Art & science respiratory supplement
Chronic obstructive pulmonary
disease: diagnosis and management
Kaufman G (2013) Chronic obstructive pulmonary disease: diagnosis and management.
Nursing Standard. 27, 21, 53-62. Date of submission: April 4 2012; date of acceptance: October 1 2012.
Abstract
Chronic obstructive pulmonary disease (COPD) is a major cause of
morbidity and mortality worldwide. However, despite being one of
the most common causes of hospital admission, COPD has been a
neglected respiratory condition. Nurses working in all care settings
can make an important contribution to the care of patients with
COPD. This article discusses assessment, diagnosis and management
of COPD. Reference is made to recent policy developments,
emphasising the importance of transforming care, and improving
quality of life and health outcomes for patients.
Author
Gerri Kaufman
Lecturer in health sciences, Department of Health Sciences,
University of York, York
Correspondence to: gerri.kaufman@york.ac.uk
Keywords
Chronic obstructive pulmonary disease, differential diagnosis,
drug treatment, respiratory diseases, smoking
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Chronic obstructive pulmonary disease
(COPD) is a major global epidemic (Barnes
2011), and the fourth leading cause of death in
the United States and Europe (Devereux 2011).
The Global Initiative for Chronic Obstructive
Lung Disease (GOLD) (2011) has predicted
that COPD will be the third leading cause of
death worldwide by 2020. In the UK, COPD
affects approximately 10% of men and women
over the age of 40 (Department of Health (DH)
2010), and is one of the most common causes
of admission to hospital. The direct cost of
COPD to the UK healthcare system is estimated
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to be between 810 million and 930 million
annually, with an economic burden as a result
of lost productivity estimated at 3.8 billion
annually (DH 2010).
In a quarter of people with COPD, the disease
prevents them from working. COPD causes the
loss of 20.4 million working days annually in the
male workforce and 3.5 million working days
in the female workforce, which is more than any
other respiratory condition (DH 2010). There is
also a social cost as COPD can diminish quality
of life by adversely affecting important activities
such as walking, shopping, gardening, exercise and
participation in family life (British Lung Foundation
2006). In addition, COPD is associated with
anxiety and depression (Bellamy and Booker 2011).
Despite these bleak statistics, COPD has been
neglected and continues to be underdiagnosed in
primary care (Barnes 2011). However, the COPD
quality standard, published by the National Institute
for Health and Clinical Excellence (NICE) (2011),
and the Outcomes Strategy for People with COPD
and Asthma in England (DH 2011) emphasise the
need to improve the health of patients with this
condition. The COPD quality standard (NICE
2011) describes markers of high quality care which,
if implemented, should enhance the effectiveness,
safety and experience of care for patients. The
outcomes strategy (DH 2011) has a broader scope
that encompasses prevention, case identification,
early detection and organisation of care.
Nurses have a pivotal role in meeting the COPD
quality standards (NICE 2011) in assessment,
diagnosis and clinical management of the condition.
They also provide guidance, education and support
for people with COPD.
Chronic obstructive pulmonary disease
COPD is an umbrella term for airflow obstruction
associated with chronic respiratory diseases such
as chronic bronchitis and emphysema (Viegi et al
2007). Chronic bronchitis is characterised by
an inflammatory response in the small airways,
which causes narrowing and reduced airflow
(Lynes 2007). Emphysema causes destruction of
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the alveoli, the small grape-like sacs in the lungs
that have a key role in oxygen absorption and
carbon dioxide elimination (Lynes 2007).
The American Thoracic Society and the European
Respiratory Society define COPD as a preventable
and treatable disease state characterised by airflow
limitation that is not fully reversible. The airflow
limitation is usually progressive and associated
with an abnormal inflammatory response of the
lungs to noxious particles or gases, primarily caused
by cigarette smoking. Although COPD affects
the lungs, it also produces significant systemic
consequences (Celli et al 2004). The airway
remodelling processes associated with asthma
can result in irreversible progressive airflow
obstruction. Both asthma and COPD co-exist
in a large proportion of individuals, which can
lead to diagnostic uncertainty (Devereux 2011).
Risk factors
Cigarette smoking is the most important risk
factor in the development of COPD, followed
by occupational exposure to dust, chemical
agents and fumes, and air pollution (Viegi et al
2007). All people who smoke cigarettes show
inflammatory changes in their lungs, but those who
develop COPD exhibit an enhanced or abnormal
inflammatory response to the toxic agents in
cigarette smoke (MacNee 2011). Approximately
50% of people who smoke cigarettes develop
airflow obstruction and 10-20% of these develop
clinically significant COPD (Devereux 2011).
Occupational environments in which there
is intense and prolonged exposure to irritant
dust, gases and fumes are associated with the
development of COPD. Although this association
is independent of cigarette smoking, smoking is
likely to exacerbate the effects of occupational
exposure. Mining (coal and hard rock), farming,
construction, manufacturing (plastics, concrete,
textiles, rubber and food products), transportation
and foundry working are all associated with an
increased prevalence of COPD (Devereux 2011).
Indoor and outdoor air pollution are also
associated with the development of COPD (Viegi
et al 2007). Urban air pollution may affect the
development of lung function in children and may
therefore be a risk factor for COPD (Devereux
2011). Biomass fuels used for cooking, such as wood,
charcoal and vegetable matter, generate indoor
pollution that is implicated in the development of
COPD. Biomass smoke exposure is responsible for
approximately 50% of cases of diagnosed COPD
in developing countries (Devereux 2011).
An inherited deficiency of the glycoprotein alpha
1-antitrypsin, which helps to protect lung tissue
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from the enzymes produced by inflammatory cells,
can also cause COPD. Severe alpha 1-antitrypsin
deficiency causes premature and accelerated
development of COPD in both smokers and
non-smokers. Severe alpha 1-antitrypsin deficiency
is rare and is only found in 1-2% of patients with the
disease (Devereux 2011). However, it is important
to determine the alpha 1-antitrypsin status of
anyone with severe COPD aged under 40, as over
50% of this patient group are alpha 1-antitrypsin
deficient (Devereux 2011).
Pathophysiology
The two main pathophysiological changes
underlying COPD are chronic inflammation of the
small airways, resulting in reduced airflow, and
gradual destruction of the alveoli (Lynes 2007).
Although COPD can affect different people in
different ways, there are some pathological processes
that are common to most patients (Lynes 2007).
In patients with chronic bronchitis, the epithelial
lining of the airways becomes chronically inflamed
and can peel away. The mucus-secreting cells in
the large airways multiply and expand in number
and size, increasing the viscosity and production of
mucus. The cilia tiny hairs that line the airways
and carry foreign material to the pharynx to be
swallowed or expectorated are destroyed and the
ability of the lungs to remove mucus is impaired
(Lynes 2007).
In patients with emphysema, the smooth muscle
in the medium-sized airways becomes thickened
and contracted, causing narrowing of the airways.
The smaller airways become inflamed, oedematous
and infiltrated with white blood cells such as
macrophages and neutrophils. Inflammation and
repeated infection cause irreversible damage to
the walls and sub-mucosa of the smaller airways.
Enzymes such as proteases are released by
neutrophils in response to toxins in cigarette smoke
and these damage the alveoli. Enzymatic damage
to the alveolar walls causes coalescence, where the
smaller, highly elastic alveolar sacs merge to form
large inelastic sacs (Lynes 2007). The surface area
of the alveolar membrane is reduced resulting in
impaired gaseous exchange.
The smaller airways that supply air to the alveoli
have microscopically thin walls. Their shape and
patency is maintained by attachments that act like
guy ropes applying radial traction. Emphysema
causes a reduction in radial traction and, because the
small airways are unsupported, they can collapse
and close up, particularly during expiration. This
makes breathing more difficult and results in a lack
of ventilation in some areas of the lung (Lynes 2007).
Consequently, gaseous exchange is further impaired.
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 Associated conditions
COPD is not just a disease of the lungs, it produces
systemic inflammation and effects throughout the
body (Bellamy and Booker 2011). Cardiovascular
disease associated with COPD includes myocardial
infarction, hypertension, chronic heart failure,
atrial fibrillation, pulmonary embolism and
stroke. The incidence of lung cancer in patients
with moderate and severe COPD is two to five
times higher than in smokers who do not have
COPD (Bellamy and Booker 2011). Skeletal
muscle wasting is also associated with COPD
(MacNee 2011), causing muscle weakness, exercise
intolerance and impaired quality of life (Bellamy
and Booker 2011). Male patients with COPD have
lower testosterone levels and therefore an increased
risk of hypogonadism, which can contribute to
muscle wasting (Bellamy and Booker 2011).
Osteoporosis is also more common in COPD:
risk increases with the severity of the condition
and is higher in women than in men (Bellamy and
Booker 2011). Obesity is more common in patients
with COPD, and consequently the risk of metabolic
syndrome and diabetes is greater (Bellamy and
Booker 2011). Anaemia is present in 13-17% of
patients with COPD, presumably as a result of
chronic systemic inflammation (Bellamy and
Booker 2011).
Anxiety and depression are also common in
patients with COPD, but these symptoms often
remain undiagnosed and untreated: the prevalence
of depression varies between 10% and 42% and
10% and 19% for anxiety (Bellamy and Booker
2011). Depression adversely affects patients quality
of life. It can also affect adherence to treatment
and increase the frequency of hospital admissions
(Bellamy and Booker 2011).
Patient assessment and diagnosis
A thorough patient history should be taken and a
full examination performed before undertaking
any investigations in a patient with suspected
COPD (Currie and Chetty 2011). A diagnosis of
COPD should be considered in any patient over the
age of 35 with a history of smoking, or any other
significant risk factor, who presents with one or
more of the following symptoms (NICE 2010):
Exertional
 breathlessness.
Chronic
 cough.
Regular
 sputum production.
Frequent
 winter bronchitis.
Wheeze.
 fumes or biomass fuel.
Other factors that should be considered when
taking a patient history are summarised in Box 1.
The most common presenting symptoms of
COPD are breathlessness on exertion and cough,
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with or without sputum production (Bellamy and
Booker 2011). The NICE (2011) COPD quality
standard requires that service providers ensure
a diagnosis of COPD includes a record of one or
more indicative symptoms. It is important to note
that COPD progresses slowly and significant loss
of lung function can occur before symptoms of the
disease become apparent. Individuals gradually
adapt their lives to the disability caused by COPD
and may not notice breathlessness until it has
a significant effect on their daily functioning
(Bellamy and Booker 2011). According to
Frankland and Lynes (2007), lung function can
be reduced by as much as 50% before the patient
presents with symptoms. In addition, many
smokers expect to cough and be short of breath,
and they often dismiss symptoms of progressive
airflow obstruction as a normal consequence of
smoking (Bellamy and Booker 2011).
It is useful to determine how breathlessness
affects activities of daily life as it is one of the
primary symptoms of COPD (Currie and Chetty
2011). NICE (2010) recommend the use of The
Medical Research Council (MRC) dyspnoea scale
to grade breathlessness (Table 1).
Smoking history COPD is unusual in a non-smoker
and therefore it is essential to establish the patients
smoking history (Frankland and Lynes 2007). It
is important to quantify an individuals exposure
to cigarettes as accurately as possible in terms of
pack years (Bellamy and Booker 2011). Pack years
are calculated by multiplying the number of packs
(one pack is 20 cigarettes) smoked each day by the
number of years the patient has smoked (Frankland
and Lynes 2007). For example, a man who has
smoked 40 cigarettes a day for 25 years has 50 pack
years. A significant smoking history for the diagnosis
of COPD is defined as more than 15-20 pack years
(Bellamy and Booker 2011).
BOX 1
Factors to be considered in the diagnosis of chronic obstructive
pulmonary disease
Smoking history.
Other medical conditions, for example asthma.
Symptoms such as weight loss, waking at night, ankle swelling,
fatigue, chest pain, haemoptysis.
Current medications.
Previous hospital admissions.
Exercise limitation.
Occupational and environmental exposure to dust, chemicals,
Previous chest problems, for example chronic asthma or tuberculosis.
Number of days missed from work.
Financial effect and the extent of social, family support.
Anxiety and depression.
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Differential diagnosis Diagnosing COPD can be
difficult (Frankland and Lynes 2007) and attention
should be paid to any features in the patient
history that may suggest an alternative diagnosis.
Symptoms such as haemoptysis, chest pain and
weight loss require urgent referral to secondary
care to exclude lung cancer or a cardiorespiratory
problem (Currie and Chetty 2011). It can be
especially challenging to differentiate COPD from
asthma and a careful history must be taken to help
distinguish between the two disorders (Currie and
Chetty 2011) (Table 2).
Spirometry Spirometry is the most accurate
method of identifying airflow obstruction and
diagnosing COPD (NICE 2010, Bellamy 2011).
Spirometry measures two parameters: the airflow
from fully inflated lungs and the total volume of air
(vital capacity) that can be exhaled from maximum
inhalation to maximum exhalation (Bellamy and
Booker 2011). Vital capacity is measured following
TABLE 1
Medical Research Council dyspnoea scale
Grade Degree of breathlessness related to activity
1 Not troubled by breathlessness except on strenuous exercise.
2 Short of breath when hurrying or walking up a slight hill.
3 Walks slower than contemporaries on level ground because
of breathlessness, or has to stop for breath when walking
at own pace.
4 Stops for breath after walking about 100 metres or after
a few minutes on level ground.
5 Too breathless to leave the house, or breathless when
dressing or undressing.
(Adapted from Fletcher et al 1959)
TABLE 2
Clinical features differentiating chronic obstructive pulmonary
disease and asthma
Clinical feature or risk factor Chronic obstructive Asthma
pulmonary disease
Smoker or ex-smoker Nearly all Possibly
Symptoms under age 35 Rare Often
Chronic productive cough Common Uncommon
Breathlessness Persistent and Variable
progressive
Night time waking with Uncommon Common
breathlessness and/or wheeze
Significant diurnal or day-to-day Uncommon Common
variability of symptoms
(National Institute for Health and Clinical Excellence 2011)
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a relaxed and forced inhalation and exhalation.
During the forced manoeuvre, the patient uses
maximum force to expel all the air from his or her
lungs as hard and fast as possible. The volume of
air exhaled is plotted on a graph against the time
taken to achieve maximum exhalation. Volume is
plotted on the x (vertical) axis and time on the y
(horizontal axis). This is referred to as the volume/
time trace and three indices can be derived from it:
FEV1:
 forced expired volume in the first second.
FVC:
 forced vital capacity (total volume of air
that can be forcibly exhaled from maximum
inhalation to maximum exhalation).
FEV1/FVC:
 FEV1 expressed as a percentage of
the FVC (for example, 76%) or as a ratio
(for example, 0.76).
The presence or absence of COPD and its severity
can be confirmed by comparing these values with
predicted normal values (Bellamy 2011). The ratio
of FEV1 to FVC provides a useful measure of airway
obstruction. Forced expiration normally results in
FEV1/FVC ratios of more than 70%. Ratios below
70% are indicative of airway obstruction; the lower
the ratio, the more severe the obstruction.
Obstructive spirometry traces are seen in asthma
and COPD, the crucial difference being that in
asthma the airflow obstruction is variable and
can be reversed by the use of bronchodilators or
corticosteroids. If the patient history is suggestive
of asthma, a reversibility test can help to confirm
diagnosis. An improvement of >400ml in FEV1
following administration of a beta2 agonist suggests
a diagnosis of asthma (Bellamy 2011).
Guidelines for the diagnosis and classification of
COPD, such as GOLD (2011) and NICE (2011),
use a post-bronchodilator FEV1/FVC of less than
70% (0.7) to indicate airflow obstruction, and
post-bronchodilator FEV1 as a percentage of
predicted value to classify the severity of obstruction
(Bellamy and Booker 2011). The NICE (2011)
COPD quality standard recommends that service
providers ensure diagnosis of COPD is confirmed
by post-bronchodilator spirometry, carried out
by practitioners who are competent in the use
and interpretation of spirometry, and that the
spirometer used is correctly maintained with regular
verification and appropriate cleaning in line with
infection control procedures.
Pharmacological therapy
It is generally agreed that treatment of COPD should
follow evidence-based recommendations and be
linked to disease severity (Jones and Ostrem 2011).
Choice of drug therapy should be based on the
individuals symptomatic response and preference,
side effects, cost and the potential of the drug to
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 reduce exacerbations (NICE 2010). Service providers
should have systems in place to ensure that inhaled
therapies are offered in accordance with NICE
(2010) guidance, and as part of an individualised
and comprehensive management plan.
Beta2 agonists and muscarinic agents
NICE (2010) recommends use of short-acting
beta2 agonists, such as salbutamol and terbutaline,
in combination with ipratropium (a muscarinic
antagonist), for the relief of breathlessness and
exercise limitation. Beta2 agonists and muscarinic
antagonists reduce breathlessness by direct
bronchodilation (Greener 2011). According to
NICE (2010), the effectiveness of bronchodilator
therapy should not be assessed by lung function
alone, but should include a variety of other
measures such as improvement in symptoms,
ability to undertake activities of daily living,
exercise capacity and rapidity of symptom relief.
Patients with stable COPD who remain breathless
or experience exacerbations despite using
short-acting bronchodilators, and who have an
FEV1 at least 50% predicted, should be prescribed
either a long-acting beta2 agonist (LABA), such
as salmeterol or formoterol, or a long-acting
muscarinic antagonist (LAMA), such as tiotropium.
Both classes of drugs have been shown to relieve
symptoms, increase exercise capacity, improve
quality of life and reduce exacerbations to a greater
extent than short-acting bronchodilators (Jones and
Ostrem 2011). However, the concomitant use of
short and long-acting muscarinic antagonists is not
recommended because ipratropium and tiotropium
block the same subtype of muscarinic receptors
in smooth muscle of the airways. Ipratropium can
minimise the effect of tiotropium because the two
drugs compete to bind to the same receptor subtype
(Kaufman 2010). Ipratropium should therefore
be discontinued in patients who are commencing
tiotropium because of persistent breathlessness or
an exacerbation.
In patients with a FEV1 <50% predicted,
NICE (2010) recommends treatment with either
a LAMA or a combination of a LABA with a
corticosteroid. In addition, NICE (2010) suggests
adding a LAMA to the treatment regimen of
patients who remain breathless or experience
acute exacerbations despite taking a LABA
with a corticosteroid and irrespective of their
FEV1 (Table 3).
New pharmacological treatments for COPD
include indacaterol and roflumilast (NICE 2012a).
Indacterol is an inhaled beta2 agonist that, when
administered once daily, improves patients
lung function and quality of life, and reduces
exacerbations (Jones and Ostrem 2011). Roflumilast
is an oral phosphodiesterase type-4 inhibitor and
can be used as an add-on treatment for severe
COPD defined as a post-bronchodilator FEV1
less than 50% predicted associated with chronic
bronchitis in adults with a history of frequent
exacerbations (Greener 2011). Indacaterol may be
a potential candidate for future NICE guidance
reviews (NICE 2012a). However, a NICE (2012b)
technology appraisal recommended that roflumilast
should only be used in the context of research as
part of clinical trials in patients with severe COPD.
Other pharmacological therapies Other
pharmacological therapies used in the management
of COPD include the oral bronchodilator
theophylline, inhaled and oral corticosteroids such
as beclometasone or prednisolone, and mucolytics

TABLE 3
Beta2 agonists and muscarinic antagonists used to treat chronic obstructive pulmonary disease (COPD)
Drug class Drug name Typical dose Use in COPD
Short-acting Salbutamol 100-200mcg as required, or in regular Breathlessness and/or exercise limitation
beta agonist doses
Terbutaline 500mcg as required, or in regular doses
Long-acting Salmeterol 50mcg twice daily Persistent breathlessness or exacerbations
beta2 agonist
Formoterol 12mcg twice daily
Short-acting Ipratropium 40mcg four times daily Breathlessness and/or exercise limitation
muscarinic
antagonist
Long-acting Tiotropium Dose is dependent on the inhaler device Persistent breathlessness or exacerbations:
muscarinic used. For example, 18mcg once daily via offer long-acting muscarinic antagonists in
antagonist a HandiHaler or 5mcg once daily via a preference to regular short-acting muscarinic
Respimat antagonists (four times a day)

(Adapted from Kaufman 2010)

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such as carbocisteine. Treatment with theophylline
should only be considered if short and long-acting
bronchodilators have no effect, or in patients
who are unable to use inhaled therapy. In those
where disease is extensive, inhaled therapies may
not be sufficient. Patients may also have difficulty
manipulating inhalers because of disability (NICE
2010). Theophylline has a narrow therapeutic index
the toxic dose is only slightly higher than the
therapeutic dose and toxic levels can cause fatal
side effects, for example arrhythmias and seizures
(Sparrow 2007). Consequently, plasma levels of
theophylline need to be monitored carefully.
Regular use of oral corticosteroids is not
normally recommended in patients with COPD,
but some patients with advanced COPD may
need a maintenance dose of oral corticosteroids
(NICE 2010). The most serious limitation of oral
corticosteroid therapy is the risk of long-term
side effects, which can include osteoporosis,
adrenal suppression, peptic ulceration, muscle
wasting, diabetes, weight gain, skin atrophy and
impaired healing (Sparrow 2007). Mucolytic
agents should be considered in patients with a
chronic productive cough and treatment should
be continued if there is symptomatic improvement
(NICE 2010).
Inhaler devices and technique
Poor inhaler technique can reduce significantly
the proportion of drug that reaches the target site
in the lungs. Therefore, correct inhaler technique
with the use of an appropriate inhaler device are
essential in the effective management of COPD
(Kaufman 2011). Various devices are available for
the administration of inhaled therapies, including:
Pressurised
 metered dose inhalers.
Spacer
 devices (to be used with pressurised
metered dose inhalers).
Breath-actuated
 metered dose inhalers.
 powder inhalers.
Dry
The selection of a particular device is determined
by the choice of drug, patient preference and the
experience and knowledge of the prescribing
clinician. No single device will satisfy the needs
of all patients (Kaufman 2011). Each device
has advantages and limitations; for example,
pressurised metered dose inhalers are quick to
use and easy to carry because they are compact.
However, common errors when using a metered
dose inhaler are failure to co-ordinate inhalation
with actuation of the device and rapid inhalation.
Difficulties with co-ordination can be managed
by using a breath-actuated device or spacer, and
the problem of rapid inhalation can be improved
by training (Corrigan 2011).
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Dry powder inhalers require rapid and forceful
inhalation for best use. Failure to inhale deeply
and forcibly at the start of inhalation results in
the generation of drug particles that are too big
to enter the lungs. In addition, if the patient does
not inhale fast or long enough, not all of the dose
is emitted from the device (Haughney et al 2008).
Most patients, regardless of age, can learn how
to use an inhaler, unless they have significant
cognitive impairment (NICE 2010).
Healthcare professionals caring for patients with
COPD should discuss any preferences for inhaler
device with the patient. Practical training should
be provided when a device is first prescribed and
inhaler technique should be checked regularly
(NICE 2010). Teaching and checking inhaler
technique should be undertaken by competent
professionals, who are trained to use all of the
devices, to avoid subtle problems with technique
going unnoticed (Corrigan 2011). If a patient
cannot use a particular device, even after training,
another device should be tried. It is also important
to check whether the patient is adhering to his or
her treatment.
Other approaches to treatment of
chronic obstructive pulmonary disease
Pharmacological therapy is only one element of
COPD management. Other interventions are also
crucial in managing symptoms and improving the
quality of life of patients.
Oxygen therapy It is important to remember that
oxygen is not a treatment for the symptomatic
relief of breathlessness and should only be used
for the correction of hypoxia. To be considered
for long-term oxygen therapy (LTOT), patients
should have a definite diagnosis of COPD, should
be receiving optimum pharmacological therapy
already and their condition should be stable (NICE
2010). Pulse oximetry should be available in all
healthcare settings to ensure that patients eligible
for LTOT are identified. Patients with oxygen
saturation persistently below 92% when stable and
on optimum drug treatment should be referred to
specialist respiratory teams for blood gas analysis.
Arterial blood gases should be measured on two
occasions, at least three weeks apart (NICE 2010).
LTOT (15 hours each day) has been shown to
improve survival and quality of life in hypoxaemic
patients with COPD (Douglas and Currie 2011).
Patients receiving LTOT should be reviewed
annually. Review should include pulse oximetry
(NICE 2010).
Short-burst oxygen therapy is often prescribed
for breathlessness at rest or recovery after exercise.
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 However, according to Douglas and Currie
(2011), giving oxygen after exercise does not
consistently influence breathlessness scores or rate
of symptomatic recovery in patients who do not
fulfil the arterial blood gas criteria for LTOT. The
role of short-burst oxygen therapy in COPD is
controversial and it should only be prescribed if clear
improvement in breathlessness or exercise tolerance
can be demonstrated (Douglas and Currie 2011).
NICE 2010 makes clear recommendations about the
use of long term, ambulatory and short-burst oxygen
therapy in patients with COPD.
Smoking cessation Stopping smoking is the most
important intervention because it is the only one that
alters progression of COPD (Bellamy and Booker
2011). All patients with COPD, regardless of age or
disease severity, should be encouraged actively and
continually to stop smoking (NICE 2010, 2012a).
Service providers should ensure systems are in
place regularly to encourage people with COPD
who smoke to stop smoking, and that the full
range of evidence-based smoking cessation support
is available (NICE 2011). Evidence-based stop
smoking interventions, which combine behavioural
support such as counselling or cognitive behavioural
therapies (Greener 2011) with pharmacotherapy,
offer the best chance of success.
Pharmacological aids to smoking cessation include
nicotine replacement therapy (NRT), bupropion and
varenicline (Bellamy and Booker 2011). The principle
of NRT is to provide nicotine at a much lower level
than that obtained by smoking. NRT replacement
helps to reduce withdrawal symptoms and allows
the smoker to concentrate on breaking the habit of
smoking. Once the habit is broken, NRT can be
reduced over a period of time and then withdrawn.
Bupropion was originally developed as an
antidepressant, but is now also used to aid
smoking cessation. Bupropion works directly on
the addiction pathways in the brain and helps to
prevent nicotine cravings. The drug is generally
well tolerated, but there are contraindications
as identified in the British National Formulary
(Joint Formulary Committee 2012).
Varenicline is the newest addition to the
pharmacological therapies available to aid
smoking cessation. It is a partial agonist at the
nicotine receptor so it reduces the craving for
cigarettes and decreases their pleasurable effects
(Bellamy and Booker 2011). Concerns about side
effects of varenicline, for example depression and
suicidal thoughts and actions, mean that it remains
controversial, although some studies have found
no increased risk (Bellamy and Booker 2011).
Nevertheless, the drug must be used with caution
in patients with a history of psychiatric illness
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(depression, bipolar disorder or schizophrenia).
Bellamy and Booker (2011) suggested that the
risks of continuing to smoke in patients with
COPD far outweigh the risks of using bupropion
or varenicline provided they are given to carefully
selected patients.
Pulmonary rehabilitation Pulmonary rehabilitation
is a holistic approach to the management of COPD.
It requires the co-ordinated efforts of several
healthcare professionals to deliver an individualised
rehabilitation programme (Cazzola et al 2007).
The NICE (2011) COPD quality standard requires
that service providers ensure multidisciplinary
pulmonary rehabilitation programmes are timely
and accessible, and that health outcomes are
monitored to establish their effectiveness.
There are three main components of pulmonary
rehabilitation: exercise training, education about
COPD and its management, and psychosocial
support. NICE (2010) recommends that pulmonary
rehabilitation should be offered to all appropriate
patients with COPD, including those who consider
themselves functionally disabled with the condition
(usually MRC grade 3 and above on the dyspnoea
scale) and those recently hospitalised as a result of an
acute exacerbation. Pulmonary rehabilitation is not
suitable for patients who are unable to walk, have
unstable angina or have had a recent myocardial
infarction (NICE 2010). Pulmonary rehabilitation is
associated with reductions in breathlessness and use
of health services, and improved exercise tolerance
and health-related quality of life (DH 2010).
Aerobic exercise to recondition skeletal muscles
and improve exercise endurance forms the
cornerstone of most pulmonary rehabilitation
programmes (Bellamy and Booker 2011). Cycling,
walking and exercises that train specific muscle
groups, such as lower and upper limb training,
feature in such programmes (Kelly 2007a, Bellamy
and Booker 2011).
Patient-centred care
Good communication and partnership working
between patients, healthcare professionals, and
carers and families, if appropriate, are essential
in the management of COPD. Clinical efficacy
and outcomes should not detract from the
patient experience or patient-centred care (NICE
2012c). Patients with COPD should be given the
opportunity to discuss their health beliefs and
concerns and so make informed decisions about
their care and treatment. They should also have
access to evidence-based written information
about their condition that is tailored to their
individual needs (NICE 2010).
18/01/2013 10:57
 Art & science respiratory supplement

As well as managing physical symptoms it is Conclusion

important to consider the patients psychological
state. A diagnosis of COPD can generate physical,
psychological and spiritual responses that
challenge coping mechanisms (Kelly 2007b).
A diagnosis of COPD can change how people
view themselves, their lives and the future. Some
patients may find it difficult to adjust, which can
lead to social isolation and a sedentary lifestyle as
a result of progressive breathlessness and fatigue
(Kelly 2007b). Healthcare professionals need
to remain alert to the potential psychological
problems that patients may experience so they can
be addressed in a timely manner (Kelly 2007b).
COPD is an umbrella term for the airflow
obstruction associated with chronic bronchitis
and emphysema. Cigarette smoking is the single
most important cause of COPD, but other risk
factors include occupation and air pollution.
Nurses working in all care settings can
make an important contribution to the care
of people with COPD by providing guidance,
education and support. It is hoped that
evidence-based practice in the diagnosis,
treatment and management of the disease will
improve care, quality of life and health outcomes
for patients NS

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