CASE STUDY:

COPD
(CHRONIC OBSTRUCTIVE PULMONARY DISEASE)

INTRODUCTION
Chronic obstructive pulmonary disease (COPD) also known as chronic obstructive
lung disease (COLD), chronic obstructive airway disease (COAD), chronic airflow
limitation (CAL) and chronic obstructive respiratory disease (CORD), refers to
chronic bronchitis and emphysema, a pair of commonly co-existing diseases of the
lungs in which the airways become narrowed. This leads to a limitation of the flow of
air to and from the lungs causing shortness of breath. In clinical practice, COPD is
defined by its characteristically low airflow on lung function tests. In contrast to
asthma, this limitation is poorly reversible and usually gets progressively worse over
time. In England, an estimated 842,100 of 50 million people have a diagnosis of COPD;
translating into approximately one person in 59 receiving a diagnosis of COPD at some
point in their lives.

COPD is caused by noxious particles or gas, most commonly from tobacco smoking,
which triggers an abnormal inflammatory response in the lung. The inflammatory
response in the larger airways is known as chronic bronchitis, which is diagnosed
clinically when people regularly cough up sputum. In the alveoli, the inflammatory
response causes destruction of the tissues of the lung, a process known as emphysema.
The natural course of COPD is characterized by occasional sudden worsening’s of
symptoms called acute exacerbations, most of which are caused by infections or air
pollution.

The diagnosis of COPD requires lung function tests. Important management strategies
are smoking cessation, vaccinations, rehabilitation, and drug therapy (often using
inhalers). Some patients go on to require long-term oxygen therapy or lung
transplantation.

Worldwide, COPD ranked as the sixth leading cause of death in 1990. It is projected to
be the fourth leading cause of death worldwide by 2030 due to an increase in smoking
rates and demographic changes in many countries. COPD is the fourth leading cause of
death in the U.S. and the economic burden of COPD in the U.S. in 2007 was $42.6 billion
in health care costs and lost productivity.

ANATOMY AND PHYSIOLOGY

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In humans, the trachea divides into the two main bronchi that enter the roots of the
lungs. The bronchi continue to divide within the lung, and after multiple divisions, give
rise to bronchioles. The bronchial tree continues branching until it reaches the level of
terminal bronchioles, which lead to alveolar sacs. Alveolar sacs are made up of clusters
of alveoli, like individual grapes within a bunch. The individual alveoli are tightly
wrapped in blood vessels and it is here that gas exchange actually occurs.
Deoxygenated blood from the heart is pumped through the pulmonary artery to the
lungs, where oxygen diffuses into blood and is exchanged for carbon dioxide in the
hemoglobin of the erythrocytes. The oxygen-rich blood returns to the heart via the
pulmonary veins to be pumped back into systemic circulation.

Human lungs are located in two cavities on either side of the heart. Though similar in
appearance, the two are not identical. Both are separated into lobes by fissures, with
three lobes on the right and two on the left. The lobes are further divided into segments
and then into lobules, hexagonal divisions of the lungs that are the smallest subdivision
visible to the naked eye. The connective tissue that divides lobules is often blackened in
smokers. The medial border of the right lung is nearly vertical, while the left lung
contains a cardiac notch. The cardiac notch is a concave impression molded to
accommodate the shape of the heart. Lungs are to a certain extent 'overbuilt' and have a
tremendous reserve volume as compared to the oxygen exchange requirements when at
rest. Such excess capacity is one of the reasons that individuals can smoke for years
without having a noticeable decrease in lung function while still or moving slowly; in
situations like these only a small portion of the lungs are actually perfused with blood
for gas exchange. As oxygen requirements increase due to exercise, a greater volume of
the lungs is perfused, allowing the body to match its CO2/O2 exchange requirements.
Additionally, due to the excess capacity, it is possible for humans to live with only one
lung, with the other compensating for its loss.

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FORMS OF COPD

I. 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 two consecutive years.

PATHOPHYSIOLOGY

SMOKING

.Irritation in the respiratory tract

Increase in mucus secreting

glands and goblet cells

Increase mucus secretion

Thickening of bronchial wall

Bronchial lumen narrows

Mucus plugged the airway

Alveoli damaged and fibrosed

Altered function of alveolar

macrophages

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CLINICAL MANIFESTATIONS

 Excessive chronic sputum production

 Cough and ronchi
 Dyspnea
 Anorexia
 Weight loss
 Classic appearance of “blue bloater”

DIAGNOSTIC EXAM

 CBC – elevated red blood cell count; hemoglobin and hematocrit elevated in later
stages
 Chest X-ray – reveals enlarged heart, congested lung fields and normal or flatted
diaphragm
 Pulmonary Function Test (PFT) (Spirometry) – indicates increased residual
volume, decreased vital capacity, FEV1, and FEV1/FVC ratio

MEDICATION THERAPY

 Immunization against pneumonia and influenza

 Adjunct theraphy
 Antibiotics
 Bronchodilators
o Symphatomimetic
o Aminophylline
o Xanthine derivatives
 Chest physiotherapy
 Corticosteroids
 Anticholinergics – ipratropium(atrovent)

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 II. EMPHYSEMA

Emphysema is a pathologic 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.

PATHOPHYSIOLOGY

SMOKING FOR MANY YEARS

Recurrent in infections

Repeated inflammations

Disappearance of ciliary
function

Hypertrophy of goblet cells in

abnormal sites of the terminal
bronchiole

Obstruction of airflow

Progressive destruction of
alveoli

Deacrease in contact of alveolar

surface area with capillaries

Increase in dead space and

impaired oxygen diffusion

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CLINICAL MANIFESTATION

 “Pink puffer” characterized by:

o barrel chest
o pursed-lip breathing (caused by force exhalation)
o obvious use of accessory muscles
o weight loss
 exertional dyspnea progresses with advancing disease
 persistent tachycardia related to inadequate oxygenation
 diminished breath sounds
 wheezes or crackles

DIAGNOTIS EXAM

 ABG analysis – reveals slightly decreased PO2; PCO2 is elevated in later stage
 Chest X-ray – indicates hyperinflated lungs with a flattened diaphragm; heart
size is normal or small
 Spirometry
 DLCO

MEDICATION THERAPHY

 Bronchodilators
 Beta-adrenergic agonists
 Anticholinergics
 Long-acting theophylline
 Corticosteroids

NURSING CARE FOR COPD

 Patient education
o Breathing exercises
o Inspiratory muscle training
o Self-care activities
o Physical conditioning
o Oxygen therapy
o Nutritional therapy
o Coping measures

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NURSING RESPONSIBILITIES FOR COPD

 Promoting smoking cessation

 Improving gas exchange
 Improving breathing patterns
 Improving activity intolerance
 Enhancing self-care strategies
 Enhancing individual coping strategies
 Monitor and managing potential complications
 Promoting home and community-based care

LATEST TREATMENT FOR COPD

Currently, there is no latest treatment for COPD

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