Smoking out the dangers of COPD

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2.5
ANCC CONTACT HOURS
THE GLOBAL INITIATIVE for
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.
goldcopd.org. 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
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www.Nursing2011.com 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 www.Nursing2011.com
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
pulmonale).1
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.
Trachea
Intrapulmonary
bronchus
Respiratory
bronchiole
Diaphragm
Esophagus
Alveoli
Larynx
bronchus
Epiglottis
Oropharynx
Nasopharynx
Extrapulmonary
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
TB
RB
A
TB
RB
A
TB
RB
A
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www.Nursing2011.com 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
inorganic
• Indoor air pollution from heating
and cooking with biomass fuels such
as wood and dung in poorly vented
dwellings
• Outdoor air pollution
• Lung growth and development
problems
• 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
predicted
50%–79% of
predicted
30%–49%
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 www.Nursing2011.com
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.
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www.Nursing2011.com 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 long-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 www.Nursing2011.com
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.
www.Nursing2011.com 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 for 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://
www.goldcopd.org. http://www.g

Smoking out the dangers of COPD

Paper details:

provide a basic summary of the article using APA citations as necessary

32 l Nursing2011 l April www.Nursing2011.com
2.5
ANCC CONTACT HOURS
THE GLOBAL INITIATIVE for
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.
goldcopd.org. 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
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www.Nursing2011.com 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 www.Nursing2011.com
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
pulmonale).1
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.
Trachea
Intrapulmonary
bronchus
Respiratory
bronchiole
Diaphragm
Esophagus
Alveoli
Larynx
bronchus
Epiglottis
Oropharynx
Nasopharynx
Extrapulmonary
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
TB
RB
A
TB
RB
A
TB
RB
A
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www.Nursing2011.com 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
inorganic
• Indoor air pollution from heating
and cooking with biomass fuels such
as wood and dung in poorly vented
dwellings
• Outdoor air pollution
• Lung growth and development
problems
• 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
predicted
50%–79% of
predicted
30%–49%
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 www.Nursing2011.com
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.
www.Nursing2011.com 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 long-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 www.Nursing2011.com
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.
www.Nursing2011.com 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 for 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://
www.goldcopd.org. http://www.goldcopd.org/
GuidelineItem.asp?intID=989.
2. National Heart, Lung and Blood Institute. COPD:
What is COPD? 2010. Diseases and Conditions
Index. http://www.nhlbi.nih.gov/health/dci/
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. http://www.goldcopd.com/Guidelineitem.
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
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Smoking out the dangers of COPD

Paper details:

provide a basic summary of the article using APA citations as necessary

32 l Nursing2011 l April www.Nursing2011.com
2.5
ANCC CONTACT HOURS
THE GLOBAL INITIATIVE for
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.
goldcopd.org. 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.
www.Nursing2011.com 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 www.Nursing2011.com
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
pulmonale).1
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.
Trachea
Intrapulmonary
bronchus
Respiratory
bronchiole
Diaphragm
Esophagus
Alveoli
Larynx
bronchus
Epiglottis
Oropharynx
Nasopharynx
Extrapulmonary
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
TB
RB
A
TB
RB
A
TB
RB
A
Copyright © 2011 Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.
www.Nursing2011.com 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
inorganic
• Indoor air pollution from heating
and cooking with biomass fuels such
as wood and dung in poorly vented
dwellings
• Outdoor air pollution
• Lung growth and development
problems
• 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
predicted
50%–79% of
predicted
30%–49%
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 www.Nursing2011.com
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.
www.Nursing2011.com 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 long-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 www.Nursing2011.com
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.
www.Nursing2011.com 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 for 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://
www.goldcopd.org. http://www.goldcopd.org/
GuidelineItem.asp?intID=989.
2. National Heart, Lung and Blood Institute. COPD:
What is COPD? 2010. Diseases and Conditions
Index. http://www.nhlbi.nih.gov/health/dci/
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. http://www.goldcopd.com/Guidelineitem.
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
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Smoking out the dangers of COPD
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