Chronic Obstructive Pulmonary Disease
Overview
• Chronic obstructive pulmonary disease
(COPD) encompasses two diseases:
emphysema and chronic bronchitis.
Most clients who have emphysema also
have chronic bronchitis. COPD is
irreversible.
• Emphysema is characterized by the loss
of lung elasticity and hyperinflation of
lung tissue.
• Emphysema causes destruction of the
alveoli, leading to a decreased surface
area for gas exchange, carbon dioxide
retention, and respiratory acidosis.
• Chronic bronchitis is an inflammation of
the bronchi and bronchioles due to
chronic exposure to irritants.
• COPD typically affects middle age to
older adults.
COPD
• Also called Chronic Airflow limitation is a
group of chronic respiratory disease
characterized by obstruction of airflow
that is not fully reversible
• Although each of the disorders may
occur individually, it is more common
for tow or more problems to co-exist
and the symptoms to overlap
• COPD may include diseases that cause
airflow obstruction (eg, emphysema,
chronic bronchitis) or a combination of
these disorders.
• Other diseases such as cystic fibrosis,
bronchiectasis, and asthma were
previously classified as types of chronic
obstructive lung disease.
• However, asthma is now considered a
separate disorder and is classified as an
abnormal airway condition
characterized primarily by reversible
inflammation.
• COPD can coexist with asthma. Both of
these diseases have the same major
symptoms; however, symptoms are
generally more variable in asthma than
in COPD.
Pathophysiology
Since the condition is chronic, this
process is repeated overtime, the
injury-repair process causes scar tissue
that narrows the airway lumen and
parenchymal destruction, plus mucous
production due to inflammation,
obstruction of the airway is more hasten.
Chronic Bronchitis
• Chronic bronchitis, a disease of the
airways, is defined as the presence of
cough and sputum production for at
least 3 months in each of 2 consecutive
years.
o In many cases, smoke or other
environmental pollutants irritate
the airways, resulting in
hypersecretion of mucus and
inflammation.
• This constant irritation causes the
mucus-secreting glands and goblet cells
to increase in number, ciliary function is
reduced, and more mucus is produced.
• The bronchial walls become thickened,
the bronchial lumen is narrowed, and
mucus may plug the airway.
• Alveoli adjacent to the bronchioles may
become damaged and fibrosed,
resulting in altered function of the
alveolar macrophages.
• This is significant because the
macrophages play an important role in
destroying foreign particles, including
bacteria. As a result, the patient
becomes more susceptible to
respiratory infection.
• A wide range of viral, bacterial, and
mycoplasmal infections can produce
acute episodes of bronchitis.
Exacerbations of chronic bronchitis are
most likely to occur during the cold
weathers.
Emphysema
• In emphysema, impaired gas exchange
(oxygen, carbon dioxide) results from
destruction of the walls of
overdistended alveoli.
• “Emphysema” is a pathological term
that describes an abnormal distention of
the air spaces beyond the terminal
bronchioles, with destruction of the
walls of the alveoli.
• It is the end stage of a process that has
progressed slowly for many years.
• As the walls of the alveoli are destroyed
(a process accelerated by recurrent
infections), the alveolar surface area in
direct contact with the pulmonary
capillaries continually decreases,
causing an increase in dead space (lung
area where no gas exchange can occur)
and impaired oxygen diffusion, which
leads to hypoxemia.
• In the later stages of the disease, carbon
dioxide elimination is impaired, resulting
in increased carbon dioxide tension in
arterial blood (hypercapnia) and causing
respiratory acidosis.
• As the alveolar walls continue to break
down, the pulmonary capillary bed is
reduced. Consequently, pulmonary
blood flow is increased, forcing the right
ventricle to maintain a higher blood
pressure in the pulmonary artery.
• Hypoxemia may further increase
pulmonary artery pressure. Thus,
right-sided heart failure (cor pulmonale)
is one of the complications of
emphysema.
• Congestion, dependent edema,
distended neck veins, or pain in the
region of the liver suggests the
development of cardiac failure.
Two main types of emphysema
• Based on the changes taking place in the
lung:
o panlobular (panacinar) and
o centrilobular (centroacinar) .
• Both types may occur in the same
patient.
In the panlobular (panacinar) type
• there is destruction of the respiratory
bronchiole, alveolar duct, and alveoli.
• All air spaces within the lobule are
essentially enlarged, but there is little
 inflammatory disease.
• The patient with this type of
emphysema typically has a hyperinflated
(hyperexpanded) chest (barrel chest on
physical examination), marked dyspnea
on exertion, and weight loss.
• To move air into and out of the lungs,
negative pressure is required during
inspiration, and an adequate level of
positive pressure must be attained and
maintained during expiration.
• The resting position is one of inflation.
Instead of being an involuntary passive
act, expiration becomes active and
requires muscular effort.
• The patient becomes increasingly short
of breath, the chest becomes rigid, and
the ribs are fixed at their joints.
In the centrilobular (centroacinar) form
• pathologic changes take place mainly in
the center of the secondary lobule,
preserving the peripheral portions of
the acinus.
• there is a derangement of
ventilation–perfusion ratios, producing:
o chronic hypoxemia,
o hypercapnia (increased CO2 in
the arterial blood),
o polycythemia, and
o episodes of right-sided heart
failure.
• (This leads to central cyanosis,
peripheral edema, and respiratory
failure).
• The patient may receive diuretic therapy
for edema.
Risk factors for COPD
• Cigarette smoking (first hand and
second hand)
• Chronic infection
• Inhaled irritants (occupational exposure
and air pollutants [indoors and
outdoors])
• Alpha, antitrypsin deficiency (enzyme
deficiency at an early age that leads to
COPD)
# a deficiency of alpha1 antitrypsin, an
enzyme inhibitor that protects the lung
parenchyma from injury. This deficiency
predisposes young patients to rapid
development of lobular emphysema even in
the absence of smoking. Alpha1 antitrypsin
deficiency is one of the most common
genetically linked lethal diseases among
Caucasians and affects approximately one in
every 3,000 Americans or approximately
80,000 to 100,000 cases (George, San Pedro
& Stoller, 2000). Genetic counseling should
also be offered. Alpha-protease inhibitor
replacement therapy, which slows the
progression of the disease, is available for
patients with this genetic defect and for
those with severe disease. This intermittent
infusion therapy is costly and is required on
an ongoing basis.
Clinical manifestations risk for acute and chronic respiratory
• Orthopnea failure
• Barrel chest • In COPD patients with a primary
• Prolonged expirator time emphysematous component, chronic
• Diminished breath sounds hyperinflation leads to the “barrel
• Thorax is hyperresonant to percussion chest” thorax configuration. This results
• Exertional dyspnea progressing to from fixation of the ribs in the
dyspnea at rest inspiratory position (due to
• Increased expiratory rate hyperinflation) and from loss of lung
• Distended neck veins elasticity (slide 17).
• Retraction of the supraclavicular fossae
COPD is characterized by three primary occurs on inspiration, causing the
symptoms: shoulders to heave upward (slide 18). In
• Cough advanced emphysema, the abdominal
• sputum production, and muscles also contract on inspiration.
• dyspnea on exertion (NIH, 2001).
o These symptoms often worsen over
time.
o Chronic cough and sputum
production often precede the
development of airflow limitation
by many years.
o However, not all individuals with
cough and sputum production will
develop COPD.
o Dyspnea may be severe and often
interferes with the patient’s
activities.
o Weight loss is common because
dyspnea interferes with eating,
and the work of breathing is
energy-depleting.
o Often the patient cannot participate
in even mild exercise because of
dyspnea; as COPD progresses,
dyspnea occurs even at rest. As
the work of breathing increases
over time, the accessory muscles
are recruited in an effort to
breathe.
• The patient with COPD is at risk for
respiratory insufficiency and respiratory
infections, which in turn increase the

Assessment and Diagnostics
• Key Factors to Assess in the COPD
Patient’s Health History
o Exposure to risk factors—types,
intensity, duration
o Past medical history—respiratory
diseases/problems, including
asthma, allergy, sinusitis, nasal
polyps, history of respiratory
infections
o Family history of COPD or other
chronic respiratory diseases
o Pattern of symptom development
o History of exacerbations or previous
hospitalizations for respiratory
problems
o Presence of comorbidities
o Appropriateness of current medical
treatments
o Impact of the disease on quality of
life
o Available social and family support
for patient
o Potential for reducing risk factors
(eg, smoking cessation)
Diagnostic findings cont….
• Pulmonary function studies are used to :
o help confirm the diagnosis of COPD,
o determine disease severity, and
o follow disease progression.
o Spirometry is used to evaluate
airflow obstruction, which is
determined by the ratio of FEV1
(volume of air that the patient can
forcibly exhale in 1 second) to
forced vital capacity (FVC).
Spirometric results are expressed as
an absolute volume and as
percent-predicted using appropriate
normal values for gender, age, and
height. With obstruction, the
patient either has difficulty exhaling
or cannot forcibly exhale air from
the lungs, reducing the FEV1.
o Obstructive lung disease is defined
as a FEV1/FVC ratio of less than
70%.
• Bronchodilator reversibility testing may
be performed to rule out the diagnosis
of asthma and to guide initial treatment.
o With this type of testing, spirometry
is first obtained,
o then the patient is given an inhaled
bronchodilator per a protocol,
o and finally spirometry is repeated.
o The patient demonstrates a degree
of reversibility if the pulmonary
function values improve after
administration of the
bronchodilator.
• Arterial blood gas measurements may
also be obtained to assess baseline
oxygenation and gas exchange.
• Chest x-ray may be obtained to exclude
alternative diagnoses.
• Alpha1 antitrypsin deficiency screening
may be performed for patients under
age 45 or for those with a strong family
history of COPD.
The Stages of COPD:
• 0 - normal spirometry, chronic
symptoms of cough, sputum production
• Mild COPD or Stage 1—Mild COPD with
a FEV1 about 80 percent or more of
normal. You may have no symptoms.
You might be short of breath when
walking fast on level ground or climbing
a slight hill.
• Moderate COPD or Stage 2—Moderate
COPD with a FEV1 between 50 and 80
percent of normal. If you’re walking on
level ground, you might have to stop
every -few minutes to catch your breath.
• Severe COPD or Stage 3—Severe
emphysema with a FEV1 between 30
and 50 percent of normal plus
respiratory failure or clinical signs of
right heart failure. You may be too short
of breath to leave the house. You might
get breathless doing something as
simple as dressing and undressing.
• Very Severe COPD or Stage 4—Very
severe or End-Stage COPD with a lower
FEV1 than Stage 3, or people with low
blood oxygen levels and a Stage 3 FEV1.
This can make it hard to catch your
breath even when you’re resting.
Important notes
• In diagnosing COPD, several differential
diagnoses must be ruled out.
• The primary differential diagnosis is
asthma.
• Key characteristics of asthma include
onset often early in life, variation in
daily symptoms and day-to-day
occurrence or timing of symptoms,
family history of asthma, and a largely
reversible airflow obstruction.
• It may be difficult to differentiate
between a patient with COPD and one
with chronic asthma.
• A key part of differentiation is the
patient history, as well as the patient’s
responsiveness to bronchodilators.
• Other diseases that must be considered
in the differential diagnosis include
heart failure, bronchiectasis, and
tuberculosis (NIH, 2001).
Medical Management
RISK REDUCTION
• Smoking cessation - is the single most
effective intervention to prevent COPD
or slow its progression (NIH, 2001).
PHARMACOTHERAPY
• Bronchodilators (inhalers)
o Short-acting beta2 agonists, such
as albuterol (Proventil, Ventolin)
provide rapid relief.
o Cholinergic antagonists
(anticholinergic medications),
such as ipratropium (Atrovent),
block the parasympathetic
nervous system. This allows for
the sympathetic nervous system
effects of increased
bronchodilation and decreased
pulmonary secretions. These
medications are long acting and
are used to prevent
bronchospasms.
o Methylxanthines, such as
 theophylline (Theo-24), relax
smooth muscles of the bronchi.
• Leukotriene antagonists, such as
montelukast (Singulair); mast cell
These medications require close
stabilizers, such as cromolyn sodium
monitoring of serum medication
(Intal); and monoclonal antibodies, such
levels due to narrow therapeutic
as omalizumab (Xolair), can be used.
ranges. Use only when other
Nursing Considerations
treatments are ineffective.
• Watch the client for a decrease in
Nursing Considerations immunity function.
• Monitor the client’s serum levels for • Monitor the client for hyperglycemia.
toxicity when taking theophylline. Side
effects will
• Advise the client to report black, tarry
stools.
• include tachycardia, nausea, and
• Observe the client for fluid retention
diarrhea.
and weight gain. This is common.
• Watch the client for tremors and
• Check the client’s throat and mouth for
tachycardia when taking albuterol.
aphthous lesions (cold sores).
• Observe the client for dry mouth when
• Omalizumab (Xolair) can cause
taking ipratropium.
anaphylaxis.
Patient Education
Client Education
• Encourage the client to suck on hard
• Encourage the client to drink plenty of
candies to help moisten dry mouth
fluids to promote hydration.
while taking ipratropium.
• Encourage client to increase fluid intake,
• Encourage the client to take
glucocorticoids (prednisone) with food.
report headaches, or blurred vision.
• Monitor heart rate. Palpitations can
• Advise client to use medication to
prevent and control bronchospasms.
occur, which may indicate toxicity of
ipratropium. • Advise client to avoid people who have
respiratory infections.
Anti-inflammatory agents
• Use good mouth care.
• These medications decrease airway
• Use medication as a prophylactic
inflammation.
prevention of COPD symptoms.
• If corticosteroids, such as fluticasone
• Instruct the client not to stop use of
(Flovent) and prednisone (Deltasone),
medication suddenly.
are given systemically, monitor for
serious side effects
Mucolytic Agents
(immunosuppression, fluid retention,
hyperglycemia, hypokalemia, poor • These agents help thin secretions
wound healing). making it easier for the client to expel.

• Nebulizer treatments include
acetylcysteine (Mucomyst), or dornase
alfa (Pulmozyme).
• An oral agent that can be taken is
guaifenesin (Mucinex, Robitussin).
• A combination of guaifenesin and
dextrommorphan (Mucinex DM) also
can be taken orally to loosen secretions.
Interprofessional Care
• Respiratory services should be consulted
for inhalers, breathing treatments, and
suctioning for airway management.
• Nutritional services should be contacted
for weight loss or gain related to
medications or diagnosis.
• Rehabilitative care can be consulted if
the client has prolonged weakness and
needs assistance with increasing level of
activity.
Therapeutic Procedures
• Chest physiotherapy uses percussion
and vibration to mobilize secretions.
• Raising the foot of the bed slightly
higher than the head can facilitate
optimal drainage and removal of
secretions by gravity ****
Care after Discharge
• COPD is debilitating for older adult
clients. Referrals to assistance programs,
such as food delivery services, can be
indicated.
• Set-up referral services, including home
care services such as portable oxygen.
o Client Education
§ Encourage the client to eat
high-calorie foods to promote
energy.
§ Encourage rest periods as
needed.
§ Promote hand hygiene to
prevent infection.
§ Reinforce the importance of
taking medications (inhalers, oral
medications) as prescribed.
§ Promote smoking cessation if the
client is a smoker.
§ Encourage immunizations, such
as influenza and pneumonia, to
decrease the risk of infection.
§ Clients should use oxygen as
prescribed. Inform other
caregivers not to smoke around
the oxygen due to flammability.
§ Provide support to the client and
family.
Complications
v Respiratory infection
- Respiratory infections result from
increased mucus production and
poor oxygenation levels.
• Nursing Actions
o Administer oxygen therapy.
o Monitor oxygenation levels.
o Administer antibiotics and other
medications as prescribed.
o Advise client to avoid crowds and
people who have respiratory
infections.
o Encourage client to obtain
pneumonia and influenza
immunizations.
v Right-sided heart failure (cor pulmonale)
- Air trapping, airway collapse, and
stiff alveoli lead to increased
pulmonary pressures.
- Blood flow through the lung tissue is
difficult. This increased workload
leads to enlargement and thickening
 of the right atrium and ventricle.
- Manifestations include the
following:
• Low oxygenation levels
• Cyanotic lips
• Enlarged and tender liver
• Distended neck veins
• Dependent edema

• Nursing Actions
o Monitor respiratory status and
administer oxygen therapy.
o Monitor heart rate and rhythm.
o Administer medications as
prescribed.
o Administer IV fluids and diuretics to
maintain fluid balance.