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Assessment and Management of Suspected Chronic Obstructive Pulmonary Disease in the Primary Care Setting
The Journal for Nurse Practitioners 15 (2019) 701e708
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The Journal for Nurse Practitioners journal homepage: www.npjournal.org
Continuing Education
Assessment and Management of Suspected Chronic Obstructive Pulmonary Disease in the Primary Care Setting Michael F. Potnek, DNP, AGPCNP-BC a b s t r a c t Keywords: chronic obstructive pulmonary disease diagnosis management primary care pulmonary function testing
Chronic obstructive pulmonary disease (COPD) is a chronic, progressive disease process characterized by dyspnea, chronic cough, and mucus production. Despite frequent referral of these patients, COPD does not require specialty management under most conditions. This article provides primary care providers with a concise review on the diagnosis and management of COPD in the primary care setting, including pulmonary function test interpretation and indications for when specialist referral is appropriate. © 2019 Elsevier Inc. All rights reserved.
This CE learning activity is designed to augment the knowledge, skills, and attitudes of nurse practitioners and assist in their assessment and treatment decisions related to chronic obstructive pulmonary disease in primary care settings. At the conclusion of this activity, the participant will be able to: A. Describe the pathophysiology of COPD B. Elaborate on the clinical presentation and testing used to diagnose COPD C. Evaluate the appropriate treatment for the patient with COPD The author, reviewers, editors, and nurse planners all report no financial relationships that would pose a conflict of interest. This activity has been awarded 1 Contact Hours of which 0.25 credit are in the area of Pharmacology. The activity is valid for CE credit until January 1, 2021. To receive CE credit, read the article and pass the CE test online at www.npjournal.org/cme/home for a $5 fee.
early diagnosis and successful management of this chronic progressive disease process.5 Primary care providers are in a unique position to affect change in the area of COPD. This includes primary prevention strategies (such as smoking cessation, and avoidance of environmental factors that can contribute to the development of COPD), evidence-based routine screening, early diagnosis, and evidence-based management and follow-up with specialist referral when appropriate. Unfortunately, the accuracy of COPD diagnosis in the primary care setting is suboptimal, with several studies showing misdiagnosis of COPD among patients.6-8 For example, in a 2010 multicenter crosssectional study, Izquierdo et al9 found that among all patients within the study who were being treated for COPD, only 13.9% met Global Initiative for Chronic Obstructive Lung Disease (GOLD) diagnostic criteria.9 The purpose of this article is to provide primary care providers with the knowledge necessary to prevent, identify early, and treat appropriately COPD among their patient population. By following these steps, both the trajectory of the disease, as well as the quality of life of those with COPD, can be impacted dramatically for the better.
Pathophysiology National prevalence estimates for chronic obstructive pulmonary disease (COPD) in the United States range from 12 million to 16 million people, with up to an additional 12 million individuals living with undiagnosed COPD.1,2 In 1999, 8.2 million Americans were diagnosed with COPD; this increased to approximately 15.9 million Americans by 2015.3,4 Morbidity aside, COPD is also the third leading cause of death in the United States (U.S.). The risk COPD poses to morbidity and mortality has led the Office of Disease Prevention and Health Promotion to dedicate several Healthy People 2020 objectives to this topic, bringing more attention to the https://doi.org/10.1016/j.nurpra.2019.08.016 1555-4155/© 2019 Elsevier Inc. All rights reserved.
COPD is a diagnosis used to categorize a collection of chronic respiratory disorders, primarily chronic bronchitis and emphysema, both of which impair airflow in either the lung parenchyma or airways. Although these 2 disorders can occur independent of one another, the majority of patients exhibit features of both conditions. Chronic bronchitis is characterized by hyperplasia and hypertrophy of goblet cells and mucus-producing glands that line the epithelium of the airway. Although mucus is not produced in the most distal airways, columnar secretory cells of the adjacent
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distal airways do secrete a modest amount of thinner mucus, which combines with mucus produced in the larger airways via ciliary transport.10 This results in an excess amount of airway mucus, which often has an increased viscosity. Decreased luminal diameter of the bronchioles also occurs in chronic bronchitis as a result of fibrosis and inflammation. These changes result in impaired airflow.11 Unlike the chronic bronchitis aspect of COPD, the effects of emphysema are at the alveolar level. Emphysema leads to the destruction of the alveolar walls and subsequent enlargement of the terminal air spaces, resulting in the loss of alveolar and capillary surface area, which leads to decreased gas exchange.11,12 Loss of elastic tissue during alveolar wall destruction diminishes elastic recoil of the lungs. Enlarged terminal air spaces and loss of elastic recoil cause resting hyperinflation of the lungs in patients with emphysema, resulting in diminished expiratory flow rates.12 COPD can be confused with asthma by patients and providers, and although there can be an overlap between the 2 conditions, they are separate and distinct diseases. Although COPD and asthma are both obstructive pulmonary diseases, for the purposes of this article, the primary difference between them is that COPD obstruction is the result of increased mucus within the airways along with a decreased luminal diameter caused by inflammation (chronic bronchitis) and enlargement and destruction of the alveoli impacting gas exchange (emphysema). The obstruction in asthma is caused primarily by bronchial smooth muscle constriction, airway hyperreactivity, and inflammation with antigen response (eosinophilia and influx of activated T cells) within the airway. The obstruction of asthma is more reversible, and patients with asthma have a more pronounced response to bronchodilation than those with COPD.13 Clinical Features COPD can present along a spectrum anywhere from asymptomatic to severe. COPD should be recognized as a possible diagnosis in any patient who presents with complaints of dyspnea (which is typically present only with exertion in early disease, eventually progressing to dyspnea at rest with disease progression), sputum production, chronic cough, and/or a history that is positive for exposure to COPD risk factors, such as cigarette smoke, industrial exposures, or air pollution.14 Other symptoms may include wheezing, chest tightness, frequent respiratory infections, and fatigue.11
Diagnosis Although COPD is diagnosed in part through careful medical history and physical examination that show the clinical features described earlier, pulmonary function testing (PFT) is required to make the diagnosis. Note that chest radiographs do not serve a purpose in the diagnosis of COPD. Their usefulness is limited to differentiating other pulmonary diseases when a COPD diagnosis is in question, as well as identifying simultaneous comorbidities in patients with COPD.14 Diagnosis of COPD by PFT is characterized by a postbronchodilator forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) of < 70%.14 There are many intricacies that exist on a PFT report, as well as evidence to support other conditions, including restrictive and mixed pulmonary disease; however, for the purpose of this article, the focus will be specifically on COPD, which is only 1 type of obstructive disease that can be diagnosed with PFT.15 Despite the necessity of PFT in the confirmation of a COPD diagnosis, it is widely underused in the primary care setting, with even fewer primary care providers feeling confident in their ability to accurately interpret the results. For this reason, a stepwise approach has been presented for use in the primary care setting to help guide providers through PFT interpretation (Table 1). Vignette To apply this process, let us assess a hypothetical patient whose pulmonary function report is seen in Figure 1. 1. Step 1: determine the postbronchodilator FEV1/FVC; we can see that this patient is obstructed with a postbronchodilator FEV1/ FVC of 60%. 2. Step 2: assess FEV1 and FVC postbronchodilator response; we can also see that this obstruction is not reversible with bronchodilation as evidenced by the less than 12% difference between pre- and postbronchodilation FEV1 (58% vs 59%). 3. Step 3: assess lung volumes; the patient’s total lung capacity is 4.92, which is 103% of the reference value of 4.77, indicating that she is hyperinflated. Her residual volume (RV)/total lung capacity (TLC) is also > 40% at 42%, telling us that she has mild air trapping. 4. Step 4: assess diffusing capacity; this patient’s diffusing capacity of the lung for carbon monoxide (DLCO) is currently 47 mL/mm Hg/min, which suggests that she is experiencing impaired gas exchange at this point.
Table 1 Stepwise Approach to Pulmonary Function Test (PFT) Interpretation Step 1: determine the postbronchodilator If this is < 70%, obstruction is present. FEV1/FVC If this measurement is greater than 70%, the patient does not have COPD. Step 2: assess FEV1 and FVC postbronchodilator response
A change 12% and 200 mL in FEV1 or FVC indicates reversibility in obstruction (consistent with an asthma diagnosis). Although there can be some degree of airway reactivity to bronchodilation in COPD, a value less than 12% and 200 mL indicates that the obstruction is not responsive to bronchodilation and supports a COPD diagnosis.
Step 3: assess lung volumes
If total lung capacity is greater than the normal reference provided by the laboratory report, hyperinflation is present. If residual volume/total lung capacity is > 40%, air trapping is present (indicative of emphysema).
Step 4: assess diffusing capacity
If diffusing capacity of the lung for carbon monoxide is < 70 mL/mm Hg/min, impaired gas exchange is present.
Step 5: assess FEV1 (degree of airflow limitation)
If the PFT report indicates COPD, we can classify the severity based on Global Initiative for Chronic Obstructive Lung Disease (GOLD) grade. GOLD 1, mild airflow limitation: FEV1 80% GOLD 2, moderate airflow limitation: FEV1 50% to <80% GOLD 3, severe airflow limitation: FEV1 30% to <50% GOLD 4, very severe airflow limitation: FEV1 <30%
COPD ¼ chronic obstructive pulmonary disease; FEV1 ¼ forced expiratory volume in 1 second; FVC ¼ forced vital capacity.
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COPD group (Figure 3). The patient who has had either 0 or 1 exacerbations in the last year, without hospitalization, will fall within 1 row of the COPD grading tool, whereas a patient who has experienced 2 or more moderate or severe exacerbations within the past year or 1 or more hospitalizations because of their COPD will fall within another row of the COPD grading tool.14 Patients with CAT scores less than 10 are in the first column, and those with scores equal to or greater than 10 are in the second column. The GOLD ABCD assessment tool can be used with the GOLD group pharmacologic treatment algorithms to determine the patient’s plan of care (Figure 4). Vignette
Figure 1. Pulmonary function report.
5. Step 5: FEV1 (degree of airflow limitation); based on this patient’s postbronchodilation FEV1 of 59%, she would be classified as having moderate COPD (GOLD 2) per GOLD grade guidelines.
Assessment Although PFT is necessary for COPD diagnosis and provides the practitioner with an objective measure of the severity of the patient’s level of airflow impairment, the assessment of symptoms and exacerbation history is critical to determine the patient’s COPD severity of symptom group, which is required to guide treatment.14 The original assessment scale used to quantify COPD symptom severity was the Modified British Medical Research Council Questionnaire. The provider would read 5 statements related to dyspnea to the patient, with the severity group being assigned based on the patient’s responses.16 Although this tool is still used today and is attractive to many providers because of its simplicity and the speed with which it can be administered, the COPD Assessment Test (CAT; GlaxoSmithKline [GSK], Brentford, UK) has since emerged and is now the recommended symptom severity scale in the GOLD guidelines. The CAT assessment considers symptoms other than severity of dyspnea alone, making it a more useful tool for comprehensive assessment of symptoms and a more accurate COPD group assignment (Figure 2). The CAT assessment asks the patient to rate 8 questions on a scale of 0 to 5, with his or her CAT score being the sum of each of the values. A score greater than or equal to 10 indicates the presence of significant symptoms.17 The final assessment needed to determine the patient’s COPD group is his or her exacerbation history. This history includes how many moderate (requiring a short-acting beta-agonist plus antibiotics and/or oral corticosteroids) or severe (requiring hospitalization or emergency department visit) exacerbations the patient experienced in the past year, as well as whether any exacerbations led to hospitalization (ie, severe exacerbations). Exacerbation history and symptom severity (score on CAT) is applied to the GOLD ABCD assessment tool to identify the patient’s
To help illustrate this concept of grading a patient’s COPD, let’s examine the patient featured earlier in the PFT report. She has already been given a diagnosis of COPD based on her postbronchodilator FEV1/FVC of 60%. It has also been established that her airflow limitation grade is GOLD 2 based on her FEV1 of 59%. We can now determine her COPD GOLD group based on our assessment. While conducting the symptom assessment with the CAT tool, the patient rated the questions on the form starting from the top as follows: 2-2-2-4-1-2-2-3, with a total CAT score of 18. She had 1 exacerbation in the last year that was treated with an inhaler and an oral corticosteroid, and after a few days of rest, she felt much better. With this information, we can look at the ABCD assessment tool in Figure 3 and see that this patient falls within the group B box; thus, this patient can be labeled GOLD grade 2, group B. Management It is important to recognize that once a patient has formally been diagnosed with COPD, the goal of the primary care provider and patient becomes twofold: reduce risk and reduce symptoms. Risk reduction includes slowing and/or preventing progression of the disease, preventing exacerbations and effectively treating them when they do occur, and reducing mortality from COPD. Symptom reduction includes providing relief from COPD symptoms, enhancing the patient’s activity and exercise tolerance, and optimizing their overall health status.14 It is well established in the literature that tobacco abuse, particularly cigarette smoking, is the most significant cause of chronic bronchitis and is also responsible for the majority of cases of emphysema.11 For this reason, the most crucial intervention for any COPD patient who is still smoking is to achieve complete cessation. Not only is smoking cessation a key preventive measure for COPD, but also patients who are able to quit smoking even after COPD diagnosis have been shown to experience a slower progression of the disease process. 2 Another intervention suggested for all patients with COPD, regardless of COPD group, is to maintain an active lifestyle and engage in physical activities including pulmonary rehabilitation, which has been shown to improve exercise tolerance, dyspnea, and overall health status.14 Pulmonary rehabilitation consists of strength, exercise and endurance training, breathing, and ventilatory muscle training, as well as health promotion counseling and psychological support. The ideal candidate for pulmonary rehabilitation is the COPD patient who is stable but still experiencing dyspnea and as a result has a limited exercise tolerance despite being on optimized pharmacologic treatment.18 It is also recommended that all individuals with COPD be vaccinated annually for influenza, as well as receive the 13valent conjugated pneumococcal vaccine and the 23-valent pneumococcal polysaccharide vaccine per Centers for Disease Control and Prevention guidelines.14 Influenza vaccination
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Figure 2. The COPD Assessment Test (CAT).
has been shown to reduce the risk of serious illness in those with COPD, including respiratory infection leading to hospitalization,19 whereas the 13-valent conjugated pneumococcal vaccine and 23-valent pneumococcal polysaccharide vaccine have shown efficacy in reducing the incidence of communityacquired pneumonia, bacteremia, and invasive pneumococcal disease among COPD patients.14 Regardless of smoking and vaccination status, pharmacologic management of COPD is the rule of treatment rather than the exception. Pharmacologic treatment selection is based on the GOLD group (A, B, C, or D), with the drug classes consisting of short-acting beta-2 agonists (SABA) (eg, albuterol), longacting beta-2 agonists (LABAs [eg, salmeterol and formoterol]), short-acting muscarinic antagonists (SAMA)/anticholinergics (eg, ipratropium), long-acting muscarinic antagonists/anticholinergics (LAMAs [eg, tiotropium and umeclidinium]), inhaled
corticosteroids (ICS) (eg, fluticasone and budesonide), N-acetylcysteine, phosphodiesterase-4 inhibitors (eg, roflumilast), maintenance oral antibiotics (azithromycin), and oral corticosteroids. Combination medications such as DuoNeb (Mylan Specialty L.P., Canonsburg, PA) (albuterol and ipratropium), Anoro Ellipta (GSK) (umeclidinium and vilanterol), and Symbicort (AstraZeneca, Cambridge, UK) (budesonide and formoterol) are also available.14 See Table 2 for a list of COPD drug classes and names. The patient’s group category is used with the GOLD group pharmacologic treatment algorithms to determine which medication regimen is initiated (Figure 4). New to the 2019 GOLD guidelines is the use of blood eosinophil counts to guide treatment. Eosinophil counts may predict the efficacy of inhaled corticosteroid use in a patient with COPD. Both treatment algorithms (Figures 4 and 5) make use of eosinophil counts to help guide treatment.14
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Let us now return to our patient scenario to select an appropriate therapy. We stated earlier that based on the patient’s exacerbation history and CAT score, she was a patient with COPD group B. If we look at the group B box algorithm in Figure 4, we can see that a long-acting bronchodilator is indicated. With regard to which drug class (LABA or LAMA) would be most appropriate, this is based largely on patient preference because either class is supported by the literature. It may be appealing to choose an LAMA because this class offers several once-per-day administration options, and LAMAs have been shown to do a slightly better job at preventing exacerbations than LABAs. The GOLD guidelines also include an algorithm for follow-up pharmacologic treatment (Figure 5). If a patient’s response to treatment is not favorable, providers can use the algorithm to adjust treatment based on if the patient is experiencing increased dyspnea, exacerbations, or both. Returning to our patient example, if she were to start experiencing increased dyspnea despite an optimal dose of an LAMA, we could escalate treatment to a LAMA/ LABA combination.14 Oxygen Therapy
Figure 3. GOLD ABCD assessment tool.
It is well established that oxygen therapy improves survival among patients with chronic severe hypoxemia. Long-term (> 15 h/d) oxygen therapy is indicated for COPD patients who have
Figure 4. GOLD group initial pharmacologic treatment algorithm.
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Table 2 Chronic Obstructive Pulmonary Disease Drug Classes and Names13,21 Drug Class
Generic Medications (Brand)
Usual Route and Frequency
Short-acting beta-2 agonists (SABAs) Albuterol (ProAir HFA, RespiClick [Teva Pharmaceuticals, North Wales, PA]; Proventil HFA [Merck & Co, Whitehouse Station, NJ]; Ventolin HFA [GlaxoSmithKline, Research Triangle Park, NC]) Levalbuterol (Xopenex HFA [Sunovion, Marlborough, MA], neb [Akorn, Buffalo Grove, IL]) Long-acting beta-2 agonists (LABAs) Arformoterol (Brovana neb [Sunovion]) Formoterol (Perforomist neb [Mylan Specialty, Basking Ridge, NJ]) Indacaterol (Arcapta Neohaler [Sunovion]) Olodaterol (Striverdi Respimat [Boehringer Ingelheim Pharmaceuticals, Ridgefield, CT]) Salmeterol (Serevent Diskus [GlaxoSmithKline]) Short-acting muscarinic antagonists/anticholinergic (SAMAs) Ipratropium (Atrovent HFA [Boehringer Ingelheim Pharmaceuticals], neb) Long-acting muscarinic antagonists/anticholinergic (LAMAs) Aclidinium (Tudorza Pressair [AstraZeneca Pharmaceuticals, Wilmington, DE]) Glycopyrrolate (Seebri Neohaler [Sunovion], Lonhala Magnair [Sunovion]) Revefenacin (Yupelri [Mylan Inc, Morgantown, WV])a Tiotropium (Spiriva HandiHaler, Respimat [Boehringer Ingelheim Pharmaceuticals]) Umeclidinium (Incruse Ellipta [GlaxoSmithKline]) Inhaled corticosteroids (ICS)b Beclomethasone (Qvar RediHaler [Teva Pharmaceuticals]) Budesonide (Pulmicort Flexhaler, neb, Respulesa [AstraZeneca Pharmaceuticals]) Fluticasone (ArmonAir RespiClick [Teva Pharmaceuticals]; Flovent Diskus, HFA [GlaxoSmithKline]) Combination medications SABA/SAMA Albuterol/ipratropium (Combivent Respimat [Boehringer Ingelheim Pharmaceuticals]; Duoneb [Mylan Inc] neb) LABA/LAMA Formoterol/glycopyrrolate (Bevespi Aerosphere [AstraZeneca Pharmaceuticals]) Indacaterol/glycopyrrolate (Utibron Neohaler [Sunovion]) Olodaterol/tiotropium (Stiolto Respimat [Boehringer Ingelheim Pharmaceuticals]) Vilanterol/umeclidinium (Anoro Ellipta [GlaxoSmithKline]) LABA/ICS Formoterol/budesonide (Symbicort [AstraZeneca Pharmaceuticals]) Formoterol/mometasone (Dulera [Merck & Co, Whitehouse Station, NJ])c Salmeterol/fluticasone (Advair Diskus, HFAb [GlaxoSmithKline]; Wixela Inhubc [Mylan Inc]) Vilanterol/fluticasone (Breo Ellipta [GlaxoSmithKline]) ICS/LAMA/LABA Fluticasone/umeclidinium/vilanterol (Trelegy Ellipta [GlaxoSmithKline]) Phosphodiesterase-4 inhibitor Roflumilast (Daliresp [AstraZeneca Pharmaceuticals]) Mucolytic N-acetylcysteine Corticosteroids Methylprednisolone (Medrol [Pfizer Inc, New York, NY]) Prednisolone Prednisone Macrolides Azithromycind
2 puffs every 4-6 h PRN
2 puffs every 4-6 h PRN or 1 neb vial TID
1 1 1 2
neb vial BID neb vial BID capsule inhaled daily puffs BID
1 puff BID 2 puffs QID or 1 neb vial every 6-8 h 1 puff BID 1 capsule inhaled BID or 1 neb vial BID daily nebulizer 1 capsule inhaled daily or 2 puffs daily 1 puff daily 50-400 mg daily, in divided doses BID 1 puff BID or 1 neb vial BID 50-500 mg daily in divided doses BID
1 puff QID or 1 neb vial every 6 h 2 puffs BID 1 capsule inhaled BID 2 puffs daily 1 2 1 1
puff daily puffs BID puff BID puff BID
1 puff daily 1 puff daily 250 mg PO daily x 4 weeks, then 500 mg PO daily Via nebulizer TID to QID 32 mg PO daily for 5-7 days 40 mg PO daily for 5-7 days 40 mg PO daily for 5-7 days 250 mg PO QOD, 250-500 mg PO 3 times per week, or 250 mg PO daily
BID ¼ 2 times a day; neb ¼ nebulizer; PO ¼ by mouth; QID ¼ 4 times a day; TID ¼ 3 times a day. a Approved but not yet available at the time of publication. b Not used as monotherapy. c Off-label. d Prevention of exacerbations.
shown oxygen saturation of 88% or less on 2 occasions over a 3week period. Patients receiving long-term oxygen therapy should be reevaluated every 2 to 3 months via oxygen saturation while breathing with oxygen and then on room air to assess the appropriateness of the prescribed oxygen flow, as well as the continued need for supplemental oxygen. Oxygen therapy should not be routinely prescribed for the patient with COPD who does not meet arterial hypoxemia criteria (partial pressure of oxygen in the alveoli < 55 mm Hg or oxygen saturation < 88%) because the use of oxygen in this population does not confer any improvement in dyspnea symptoms, quality of life, or functional status.14
Referral Although most cases of COPD can be managed in the primary care setting, there are instances in which referral to a specialist is warranted. While the 2019 GOLD guidelines do not address this topic, the Canadian Thoracic Society provides suggestions for primary care providers regarding when to refer. The society’s recommendations for management of chronic obstructive pulmonary disease (2008) provide 7 situations in which specialist referral would be the prudent course of action. These situations include patients who present with COPD symptoms disproportionate to the degree of obstruction measured by PFT, patients
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Figure 5. GOLD group follow-up pharmacologic treatment algorithm.
who are suspect for alpha-1 antitrypsin deficiency, patients who experience a sudden and rapid decline in their pulmonary function, patients who present with symptom onset at a young age ( 45 years old), those who experience either recurrent or severe exacerbations, and any patients who fail to respond to treatment initiated in the primary care setting.19 Conclusion Although COPD is a complex and life-altering chronic disease process, it is a disease that can and should be diagnosed and managed in the primary care setting, at least initially. Primary care providers have the opportunity to vigilantly screen for tobacco abuse, discourage the start of tobacco use, and promote cessation for those who do use tobacco. Primary care providers are also well positioned to identify patients with COPD early in the disease process, allowing for prompt initiation of appropriate management, thus decreasing the future burden of the disease by slowing its progression.20
References 1. National Institutes of Health. Fact sheet: chronic obstructive pulmonary disease (COPD). Department of Health and Human Services. https://report.nih. govnihfactsheets/ViewFactSheet.aspx?csid¼77. October 2010. Accessed October 16, 2018. 2. Wheaton A, Cunningham T, Ford E, Croft J. Employment and activity limitations among adults with chronic obstructive pulmonary disease e United States, 2013. MMWR Morb Mortal Wkly Rep. 2015;64(11):289-295. https:// www.cdc.gov/mmwr/pdf/wk/mm6411.pdf. March 27, 2015. Accessed October 16, 2018. 3. Sullivan J, Pravosud V, Mannino DM, Siegel K, Choate R, Sullivan T. National and state estimates of COPD morbidity and mortality - United States, 20142015. Chronic Obstr Pulm Dis. 2018;5(4):324-333. https://doi.org/10.15326/ jcopdf.5.4.2018.0157. 4. Ford E, Croft J, Mannino D, Wheaton A, Zhang X, Giles W. COPD surveillance– United States, 1999-2011. Chest. 2013;144(1):284-305. 5. HealthyPeople 2020. Chronic obstructive pulmonary disease. Department of Health and Human Services. https://www.healthypeople.gov/node/3503/ objectives#5166. November 20, 2018. Accessed October 14, 2018. 6. Ghattas C, Gemmel DJ, Awad MH. Overdiagnosis of chronic obstructive pulmonary disease in an underserved patient population. Int J Chron Obstruct Pulmon Dis. 2013;8:545-549. https://doi.org/10.2147/COPD.S45693. 7. Jain V, Allison D, Andrews S, Mejia J, Mills P, Peterson M. Misdiagnosis among frequent exacerbators of clinically diagnosed asthma and COPD in absence of
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M.F. Potnek / The Journal for Nurse Practitioners 15 (2019) 701e708 confirmation of airflow obstruction. Lung. 2015;193(4):505-512. https:// doi.org/10.1007/s00408-015-9734-6. s M, Jae n J, Almagro P, et al. Prevalence, risk factors and diagnostic acLlorde curacy of COPD among smokers in primary care. COPD. 2015;12(4):404-412. https://doi.org/10.3109/15412555.2014.974736. Izquierdo J, Martin A, Rodriguez-Gonzalez-Moro J, Almonacid C, Paravisini A. Misdiagnosis of patients receiving inhaled therapies in primary care. Int J Chron Obstruct Pulmon Dis. 2010;5:241-249. https://www.ncbi.nlm.nih.gov/ pmc/articles/PMC2921692/pdf/copd-5-241.pdf. August 9, 2010. Accessed November 3, 2018. Fahy JV, Dickey BF. Airway mucus function and dysfunction. N Engl J Med. 2010;363(23):2233-2247. https://doi.org/10.1056/NEJMra0910061. Weinberger S, Cockrill B, Mandel J. Chronic obstructive pulmonary disease. In: Principles of Pulmonary Medicine. 7th ed. Philadelphia, PA: Elsevier; 2019:93. O’Donnell DE, Laveneziana P. Physiology and consequences of lung hyperinflation in COPD. Eur Respir Rev. 2006;15(100):61-67. https://doi.org/10.1183/ 09059180.00010002. Barnes P. Similarities and differences in inflammatory mechanisms of asthma and COPD. Breathe. 2011;7(3):229-238. https://doi.org/10.1183/20734735.026410. Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management and prevention of chronic obstructive pulmonary disease: 2019 report. Global Initiative for Chronic Obstructive Lung Disease, Inc. 2018. https://goldcopd.org/wp-content/uploads/2017/11/GOLD-2018-v6. 0-FINAL-revised-20-Nov_WMS.pdf. Accessed December 17, 2018. Pellegrino R, Viegi G, Brusasco V, et al. Interpretive strategies for lung function tests. Eur Respir J. 2005;26(5):948-963. https://doi.org/10.1183/ 09031936.05.00035205. Fletcher CM. Standardised questionnaires on respiratory symptoms: a statement prepared and approved by the MRC committee on the etiology of chronic bronchitis (MRC breathlessness score). BMJ. 1960;2:1662. https://
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Michael F. Potnek, DNP, AGPCNP-BC, is a primary care nurse practitioner at Outreach Community Health Centers and adjunct faculty member at Marquette University College of Nursing in Milwaukee, WI, and can be contacted at Michael.potnek@marquette. edu. In compliance with national ethical guidelines, the author reports no relationships with business or industry that would pose a conflict of interest.
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The Journal for Nurse Practitioners journal homepage: www.npjournal.org
Continuing Education
Assessment and Management of Suspected Chronic Obstructive Pulmonary Disease in the Primary Care Setting Michael F. Potnek, DNP, AGPCNP-BC a b s t r a c t Keywords: chronic obstructive pulmonary disease diagnosis management primary care pulmonary function testing
Chronic obstructive pulmonary disease (COPD) is a chronic, progressive disease process characterized by dyspnea, chronic cough, and mucus production. Despite frequent referral of these patients, COPD does not require specialty management under most conditions. This article provides primary care providers with a concise review on the diagnosis and management of COPD in the primary care setting, including pulmonary function test interpretation and indications for when specialist referral is appropriate. © 2019 Elsevier Inc. All rights reserved.
This CE learning activity is designed to augment the knowledge, skills, and attitudes of nurse practitioners and assist in their assessment and treatment decisions related to chronic obstructive pulmonary disease in primary care settings. At the conclusion of this activity, the participant will be able to: A. Describe the pathophysiology of COPD B. Elaborate on the clinical presentation and testing used to diagnose COPD C. Evaluate the appropriate treatment for the patient with COPD The author, reviewers, editors, and nurse planners all report no financial relationships that would pose a conflict of interest. This activity has been awarded 1 Contact Hours of which 0.25 credit are in the area of Pharmacology. The activity is valid for CE credit until January 1, 2021. To receive CE credit, read the article and pass the CE test online at www.npjournal.org/cme/home for a $5 fee.
early diagnosis and successful management of this chronic progressive disease process.5 Primary care providers are in a unique position to affect change in the area of COPD. This includes primary prevention strategies (such as smoking cessation, and avoidance of environmental factors that can contribute to the development of COPD), evidence-based routine screening, early diagnosis, and evidence-based management and follow-up with specialist referral when appropriate. Unfortunately, the accuracy of COPD diagnosis in the primary care setting is suboptimal, with several studies showing misdiagnosis of COPD among patients.6-8 For example, in a 2010 multicenter crosssectional study, Izquierdo et al9 found that among all patients within the study who were being treated for COPD, only 13.9% met Global Initiative for Chronic Obstructive Lung Disease (GOLD) diagnostic criteria.9 The purpose of this article is to provide primary care providers with the knowledge necessary to prevent, identify early, and treat appropriately COPD among their patient population. By following these steps, both the trajectory of the disease, as well as the quality of life of those with COPD, can be impacted dramatically for the better.
Pathophysiology National prevalence estimates for chronic obstructive pulmonary disease (COPD) in the United States range from 12 million to 16 million people, with up to an additional 12 million individuals living with undiagnosed COPD.1,2 In 1999, 8.2 million Americans were diagnosed with COPD; this increased to approximately 15.9 million Americans by 2015.3,4 Morbidity aside, COPD is also the third leading cause of death in the United States (U.S.). The risk COPD poses to morbidity and mortality has led the Office of Disease Prevention and Health Promotion to dedicate several Healthy People 2020 objectives to this topic, bringing more attention to the https://doi.org/10.1016/j.nurpra.2019.08.016 1555-4155/© 2019 Elsevier Inc. All rights reserved.
COPD is a diagnosis used to categorize a collection of chronic respiratory disorders, primarily chronic bronchitis and emphysema, both of which impair airflow in either the lung parenchyma or airways. Although these 2 disorders can occur independent of one another, the majority of patients exhibit features of both conditions. Chronic bronchitis is characterized by hyperplasia and hypertrophy of goblet cells and mucus-producing glands that line the epithelium of the airway. Although mucus is not produced in the most distal airways, columnar secretory cells of the adjacent
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distal airways do secrete a modest amount of thinner mucus, which combines with mucus produced in the larger airways via ciliary transport.10 This results in an excess amount of airway mucus, which often has an increased viscosity. Decreased luminal diameter of the bronchioles also occurs in chronic bronchitis as a result of fibrosis and inflammation. These changes result in impaired airflow.11 Unlike the chronic bronchitis aspect of COPD, the effects of emphysema are at the alveolar level. Emphysema leads to the destruction of the alveolar walls and subsequent enlargement of the terminal air spaces, resulting in the loss of alveolar and capillary surface area, which leads to decreased gas exchange.11,12 Loss of elastic tissue during alveolar wall destruction diminishes elastic recoil of the lungs. Enlarged terminal air spaces and loss of elastic recoil cause resting hyperinflation of the lungs in patients with emphysema, resulting in diminished expiratory flow rates.12 COPD can be confused with asthma by patients and providers, and although there can be an overlap between the 2 conditions, they are separate and distinct diseases. Although COPD and asthma are both obstructive pulmonary diseases, for the purposes of this article, the primary difference between them is that COPD obstruction is the result of increased mucus within the airways along with a decreased luminal diameter caused by inflammation (chronic bronchitis) and enlargement and destruction of the alveoli impacting gas exchange (emphysema). The obstruction in asthma is caused primarily by bronchial smooth muscle constriction, airway hyperreactivity, and inflammation with antigen response (eosinophilia and influx of activated T cells) within the airway. The obstruction of asthma is more reversible, and patients with asthma have a more pronounced response to bronchodilation than those with COPD.13 Clinical Features COPD can present along a spectrum anywhere from asymptomatic to severe. COPD should be recognized as a possible diagnosis in any patient who presents with complaints of dyspnea (which is typically present only with exertion in early disease, eventually progressing to dyspnea at rest with disease progression), sputum production, chronic cough, and/or a history that is positive for exposure to COPD risk factors, such as cigarette smoke, industrial exposures, or air pollution.14 Other symptoms may include wheezing, chest tightness, frequent respiratory infections, and fatigue.11
Diagnosis Although COPD is diagnosed in part through careful medical history and physical examination that show the clinical features described earlier, pulmonary function testing (PFT) is required to make the diagnosis. Note that chest radiographs do not serve a purpose in the diagnosis of COPD. Their usefulness is limited to differentiating other pulmonary diseases when a COPD diagnosis is in question, as well as identifying simultaneous comorbidities in patients with COPD.14 Diagnosis of COPD by PFT is characterized by a postbronchodilator forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) of < 70%.14 There are many intricacies that exist on a PFT report, as well as evidence to support other conditions, including restrictive and mixed pulmonary disease; however, for the purpose of this article, the focus will be specifically on COPD, which is only 1 type of obstructive disease that can be diagnosed with PFT.15 Despite the necessity of PFT in the confirmation of a COPD diagnosis, it is widely underused in the primary care setting, with even fewer primary care providers feeling confident in their ability to accurately interpret the results. For this reason, a stepwise approach has been presented for use in the primary care setting to help guide providers through PFT interpretation (Table 1). Vignette To apply this process, let us assess a hypothetical patient whose pulmonary function report is seen in Figure 1. 1. Step 1: determine the postbronchodilator FEV1/FVC; we can see that this patient is obstructed with a postbronchodilator FEV1/ FVC of 60%. 2. Step 2: assess FEV1 and FVC postbronchodilator response; we can also see that this obstruction is not reversible with bronchodilation as evidenced by the less than 12% difference between pre- and postbronchodilation FEV1 (58% vs 59%). 3. Step 3: assess lung volumes; the patient’s total lung capacity is 4.92, which is 103% of the reference value of 4.77, indicating that she is hyperinflated. Her residual volume (RV)/total lung capacity (TLC) is also > 40% at 42%, telling us that she has mild air trapping. 4. Step 4: assess diffusing capacity; this patient’s diffusing capacity of the lung for carbon monoxide (DLCO) is currently 47 mL/mm Hg/min, which suggests that she is experiencing impaired gas exchange at this point.
Table 1 Stepwise Approach to Pulmonary Function Test (PFT) Interpretation Step 1: determine the postbronchodilator If this is < 70%, obstruction is present. FEV1/FVC If this measurement is greater than 70%, the patient does not have COPD. Step 2: assess FEV1 and FVC postbronchodilator response
A change 12% and 200 mL in FEV1 or FVC indicates reversibility in obstruction (consistent with an asthma diagnosis). Although there can be some degree of airway reactivity to bronchodilation in COPD, a value less than 12% and 200 mL indicates that the obstruction is not responsive to bronchodilation and supports a COPD diagnosis.
Step 3: assess lung volumes
If total lung capacity is greater than the normal reference provided by the laboratory report, hyperinflation is present. If residual volume/total lung capacity is > 40%, air trapping is present (indicative of emphysema).
Step 4: assess diffusing capacity
If diffusing capacity of the lung for carbon monoxide is < 70 mL/mm Hg/min, impaired gas exchange is present.
Step 5: assess FEV1 (degree of airflow limitation)
If the PFT report indicates COPD, we can classify the severity based on Global Initiative for Chronic Obstructive Lung Disease (GOLD) grade. GOLD 1, mild airflow limitation: FEV1 80% GOLD 2, moderate airflow limitation: FEV1 50% to <80% GOLD 3, severe airflow limitation: FEV1 30% to <50% GOLD 4, very severe airflow limitation: FEV1 <30%
COPD ¼ chronic obstructive pulmonary disease; FEV1 ¼ forced expiratory volume in 1 second; FVC ¼ forced vital capacity.
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COPD group (Figure 3). The patient who has had either 0 or 1 exacerbations in the last year, without hospitalization, will fall within 1 row of the COPD grading tool, whereas a patient who has experienced 2 or more moderate or severe exacerbations within the past year or 1 or more hospitalizations because of their COPD will fall within another row of the COPD grading tool.14 Patients with CAT scores less than 10 are in the first column, and those with scores equal to or greater than 10 are in the second column. The GOLD ABCD assessment tool can be used with the GOLD group pharmacologic treatment algorithms to determine the patient’s plan of care (Figure 4). Vignette
Figure 1. Pulmonary function report.
5. Step 5: FEV1 (degree of airflow limitation); based on this patient’s postbronchodilation FEV1 of 59%, she would be classified as having moderate COPD (GOLD 2) per GOLD grade guidelines.
Assessment Although PFT is necessary for COPD diagnosis and provides the practitioner with an objective measure of the severity of the patient’s level of airflow impairment, the assessment of symptoms and exacerbation history is critical to determine the patient’s COPD severity of symptom group, which is required to guide treatment.14 The original assessment scale used to quantify COPD symptom severity was the Modified British Medical Research Council Questionnaire. The provider would read 5 statements related to dyspnea to the patient, with the severity group being assigned based on the patient’s responses.16 Although this tool is still used today and is attractive to many providers because of its simplicity and the speed with which it can be administered, the COPD Assessment Test (CAT; GlaxoSmithKline [GSK], Brentford, UK) has since emerged and is now the recommended symptom severity scale in the GOLD guidelines. The CAT assessment considers symptoms other than severity of dyspnea alone, making it a more useful tool for comprehensive assessment of symptoms and a more accurate COPD group assignment (Figure 2). The CAT assessment asks the patient to rate 8 questions on a scale of 0 to 5, with his or her CAT score being the sum of each of the values. A score greater than or equal to 10 indicates the presence of significant symptoms.17 The final assessment needed to determine the patient’s COPD group is his or her exacerbation history. This history includes how many moderate (requiring a short-acting beta-agonist plus antibiotics and/or oral corticosteroids) or severe (requiring hospitalization or emergency department visit) exacerbations the patient experienced in the past year, as well as whether any exacerbations led to hospitalization (ie, severe exacerbations). Exacerbation history and symptom severity (score on CAT) is applied to the GOLD ABCD assessment tool to identify the patient’s
To help illustrate this concept of grading a patient’s COPD, let’s examine the patient featured earlier in the PFT report. She has already been given a diagnosis of COPD based on her postbronchodilator FEV1/FVC of 60%. It has also been established that her airflow limitation grade is GOLD 2 based on her FEV1 of 59%. We can now determine her COPD GOLD group based on our assessment. While conducting the symptom assessment with the CAT tool, the patient rated the questions on the form starting from the top as follows: 2-2-2-4-1-2-2-3, with a total CAT score of 18. She had 1 exacerbation in the last year that was treated with an inhaler and an oral corticosteroid, and after a few days of rest, she felt much better. With this information, we can look at the ABCD assessment tool in Figure 3 and see that this patient falls within the group B box; thus, this patient can be labeled GOLD grade 2, group B. Management It is important to recognize that once a patient has formally been diagnosed with COPD, the goal of the primary care provider and patient becomes twofold: reduce risk and reduce symptoms. Risk reduction includes slowing and/or preventing progression of the disease, preventing exacerbations and effectively treating them when they do occur, and reducing mortality from COPD. Symptom reduction includes providing relief from COPD symptoms, enhancing the patient’s activity and exercise tolerance, and optimizing their overall health status.14 It is well established in the literature that tobacco abuse, particularly cigarette smoking, is the most significant cause of chronic bronchitis and is also responsible for the majority of cases of emphysema.11 For this reason, the most crucial intervention for any COPD patient who is still smoking is to achieve complete cessation. Not only is smoking cessation a key preventive measure for COPD, but also patients who are able to quit smoking even after COPD diagnosis have been shown to experience a slower progression of the disease process. 2 Another intervention suggested for all patients with COPD, regardless of COPD group, is to maintain an active lifestyle and engage in physical activities including pulmonary rehabilitation, which has been shown to improve exercise tolerance, dyspnea, and overall health status.14 Pulmonary rehabilitation consists of strength, exercise and endurance training, breathing, and ventilatory muscle training, as well as health promotion counseling and psychological support. The ideal candidate for pulmonary rehabilitation is the COPD patient who is stable but still experiencing dyspnea and as a result has a limited exercise tolerance despite being on optimized pharmacologic treatment.18 It is also recommended that all individuals with COPD be vaccinated annually for influenza, as well as receive the 13valent conjugated pneumococcal vaccine and the 23-valent pneumococcal polysaccharide vaccine per Centers for Disease Control and Prevention guidelines.14 Influenza vaccination
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Figure 2. The COPD Assessment Test (CAT).
has been shown to reduce the risk of serious illness in those with COPD, including respiratory infection leading to hospitalization,19 whereas the 13-valent conjugated pneumococcal vaccine and 23-valent pneumococcal polysaccharide vaccine have shown efficacy in reducing the incidence of communityacquired pneumonia, bacteremia, and invasive pneumococcal disease among COPD patients.14 Regardless of smoking and vaccination status, pharmacologic management of COPD is the rule of treatment rather than the exception. Pharmacologic treatment selection is based on the GOLD group (A, B, C, or D), with the drug classes consisting of short-acting beta-2 agonists (SABA) (eg, albuterol), longacting beta-2 agonists (LABAs [eg, salmeterol and formoterol]), short-acting muscarinic antagonists (SAMA)/anticholinergics (eg, ipratropium), long-acting muscarinic antagonists/anticholinergics (LAMAs [eg, tiotropium and umeclidinium]), inhaled
corticosteroids (ICS) (eg, fluticasone and budesonide), N-acetylcysteine, phosphodiesterase-4 inhibitors (eg, roflumilast), maintenance oral antibiotics (azithromycin), and oral corticosteroids. Combination medications such as DuoNeb (Mylan Specialty L.P., Canonsburg, PA) (albuterol and ipratropium), Anoro Ellipta (GSK) (umeclidinium and vilanterol), and Symbicort (AstraZeneca, Cambridge, UK) (budesonide and formoterol) are also available.14 See Table 2 for a list of COPD drug classes and names. The patient’s group category is used with the GOLD group pharmacologic treatment algorithms to determine which medication regimen is initiated (Figure 4). New to the 2019 GOLD guidelines is the use of blood eosinophil counts to guide treatment. Eosinophil counts may predict the efficacy of inhaled corticosteroid use in a patient with COPD. Both treatment algorithms (Figures 4 and 5) make use of eosinophil counts to help guide treatment.14
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Let us now return to our patient scenario to select an appropriate therapy. We stated earlier that based on the patient’s exacerbation history and CAT score, she was a patient with COPD group B. If we look at the group B box algorithm in Figure 4, we can see that a long-acting bronchodilator is indicated. With regard to which drug class (LABA or LAMA) would be most appropriate, this is based largely on patient preference because either class is supported by the literature. It may be appealing to choose an LAMA because this class offers several once-per-day administration options, and LAMAs have been shown to do a slightly better job at preventing exacerbations than LABAs. The GOLD guidelines also include an algorithm for follow-up pharmacologic treatment (Figure 5). If a patient’s response to treatment is not favorable, providers can use the algorithm to adjust treatment based on if the patient is experiencing increased dyspnea, exacerbations, or both. Returning to our patient example, if she were to start experiencing increased dyspnea despite an optimal dose of an LAMA, we could escalate treatment to a LAMA/ LABA combination.14 Oxygen Therapy
Figure 3. GOLD ABCD assessment tool.
It is well established that oxygen therapy improves survival among patients with chronic severe hypoxemia. Long-term (> 15 h/d) oxygen therapy is indicated for COPD patients who have
Figure 4. GOLD group initial pharmacologic treatment algorithm.
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Table 2 Chronic Obstructive Pulmonary Disease Drug Classes and Names13,21 Drug Class
Generic Medications (Brand)
Usual Route and Frequency
Short-acting beta-2 agonists (SABAs) Albuterol (ProAir HFA, RespiClick [Teva Pharmaceuticals, North Wales, PA]; Proventil HFA [Merck & Co, Whitehouse Station, NJ]; Ventolin HFA [GlaxoSmithKline, Research Triangle Park, NC]) Levalbuterol (Xopenex HFA [Sunovion, Marlborough, MA], neb [Akorn, Buffalo Grove, IL]) Long-acting beta-2 agonists (LABAs) Arformoterol (Brovana neb [Sunovion]) Formoterol (Perforomist neb [Mylan Specialty, Basking Ridge, NJ]) Indacaterol (Arcapta Neohaler [Sunovion]) Olodaterol (Striverdi Respimat [Boehringer Ingelheim Pharmaceuticals, Ridgefield, CT]) Salmeterol (Serevent Diskus [GlaxoSmithKline]) Short-acting muscarinic antagonists/anticholinergic (SAMAs) Ipratropium (Atrovent HFA [Boehringer Ingelheim Pharmaceuticals], neb) Long-acting muscarinic antagonists/anticholinergic (LAMAs) Aclidinium (Tudorza Pressair [AstraZeneca Pharmaceuticals, Wilmington, DE]) Glycopyrrolate (Seebri Neohaler [Sunovion], Lonhala Magnair [Sunovion]) Revefenacin (Yupelri [Mylan Inc, Morgantown, WV])a Tiotropium (Spiriva HandiHaler, Respimat [Boehringer Ingelheim Pharmaceuticals]) Umeclidinium (Incruse Ellipta [GlaxoSmithKline]) Inhaled corticosteroids (ICS)b Beclomethasone (Qvar RediHaler [Teva Pharmaceuticals]) Budesonide (Pulmicort Flexhaler, neb, Respulesa [AstraZeneca Pharmaceuticals]) Fluticasone (ArmonAir RespiClick [Teva Pharmaceuticals]; Flovent Diskus, HFA [GlaxoSmithKline]) Combination medications SABA/SAMA Albuterol/ipratropium (Combivent Respimat [Boehringer Ingelheim Pharmaceuticals]; Duoneb [Mylan Inc] neb) LABA/LAMA Formoterol/glycopyrrolate (Bevespi Aerosphere [AstraZeneca Pharmaceuticals]) Indacaterol/glycopyrrolate (Utibron Neohaler [Sunovion]) Olodaterol/tiotropium (Stiolto Respimat [Boehringer Ingelheim Pharmaceuticals]) Vilanterol/umeclidinium (Anoro Ellipta [GlaxoSmithKline]) LABA/ICS Formoterol/budesonide (Symbicort [AstraZeneca Pharmaceuticals]) Formoterol/mometasone (Dulera [Merck & Co, Whitehouse Station, NJ])c Salmeterol/fluticasone (Advair Diskus, HFAb [GlaxoSmithKline]; Wixela Inhubc [Mylan Inc]) Vilanterol/fluticasone (Breo Ellipta [GlaxoSmithKline]) ICS/LAMA/LABA Fluticasone/umeclidinium/vilanterol (Trelegy Ellipta [GlaxoSmithKline]) Phosphodiesterase-4 inhibitor Roflumilast (Daliresp [AstraZeneca Pharmaceuticals]) Mucolytic N-acetylcysteine Corticosteroids Methylprednisolone (Medrol [Pfizer Inc, New York, NY]) Prednisolone Prednisone Macrolides Azithromycind
2 puffs every 4-6 h PRN
2 puffs every 4-6 h PRN or 1 neb vial TID
1 1 1 2
neb vial BID neb vial BID capsule inhaled daily puffs BID
1 puff BID 2 puffs QID or 1 neb vial every 6-8 h 1 puff BID 1 capsule inhaled BID or 1 neb vial BID daily nebulizer 1 capsule inhaled daily or 2 puffs daily 1 puff daily 50-400 mg daily, in divided doses BID 1 puff BID or 1 neb vial BID 50-500 mg daily in divided doses BID
1 puff QID or 1 neb vial every 6 h 2 puffs BID 1 capsule inhaled BID 2 puffs daily 1 2 1 1
puff daily puffs BID puff BID puff BID
1 puff daily 1 puff daily 250 mg PO daily x 4 weeks, then 500 mg PO daily Via nebulizer TID to QID 32 mg PO daily for 5-7 days 40 mg PO daily for 5-7 days 40 mg PO daily for 5-7 days 250 mg PO QOD, 250-500 mg PO 3 times per week, or 250 mg PO daily
BID ¼ 2 times a day; neb ¼ nebulizer; PO ¼ by mouth; QID ¼ 4 times a day; TID ¼ 3 times a day. a Approved but not yet available at the time of publication. b Not used as monotherapy. c Off-label. d Prevention of exacerbations.
shown oxygen saturation of 88% or less on 2 occasions over a 3week period. Patients receiving long-term oxygen therapy should be reevaluated every 2 to 3 months via oxygen saturation while breathing with oxygen and then on room air to assess the appropriateness of the prescribed oxygen flow, as well as the continued need for supplemental oxygen. Oxygen therapy should not be routinely prescribed for the patient with COPD who does not meet arterial hypoxemia criteria (partial pressure of oxygen in the alveoli < 55 mm Hg or oxygen saturation < 88%) because the use of oxygen in this population does not confer any improvement in dyspnea symptoms, quality of life, or functional status.14
Referral Although most cases of COPD can be managed in the primary care setting, there are instances in which referral to a specialist is warranted. While the 2019 GOLD guidelines do not address this topic, the Canadian Thoracic Society provides suggestions for primary care providers regarding when to refer. The society’s recommendations for management of chronic obstructive pulmonary disease (2008) provide 7 situations in which specialist referral would be the prudent course of action. These situations include patients who present with COPD symptoms disproportionate to the degree of obstruction measured by PFT, patients
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Figure 5. GOLD group follow-up pharmacologic treatment algorithm.
who are suspect for alpha-1 antitrypsin deficiency, patients who experience a sudden and rapid decline in their pulmonary function, patients who present with symptom onset at a young age ( 45 years old), those who experience either recurrent or severe exacerbations, and any patients who fail to respond to treatment initiated in the primary care setting.19 Conclusion Although COPD is a complex and life-altering chronic disease process, it is a disease that can and should be diagnosed and managed in the primary care setting, at least initially. Primary care providers have the opportunity to vigilantly screen for tobacco abuse, discourage the start of tobacco use, and promote cessation for those who do use tobacco. Primary care providers are also well positioned to identify patients with COPD early in the disease process, allowing for prompt initiation of appropriate management, thus decreasing the future burden of the disease by slowing its progression.20
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Michael F. Potnek, DNP, AGPCNP-BC, is a primary care nurse practitioner at Outreach Community Health Centers and adjunct faculty member at Marquette University College of Nursing in Milwaukee, WI, and can be contacted at Michael.potnek@marquette. edu. In compliance with national ethical guidelines, the author reports no relationships with business or industry that would pose a conflict of interest.