Chronic Obstructive ❑ There are two main types of

emphysema: panlobular and

Pulmonary Disease (COPD) centrilobular.
❑ A condition of chronic dyspnea with
In panlobular, there is destruction of the
expiratory airflow limitation that
respiratory bronchiole, alveolar duct, and
does not significantly fluctuate.
alveolus.
❑ Defined by The Global Initiative for
All spaces in the lobule are enlarged.
Chronic Obstructive Lung Disease as
“a preventable and treatable disease
In centrilobular, pathologic changes occur
with some significant extrapulmonary
mainly in the center of the secondary
effects that may contribute to the
lobule.
severity in individual patients.”

 Pathophysiology
 Classification
❑ There are two classifications of COPD:
chronic bronchitis and emphysema.
❑ These two types of COPD can be
sometimes confusing because there
are patients who have overlapping
signs and symptoms of these two
distinct disease processes.
Chronic Bronchitis
❑ Chronic bronchitis is a disease of the
airways and is defined as the
presence of cough and sputum
production for at least 3 months in
each of 2 consecutive years.
❑ Chronic bronchitis is also termed as
“blue bloaters”.
❑ Pollutants or allergens irritate the
airways and leads to the production
of sputum by the mucus-secreting
glands and goblet cells.
❑ A wide range of viral, bacterial, and
mycoplasmal infections can produce
acute episodes of bronchitis.
Emphysema
❑ Pulmonary Emphysema is a
pathologic term that describes an
abnormal distention of airspaces
beyond the terminal bronchioles and
destruction of the walls of the alveoli.
❑ People with emphysema are also
called “pink puffers”.
❑ There is impaired carbon dioxide and
oxygen exchange, and the exchange
results from the destruction of the
walls of over distended alveoli.
In COPD, the airflow limitation is both
progressive and associated with an
abnormal inflammatory response of the
lungs to noxious gases or particles.
❑ An inflammatory response occurs
throughout the proximal and
peripheral airways, lung parenchyma,
and pulmonary vasculature.
❑ Due to the chronic inflammation,
changes and narrowing occur in the
airways.
❑ There is an increase in the number of
goblet cells and enlarged submucosal
glands leading to hypersecretion of
mucus.
❑ Scar formation. This can cause scar
formation in the long term and
narrowing of the airway lumen.
❑ Wall destruction. Alveolar wall
destruction leads to loss of alveolar
attachments and a decrease in elastic
recoil.
❑ The chronic inflammatory process
affects the pulmonary vasculature
and causes thickening of the vessel
lining and hypertrophy of smooth
muscle.
 Epidemiology
Mortality for COPD has been increasing
ever since while other diseases have
decreasing mortalities.
❑ COPD is the fourth leading cause of
death in the United States.
❑ COPD also account for the death of
125, 000 Americans every year.
❑ Mortality from COPD among women
has increased, and in 2005, more
women than men died of COPD
 ❑ Approximately 12 million Americans
live with a diagnosis of COPD.
❑ An additional 2 million may have COPD
but remain undiagnosed.
❑ The annual cost of COPD is
approximately $42.6 billion with
overall healthcare expenditures of
$26.7 billion.
❑ In the 2016 update of the GOLD
guidelines, a rubric is used that
assesses symptoms, breathlessness,
spirometric classification, and risk of
exacerbations to classify patients
according to the following groups
What is the Gold classification for
COPD?
❑ Group A (low risk/less symptoms):
Stage I or II, 1 or fewer exacerbation
per year no hospitalization, modified
Medical Research Council (mMRC) 0-
1 or COPD Assessment Test (CAT) less
than 10
❑ Group B (low risk/more symptoms):
Stage I or II, 1 or fewer exacerbation
per year no hospitalization, mMRC 2
or higher or CAT 10 or higher.
❑ Group C (high risk/less symptoms):
Stage III or IV, 2 or more per year 1 or
more exacerbation with
hospitalization, mMRC 0-1 or CAT less
than 10.
 Causes
Causes of COPD includes environmental
factors and host factors. These includes:
❑ Smoking depresses the activity of
scavenger cells and affects the
respiratory tract’s ciliary cleansing
mechanism
❑ Occupational exposure. Prolonged
and intense exposure to occupational
dust and chemicals, indoor air
pollution, and outdoor air pollution
all contribute to the development of
COPD.
❑ Genetic abnormalities. The well-
documented genetic risk factor is a
deficiency of alpha1- antitrypsin, an
enzyme inhibitor that protects the
lung parenchyma from injury.
 Clinical Manifestations
The natural history of COPD is variable
but is a generally progressive disease.
❑ Genetic abnormalities. The well-
documented genetic risk factor is a
deficiency of alpha1- antitrypsin, an
enzyme inhibitor that protects the
lung parenchyma from injury.
❑ Chronic cough. Chronic cough is one
of the primary symptoms of COPD.
❑ Sputum production. There is a
hyperstimulation of the goblet cells
and the mucus-secreting gland
leading to overproduction of sputum.
❑ Dyspnea on exertion. Dyspnea is
usually progressive, persistent, and
worsens with exercise.
❑ Dyspnea at rest. As COPD progress,
dyspnea at rest may occur.
❑ Weight loss. Dyspnea interferes with
eating and the work of breathing is
energy depleting.
❑ Barrel chest. In patients with
emphysema, barrel chest thorax
configuration results from a more
fixed position of the ribs in the
inspiratory position and from loss of
elasticity.
❑ Barrel chest is a condition in which
the chest appears to be partially
inflated all the time, with the rib cage
broadened as if in the middle of a
deep breath. The person may find it
hard to breathe normally.
 Prevention
Prevention of COPD is never impossible.
Discipline and consistency are the keys to
achieving freedom from chronic
pulmonary diseases.
❑ Smoking cessation. This is the single
most cost-effective intervention to
reduce the risk of developing COPD
and to stop its progression.
❑ Healthcare providers should promote
cessation by explaining the risks of
smoking and personalizing the “at-
risk” message to the patient.
 Complications
There are two major life-threatening
complications of COPD: respiratory
insufficiency and failure.
 ❑ Respiratory failure. The acuity and
the onset of respiratory failure
depend on baseline pulmonary
function, pulse oximetry or arterial
blood gas values, comorbid
conditions, and the severity of other
complications of COPD.
❑ Respiratory insufficiency. This can be
acute or chronic, and may necessitate
ventilator support until other acute
complications can be treated.
 Assessment and Diagnostic
Findings
Diagnosis and assessment of COPD must be
done carefully since the three main
symptoms are common among chronic
pulmonary disorders.
Health History
❑ The nurse should obtain a thorough
health history from patients with
known or potential COPD.
Pulmonary function studies
❑ Pulmonary function studies are used
to help confirm the diagnosis of
COPD, determine disease severity,
and monitor disease progression.
Spirometry
❑ Spirometry is used to evaluate airway
obstruction, which is determined by
the ratio of FEV1 to forced vital
capacity.
❑ FEV1 (Forced Expiratory Volume) is
the amount of air you can force from
your lungs in one second.
❑ It's measured during a spirometry
test, also known as a pulmonary
function test, which involves
forcefully breathing out into a
mouthpiece connected to a
spirometer machine.
❑ If the FVC (Forced Vital Capacity) and
the FEV1 are within 80% of the
reference value, the results are
considered normal.
❑ The normal value for the FEV1/FVC
ratio is 70% (and 65% in persons
older than age 65).
❑ When compared to the reference
value, a lower measured value
corresponds to a more severe lung
abnormality.
ABG
❑ Arterial blood gas measurement is
used to assess baseline oxygenation
and gas exchange and is especially
important in advanced COPD.
❑ According to the National Institute of
Health, typical normal values are: pH:
7.35-7.45. Partial pressure of oxygen
(PaO2): 75 to 100 mmHg. Partial
pressure of carbon dioxide (PaCO2):
35-45 mmHg
❑ Arterial blood gases (ABGs):
Determines degree and severity of
disease process, e.g., most often
Pao2is decreased, and Paco2 is
normal or increased in chronic
bronchitis and emphysema, but is
often decreased in asthma; pH
normal or acidotic, mild respiratory
alkalosis secondary to
hyperventilation (moderate
emphysema or asthma).
CT Scan
❑ Computed tomography chest scan
may help in the differential diagnosis.
Screening for alpha1-antitrypsin
deficiency
❑ Screening can be performed for
patients younger than 45 years old
and for those with a strong family
history of COPD.
❑ This test measures the amount of
alpha-1 antitrypsin (AAT) in the
blood. AAT is a protein that is made
in the liver. It helps protect your
lungs from damage and diseases,
such as emphysema and chronic
obstructive pulmonary disease
(COPD). AAT is made by certain genes
in your body.
Chest x-ray
❑ A chest x-ray may be obtained to
exclude alternative diagnoses.
❑ May reveal hyperinflation of lungs,
flattened diaphragm, increased
retrosternal air space, decreased
vascular markings/bullae
(emphysema), increased
 bronchovascular markings Lung scan
(bronchitis), normal findings during
❑ Perfusion/ventilation studies may be
periods of remission (asthma).
done to differentiate between the
various pulmonary diseases.
Pulmonary function tests ❑ COPD is characterized by a mismatch
❑ Done to determine cause of dyspnea, of perfusion and ventilation (i.e.,
whether functional abnormality is areas of abnormal ventilation in area
obstructive or restrictive, to estimate of perfusion defect).
degree of dysfunction and to
evaluate effects of therapy, e.g., Complete blood count (CBC) and
bronchodilators.
differential
❑ Exercise pulmonary function studies
may also be done to evaluate activity ❑ Increased hemoglobin (advanced
tolerance in those with known emphysema), increased eosinophils
pulmonary impairment/progression (asthma).
of disease
❑ The forced expiratory volume over 1 Blood chemistry
second (FEV1): Reduced FEV1 not
only is the standard way of assessing ❑ alpha1-antitrypsin is measured to
the clinical course and degree of verify deficiency and diagnosis of
reversibility in response to therapy, primary emphysema.
but also is an important predictor of
prognosis. Sputum culture
❑ Total lung capacity (TLC), functional
residual capacity (FRC), and residual ❑ Determines presence of infection,
volume (RV): May be increased, identifies pathogen.
indicating air-trapping. In obstructive
lung disease, the RV will make up the Cytologic examination
greater portion of the TLC.
❑ Rules out underlying malignancy or
allergic disorder.
DL CO test
❑ Assesses diffusion in lungs. Carbon Electrocardiogram (ECG)
monoxide is used to measure gas
❑ Right axis deviation, peaked P waves
diffusion across the alveocapillary
(severe asthma); atrial dysrhythmias
membrane. Because carbon
(bronchitis), tall, peaked P waves in
monoxide combines with hemoglobin
leads II, III, AVF (bronchitis,
200 times more easily than oxygen, it
emphysema); vertical QRS axis
easily affects the alveoli and small
(emphysema).
airways where gas exchange occurs.
Emphysema is the only obstructive
disease that causes diffusion Exercise ECG, stress test
dysfunction.
❑ Helps in assessing degree of
pulmonary dysfunction, evaluating
Bronchogram effectiveness of bronchodilator
therapy, planning/evaluating exercise
❑ a radiograph of the bronchial tree
program
after injection of a radiopaque
substance.
❑ Can show cylindrical dilation of
bronchi on inspiration; bronchial
collapse on forced expiration
(emphysema); enlarged mucous
ducts (bronchitis).
 Medical Management
Pharmacologic Therapy
Bronchodilators
❑ Bronchodilators relieve
bronchospasm by altering the
smooth muscle tone and reduce
airway obstruction by allowing
increased oxygen distribution
throughout the lungs and improving
alveolar ventilation.
❑ The 3 most widely used
bronchodilators are:
▪ beta-2 agonists, such as
salbutamol, salmeterol,
formoterol and vilanterol.
▪ anticholinergics, such as
ipratropium, tiotropium,
aclidinium and glycopyrronium.
▪ theophylline
❑ Example of a short acting
bronchodilator?
 Beta2-agonists (bronchodilators)
are a group of drugs prescribed to
treat asthma. ... Examples of these
short-acting medications include:
albuterol (AccuNeb, Proventil HFA,
ProAir HFA, Ventolin HFA) and
levalbuterol (Xopenex, Xopenex
HFA).
 The preferred route of
administration for beta-2 agonists
in the treatment of asthma and
COPD is through inhalation.
 Inhalation localizes the drug to the
lung tissue, concentrating the
therapeutic effect on the airway
smooth muscles while minimizing
the distribution of the drug to the
systemic circulation.
Possible side effects of salbutamol
▪ headache.
▪ feeling nervous, restless, excitable
and/or shaky.
▪ fast, slow or uneven heartbeat.
▪ bad taste in the mouth.
▪ dry mouth.
▪ sore throat and cough.
▪ inability to sleep.
Anticholinergics
❑ Anticholinergics are a group of
substances that blocks the action of
the neurotransmitter called
acetylcholine at synapses in the
central and peripheral nervous
system. These agents inhibit the
parasympathetic nervous system by
selectively blocking the binding of
ACh to its receptor in nerve cells
✔ Anticholinergics have an
important role in the acute
treatment of COPD
exacerbations.
✔ The anticholinergics reduce
airway tone and improve
expiratory flow limitation,
primarily by blocking
parasympathetic activity in the
large and medium-sized airways.
▪ Anticholinergic inhalers include
✔ Aclidinium (Tudorza Pressair)
✔ Glycopyrronium (Seebri
Neohaler)
✔ Ipratropium (Atrovent)
✔ Tiotropium (Spiriva)
✔ Umeclidinium (Incruse Ellipta)
Theophylline
❑ Theophylline, also known as 1,3-
dimethylxanthine, is a
phosphodiesterase inhibiting drug
used in therapy for respiratory
diseases such as chronic obstructive
pulmonary disease (COPD) and
asthma under a variety of brand
names.
✔ Theophylline is indicated for the
treatment of the symptoms and
reversible airflow obstruction
associated with chronic asthma
and other chronic lung diseases,
e.g., emphysema and chronic
bronchitis.
✔ Theophylline is used to prevent
and treat wheezing, shortness of
breath, and chest tightness
caused by asthma, chronic
bronchitis, emphysema, and
other lung diseases. It relaxes
and opens air passages in the
lungs, making it easier to
breathe.
Corticosteroids
❑ A short trial course of oral
corticosteroids may be prescribed for
patients to determine whether
 pulmonary function improves and
symptoms decrease.
❑ People with COPD have airways that
are irritated and swollen, which can
make it hard to breathe.
Corticosteroids reduce inflammation,
so they can help to reduce the
amount of swelling in the airways and
make breathing easier
❑ Corticosteroids are a class of drug
that lowers inflammation in the body.
They also reduce immune system
activity. Because corticosteroids ease
swelling, itching, redness, and allergic
reactions, doctors often prescribe
them to help treat diseases like:
asthma.
❑ Examples of inhaled steroids for
COPD include:
✔ beclomethasone dipropionate
(Qvar Redihaler)
✔ budesonide (Pulmicort Flexhaler)
✔ ciclesonide (Alvesco)
✔ flunisolide (Aerospan)
✔ fluticasone propionate (Flovent)
✔ mometasone (Asmanex)
Other medications
❑ Other pharmacologic treatments that
may be used in COPD include alpha1-
antitrypsin augmentation therapy,
antibiotic agents, mucolytic agents,
antitussive agents, vasodilators, and
narcotics.
 Management of Exacerbations
❑ Optimization of bronchodilator
medications is first-line therapy and
involves identifying the best
medications or combinations of
medications taken on a regular
schedule for a specific patient
❑ Hospitalization. Indications for
hospitalization for acute exacerbation
of COPD include severe dyspnea that
does not respond to initial therapy,
confusion or lethargy, respiratory
muscle fatigue, paradoxical chest wall
movement, and peripheral edema.
❑ Oxygen therapy. Upon arrival of the
patient in the emergency room,
supplemental oxygen therapy is
administered and rapid assessment is
performed to determine if the
exacerbation is life-threatening.
❑ Antibiotics. Antibiotics have been
shown to be of some benefit to
patients with increased dyspnea,
increased sputum production, and
increased sputum purulence.
Surgical Management
Patients with COPD also have options for
surgery to improve their condition.
❑ Bullectomy is a surgical option for
select patients with bullous
emphysema and can help reduce
dyspnea and improve lung function.
❑ Lung Volume Reduction Surgery- is a
palliative surgery in patients with
homogenous disease or disease that
is focused in one area and not
widespread throughout the lungs.
❑ Lung Transplantation -is a viable
option for definitive surgical
treatment of end-stage emphysema.
❑ A patient with an acute exacerbation
of chronic obstructive pulmonary
disease (COPD) needs to receive
precise amounts of oxygen.
❑ The Venturi mask delivers precise
concentrations of oxygen and should
be selected whenever this is a priority
concern. The other methods are less
precise in terms of amount of oxygen
delivered.
 Nursing Management
Management of patients with COPD should
be incorporated with teaching and
improving the respiratory status of the
patient
Nursing Assessment
Assessment of the respiratory system
should be done rapidly yet accurately.
❑ Assess patient’s exposure to risk
factors.
❑ Assess the patient’s past and present
medical history.
❑ Assess the signs and symptoms of
COPD and their severity.
❑ Assess the patient’s knowledge of the
disease.
❑ Assess the patient’s vital signs.
❑ Assess breath sounds and pattern.
Diagnosis
Diagnosis of COPD would mainly depend
on the assessment data gathered by the
healthcare team members.
❑ Assess breath sounds and pattern.
❑ Impaired gas exchange due to chronic
inhalation of toxins.
❑ Ineffective airway clearance related
to bronchoconstriction, increased
mucus production, ineffective cough,
and other complications.
❑ Ineffective breathing pattern related
to shortness of breath, mucus,
bronchoconstriction, and airway
irritants.
❑ Self-care deficit related to fatigue.
❑ Activity intolerance related to
hypoxemia and ineffective breathing
patterns.
Planning & Goals
Goals to achieve in patients with COPD
include:
❑ Self-care deficit related to fatigue.
❑ Improvement in gas exchange.
❑ Achievement of airway clearance.
❑ Improvement in breathing pattern.
❑ Independence in self-care activities.
❑ Improvement in activity intolerance.
❑ Ventilation/oxygenation adequate to
meet self-care needs.
❑ Nutritional intake meeting caloric
needs.
❑ Infection treated/prevented.
❑ Disease process/prognosis and
therapeutic regimen understood.
❑ Plan in place to meet needs after
discharge.
Nursing Priorities
1. Maintain airway patency.
2. Assist with measures to facilitate gas
exchange.
3. Enhance nutritional intake.
4. Prevent complications, slow
progression of condition.
5. Provide information about disease
process/prognosis and treatment
regimen.
Nursing Interventions
Patient and family teaching is an
important nursing intervention to enhance
self-management in patients with any
chronic pulmonary disorder.
To achieve airway clearance
▪ The nurse must appropriately
administer bronchodilators and
corticosteroids and become alert for
potential side effects.
▪ Direct or controlled coughing. The
nurse instructs the patient in direct or
controlled coughing, which is more
effective and reduces fatigue
associated with undirected forceful
coughing.
To improve breathing pattern
▪ Inspiratory muscle training. This may
help improve the breathing pattern.
▪ Diaphragmatic breathing.
Diaphragmatic breathing reduces
respiratory rate, increases alveolar
ventilation, and sometimes helps
expel as much air as possible during
expiration.
▪ Pursed lip breathing. Pursed lip
breathing helps slow expiration,
prevents collapse of small airways,
and control the rate and depth of
respiration.
To improve activity intolerance
▪ Manage daily activities. Daily
activities must be paced throughout
the day and support devices can be
also used to decrease energy
expenditure.
▪ Exercise training. Exercise training
can help strengthen muscles of the
upper and lower extremities and
improve exercise tolerance and
endurance.
▪ Walking aids. Use of walking aids may
be recommended to improve activity
levels and ambulation.
To monitor and manage potential
complications
▪ Monitor cognitive changes. The nurse
should monitor for cognitive changes
such as personality and behavior
changes and memory impairment.
▪ Monitor pulse oximetry values. Pulse
oximetry values are used to assess
the patient’s need for oxygen and
administer supplemental oxygen as
prescribed.
▪ Prevent infection. The nurse should
encourage the patient to be
immunized against influenza and S.
pneumonia because the patient is
prone to respiratory infection.
Evaluation
During evaluation, the effectiveness of the
care plan would be measured if goals
were achieved in the end and the patient:
▪ Identifies the hazards of cigarette
smoking.
▪ Identifies resources for smoking
cessation.
▪ Enrolls in smoking cessation program.
▪ Minimizes or eliminates exposures.
▪ Verbalizes the need for fluids.
▪ Is free of infection.
▪ Practices breathing techniques.
▪ Performs activities with less shortness
of breath.
Discharge and Home Care
Guidelines
It is important for the nurse to assess the
knowledge of patient and family members
about self-care and the therapeutic
regimen
Setting goals.
▪ If the COPD is mild, the objectives of
the treatment are to increase exercise
tolerance and prevent further loss of
pulmonary function, while if COPD is
severe, these objectives are to
preserve current pulmonary function
and relieve symptoms as much as
possible.
Temperature control
▪ The nurse should instruct the patient
to avoid extremes of heat and cold
because heat increases the
temperature and thereby raising
oxygen requirements and high
altitudes increase hypoxemia.
Activity moderation
▪ The patient should adapt a lifestyle of
moderate activity and should avoid
emotional disturbances and stressful
situations that might trigger a
coughing episode.
Breathing retraining
▪ The home care nurse must provide
the education and breathing
retraining necessary to optimize the
patient’s functional status.
Documentation Guidelines
Documentation is an essential part of the
patient’s chart because the interventions
and medications given and done are
reflected on this part.
▪ Document assessment findings
including respiratory rate, character of
breath sounds; frequency, amount and
appearance of secretions laboratory
findings and mentation level.
▪ Document conditions that interfere
with oxygen supply.
▪ Document plan of care and specific
interventions.
▪ Document liters of supplemental
oxygen.
▪ Document client’s responses to
treatment, teaching, and actions
performed.
▪ Document teaching plan.
▪ Document modifications to plan of
care.
▪ Document attainment or progress
towards goals