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Smoking out the dangers of COPD

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32 l Nursing2011 l April
Chronic Obstructive Lung Disease
(GOLD) is a consortium of international
experts whose objective is to
improve worldwide awareness, education,
and care for those who suffer
from chronic obstructive pulmonary
disease (COPD). Formed in 1997 in
collaboration with the World Health
Organization (WHO) and the National
Heart, Lung and Blood Institute,
the consortium published its
initial report in 2001, following a
comprehensive review of existing
guidelines for COPD.
After reviewing the world’s literature
each year, committee members
continue to develop evidence-based
guidelines for preventing, diagnosing,
and treating COPD.1 Annual updates
are available online at http://www. This article provides an
overview of these important guidelines
and promotes their evidencebased
use in the clinical setting.
Coming to terms
The term COPD doesn’t describe one
disease process; rather, it encompasses
pathology from different disease
states that ultimately produce
chronic and irreversible limitations
in airflow. The GOLD report defines
COPD as a preventable and treatable
disease characterized by airflow limitation
that also has some extrapulmonary
(outside of the lung) effects
that may contribute to other comorbidities
in certain patients.1 Airflow
limitation is progressive.2
Chronic bronchitis and emphysema
have long been identified as the
two categories beneath the umbrella
term COPD. Interestingly, the 2010
GOLD Pocket Guide includes neither
of these disease entities in its definition
of COPD. (The full report for
2010 hasn’t been published yet.)
Bronchitis isn’t always associated
with airflow obstruction, and the
alveolar destruction that’s indicative
of emphysema is only one of multiple
lung abnormalities present in
COPD.3 However, the 2009 report
does describe the characteristic airflow
limitation of COPD developing
from small airway disease (obstructive
bronchiolitis) and lung tissue
destruction (emphysema).1
Chronic bronchitis is diagnosed by
the presence of a cough with sputum
production for 3 months a year for
2 consecutive years.1 Although this is
a disease of the small airways, its definition
doesn’t include reference to
airflow limitation, and many patients
who don’t have a chronic cough and
sputum production may develop
airflow limitation. However, the
presence of a cough and sputum
Smoking out the
By Brenda L. Smith, MSN, RN, CMSRN, and Frederick J. Tasota, MSN, RN
Bodell Communications, Inc. / Phototake
Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. April l Nursing2011 l 33
dangers of COPD
Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
34 l Nursing2011 l April
production doesn’t exclude a diagnosis
of COPD.1
Obstructive bronchiolitis involves
narrowing of the small airways that
may result from various pathologic
states.1 This broader term better reflects
the airflow limitation of COPD
as defined by the GOLD report.
Emphysema is associated with alveolar
destruction, which reduces
the surface area available for gas exchange.
This structural change decreases
the elastic recoil, the ease
with which the lung relaxes during
expiration, and results in alveolar
hyperinflation and air trapping.1,4
There are two commonly recognized
types of emphysema: centriacinar or
cerntrilobular, and panacinar. (See
The destruction of emphysema.)
COPD’s impact
Although 16 million patients in the
United States may already be diagnosed
with COPD, another 14 million
may be undiagnosed.5 In the
United States, COPD accounted for
1.5 million emergency visits and
more than 725,000 hospitalizations
in 2000 and more than $32 billion
in costs in 2002.5 According to the
WHO, the incidence of COPD is on
the rise. Currently ranked as the
fourth leading cause of morbidity
and mortality in the United States,
COPD is predicted to become number
three by the year 2020.5
Not only does this chronic disease
present a significant health burden,
it also has costly economic and social
ramifications.1 The direct healthcare
costs to treat, diagnose, and
manage the disease are burdensome
not only to patients but to the
healthcare system in this country.
This debilitating disease prevents
many patients from earning a living
and makes them rely on family, other
caregivers, and indirectly on society
as a whole for financial support.1
Structural changes
Exposure to irritating, inhaled substances
such as cigarette smoke
normally causes an inflammatory
response in the airways and lungs. In
COPD, an exaggerated response to
noxious stimuli disrupts the body’s
normal defense mechanisms. This
abnormal response results in chronic
inflammation and structural changes
in the trachea and bronchi, bronchioles,
respiratory bronchioles and alveoli,
and the pulmonary vessels.1
(See Reviewing normal lung anatomy.)
The airways narrow due to the
body’s attempts to adapt to injurious
stimuli and chronic inflammatory
changes. The inflammatory response
causes an increase in the number of
macrophages and CD8+ lymphocytes,
which combine to destroy tissue
throughout the lungs.1 In the trachea
and bronchi, an increase in goblet
cells and enlarged submucosal glands
increase mucus secretion and further
narrow the airways.1 Bronchioles narrow
from thickening of airway walls
and from increased exudate.1
Chronic airway inflammation may
also lead to pulmonary vasoconstriction
secondary to chronic hypoxemia.
This leads to pulmonary
hypertension, which in turn may
cause right-sided heart failure (cor
Continued exposure to noxious
irritants and inflammatory changes
Reviewing normal lung anatomy
Source: Porth CM. Essentials of Pathophysiology. 3rd ed. Wolters Kluwer/Lippincott Williams & Wilkins; 2010.
The destruction of emphysema
In centriacinar emphysema, the destruction is confined to the terminal bronchioles
(TB) and respiratory bronchioles (RB). In panacinar emphysema, the peripheral
alveoli (A) are also involved.
Source: Porth CM. Essentials of Pathophysiology. 3rd ed. Wolters Kluwer/Lippincott Williams & Wilkins; 2010.
Normal Centriacinar Panacinar
Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. April l Nursing2011 l 35
cause fibrotic changes in the small
airways, obstructing airflow during
expiration.1 As the alveoli become
further damaged, hyperinflation
results from loss of elasticity. As
COPD progresses, alveolar hyperinflation
makes inspiration more difficult,
reduces gas exchange, and
leads to reduced oxygen uptake and
carbon dioxide retention.1
Smoke and other risks
One of your important roles in the
prevention and treatment of COPD is
to identify patient risk factors for this
disease. Risk factors include genetics
and environmental exposures.
Of every two people with the same
smoking history, one may develop
COPD; of every six people diagnosed
with COPD, one has never smoked.
A genetic predisposition is thought
to be the reason these nonsmokers
develop COPD.1,2
Genetic risk factors for COPD
aren’t clearly understood and require
further research, but the most studied
and documented genetic risk factor
is alpha1 antitrypsin deficiency.1,2
Alpha1 antitrypsin is an enzyme produced
mostly in the liver that primarily
protects the lungs from injury.
A deficiency of this enzyme predisposes
adults to the early development
of emphysema.2
An estimated 100,000 people in the
United States have this enzyme deficiency,
but only about 10% of them
have been diagnosed.2 Although both
smokers and nonsmokers with the
deficiency experience a decline in lung
function, smokers have an increased
risk of rapid disease progression.1
Cigarette smoking is by far the
most common cause for the development
and progression of COPD.1,2 In
addition, exposure to secondhand
smoke (passive smoking) increases
the risk of COPD in nonsmokers.1
Exposure to cigarette smoke initiates
the inflammatory cascade in the airways
and lungs, and the continued
exposure to noxious irritants may result
in obstructive airflow limitation.
Carbon monoxide, a byproduct of
cigarette smoking, adds to a patient’s
problems. In the body, carbon monoxide
combines with hemoglobin to
form carboxyhemoglobin. These
hemoglobin molecules are inefficient
carriers of oxygen to the body’s tissues
and only worsen hypoxemia. Other
environmental risk factors include
exposure to occupational dusts and
chemicals, and indoor and outdoor
air pollution.1 An estimated 19% of
those with COPD develop the disease
secondary to occupational exposure,
and 31% of them are nonsmokers.1
The GOLD report cites several other
risk factors that have been identified
through research, including respiratory
injuries during gestation
and childhood that interfere with
normal lung growth and development,
asthma, lower socioeconomic
status, viral and bacterial infections,
and poor nutrition.1
(See What are the
risks for developing COPD?)
Whether gender is a risk factor is
unclear. Historically, COPD has been
more prevalent in men than in women,
but recent studies reveal that women
have almost achieved equality with
men in terms of COPD.1 Causes for
this rise are thought to be related to
women having smaller airways and
more women smoking cigarettes over
the past few decades.1
Assessing your patient
If you suspect your patient has
COPD, obtain a thorough health
history and physical assessment. The
health history should include risk
factors, pattern of signs and symptoms
(progressive, persistent dyspnea;
chronic cough; and sputum
production), and the presence of
comorbidities.1 Possible physical
assessment findings include decreased
breath sounds, “barrel-shaped” chest,
and pursed-lip breathing.1 (See What’s
a barrel-shaped chest?)
The healthcare provider will confirm
diagnosis of COPD with spirometry.
Considered the gold standard
for diagnosing and monitoring
disease progression, spirometry is the
most accurate and objective means
to measure airflow limitation.1 It also
helps to differentiate COPD from
other pulmonary diseases.
Spirometry includes measurement
of forced vital capacity (FVC), the
maximal amount of air that can be
rapidly and forcefully exhaled from
the lungs after maximal inspiration,
and forced expired volume achieved
in 1 second (FEV1), the volume of air
expired in the first second of FVC.
The ratio of FEV1/FVC is then calculated.
A normal FEV1/FVC ratio is
greater than or equal to 70% of the
predicted value based on height, age,
and gender. A calculated ratio of less
What are the risks for
developing COPD?4
• Genetic factors
• Exposure to particles
• Tobacco smoke
• Occupational dusts, organic and
• Indoor air pollution from heating
and cooking with biomass fuels such
as wood and dung in poorly vented
• Outdoor air pollution
• Lung growth and development
• Oxidative stress
• Respiratory infections
• Lower socioeconomic status
• Poor nutrition
• Comorbidities
Using GOLD staging for COPD3
Stage I:
mild COPD
Stage II:
moderate COPD
Stage III:
severe COPD
Stage IV: very
severe COPD
FEV1/FVC <70% <70% <70% <70%
FEV1 =80% of
50%–79% of
of predicted
<30% of predicted or
<50% of predicted AND chronic respiratory failure Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 36 l Nursing2011 l April than 70% confirms airflow obstruction. 1,4 COPD severity is classified as stages I through IV based on spirometry measurements (see Using GOLD staging for COPD).1 Smoking cessation Annually, smoking is responsible for more than 435,000 deaths in the United States, with tobacco-related disease accounting for $96 billion in medical expenses. Approximately 20% of U.S. adults currently smoke, and 4,000 children and adolescents will smoke their first cigarette today.6 Smoking cessation is the single most cost-effective strategy to reduce the risk of developing COPD or to slow its progression. More than 70% of current smokers have a desire to stop smoking. Take advantage of an opportunity to help them achieve this goal.6 Dependence on tobacco is both a chronic disease and an addiction.1,6 Stopping tobacco use is difficult and relapse is common, mainly because nicotine is highly addictive.1 To prevent or minimize the development of chronic disease, be proactive in assessing, educating, and intervening to help stop tobacco use. Be sure to consistently identify and document the smoking habits of each patient. Determine the age at which the patient began smoking, current smoking status, and the desire to stop smoking. Inform the patient about effective treatment options for smoking prevention and cessation.1,6 The U.S. Public Health Service has compiled guidelines for smoking cessation entitled Treating Tobacco Use and Dependence: 2008 Update. Quick Reference Guide for Clinicians. These guidelines outline a five-step approach known as the 5 A’s (see When smokers want to quit, use the 5 A’s) for clinicians to help their patients stop smoking.6 Use the guidelines with every patient encounter to identify tobacco users and encourage them to quit.6 Once a patient has expressed the desire to quit smoking, discuss the preparatory STAR quit plan with the patient.6 (See The patient’s STAR quit plan for smoking cessation.) For other key elements, see Treating tobacco use and dependence: Key findings of U.S. Public Health Service. Also included in the guidelines are specific interventions, known as the 5 R’s, which the clinician can use to educate and enhance motivation to stop smoking for smokers who don’t want to quit.3 (See The 5 R’s for those who don’t want to quit smoking.) Drug therapy for COPD The goals of effective COPD management are to relieve signs and symptoms, prevent disease progression, improve exercise tolerance and health status, prevent and treat complications and exacerbations, and reduce mortality. 1 Reaching the goals requires an individualized approach for every patient. To maximize the patient’s quality of life, weigh the benefits against the risks of pharmacologic and nonpharmacologic therapies for each patient. Pharmacologic therapy for COPD focuses on controlling signs and symptoms and decreasing complications. 1 Bronchodilators, a mainstay for symptom management, include beta2-agonists, anticholinergics, and methylxanthines. The medications are typically prescribed for patients in this order, escalating the number of medications used for treatment as needed, based on signs and symptoms, presence of comorbidities, and the patient’s general health.1 Short- and long-acting bronchodilators manage signs and symptoms and prevent exacerbations. Shortacting or rescue inhalers are used as needed for the immediate relief of worsening symptoms. Salbutamol is an example of a short-acting beta2- agonist with a 4- to 6-hour duration of action. Long-acting bronchodilators are prescribed for patients who must use medications on a regular schedule to What’s a barrel-shaped chest? A normal chest and cross section are shown on the left, and barrel-shaped chest and cross section seen in emphysema are on the right. Source: Smeltzer SC, Bare BG. Medical-Surgical Nursing. 10th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2004. Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. April l Nursing2011 l 37 control their signs and symptoms. These are more effective and convenient than short-acting bronchodilators used frequently. Salmeterol, a long-acting bronchodilator, has a duration of action of 12 hours or longer.1 The preferred route of administration is via inhalation to maximize medication effectiveness and minimize systemic adverse reactions. To promote optimal therapy, teach the patient to correctly use inhalers, then reinforce your teaching. Be sure to present education consistently as appropriate for the individual.1 Regardless of a beta2-agonist’s duration of action, the mechanism of action is to relax smooth muscles in the airway.1 The resulting bronchodilation promotes expiratory flow and improves exhalation. This subsequently decreases hyperinflation and improves symptoms both at rest and with exercise. The predominant adverse reactions to beta2-agonists are sinus tachycardia, which may cause more serious cardiac dysrhythmias in some patients, and exaggerated tremors, a particular risk in older adults taking high doses.1 Several of the short-acting beta2-agonists also come in oral preparations, but their onset of action is much slower and they’re associated with more systemic adverse reactions than the inhaled formulations.1 Inhaled anticholinergics facilitate bronchodilation by blocking acetylcholine receptor sites and preventing bronchcoconstriction.1 Ipratropium is a short-acting anticholinergic whose effects last up to 8 hours. Long-acting tiotropium has a duration of action greater than 24 hours, making it an appropriate choice for once-daily dosing.1,4 Treatment with a long-acting anticholinergic such as tiotropium helps to produce clinically significant improvement in lung function, reduce COPD exacerbations, and improve the effectiveness of pulmonary rehabilitation.1 The main adverse reaction to anticholinergics is dry mouth. Some patients taking ipratropium report a bitter metallic taste.1 Methylxanthines inhibit phosphodiesterase, which increases cyclic adenosine monophosphate, relaxes bronchial smooth muscle, and promotes bronchodilation.1,4 Theophylline, the best-known drug in this class, was once a mainstay of COPD management. Today it’s prescribed much less frequently because of its narrow therapeutic window, which outweighs its potential benefits for many patients. However, theophylline is still sometimes prescribed for additional symptom control.1 Methylxanthines are given via the oral and I.V. route, and the most common adverse reactions they cause are headache, insomnia, nausea, and heartburn. Atrial and ventricular dysrhythmias and seizures are possible signs of toxicity. Combination therapy using bronchodilators with varied mechanisms and durations of action may improve symptom control. But combination therapy also increases costs, requires a higher level of adherence to the prescribed therapy, and may be no better than using a higher dose of a single medication—as long as adverse reactions aren’t an issue. Treatment is individualized to each patient’s condition and response. Glucocorticosteroids are commonly used for their anti-inflammatory effects, but according to the GOLD report, their role in managing COPD is limited. Patients benefitting the most are those with advanced stages of COPD—stages III and IV—as they tend to have more severe signs and symptoms and more frequent exacerbations. The regular use of inhaled glucocorticosteroids reduces the frequency of exacerbations. Using an inhaled glucocorticosteroid in combination with an inhaled long-acting beta2-agonist is more effective than using either of them alone to reduce exacerbations and slow the decline in lung function. Inhaled glucocorticosteroids may increase the risk of pneumonia, particularly when combined with a long-acting beta2-agonist. The use of oral glucocorticosteroids hasn’t proved to be effective as either a short- or l

ong-term treatment for patients with COPD. Furthermore, chronic treatment with oral systemic glucocorticosteroids may induce a steroid myopathy. This increase in muscle weakness may contribute to respiratory failure in patients with end-stage COPD, who are already suffering from a decline in overall physical functioning.1 For these reasons, the chronic use of systemic steroids should be avoided. Minimize the risk of infections Patients diagnosed with COPD should receive a yearly seasonal influenza When smokers want to quit, use the 5 A’s 1. ASK: Ask about tobacco use at every new encounter. 2. ADVISE: Urge every tobacco user to quit. 3. ASSESS: Determine willingness to quit. 4. ASSIST: Develop a quit plan. 5. ARRANGE: Follow up. Adapted from Fiore MC, Jaén CR, Baker TB, et al. Treating Tobacco Use and Dependence: 2008 Update. Quick Reference Guide for Clinicians. Rockville, MD: U.S. Department of Health and Human Services, Public Health Service; 2009. The patient’s STAR quit plan for smoking cessation Set a quit date within 2 weeks of the decision to stop smoking. Tell family, friends, and coworkers about the decision to quit and enlist their support. Anticipate challenges to quitting, especially during the first few weeks. Remove all tobacco products from your environment (work, home, and car). Adapted from Fiore MC, Jaén CR, Baker TB, et al. Treating Tobacco Use and Dependence: 2008 Update. Quick Reference Guide for Clinicians. Rockville, MD: U.S. Department of Health and Human Services, Public Health Service; 2009. Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. 38 l Nursing2011 l April vaccine. This has proved to reduce illness and death by 50%. Patients age 65 or older should also receive the pneumococcal vaccine to reduce the risk of community-acquired pneumonia. Routine prophylaxis with other medications sometimes prescribed for patients with COPD isn’t indicated. The GOLD report recommends that antibiotic use be reserved for COPD exacerbations in the presence of a bacterial infection, and doesn’t promote the use of mucolytics and cough suppressants in the management of stable COPD.1 Nonpharmacologic treatment Pulmonary rehabilitation involves a multidisciplinary team approach that includes assessment, exercise training, nutrition counseling, smoking cessation, and education for the patient. Many clinical trials have shown that participating in a pulmonary rehabilitation program reduces dyspnea and fatigue and improves exercise tolerance and quality of life for patients with COPD. Patients with COPD at all disease stages benefit from pulmonary rehabilitation programs lasting at least 6 weeks; the longer the program, the better the results.1 Oxygen therapy is usually reserved for patients with end-stage (stage IV) COPD and can be used as long-term continuous therapy, during activity, and to relieve shortness of breath.1 The goal of oxygen therapy is to achieve an SaO2 of 90% or greater.1,4 The prescription for oxygen must specify liters/minute at rest, during activity, and while sleeping. Long-term administration of oxygen in patients with end-stage COPD and respiratory failure has demonstrated prolonged survival. However, like other COPD treatments, it doesn’t reverse the disease process.1 Surgical treatment may be an option for select patients who have COPD. Bullae (the enlarged alveolar air spaces that don’t contribute to gas exchange and compress functional lung tissue) may be excised with a bullectomy. This surgery reduces dyspnea and improves lung function by allowing reexpansion of the compressed lung region.1 Lung volume reduction surgery removes part of the lung that’s nonfunctional due to hyperinflation, reducing overcrowding of the chest cavity and improving elastic recoil of functional lung tissue.1,4 This surgery has improved survival by more than 50 months compared with medical treatment.1 Lung transplantation is another surgical option for some patients with advanced COPD, but this therapy is limited by a shortage of donor organs. Maintaining immunosuppression is also very costly and is associated with serious risks, including infections and malignancies.1 Although data show that lung transplantation doesn’t improve longevity, it may improve the quality of life for select groups of patients with end-stage COPD.4 The potential benefits of any surgery must be weighed against the risks, based on the patient’s existing pulmonary status, comorbidities such as obesity or diabetes, and overall health. Managing exacerbations The GOLD report defines an exacerbation of COPD as “an event in the natural course of the disease characterized by a change in the patient’s baseline dyspnea, cough, and/or sputum that’s beyond normal day-to-day variations, is acute in onset, and may warrant a change in regular medication in a patient with underlying COPD.”1 All patients with COPD, regardless of the stage, are at risk for an exacerbation. Triggers for an exacerbation include respiratory infection and air pollution. Approximately one-third of exacerbations are from an unknown cause.1 When a patient is admitted with a COPD exacerbation, the first-line treatment includes providing oxygen Treating tobacco use and dependence: Key findings of U.S. Public Health Service 1. Individual, group, and telephone counseling are effective measures to help patients stop smoking. 2. The medications that are effective for treatment in smoking cessation are bupropion SR, nicotine gum, nicotine inhaler, nicotine lozenge, nicotine nasal spray, nicotine patch, and varenicline. These medications increase long-term smoking abstinence and, in the absence of contraindications, one should be prescribed as part of the treatment regimen. 3. Patients should be encouraged to use counseling and medication as part of their treatment plan to stop smoking; the combination is more effective than either measure alone. 4. The measures to treat smoking and tobacco dependence are more cost-effective than treating and managing a chronic disease resulting from tobacco use. Adapted from Fiore MC, Jaén CR, Baker TB, et al. Treating Tobacco Use and Dependence: 2008 Update. Quick Reference Guide for Clinicians. Rockville, MD: U.S. Department of Health and Human Services, Public Health Service; 2009. 5 R’s for those who don’t want to quit smoking 1. RELEVANCE: Ask the patient why quitting is personally relevant (such as family or health concerns). 2. RISKS: Ask the patient to identify risks of tobacco use (such as shortness of breath or lung cancer). 3. REWARDS: Ask the patient to identify rewards or benefits of quitting smoking (such as improving health, saving money). 4. ROADBLOCKS: Ask the patient to identify barriers or roadblocks to quitting smoking (such as weight gain, losing the enjoyment of smoking). 5. REPETITION: Repeat this process with every new encounter with the patient. Adapted from Fiore MC, Jaén CR, Baker TB, et al. Treating Tobacco Use and Dependence: 2008 Update. Quick Reference Guide for Clinicians. Rockville, MD: U.S. Department of Health and Human Services, Public Health Service; 2009. Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited. April l Nursing2011 l 39 and determining if the patient requires intensive care. If admission to an ICU is warranted, the need for invasive versus noninvasive mechanical ventilation and hemodynamic stability must be quickly evaluated, followed by appropriate treatment.1 To determine adequate oxygenation and ventilation, obtain arterial blood gases 30 minutes after initiating oxygen therapy. Start bronchodilator therapy with a short-acting inhaled beta2-agonist as prescribed. In addition, glucocorticosteroids are recommended for 7 to 10 days. As prescribed, administer antibiotics to patients who present with one of the following: • the three cardinal signs of COPD: increased dyspnea, increased sputum production, and increased sputum purulence • two of the cardinal signs, with one of them being increased sputum purulence • the need f

or invasive or noninvasive mechanical ventilation. Evaluate the patient for pulmonary embolism, which must be ruled out with every COPD exacerbation that requires hospitalization.1 Following the acute stage of exacerbation, educate the patient about preventing future exacerbations as part of the discharge planning and teaching. Review smoking cessation, medication administration, inhaler technique, and recognition and management of worsening COPD symptoms. Initiating or continuing a pulmonary rehabilitation program is also highly recommended.1 Because pharmacotherapy reduces the frequency of exacerbations and hospitalizations, pay special attention to instructing the patient about taking medications as prescribed to control COPD symptoms.1 Explain the importance of regular follow-up with the healthcare provider. The prevalence of COPD is increasing, but thanks to improved management strategies, many patients are surviving longer with a better quality of life. Keep your knowledge and skills up to date by reviewing ever-evolving evidence-based best practices. By investing your time and educating yourself, you can have a greater impact on the quality of life for patients who must cope with COPD for the rest of their lives. ¦ REFERENCES 1. Global Initiative for Chronic Obstructive Lung Disease (GOLD). Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: Updated 2009. http:// GuidelineItem.asp?intID=989. 2. National Heart, Lung and Blood Institute. COPD: What is COPD? 2010. Diseases and Conditions Index. Diseases/Copd/Copd_WhatIs.html. 3. GOLD: Global Initiative for Chronic Obstructive Lung Disease. Guidelines. Pocket Guide to COPD Diagnosis, Management, and Prevention: Updated 2010. asp?l1=2&l2=1&intId=1116. 4. Bauldoff GS. When breathing is a burden: how to help patients with COPD. Am Nurse Today. 2009; 4(9):17-23. 5. COPD International. http://www.copd-international. com/Library/statistics.htm. 6. Fiore MC, Jaén CR, Baker TB, et al. Treating Tobacco Use and Dependence: 2008 Update. Quick Reference Guide for Clinicians. Rockville, MD: U.S. Department of Health and Human Services, Public Health Service; 2009. Brenda L. Smith is a nursing instructor I at UPMC Shadyside School of Nursing in Pittsburgh, Pa. Frederick J. Tasota is a critical care clinical specialist at UPMC Presbyterian Hospital in Pittsburgh, Pa. The authors have disclosed that they have no financial relationships pertaining to this article. DOI-10.1097/01.NURSE.0000395203.80613.e2 INSTRUCTIONS Smoking out the dangers of COPD DISCOUNTS and CUSTOMER SERVICE • Send two or more tests in any nursing journal published by Lippincott Williams & Wilkins together by mail, and deduct $0.95 from the price of each test. • We also offer CE accounts for hospitals and other healthcare facilities on nursingcenter. com. Call 1-800-787-8985 for details. PROVIDER ACCREDITATION Lippincott Williams & Wilkins, publisher of Nursing2011 journal, will award 2.5 contact hours for this continuing nursing education activity. Lippincott Williams & Wilkins is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center’s Commission on Accreditation. Lippincott Williams & Wilkins is also an approved provider of continuing nursing education by the District of Columbia and Florida #FBN2454. This activity is also provider approved by the California Board of Registered Nursing, Provider Number CEP 11749 for 2.5 contact hours. Your certificate is valid in all states. The ANCC’s accreditation status of Lippincott Williams & Wilkins Department of Continuing Education refers only to its continuing nursing educational activities and does not imply Commission on Accreditation approval or endorsement of any commercial product. TEST INSTRUCTIONS • To take the test online, go to our secure Web site at • On the print form, record your answers in the test answer section of the CE enrollment form on page 40. Each question has only one correct answer. You may make copies of these forms. • Complete the registration information and course evaluation. Mail the completed form and registration fee of $24.95 to: Lippincott Williams & Wilkins, CE Group, 2710 Yorktowne Blvd., Brick, NJ 08723. We will mail your certificate in 4 to 6 weeks. For faster service, include a fax number and we will fax your certificate within 2 business days of receiving your enrollment form. • You will receive your CE certificate of earned contact hours and an answer key to review your results. There is no minimum passing grade. • Registration deadline is April 30, 2013. For more than 23 additional continuing education articles related to respiratory topics, go to > <
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