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Chronic Obstructive Pulmonary

Disease (COPD)
:PREPARED BY
Miss Fatima Hirzallah RN,MSN,CNS,
PhD
 chronic obstructive pulmonary disease (COPD)

• Is a disease state characterized by airflow limitation

that is not fully reversible.

• COPD may include disease that cause airflow

obstruction (emphysema, bronchitis or chronic
obstruction) or a combination of these disorders.
Other disease as, bronchiectasis, and asthma were
previously classified as types of COPD.

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 Pathophysiology

• In COPD, the airflow imitation in both progressive &

associated with an abnormal inflammatory response
of the lungs to noxious particles or gases.

• Because of the chronic inflammation & the body’s

attempts to repair it, narrowing occurs in the small
peripheral air way. Over time, this injury & repair
process cause scar tissue formatting & narrowing of
the airway lumen.

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• Airflow obstruction may also due to parenchymal
destruction as seen with emphysema, a disease of
the alveoli or gas exchange units.

• When activated by chronic inflammation proteinases

and other substances may released & damaging the
parenchyma of the lung. Parenchyma change may be
due to inflammation, environmental, and genetic
factors

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 Chronic Bronchitis

• A disease of the airway is defined as the presence of

cough & sputum production for at least 3 months in
each of two consecutive years.

• In many cases, smoke or environmental pollutants

irritant the airway, resulting in hypersecreation of
mucus & inflammation. This constant irritation
causes the mucous-secretion glands and goblet cell
to increase in number, ciliary function is reduce, &
more mucus is produced.

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• Bronchial walls become thickened, the bronchial
lumen is narrowed, and mucus may blug the airway.

• Alveolar adjacent to the brochioles may become

damaged & fibrosed resulting in altered function of
the alveolar macrophages, which play a big role in
destroying foreign particles, including bacteria. As a
result pt. is more susceptible to respiratory infection.

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 Emphysema
• Impaired gas exchange (O2.CO2).Result from
destruction of the walls of over distended alveoli.

• It’s a pathological term that describes an

abnormal distention of the air spaces beyond the
terminal bronchioles, with destruction of the
walls of the alveoli. Its end process that has
progressed slowly for many years.

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• As the walls of the alveoli are destroyed, 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 O2 diffusion, CO2 elimination is
impaired resulting in increase CO2 tension in arterial
line & resp acidosis.

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• Consequently blood pulmonary blood flow is
increase, forcing the Rt. Ventricle to maintain a
higher blood pressure in pulmonary artery.
Hypoxemia also increase pulmonary artery pressure.

• Thus Rt.-sided heart failure (cor pulmonal) is one

complication of emphysema.

• Congestion, dependent edema, distended neck

veins, or pain in the region of liver suggests the
development of cardiac failure.

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• Rt.pulmonary hypertrophy may result, followed by
Rt. Ventricular failure.

• (In short cor pulmonary results from pulmonary

hypertension, which may causes the Rt.side of the
heart to enlarge because of the increased work
required to pump blood against high resistance
through the pulmonary vascular system).

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 There are two main types of emphysema, based on
changes taking place in the lung: pan lobular and
centrilobular.

Pan lobular…destruction of resp. bronchiole,

alveolar duct, and alveoli. All air spaces within the
lobule are essentially enlarged. In this type pt has
barrel chest, dyspnea, to move air out of the lungs,
negative pressures is required.

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 Risk Factors

• It includes environmental exposure and host factors

for COPD is cigarette smoking, pipe, cigar, & other
types of tobacco smoking.

• Smoking depress the activity of scavenger cells &

affect respiratory tract ciliary cleansing mechanism,
which keeps breathing passages free of inhaled
irritant, bacteria, & other foreign matter. When
smoking damaged this cleansing mechanism, airflow
is obstructed & air becomes trapped, behind the
obstruction.
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• Other factors include prolonged & intense exposure
to occupational dusts & chemicals.

• A host risk of factor, is a deficiency of alpha, anti-

trypsin, an enzyme inhibitor that protects the lung
parenchyma from injury. This predisposes young pt.
to rapid development of lobular emphysema even in
the abscent of smoking. Alpha, antitrypsin deficiency
is one of the most common genetically linked lethal
among causasion.

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 S&S

• It characterized by three primary symptoms:

Cough, sputum production, and dyspnea on
exertion. These symptoms often worsen over the
time.

• Often pt cannot participate in even mild exercise

because of dyspnea, as COPD progress, dyspnea
occur at rest.

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• Pt with COPD is at risk respiratory insufficiency &
infections.

• In COPD Pt with a primary emphysematous component,

chronic hyperinflation leads to the barrel chest. This
results from fixation of the ribs in the inspiration position
(due to hyperinflation) and from loss of lung elasticity.

• Retraction of the supraclavicular fossae occurs on

inspiration, causing the shoulder to have upwared.
Advance emphysema, the abdominal muscle also
contract on inspiration.
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 Assessment and diagnostic finding

• Health history for pt with potential COPD.

• Spirometry is used to evaluate airflow obstruction
• ABGS.
• Chest x-ray.
• alpha, anti-trypsin screening may be performed for
pt under age 45, or those with strong family history.

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• In DX of COPD, several differential DX must be ruled.
( the primary differential DX is asthma).

• The key part of differentiation is the pt history, as

well as pt responsiveness to bronchodilators.

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 Complication

• Respiratory insufficiency & failure are major life

threatening complication of COPD.

• Pneumothorax, pneumonia, atelactasis, & cor

pulmonale.

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 Medical Management

• Risk reduction, cessation of smoking is the most

effective intervention to prevent COPD. (nicotin gum,
inhaler, patches, nasal spray)

• Pharmacological therapy: bronchodilator, relieve

bronchospasm and relieve airway obstruction by
allowing increased oxygen distribution through out
the lungs and improving alveolar ventilation.

• A metered-dose inhaler (MDI) is a pressurized device

containing an aerosolized powder of medication. Pt
instructed on the correct use of the device. (holding
chamber).

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• Corticosteroids: inhaled and systemic corticosteroid
(oral or IV) may be used in COPD, but are used more
frequently in asthma.

• It has been shown that corticosteroid don’t slow the

decline in lung infection, these medication may
improve symptoms.

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• Medication regimens used to manage COPD
are based on disease severity.
• For stage one or mild, a short acting
bronchodilator.
• For stage II bronchodilator with inhaled
corticosteroid.
• For stage III or sever regular treatment with
one or more bronchodilator and inhaled
corticosteroid.
• Pt should receive a yearly influenza vaccine &
pneumococcal vaccine every 5-7 years as preventive
measures.

• Management of exacerbation: its difficult to DX,

primary causes is tracheobronchial infection & air
pollution. Secondary causes are pneumonia,
pneumothorac, rib fracture. Optimizing of
bronchodilator therapy is the first line. Depending on
S&S antibiotic agent, corticosteroid, O2 therapy &
respiratory intervention may be used
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• O2 therapy: can be administered as long-term
continuous therapy, during exercise or to prevent
acute dyspnea.
• Because hypoxemia stimulates respiration in the pt
with sever COPD, increasing O2 flow to a high rate
may greatly raise the pt blood oxygen level at the
same time, this will suppress the respiratory drive,
causing increase retention of CO2.
• The nurse should closely monitor the pt respiratory
response to O2 administration via physical
assessment, pulse oximetry, and \or arterial blood
gases.

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 :Surgical management

• bullectomy is a surgical option for select pt with

bolous emphysema. Bullae are enlarged airspaces
that don’t contribute to ventilation but occupy space
in the thorax.

• Lung volume reduction surgery: involves the removal

of a portion of the diseased lung parenchyma. This
allows functional tissue to expand, resulting in
improved elastic recoil of the lung, improved chest
wall & diaphragmatic mechanism.

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• Lung transplantation

• Pulmonary rehabilitation: it’s well established &

widely accepted as a means to alleviate symptoms
and optimizing functional status. Most rehabilitation
program includes educational, psychosocial,
behavioral, & physical competent. Breathing exercise
is used to improve functional status.

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 NSG Management

• The nurse plays a key role in identifying potential

candidates for pulmonary rehabilitation and in
facilitating, & reinforcement the material learned in
program.

• PT Education: is a major component of pulmonary

rehabilitation program. It may include normal
anatomy & physiology of the lung, path., medication,
home O2 therapy, nutrition, coping with chronic
disease & communication with health team.

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• Breathing exercises: the breathing of most people
with COPD is shallow, rapid, & inefficient. With
practice this type of upper chest breathing can be
changed to diaphragmatic breathing.

• Inspiratory muscle training. Once the pt

diaphragmatic breathing, a program of inspiratory
muscle training may be prescribed to help
strengthen the muscles used in breathing.

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• Activity pacing: pt with COPD has decrease exercise
tolerance during specific periods of day. This true on
arising in the morning, because bronchial secretion
collect in the lungs during night while pt is lying
down.

• Self-care activities: pt encourage to precipitate.

• Physical conditioning: its include breathing exercise

& general exercise.

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• Oxygen therapy: Portable O2 is allow pt to exercise,
work, and travel.

• Nutritional therapy: 25% of COPD undernourished,

also assessment of caloric need & meal planning.

• Coping measures: frustration of having to work to

breath & realization that the disease is prolonged.
Nurse needs to provide education, and support to
family. (NSG Process-discuss).

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THANKS