NURSING RESPIRATORY SYSTEM

COPD (Chronic Obstructive Pulmonary Disease)

LECTURER:
Vetty Priscilla, Skp, Mkep, Spmat, Mph

MEMBERS OF GROUP I
Muhammad Ilham Zul (1511314001)
Suci Raesman (1511314021)
Balqis Qisty (1511314016)
Dwi Yani Adinda (1511314006)
Siti Sarah Nurfalah (1511314011)

NURSING FACULTY
ANDALAS UNIVERSITY
PADANG
2015/2016

PREFACE
Thank to Almighty God who has given His bless to the writer for finishing the paper
entitled COPD (Chronic Obstructive Pulmonary Disease)
The writer also wish to express his deep and sincere gratitude for those who have
guided in completing this paper. This paper contains some explanation that can help the
reader to addition their knowledge. The procedures in using reading games is provided in this
paper.
Hopefully, this paper can help the readers to expand their knowledge hopelessness
and powerlessness.

Padang. November,22, 2016

Writer

CHAPTER I INTODUCTION
1.1 Background
1.2 Formulation of Problem
1.3 Purpose

CHAPTER II CONTENT

COPD (Chronic Obstructive Pulmonary Disease)

2.1 Definition
COPD (Chronic Obstructive Pulmonary Disease) is a disease state characterized by
airflow limitation that is not fully reversible. This newest definition of COPD, provided by
the Global Initiative for Chronic Obstructive Lung Disease, provides a broad description that
better explains this disorder and its signs and symptoms (National Institutes of Health [NIH],
2001).
The airflow limitation is usually progressive and associated with an abnormal
inflammatory response of the lung to noxious particles or gases, resulting in narrowing of
airways, hypersecretion of mucus, and changes in the pulmonary vasculature. Other diseases
such as cystic fibrosis, bronchiectasis, and asthma that were previously classified as types of
COPD are now classified as chronic pulmonary disorders, although symptoms may overlap
with those of COPD.
2.2 Etiology
Cigarette smoking
COPD is most often caused by smoking. Most people with COPDare long-term
smokers, and research shows that smokingcigarettes increases the risk of getting COPD:

Some studies show that up to half of long-term smokers older than age 60 get COPD.
Smoking both tobacco and marijuana increases
the
risk
of
COPD
more
than smoking either one.
Cigarette smoking induces macrophages to release neutrophil chemotactic factors and

elastases, which lead to tissue destruction. Clinically significant COPD develops in 15% of
cigarette smokers, although this number is believed to be an underestimate. Age of initiation
of smoking, total pack-years, and current smoking status predict COPD mortality.

Environmental factors
COPD does occur in individuals who have never smoked. Although the role of air
pollution in the etiology of COPD is unclear, the effect is small when compared with that of
cigarette smoking. In developing countries, the use of biomass fuels with indoor cooking and
heating is likely to be a major contributor to the worldwide prevalence of COPD. Long-term
exposure to traffic-related air pollution may be a factor in COPD in patients with diabetes and
asthma.
Airway hyperresponsiveness
Airway hyperresponsiveness (ie, Dutch hypothesis) stipulates that patients who have
nonspecific airway hyperreactivity and who smoke are at increased risk of developing COPD
with an accelerated decline in lung function. Nonspecific airway hyperreactivity is inversely
related to FEV1 and may predict a decline in lung function.
The possible role of airway hyperresponsiveness as a risk factor for the development
of COPD in people who smoke is unclear. Moreover, bronchial hyperreactivity may result
from airway inflammation observed with the development of smoking-related chronic
bronchitis. This may contribute to airway remodeling, leading to a more fixed obstruction, as
is seen in persons with COPD.
Intravenous drug use
Emphysema occurs in approximately 2% of persons who use intravenous (IV) drugs.
This is attributed to pulmonary vascular damage that results from the insoluble filler (eg,
cornstarch, cotton fibers, cellulose, talc) contained in methadone or methylphenidate.
The bullous cysts found in association with IV use of cocaine or heroin occur
predominantly in the upper lobes. In contrast, methadone and methylphenidate injections are
associated with basilar and panacinar emphysema.

Immunodeficiency syndromes
Human immunodeficiency virus (HIV) infection has been found to be an independent
risk factor for COPD, even after controlling for confounding variables such as smoking, IV
drug use, race, and age.
Apical and cortical bullous lung damage occurs in patients who have autoimmune
deficiency syndrome and Pneumocystis carinii infection. Reversible pneumatoceles are
observed in 10-20% of patients with this infection
2.3 Pathophysiology
In COPD, the airflow limitation is both progressive and associated with an abnormal
inflammatory response of the lungs to noxious particles or gases. The inflammatory response
occurs throughout the airways, parenchyma, and pulmonary vasculature (NIH, 2001).
Because of the chronic inflammation and the bodys attempts to repair it, narrowing occurs in
the small peripheral airways. Over time, this injury-and-repair process causes scar tissue
formation and narrowing of the airway lumen. Airflow obstruction may also be due to
parenchymal destruction as seen with emphysema, a disease of the alveoli or gas exchange
units.
In addition to inflammation, processes relating to imbalances of proteinases and
antiproteinases in the lung may be responsible for airflow limitation. When activated by
chronic inflammation, proteinases and other substances may be released, damaging the
parenchyma of the lung. The parenchymal changes may also be consequences of
inflammation, environmental, or genetic factors (eg, alpha1 antitrypsin deficiency).
Early in the course of COPD, the inflammatory response causes pulmonary
vasculature changes that are characterized by thickening of the vessel wall. These changes
may occur as a result of exposure to cigarette smoke or use of tobacco products or as a
result of the release of inflammatory mediators (NIH, 2001).

Figure 2.1 Pathophysiology of chronic bronchitis as compared to a normal bronchus. The

bronchus in chronic bronchitis is narrowed and has impaired air flow due to multiple
mechanisms: inflammation, excess mucus production, and potential smooth muscle
constriction (bronchospasm).
2.4 Clinical Manifestation
COPD is characterized by three primary symptoms: cough, sputumproduction, and
dyspnea on exertion (NIH, 2001). These symptoms often worsen over time. Chronic cough
and sputum production often precede the development of airflow limitation by many years.
However, not all individuals with cough and sputum production will develop COPD.
Dyspnea may be severe and often interferes with the patients activities. Weight loss is
common because dyspnea interferes with eating, and the work of breathing is energydepleting. 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 risk for
acute and chronic respiratory failure.
2.5 Risk Factor
Tobacco smoking
Tobacco smoking is the most important risk factor for COPD. Compared to smoking,
other risks are minor.

Pipe and cigar smokers have less risk of getting COPD than cigarette smokers.

But they still have more risk than nonsmokers.

The risk for COPD increases with both the amount of tobacco you smoke each
day and the number of years you have smoked.

Family history
Some people may be more at risk than others for getting the disease, especially if they
have low levels of the protein alpha-1 antitrypsin (alpha-1 antitrypsin deficiency), a disorder
that runs in families.

Asthma
Asthma and COPD are different diseases, even though both of them involve breathing
problems. People with asthma may have a greater risk for getting COPD, but the reasons for
this are not fully understood.
Risks in the environment

Outside air pollution. Air pollution may make COPD worse. It may increase the risk of a
flare-up, or COPD exacerbation, when your symptoms quickly get worse and stay worse.

Try not to be outside when air pollution levels are high.

Indoor air pollution. Have good ventilation in your home to avoid indoor air pollution.
Secondhand smoke. It is not yet known whether secondhand smoke can lead to COPD.
But a large study showed that children who were exposed to secondhand smoke were
more likely to get emphysema than children who weren't exposed. And people who are
exposed to secondhand smoke for a long time are more likely to have breathing problems

and respiratory diseases. 1

Occupational hazards. If your work exposes you to chemical fumes or dust, use safety
equipment to reduce the amount of fumes and dust you breathe.
Cigarette smoking, air pollution, and occupational exposure (coal, cotton, grain) are

important risk factors that contribute to COPD development, which may occur over a 20- to
30- year span. Complications of COPD vary but include respiratory insufficiency and failure
(major complications) as well as pneumonia, atelectasis, and pneumothorax.
2.6 Prevention
Don't smoke
The best way to keep COPD from starting or from getting worse is to not smoke.
There are clear benefits to quitting, even after years of smoking. When you stop smoking,
you slow down the damage to your lungs. For most people who quit, loss of lung function is
slowed to the same rate as a nonsmoker's.
Stopping smoking is especially important if you have low levels of the protein alpha-1
antitrypsin. People who have an alpha-1 antitrypsin deficiency may lower their risk for severe

COPD if they get regular shots of alpha-1 antitrypsin. Family members of someone with
alpha-1 antitrypsin deficiency should be tested for the condition.
Avoid bad air
Other airway irritants (such as air pollution, chemical fumes, and dust) also can make
COPD worse, but they are far less important than smoking in causing the disease.
Get vaccines
1. Flu vaccines
If patient have COPD, patient need to get a flu vaccine every year. When people with
COPD get the flu, it often turns into something more serious, like pneumonia. A flu vaccine
can help prevent this from happening.
Also, getting regular flu vaccines may lower chances of having COPD flare-ups.
2. Pneumococcal vaccine
People with COPD often get pneumonia. Getting a shot can help keep from getting
very ill with pneumonia. People younger than 65 usually need only one shot. But doctors
sometimes recommend a second shot for some people who got their first shot before they
turned 65. Talk with your doctor about whether need a second shot. Two different types of
pneumococcal vaccines are recommended for people ages 65 and older.
3. Pertussis vaccine
Pertussis (also called whooping cough) can increase the risk of having a COPD flareup. So making sure you are current on pertussis vaccinations may help control COPD
2.7 Complication
Respiratory insufficiency and failure are major life-threatening complications of
COPD. The acuity of the onset and the severity of respiratory failure depend on the patients
baseline pulmonary function, pulse oximetry or arterial blood gas values, comorbid
conditions, and the severity of other complications of COPD. Respiratory insufficiency and
failure may be chronic (with severe COPD) or acute (with severe bronchospasm or

pneumonia in the patient with severe COPD). Acute respiratory insufficiency and failure may
necessitate ventilatory support until other acute complications, such as infection, can be
treated. Other complications of COPD include pneumonia, atelectasis, pneumothorax, and cor
pulmonale.
2.8 Treatment
Pharmacologic Therapy
Bronchodilators. Bronchodilators relieve bronchospasm and reduce airway
obstruction by allowing increased oxygen distribution throughout the lungs and improving
alveolar ventilation. These medications, which are central in the management of COPD (NIH,
2001), are delivered through a metered-dose inhaler, by nebulization, or via the oral route in
pill or liquid form. Bronchodilators are often administered regularly throughout the day as
well as on an as-needed basis. They may also be used prophylactically to prevent
breathlessness by having the patient use them before an activity, such as eating or walking.
Corticosteroids. Inhaled and systemic corticosteroids (oral or intravenous) may also
be used in COPD but are used more frequently in asthma. Although it has been shown that
corticosteroids do not slow the decline in lung function, these medications may improve
symptoms. A short trial course of oral corticosteroids may be prescribed for patients with
stage II or III COPD to see if pulmonary function improves and symptoms decrease. Inhaled
corticosteroids via MDI may also be used. Examples of corticosteroids in the inhaled form
are beclomethasone (Beclovent,Vanceril), budesonide (Pulmicort), flunisolide (AeroBid),
fluticasone (Flovent), and triamcinolone (Azmacort).

Table 2.1 Types of Bronchodilator Medications

Oxygen Therapy

Oxygen therapy can be administered as long-term continuous therapy, during

exercise, or to prevent acute dyspnea. Longterm oxygen therapy has been shown to improve
the patients quality of life and survival (NIH, 2001). For patients with an arterial oxygen
pressure (PaO2) of 55 mm Hg or less on room air, maintaining a constant and adequate
oxygen saturation (>90%) is associated with significantly reduced mortality and improved
quality of life. Indications for oxygen supplementation include a PaO2 of 55 mm Hg or less
or evidence of tissue hypoxia and organ damage such as cor pulmonale, secondary
olycythemia, edema from right heart failure, or impaired mental status. In patients with
exercise-induced hypoxemia, oxygen supplementation during exercise can improve
performance. Patients who are hypoxemic while awake are likely to be so during sleep.
Therefore, nighttime oxygen therapy is recommended as well, and the prescription for
oxygen therapy is for continuous, 24-hour use. Intermittent oxygen therapy is indicated for
those who desaturate only during exercise or sleep.
Surgical Management
Bullectomy. A bullectomy is a surgical option for select patients with bullous
emphysema. Bullae are enlarged airspaces that do not contribute to ventilation but occupy
space in the thorax; these areas may be surgically excised. Many times these bullae compress
areas of the lung that do have adequate gas exchange. Bullectomy may help reduce dyspnea
and improve lung function. It can be done thoracoscopically (with a video-assisted
thoracoscope) or via a limited thoracotomy incision.
Lung Volume Reduction Surgery. Treatment options for patientswith end-stage
COPD (stage III) with a primary emphysematous component are limited, although lung
volume reduction surgery is an option for a specific subset of patients. This subset includes
patients with homogenous disease or disease that is focused in one area and not widespread
throughout the lungs. Lung volume reduction surgery involves the removal of a portion of the
diseased lung parenchyma. This allows the functional tissue to expand, resulting in improved
elastic recoil of the lung and improved chest wall and diaphragmatic mechanics. This type of
surgery does not cure the disease, but it may decrease dyspnea, improve lung function, and
improve the patients overall quality of life. Careful selection of patients for this procedure is
essential to decrease the morbidity and mortality. The long-term outcomes of this surgery are
unknown.
Lung Transplantation. Lung transplantation is a viable alternative for definitive
surgical treatment of end-stage emphysema. It has been shown to improve quality of life and

functional capacity (NIH, 2001). Specific criteria exist for referral for lung transplantation;
however, organs are in short supply and many patients die while waiting for a transplant.
2.8 Nursing Management
The first step that must do Assessment is obtain information about current symptoms
as well as previous disease manifestations. In addition to the history, nurses review the results
of available diagnostic tests.
NANDA
Ineffective

Airway

NOC
Maintain

NIC
airway Auscultate breath sounds.

Clearance: Inability to clear

patency with

secretions

sounds clear/clearing.
Demonstrate behaviors

or

obstructions

from the respiratory tract to

Related to :

Bronchospasm

Increased
production

Note adventitious breath

sounds

improve airway

to

maintain a clear airway.

breath

crackles, rhonchi).
Assess
and
monitor

clearance, e.g., cough

respirations and breath

effectively

sounds, noting rate and

and

expectorate secretions
of

sounds

(tachypnea,

stridor,

crackles,

wheezes).

secretions;

Note

inspiratory and expiratory

retained
secretions;

(wheezes,

thick,

ratio.
Assist patient to assume

viscous secretions

position

Allergic airways

(elevate head of bed,

Hyperplasia

have

of

patient

comfort
lean

on

bronchial walls

overbed table or sit on

Decreased

edge of bed).
Keep
environmental

energy/fatigue

Impaired

of

pollution

Gas

Demonstrate

Exchange: Excess or deficit

improved

in oxygenation and/or carbon

and

to

minimum such

as dust,

smoke,

and

feather

pillows,

according

to

individual situation.
Assess
and
record

ventilation

respiratory rate, depth.

adequate

Note use of accessory

dioxide elimination at the

oxygenation of tissues

muscles,

alveolar-capillary membrane.

by

breathing,

Related to :

patients normal range

Altered oxygen

supply (obstruction
of airways by
secretions,
bronchospasm; airtrapping)
Alveoli destruction
Alveolar-capillary

ABGs

within

pursed-lip
inability

to

and be free of symptoms

speak or converse.
Elevate head of bed,

of respiratory distress.

assist patient to assume

Participate
treatment
within

position to ease work of

in

breathing.

regimen
level

Include

periods of time in prone

of

position

ability/situation.

as

tolerated.

Encourage deep-slow or
pursed-lip breathing as

membrane changes

individually needed or

tolerated.
Auscultate breath sounds,
noting areas of decreased
airflow and adventitious

Ineffective Breathing
Pattern related

to

will

sounds.
Place patient in semi-

fowlers position
Increase fluid intake as

a respiratory rate within

applicable
Keep patient back dry
Maintain a patent airway,

normal limits

suctioning of secretions

Patient
improve breathing

Retained Secretions

pattern.

Patient will maintain

may be done as ordered

CHAPTER III CONCLUTION

3.1 Conclution
3.2 Sugestion

REFERENCESS