnostic test: arterial blood gases, bronchodilator reversibility, chest X-ray, pulmonary function test, spirometry) mixed ANOVA. There was a main effect for diagnostic test, F (4, 776) = 83.63, p < 0.001, η2 p = 0.30 but not for area of certification, F (1, 194) = 0.48, p = 0.62, η2 p = 0.01. There was a significant interaction, F (7.39, 776) = 3.26, p = 0.002, η2 p = 0.03 (Greenhouse-Geisser correction). Pairwise post-hoc comparisons showed that the relationship of the variables in this interaction was similar to the hypothesized. Population-specific NPs identified bronchodilator reversibility significantly less frequently than family NPs (p = 0.02) and marginally less frequently than adult NPs (p = 0.05). Both family (p = 0.02) and adult (p = 0.02) NPs identified spirometry significantly more often than population-specific NPs. No significant differences in item response were observed between NP types on chest X-rays or pulmonary function test. Population-specific NPs were significantly more likely to indicate arterial blood gases as a diagnostic tool for COPD than family NPs (p = 0.01) but not adult NPs (p = 0.17).

To test treatment responses, a 3 (area of certification: adult, family, population specific) × 7 (treatment: antitussives, inhaled anticholinergics, inhaled beta2-agonists, inhaled glucocorticosteroids, methylxanthines, mucolytic agents, systemic glucocorticosteroids) mixed ANOVA was used. There was a main effect for both area of certification, F (1, 189) = 7.39, p = 0.001, η2 p = 0.07, and pharmaceutical treatment, F (6, 1134) = 51.00, p < 0.001, η2 p = 0.21. There was also a significant interaction, F (10.93, 1032.71) = 2.75, p = 0.002, η2 p = 0.03 (Greenhouse-Geisser correction). In the area of primary pharmacologic treatment, it was hypothesized that there would be significantly more endorsements by family and adult NPs than the population-specific NPs for the inhaled agents (anticholinergics, beta2-agonist, and glucocorticosteroids) but not the other treatments (antitussives, methylxanthines, mucolytic agents, or systemic glucocorticosteroids). This was the pattern that emerged after post-hoc comparisons. For inhaled anticholinergics and inhaled beta2-agonists, family and adult NPs showed no group differences but were both significantly higher than population-specific NPs ( all p values less than 0.03). For inhaled glucocorticosteroids, the only significant difference was between family NPs and population-specific NPs (p = 0.005). In all three cases, family and adult NPs more often indicated that inhaled pharmaceuticals were the primary treatments for COPD.

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Despite the limitations of this survey (such as poor return rate and confusion with survey questions), the results give a snapshot view of the knowledge of symptoms, diagnostic spirometry, and an overview of primary pharmacologic management of COPD by NP respondents in the State of Colorado. NPs, regardless of certification, have a broad knowledge regarding COPD; however, there were some differences identified by certification.

Population-based NPs were less likely to recognize that spirometry post bronchodilator was the early diagnostic test for COPD. Perhaps this difference was related to the lack of clarity in the survey question. The correct responses were spirometry and bronchodilator reversibility. Retrospectively, for clarity, the answer should have been postbronchodilator spirometry. Previously, COPD was defined by the lack of reversibility; however, the newer definition incorporates partial reversibility.8,30,31

This finding that spirometry is an early diagnostic tool is particularly salient for pediatric and women's health NPs. These NPs serve two vulnerable populations that may benefit from primary and secondary prevention, and early interventions. As reported earlier, women develop a more aggressive disease and have higher rates of mortality. Additionally, women with COPD are less frequently identified. The pediatric population is at risk for pulmonary insults (such as frequent lower respiratory tract infections or poorly controlled asthma) while the lungs are developing. Several studies suggest that children with early insults are more likely to develop obstructive disease later in life even if they never smoke.45-47 These two populations would benefit by periodic spirometry when the history suggests a risk for developing obstructive lung disease.

Overall, all NPs, regardless of certification, identified the three major symptoms (dyspnea with exertion, chronic cough, and sputum production) while later symptoms, such as nocturnal awakening and chest tightness, were less frequently identified simply because these symptoms can be confused with other conditions, such as heart disease. Often, symptoms are not specific to COPD, and these findings suggest the importance of using spirometry to aid in the early diagnosis.

Although most NPs recognized that inhaled agents such as beta2-agonist and glucocorticosteroids were used in the primary management of COPD, inhaled anticholinergic agents were less frequently identified. Recent research, however, highlights lung function improvement as well as a reduction in exacerbations when these agents are used.48,49 As anticipated, population-specific NPs as compared to family and adult NPs were less likely to identify inhaled agents as primary pharmacologic treatment. This is significant in that population-specific NPs, especially women's health and gerontologic, are likely to care for vulnerable populations at risk for COPD.

One important area identified in this study was the lack of recognition of postbronchodilator spirometry for the early diagnosis of COPD. This procedure is simple and can easily be performed in the primary care setting; therefore, NPs should learn how to perform and interpret spirometry. This can be easily accomplished through formal educational programs or continuing-education programs.

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Moving forward

Tremendous strides have been made in primary prevention through media campaigns that address smoking cessation; however, less information has been disseminated regarding other risk factors, such as alpha-1 antitrypsin deficiency, prematurity, repeated lower respiratory infections before the age of 6 years, environmental pollution, and occupational exposure. NPs, regardless of specialty, should remain current about diseases they may not always see in their practices. As in the case of COPD, recognition of risk factors, clinical presentation, and the use of postbronchodilator spirometry will facilitate early diagnosis, which can result in early pharmacologic management, and, ultimately, slow the progression of COPD.

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Risk factors15–17

  • Alpha-1 antitrypsin deficiency
  • Family history of COPD
  • Prematurity
  • Severe lower respiratory tract infections before age 5 to 6 years
  • Asthma (poorly controlled)
  • Exposure to second-hand smoke
  • Cigarette and marijuana smoking
  • Water pipe smoking
  • Women (smokers and those exposed to second-hand smoke)
  • Teen smokers
  • Indoor and outdoor pollutants
  • Occupational exposure (organic, inorganic dust, vapors, chemical, and so on)
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Clinical manifestations9,10,17–20


  • Recurrent respiratory infections
  • Smoking or a history of other risk factors


  • Dyspnea with activity
  • Sputum production
  • Persistent cough
  • Nocturnal awakening
  • Chest tightness

Physical presentation

  • Barrel chest
  • Decreased breath sounds
  • Wheezing
  • Hyperresonance
  • Decreased or absent tactile fremitus
  • Muscle wasting
  • Loss of body fat
  • Loss of bone mass
  • Peripheral edema
Table C

Table C





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Other treatment strategies30–34


  • Oral corticosteroids
  • Methylxanthines
  • Phosphodiesterase-4-inhibitor
  • Mucolytic agents
  • Antitussives
  • Antibiotics


  • Pneumococcal


  • Oxygen
  • Pulmonary rehabilitation
  • Ventilatory support
  • Lung reduction surgery


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1. Berry CE, Wise RA. Mortality in COPD: causes, risk factors, and prevention. COPD. 2010;7(5):375–382.
2. Cote CG, Chapman KR. Diagnosis and treatment considerations for women with COPD. Int J Clin Pract. 2009;63(3):486–493.
3. Ohar JA, Sadeghnejad A, Meyers DA, Donohue JF, Bleecker ER. Do symptoms predict COPD in smokers? Chest. 2010;137(6):1345–1353.
4. Blanc PO, Iribarren C, Trupin L, et al. Occupational exposures and the risk of COPD: dusty trades revisited. Thorax. 2009;64(1):6–12.
5. Camp PG, O'Donnell DE, Postma DS.. Chronic obstructive pulmonary disease in men and women: myths and reality. Proc Am Thorac Soc. 2009;6(6):535–538.
6. Weinmann S, Vollmer WM, Breen V, et al. COPD and occupational exposures: a case-control study. J Occup Environ Med. 2008;55(5):561–569.
    7. Ito K, Barnes PJ. COPD as a disease of accelerated lung aging. Chest. 2009;135(1):173–180.
    8. Tashkin D, Celli B, Kesten S, Lystig T, Decramer M. Effect of tiotropium in men and women with COPD: results of the 4-year UPLIFT trial. Respir Med. 2010;104(10):1495–1504.
    9. Verhage TL, Heijdra Y, Molema J, Vercoulen J, Dekhuijzen R. Associations of muscle depletion with health status. Another gender difference in COPD. Clin Nutr. 2011;30(3):332–338.
    10. Nussbaumer-Ochsner Y, Rabe KF. Systemic manifestations of COPD. Chest. 2011;139(1):165–173.
    11. Laghi F, Adiguzel N, Tobin MJ. Endocrinological derangements in COPD. Eur Respir J. 2009;34(4):975–996.
    12. Ekström M, Franklin KA, Ström KE. Increased relative mortality in women with severe oxygen-dependent COPD. Chest. 2010;137(1):31–36.
    13. Sørheim IC, Johannessen A, Gulsvik A, Bakke PS, Silverman EK, DeMeo DL. Gender differences in COPD: are women more susceptible to smoking effects than men? Thorax. 2010;65(6):480–485.
    14. Celli B, Vestbo J, Jenkins CR, et al. Sex differences in mortality and clinical expressions of patients with chronic obstructive pulmonary disease. The TORCH experience. Am J Respir Crit Care Med. 2011;183(3):317–322.
    15. Liu Y, Lee K, Perez-Padilla R, Hudson NL, Mannino DM. Outdoor and indoor air pollution and COPD-related diseases in high- and low-income countries. Int J Tuberc Lung Dis. 2008;12(2):115–127.
    16. Rodríguez E, Ferrer J, Martí S, Zock JP, Plana E, Morell F. Impact of occupational exposure on severity of COPD. Chest. 2008;134(6):1237–1243.
      17. Reardon JZ. Environmental tobacco smoke: respiratory and other health effects. Clin Chest Med. 2007;28(3):559–573.
      18. Bellamy D, Smith J. Role of primary care in early diagnosis and effective management of COPD. Int J Clin Pract. 2007;61(8):1380–1389.
      19. Wise RA, Tashkin DP. Optimizing treatment of chronic obstructive pulmonary disease: an assessment of current therapies. Am J Med. 2007;120(8 suppl 1):S4–S13.
      20. Kessler R, Partridge MR, Miravitlles M, et al. Symptom variability in patients with severe COPD: a pan-European cross-sectional study. Eur Respir J. 2011;37(2):264–272.
      21. Hill K, Hodder R, Blouin M, Heels-Ansdell D, Guyatt G, Goldstein R. Identifying adults at risk of COPD who need confirmatory spirometry in primary care: do symptom-based questions help. Can Fam Physician. 2011;57(2):e51–e57.
      22. Roberts NJ, Smith SF, Partridge MR. Why is spirometry underused in the diagnosis of the breathless patient: a qualitative study. BMC Pulm Med. 2011;11:37.
        23. Arne M, Lisspers K, Ställberg B, et al. How often is diagnosis of COPD confirmed with spirometry. Respir Med. 2010;104(4):550–556.
        24. Poels PJ, Schermer TR, Schellekens DP, et al. Impact of a spirometry expert system on general practitioners' decision making. Eur Respir J. 2008;31(1):84–92.
        25. Canals-Borrajo G, Martínez-Andión B, Cigüenza-Fuster ML, et al. Spirometry for detection of undiagnosed chronic obstructive pulmonary disease in primary care. Eur J Gen Pract. 2010;16(4):215–221.
        26. Yawn BP, Enright PL, Lemanske RF Jr, et al. Spirometry can be done in family physicians' offices and alters clinical decisions in management of asthma and COPD. Chest. 2007;132(4):1162–1168.
          27. Radin A, Cote C. Primary care of the patient with chronic obstructive pulmonary disease-Part 1: frontline prevention and early diagnosis. Am J Med. 2008;121(suppl 7):S3–S12.
          28. Blain EA, Craig TJ. The use of spirometry in a primary care setting. Int J Gen Med. 2009;2:183–186.
          29. Spirometry for health care providers. Global Initiative for chronic obstructive lung disease (GOLD).
          30. Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management and prevention of chronic obstructive pulmonary disease.
          31. Gross N, Levin D. Primary care of the patient with chronic obstructive pulmonary disease-Part 2: pharmacologic treatment across all stages of disease. Am J Med. 2008;121(suppl 7):S13–S24.
          32. Chavez PC, Shokar NK. Diagnosis and management of chronic obstructive pulmonary disease (COPD) in a primary care clinic. COPD. 2009;6(6):446–451.
            33. Cazzola M, Molimard M. The scientific rationale for combining long-acting beta2-agonists and muscarinic antagonists in COPD. Pulm Pharmacol Ther. 2010;23(4):257–267.
            34. Jones R, Østrem A. Optimising pharmacological maintenance treatment for COPD in primary care. Prim Care Respir J. 2011;20(1):33–45.
            35. Alifano M, Cuvelier A, Delage A, et al. Treatment of COPD: from pharmacological to instrumental therapies. Eur Respir Rev. 2010;19(115):7–23.
            36. Hatzelmann A, Morcillo EJ, Lungarella G, et al. The preclinical pharmacology of roflumilast—a selective, oral phosphodiesterase 4 inhibitor in development for chronic obstructive pulmonary disease. Pulm Pharmacol Ther. 2010;23(4):235–256.
              37. Oba Y, Lone NA Efficacy and safety of roflumilast in patients with chronic obstructive pulmonary disease: a systematic review and meta-analysis Ther Adv Respir Dis (2013) 7(1) 13–24 DOI: 10.1177/1753465812466167
              38. Maltais F, Celli B, Casaburi R, et al. Aclidinium bromide improves exercise endurance and lung hyperinflation in patients with moderate to severe COPD. Respir Med. 2011;105(4):580–587.
              39. Korn S, Kerwin E, Atis S, Amos C, Owen R, Lassen C; INSIST study group. Indacaterol once-daily provides superior efficacy to salmeterol twice-daily in COPD: a 12-week study. Respir Med. 2011;105(5):719–726.
              40. Jones PW, Mahler DA, Gale R, Owen R, Kramer B. Profiling the effects of indacaterol on dyspnoea and health status in patients with COPD. Respir Med. 2011;105(6):892–899.
              41. Bernstein JA, Liu N, Knorr BA, et al. MK-0633, a potent 5-lipoxygenase inhibitor, in chronic obstructive pulmonary disease. Respir Med. 2011;105(3):392–401.
              42. Kilgore D, Najm W. Common respiratory diseases. Prim Care. 2010;37(2):297–324.
              43. An X, Zhang AL, Yang AW, et al. Oral ginseng formulae for stable chronic obstructive pulmonary disease: a systematic review. Respir Med. 2011;105(2):165–176.
              44. Blair KA, Evelo A. Risk factors for COPD: what do nurse practitioners know. J Am Acad Nurse Pract. In press.
              45. Dharmage SC, Erbas B, Jarvis D, et al. Do childhood respiratory infections continue to influence adult respiratory morbidity? Eur Respir J. 2009;33(2):237–244.
              46. Svanes C, Sunyer J, Plana E, et al. Early life origins of chronic obstructive pulmonary disease. Thorax. 2010;65(1):14–20.
                47. Kalhan R, Arynchyn A, Colangelo LA, Dransfield MT, Gerald LB, Smith LJ. Lung function in young adults predicts airflow obstruction 20 years later. Am J Med. 2010;123(5):468.e1–468.e7.
                48. Niewoehner DE. TORCH and UPLIFT: what has been learned from the COPD “mega-trials”? COPD. 2009;6(1):1–3.
                49. Kerstjens HA, Disse B, Schröder-Babo W, et al. Tiotropium improves lung function in patients with severe uncontrolled asthma: a randomized controlled trial. J Allergy Clin Immunol. 2011;128(2):308–314.

                clinical manifestations; COPD; pharmacologic update; spirometry

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