Chronic obstructive pulmonary disease (COPD)
Abstract: 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.
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
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).
Spirometry
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).
Treatment
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
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%.
Results item response rates
A list of correct item response rates for all NPs was calculated (see Percentage
Chronic obstructive pulmonary disease (COPD)
Abstract: 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.
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
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).
Spirometry
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).
Treatment
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
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%.
Results item response rates
A list of correct item response rates for all NPs was calculated (see Percentage
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