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CHAPTER 1

I. INTRODUCTION

The Lungs are a pair of organs in the chest that are primarily responsible for the

exchange of oxygen and carbon dioxide between the air we breathe and the blood.

The lung is composed of clusters of small air sacs (alveoli) divided by thin, elastic

walls or membranes. Capillaries, the tiniest of blood vessels, run within these walls between

the alveoli and allow blood and air to come near each other. The distance between the air in

the lungs and the blood in the capillaries is very small, and allows molecules of oxygen and

carbon dioxide to transfer across the membranes.

Air reaches the alveoli via the bronchial tree. The trachea splits into the right and left

main stem bronchi, which branch further into bronchioles and finally ends in the alveolar

sacs.

When we breathe in, air enters the lung and the alveoli expands. Oxygen is transferred

onto hemoglobin molecules in the red blood cells to be transported to the rest of the body for

use. As oxygen attaches to the red blood cells, carbon dioxide be exhaled. When we breathe

out, the alveoli get squeezed by the elasticity in their walls and air is pushed out the lungs.

Normally, the lungs are very spongy and elastic. When a breath is taken, the chest

wall expands, expanding the sponge. Similar to the way a squeezed sponge will draw

water into it when released, suction draws air into the lungs when the chest wall expands.

Air is brought though the trachea (windpipe) and bronchi (the main air tubes going to

right and left lungs). These tubes divide into smaller and smaller tubes, finally ending in

alveoli. Alveoli, the tiniest structures in the lung, are very small air sacs that are arranged

like a bunch of grapes. The alveoli are at the ends of the smallest tubes called

bronchioles. The alveoli and the bronchioles are very important structures for the lungs to

function properly. It is these structures that are destroyed by emphysema.


Emphysema is a long-term progressive disease of the lung that primaly causes

shortness of breathe. In people with emphysema, the lung tissues necessary to support the

physical shape and function of the lungs are destroyed. Emphysema is called an obstructive

lung disease because the destruction of lung tissue around smaller airways, called

bronchioles, makes these airways unable to hold their shape properly when you exhale.

II. OBJECTIVES

A. GENERAL OBJECTIVE

After 6 days of exposure in the community through the intensive care practicum

(ICP), we, students must be able to identify a life long disease or chronic illness and

determine the general health problems and needs of the patient. We also intend to help

patient promote health and medical understanding of such condition through the

application if the nursing skills, managing and providing care services such as health

assessment and patient and family education. We also aim to promote wellness,

reduced the spread of illness and improve the health status groups or community

through nursing intervention.

B. SPECIFIC OBJECTIVES

b.1. NURSE-CENTERED

> to establish harmonious relationship with the patient and family.

> to obtain a nursing health history, conduct physical assessment, review

records, organize and validate data obtained from the patient .

> to know nursing diagnosis and collaborative problem statement

> to set priorities and goals or outcomes in collaboration with the client.
> to select nursing strategies or intervention appropriate for the client.

> to render nursing care and information appropriate for the client.

b. 2. PATIENT-CENTERED

> to raise the level of awareness of patient on problems that he may

encounter.

> to facilitate patient in taking necessary actions to solve and prevent the

identified problems on his own.

> to help patient in motivating him to continue the health care provider by the

health workers.

> to promote the patient`s optimum level of functioning in his daily life.

III. PATIENT`S PROFILE

Name: J. S.

Address: Block G, Marcos Village Palayan City

Age: 66 y/o

Birth: feb. 7, 1943

Sex: Male

Status: Married

Nationality: Filipino

Height : 5’7”

Weight : 65 kgs.

No.of daughters : 5

No.of son: 1 (deceased)

Occupation: Sari-sari store owner

Religion: Catholic
Educational Attainment: Elementary Graduate

Attending physician: Dr. Ramos

Hospital: Good Samaritan Hospital

Diagnosis: Emphysema

IV. PAST MEDICAL HISTORY

do before he was hospitalized due to easy fatigability. July of 2008 it started at

productive cough with thick, tenacious phlegm, colds and accompanied by nocturnal

fever, sweating and moist skin. Complaining of easy fatigability and body malaise in

which he was confined for 5 days at Good Samaritan Hospital .

After he was discharged, there was a gradual decrease of weight due to loss of

appetite. He also doesn’t be able to do all house chores that he usually

V. PRESENT HISTORY

Patient still experienced difficulty of breathing and fatigability. He is also easily

destructed by a single noise at night associated with dyspnea.

He had a continuous check-up at Good Samaritan Hospital , and be able to do a house

chores and walking for his daily exercise. Continue to take his medications at home to

prevent progression of his disease.

VI. PATIENT`S FAMILY HISTORY

According to the patient, his father also manifest signs and symptoms like productive

cough, fever, and difficulty of breathing. And his mother had asthma.

VII. ACTIVITIES OF DAILY LIVINGS

Before Hospitalization After hospitalization Analysis


A. Sleep pattern >Had enough sleep at > Easily disturb by a > Disturbance of
night and during the single noise at night. sleep pattern due to
day his cough,
uncomfortable
position and asthma.
B. Bowel > Eliminates 2-3 times Eliminates once a > elimination
elimination a day day pattern related to
decrease peristalsis
due to mobility.

C. Fluids > consumes 8-10 > consumes 10-12 > increase fluid
glasses a day glasses per day intake due to
increase fatigability.

D. Foods > Large amount of > Small amount of > decrease food
foods each meals, food intake each intake due to loss of
usually meat and fish. meal. appetite.

E. Exercise/ >doing household >walking for 10- >due to easy


Activity chores every morning 20mins. fatigability

F. Hygiene >take a bath: >take a bath: >poor hygiene


Twice a day Once a day related to decrease
in self-esteem due to
>brushes teeth: >brushes teeth: his present disease.
After each meal Once before going
to sleep

G. Lifestyle/ >use of cigarettes for >decided to quit >avoiding smoking


Personal Habits about 2-3 packs a day early illness was to prevent further
in 45 years diagnosed. complications.
>alcoholic beverages >still drinking >still, coping up
drinker once or twice a alcoholic beverages with his drinking
week in 45 years even. occasionally. problem.
Discussion:
Chronic obstructive pulmonary disease (COPD) is a disease state characterized by
airflow limitation that is not fully reversible. This newest definition COPD, provided by the
Global Initiative for Chrnonic Obstructive Lung Disease (GOLD), is a broad description that
better explains this disorder and its signs and symptoms (GOLD, World Health
Organization [WHO] & National Heart, Lung and Blood Institute [NHLBI], 2004).
Although previous definitions have include emphysema and chronic bronchitis
under the umbrella classification of COPD, this was often confusing because most patient

with COPD present with over lapping signs and symptoms of these two
distinct disease processes.
COPD may include diseases that cause airflow obstruction (e.g., Emphysema, chronic

bronchitis) or any combination of these disorders. Other diseases as cystic


fibrosis, bronchiectasis, and asthma that were previously classified as types of chronic
obstructive lung disease are now classified as chronic pulmonary disorders. However,
asthma is now considered as a separate disorder and is classified as an abnormal airway
condition characterized primarily by reversible inflammation. COPD can co-exist with

asthma. Both of these diseases have the same major symptoms; however,
symptoms are generally more variable in asthma than in COPD.
Currently, COPD is the fourth leading cause of mortality and the 12th leading cause of
disability. However, by the year 2020 it is estimated that COPD will be the third leading
cause of death and the firth leading cause of disability (Sin, McAlister, Man. Et al., 2003).
People with COPD commonly become symptomatic during the middle adult years, and the
incidence of the disease increases with age.
ANATOMY AND PHYSIOLOGY:
The respiratory system consists of all the organs involved in breathing. These include the

nose, pharynx, larynx, trachea, bronchi and lungs. The respiratory system does
two very important things: it brings oxygen into our bodies, which we need for our cells to
live and function properly; and it helps us get rid of carbon dioxide, which is a waste
product of cellular function. The nose, pharynx, larynx, trachea and bronchi all work like a
system of pipes through which the air is funneled down into our lungs. There, in very small

air sacs called alveoli, oxygen is brought into the bloodstream and carbon
dioxide is pushed from the blood out into the air. When something goes wrong with part of

the respiratory system, such as an infection like pneumonia, chronic

obstructive pulmonary diseases, it makes it harder for us to get the oxygen we

need and to get rid of the waste product carbon dioxide. Common respiratory
symptoms include breathlessness, cough, and chest pain.
The Upper Airway and Trachea
When you breathe in, air enters your body through your nose or mouth. From there, it
travels down your throat through the larynx (or voicebox) and into the trachea (or windpipe)
before entering your lungs. All these structures act to funnel fresh air down from the outside
world into your body. The upper airway is important because it must always stay open for
you to be able to breathe. It also helps to moisten and warm the air before it reaches your
lungs.
The Lungs
Structure
The lungs are paired, cone-shaped organs which take up most of the space in our chests,
along with the heart. Their role is to take oxygen into the body, which we need for our cells to

live and function properly, and to help us get rid of carbon dioxide, which is a
waste product. We each have two lungs, a left lung and a right lung. These are divided up into
‘lobes’, or big sections of tissue separated by ‘fissures’ or dividers. The right lung has three
lobes but the left lung has only two, because the heart takes up some of the space in the left
side of our chest. The lungs can also be divided up into even smaller portions, called
‘bronchopulmonary segments’.
These are pyramidal-shaped areas which are also separated from each other by membranes.
There are about 10 of them in each lung. Each segment receives its own blood supply and air
supply.
COPD VERSUS HEALTHY LUNG

How they work


Air enters your lungs through a system of pipes called the bronchi. These pipes start from the
bottom of the trachea as the left and right bronchi and branch many times throughout the
lungs, until they eventually form little thin-walled air sacs or bubbles, known as the alveoli.
The alveoli are where the important work of gas exchange takes place between the air and
your blood. Covering each alveolus is a whole network of little blood vessel called
capillaries, which are very small branches of the pulmonary arteries. It is important that the
air in the alveoli and the blood in the capillaries are very close together, so that oxygen and

carbon dioxide can move (or diffuse) between them. So, when you

breathe in, air comes down the trachea and through the bronchi into the
alveoli. This fresh air has lots of oxygen in it, and some of this oxygen will travel across the
walls of the alveoli into your bloodstream. Traveling in the opposite direction is

carbon dioxide, which crosses from the blood in the capillaries into the air in
the alveoli and is then breathed out. In this way, you bring in to your body the oxygen that

you need to live, and get rid of the waste product carbon dioxide.
Blood Supply
The lungs are very vascular organs, meaning they receive a very large blood supply. This is
because the pulmonary arteries, which supply the lungs, come directly from the right side of

your heart. They carry blood which is low in oxygen and high in carbon

dioxide into your lungs so that the carbon dioxide can be blown off, and more
oxygen can be absorbed into the bloodstream. The newly oxygen-rich blood then travels back
through the paired pulmonary veins into the left side of your heart. From there, it is pumped
all around your body to supply oxygen to cells and organs.
The Work of Breathing
The Pleurae
The lungs are covered by smooth membranes that we call pleurae. The pleurae have two
layers, a ‘visceral’ layer which sticks closely to the outside surface of your lungs, and a
‘parietal’ layer which lines the inside of your chest wall (ribcage). The pleurae are important

because they help you breathe in and out smoothly, without any friction. They
also make sure that when your ribcage expands on breathing in, your lungs expand as well to
fill the extra space.
The Diaphragm and Intercostal Muscles

When you breathe in (inspiration), your muscles need to work to fill your
lungs with air. The diaphragm, a large, sheet-like muscle which stretches across your chest
under the ribcage, does much of this work. At rest, it is shaped like a dome curving up into

your chest. When you breathe in, the diaphragm contracts and flattens out,
expanding the space in your chest and drawing air into your lungs. Other muscles, including
the muscles between your ribs (the intercostal muscles) also help by moving your ribcage in
and out. Breathing out (expiration) does not normally require your muscles to work. This is
because your lungs are very elastic, and when your muscles relax at the end of inspiration
your lungs simply recoil back into their resting position, pushing the air out as they go.

The Respiratory System and Ageing


The normal process of ageing is associated with a number of changes in both the structure

and function of the respiratory system. These include:


• Enlargement of the alveoli. The air spaces get bigger and lose their elasticity, meaning
that there is less area for gases to be exchanged across. This change is sometimes
referred to as ’senile emphysema’.
• The compliance (or springiness) of the chest wall decreases, so that it takes more
effort to breathe in and out.
• The strength of the respiratory muscles (the diaphragm and intercostal muscles)
decreases. This change is closely connected to the general health of the person.
All of these changes mean that an older person might have more difficulty coping with
increased stress on their respiratory system, such as with an infection like pneumonia, than a
younger person would.
PREDISPOSING FACTORS

Risk factors for COPD include environmental exposures and host factors. The most
important risk factor for COPD is cigarette smoking. Other risk factors are pipe, cigar, and
other types of tobacco smoking. In addition, passive smoking contributes to respiratory
symptoms and COPD. Smoking depresses the activity of scavenger cells and affects the
respiratory tract’s ciliary cleansing mechanism, which keeps breathing passages free of
inhaled irritants, bacteria, and other foreign matter. When smoking damages this cleansing
mechanism, airflow is obstructed and air becomes trapped behind the obstruction. The alveoli
greatly distend, diminished lung capacity. Smoking also irritates the goblet cells and mucus
glands, causing an increased accumulation of mucus, which in turn produces more irritation,
infection, and damage to the lung. In addition, carbon monoxide (a by product of smoking)
combines with hemoglobin to form carboxyhemoglobin. Hemoglobin that is bound by
carboxyhemoglobin cannot carry oxygen efficiently.
A host risk factor for COPD is a deficiency of alpha antitrypsin, an enzyme inhibitor that
protects the lung parenchyma from injury. This deficiency predisposes young people to rapid
development of lobular emphysema, even if they do not smoke. Genetically susceptible
people are sensitive to environmental factors (eg. Smoking, air pollution, infectious agents,
allergens) and eventually developed chronic obstructive symptoms. Carriers of this genetic
defect must be identified so that they can modify environmental risk factors to delay or
prevent overt symptoms of disease.
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. Because of the
chronic inflammation and the body’s 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 caused by parenchymal
destruction, as is seen with emphysema, a disease of the alveoli or gas exchange units.
In addition to inflammation, processes related to imbalances of proteinases and
antiproteinases in the lung may be responsible for airflow limitation. When activated by
chronic inflammation, proteiness and other substances may be released, damaging the
parenchyma of the lung. The parenchymal changes may occur as a consequence of
inflammation or 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 result
from exposure to cigarette smoke, use of tobacco products, and the release of inflammatory
medicators.

CHRONIC BRONCHITIS
Lung damage and inflammation in the large
airways results in chronic bronchitis. Chronic
bronchitis is defined in clinical terms as a cough
with sputum production on most days for 3
months of a year, for 2 consecutive years. In the
airways of the lung, the hallmark of chronic
bronchitris is an increased number (hyperplasia)
and increased size (hypertrophy) of the goblet
cells and mucous glands of the airway. As a result,
there is more mucus than usual in the airways,
contributing to narrowing of the airways and
causing a cough with sputum. Microscopically
there is infiltration of the airway walls with
inflammatory cells. Inflammation is followed by scarring and remodeling that thickens the
walls and also results in narrowing of the airways. As chronic bronchitis progresses, there is
squamous metaplasia (an abnormal change in the tissue lining the inside of the airway) and
fibrosis (further thickening and scarring of the airway wall). The consequence of these
changes is a limitation of airflow.
Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema
were commonly referred to as “blue bloaters” because of the bluish color of the skin and lips
(cyanosis) seen in them. The hypoxia and fluid retention leads to them being called “Blue
Bloaters.”
ACUTE BRONCHITIS
PHYSICAL MANIFESTATIONS
One of the most common symptoms of COPD is shortness of breath (dyspnea). People with
COPD commonly describe this as: “My breathing requires effort”, “I feel out of breath”, or
“I can not get enough air in”. People with COPD typically first notice dyspnea during
vigorous exercise when the demands on the lungs are greatest. Over the years, dyspnea tends
to get gradually worse so that it can occur during milder, everyday activities such as
housework. In the advanced stages of COPD, dyspnea can become so bad that it occurs
during rest and is constantly present. Other symptoms of COPD are a persistent cough,
sputum or mucus production, wheezing, chest tightness, and tiredness. People with advanced
(very severe) COPD sometimes develop respiratory failure. When this happens, cyanosis, a
bluish discoloration of the lips caused by a lack of oxygen in the blood, can occur. An excess
of carbon dioxide in the blood can cause headaches, drowsiness or twitching (asterixis). A
complication of advanced COPD is cor pulmonale, a strain on the heart due to the extra work
required by the heart to pump blood through the affected lungs. Symptoms of cor pulmonale
are peripheral edema, seen as swelling of the ankles, and dyspnea.
There are a few signs of COPD that a healthcare worker may detect although they can be
seen in other diseases. Some people have COPD and have none of these signs. Common
signs are:
• tachypnea, a rapid breathing rate
• wheezing sounds or crackles in the lungs heard through a stethoscope
• breathing out taking a longer time than breathing in
• enlargement of the chest, particularly the front-to-back distance (hyperinflation)
• active use of muscles in the neck to help with breathing
• breathing through pursed lips increased anteroposterior to lateral ratio of the chest (i.e.
barrel chest).

EMPHYSEMA
Emphysema is a chronic obstructive pulmonary
disease (COPD, as it is otherwise known, formerly
termed a chronic obstructive lung disease). It is
often caused by exposure to toxic chemicals,
including long-term exposure to tobacco smoke.
Emphysema is characterized by loss of elasticity
(increased pulmonary compliance) of the lung
tissue caused by destruction of structures feeding
the alveoli, owing to the action of alpha 1
antitrypsin deficiency. This causes the small
airways to collapse during forced exhalation, as
alveolar collapsibility has decreased. As a result,
airflow is impeded and air becomes trapped in the
lungs, in the same way as other obstructive lung diseases. Symptoms include shortness of
breath on exertion, and an expanded chest. However, the constriction of air passages isn’t
always immediately deadly, and treatment is available.
PHYSICAL MANIFESTATIONS
Signs of emphysema include pursed-lipped breathing, central cyanosis and finger clubbing.
The chest has hyper resonant percussion notes, particularly just above the liver, and a difficult
to palpate apex beat, both due to hyperinflation. There may be decreased breath sounds and
audible expiratory wheeze. In advanced disease, there are signs of fluid overload such as
pitting peripheral edema. The face has a ruddy complexion if there is a secondary
polycythemia. Sufferers who retain carbon dioxide have asterixis (metabolic flap) at the
wrist.
DIAGNOSTIC EVALUATION
1. PFTs demonstrative airflow obstruction – reduced forced vital capacity (FVC), FEV1,
FEV1 to FVC ration; increased residual volume to total lung capacity (TLC) ratio,
possibly increased TLC.
2. ABG levels- decreased PaO2, pH, and increased CO2.
3. Chest X-ray – in late stages, hyperinflation, flattened diaphragm, increased
rettrosternal space, decreased vascular markings, possible bullae.
4. Alpa1-antitrypsin assay useful in identifying genetically determined deficiency in
emphysema.
TREATMENT
The goals of COPD treatment are 1) to prevent further deterioration in lung function, 2) to
alleviate symptoms, 3) to improve performance of daily activities and quality of life. The
treatment strategies include 1) quitting cigarette smoking, 2) taking medications to dilate
airways (bronchodilators) and decrease airway inflammation, 3) vaccinating against flu
influenza and pneumonia and 4) regular oxygen supplementation and 5) pulmonary
rehabilitation.
Quitting cigarette smoking
The most important treatment for COPD is quitting cigarette smoking. Patients who continue
to smoke have a more rapid deterioration in lung function when compared to others who quit.
Aging itself can cause a very slow decline in lung function. In susceptible individuals,
cigarette smoking can result in a much more dramatic loss of lung function. It is important to
note that when one stops smoking the decline in lung function eventually reverts to that of a
non-smoker.
Nicotine in cigarettes is addictive, and, therefore, cessation of smoking can cause symptoms
of nicotine withdrawal including anxiety, irritability, anger, depression, fatigue, difficulty
concentrating or sleeping, and intense craving for cigarettes. Patients likely to develop
withdrawal symptoms typically smoke more than 20 cigarettes a day, need to smoke shortly
after waking up in the morning, and have difficulty refraining from smoking in non-smoking
areas. However, some 25% of smokers can stop smoking without developing these
symptoms. Even in those smokers who develop symptoms of withdrawal, the symptoms will
decrease after several weeks of abstinence.
Bronchodilators
Treating airway obstruction in COPD with bronchodilators is similar but not identical to
treating bronchospasm in asthma. Bronchodilators are medications that relax the muscles
surrounding the small airways thereby opening the airways. Bronchodilators can be inhaled,
taken orally or administered intravenously. Inhaled bronchodilators are popular because they
go directly to the airways where they work. As compared with bronchodilators given orally,
less medication reaches the rest of the body, and, therefore, there are fewer side effects.
Metered dose inhalers (MDIs) are used to deliver bronchodilators. An MDI is a pressurized
canister containing a medication that is released when the canister is compressed. A standard
amount of medication is released with each compression of the MDI. To maximize the
delivery of the medications to the airways, the patient has to learn to coordinate inhalation
with each compression. Incorrect use of the MDI can lead to deposition of much of the
medication on the tongue and the back of the throat instead of on the airways.
To decrease the deposition of medications on the throat and increase the amount reaching the
airways, spacers can be helpful. Spacers are tube-like chambers attached to the outlet of the
MDI canister. Spacer devices can hold the released medications long enough for patients to
inhale them slowly and deeply into the lungs. Proper use of spacer devices can greatly
increase the proportion of medication reaching the airways.
Oxygen Therapy
Other treatments
• Pulmonary rehabilitation has become a cornerstone in the management of moderate
to severe COPD. Pulmonary rehabilitation is a program of education regarding lung
function and dysfunction, proper breathing techniques (diaphragmatic breathing,
pursed lip breathing), and proper use of respiratory equipment and medications. An
essential ingredient in this program is the use of increasing physical exercise to
overcome the reduced physical capacity that usually has developed over time. In
addition, occupational and physical therapy are used to teach optimal and efficient
body mechanics.
• Lung volume reduction surgery (LVRS) has received much fanfare in the lay press.
LVRS is a surgical procedure used to treat some patients with COPD. The premise
behind this surgery is that the over-inflated, poorly-functioning upper parts of the lung
compress and impair function of the better-functioning lung elsewhere. Thus, if the
over-inflated portions of lung are removed surgically, the compressed lung may
expand and function better. In addition, the diaphragm and the chest cavity achieve
more optimal positioning following the surgery, and this improves breathing further.
The best criteria for choosing patients for LVRS are still uncertain. A national study
was completed in 2003. Patients primarily with emphysema at the top of their lungs,
whose exercise tolerance was low even after pulmonary rehabilitation, seemed to do
the best with this procedure. On average, lung function and exercise capacity among
surviving surgical patients improved significantly following LVRS, but after two
years returned to about the same levels as before the procedure. Patients with forced
expiratory volume in FEVI of less than 20% of predicted and either diffuse disease on
the CAT scan or lower than 20% diffusing capacity or elevated carbon dioxide levels
had higher mortality. The role of LVRS is at present is very limited.
PHARMACOLOGIC INTERVENTIONS
• Beta-agonists
○ Beta-2 agonists have the bronchodilating effects of adrenaline without many
of its unwanted side effects. Beta-2 agonists can be administered by MDI
inhalers or orally. They are called “agonists” because they activate the beta-2
receptor on the muscles surrounding the airways. Activation of beta-2
receptors relaxes the muscles surrounding the airways and opens the airways.
Dilating airways helps to relieve the symptoms of dyspnea (shortness of
breath). Beta-2 agonists have been shown to relieve dyspnea in many COPD
patients, even among those without demonstrable reversibility in airway
obstruction. The action of beta-2 agonists starts within minutes after inhalation
and lasts for about 4 hours. Because of their quick onset of action, beta-2
agonists are especially helpful for patients who are acutely short of breath.
Because of their short duration of action, these medications should be used for
symptoms as they develop rather than as maintenance. Evidence suggests that
when these drugs are used routinely, their effectiveness is diminished. These
are referred to as rescue inhalers. Examples of beta-2 agonists include
albuterol (Ventolin, Proventil), metaproterenol (Alupent), pirbuterol (Maxair),
terbutaline (Brethaire), and isoetharine (Bronkosol). Levalbuterol (Xopenex)
is a recently approved Beta-2 agonist.
○ In contrast, Beta-2 agonists with a slower onset of action but a longer period
of activity, such as salmeterol xinafoate (Serevent) and formoterol fumarate
(Foradil) may be used routinely as maintenance medications. These drugs last
twelve hours and should be taken twice daily and no more. Along with some
of these inhalers to be mentioned, these are often referred to as maintenance
inhalers.
○ Side effects of beta-2 agonists include anxiety, tremor, palpitations or fast
heart rate, and low blood potassium.
• Anti-cholinergic Agents
○ Acetylcholine is a chemical released by nerves that attaches to receptors on the
muscles surrounding the airway causing the muscles to contract and the
airways to narrow. Anti-cholinergic drugs such as ipratropium bromide
(Atrovent) dilate airways by blocking the receptors for acetylcholine on the
muscles of the airways and preventing them from narrowing. Ipratropium
bromide (Atrovent) usually is administered via a MDI. In patients with COPD,
ipratropium has been shown to alleviate dyspnea, improve exercise tolerance
and improve FEV1. Ipratropium has a slower onset of action but longer
duration of action than the shorter-acting beta-2 agonists. Ipratropium usually
is well tolerated with minimal side effects even when used in higher doses.
Tiotropium (SPIRIVA) is a long acting and more powerful version of
Ipratropium and has been shown to be more effective.
○ In comparing ipratropium with beta-2 agonists in the treatment of patients
with COPD, studies suggest that ipratropium may be more effective in dilating
airways and improving symptoms with fewer side effects. Ipratropium is
especially suitable for use by elderly patients who may have difficulty with
fast heart rate and tremor from the beta-2 agonists. In patients who respond
poorly to either beta-2 agonists or ipratropium alone, a combination of the two
drugs sometimes results in a better response than to either drug alone without
additional side effects.
• Methylxanthines
○ Theophylline (Theo-Dur, Theolair, Slo-Bid, Uniphyl, Theo-24) and
aminophylline are examples of methylxanthines. Methylxanthines are
administered orally or intravenously. Long acting theophylline preparations
can be given orally once or twice a day. Theophylline, like a beta agonist,
relaxes the muscles surrounding the airways but also prevents mast cells
around the airways from releasing bronchoconstricting chemicals such as
histamine. Theophylline also can act as a mild diuretic and increase urination.
Theophylline also may increase the force of contraction of the heart and lower
pressure in the pulmonary arteries. Thus, theophylline can help patients with
COPD who have heart failure and pulmonary hypertension. Patients who have
difficulty using inhaled bronchodilators but no difficulty taking oral
medications find theophylline particularly useful.
○ The disadvantage of methylxanthines is their side effects. Dosage and blood
levels of theophylline or aminophylline have to be closely monitored.
Excessively high levels in the blood can lead to nausea, vomiting, heart
rhythm problems, and even seizures. In patients with heart failure or cirrhosis,
dosages of methylxanthines are lowered to avoid high blood levels.
Interactions with other medications, such as cimetidine (Tagamet), calcium
channel blockers (Procardia), quinolones (Cipro), and allopurinol (Zyloprim)
also can alter blood levels of methylxanthines.
• Corticosteroids
○ When airway inflammation (which causes swelling) contributes to airflow
obstruction, anti-inflammatory medications (more specifically, corticosteroids)
may be beneficial. Examples of corticosteroids include Prednisone and
Prednisolone. Twenty to thirty percent of patients with COPD show
improvement in lung function when given corticosteroids by mouth.
Unfortunately, high doses of oral corticosteroids over prolonged periods can
have serious side effects, including osteoporosis, bone fractures, diabetes
mellitus, high blood pressure, thinning of the skin and easy bruising, insomnia,
emotional changes, and weight gain. Therefore, many doctors use oral
corticosteroids as the treatment of last resort. When oral corticosteroids are
used, they are prescribed at the lowest possible doses for the shortest period of
time to minimize side effects. When it is necessary to use long term oral
steroids, medications are often prescribed to help reduce the development of
the above side effects.
○ Corticosteroids also can be inhaled. Inhaled corticosteroids have many fewer
side effects than long term oral corticosteroids. Examples of inhaled
corticosteroids include beclomethasone dipropionate (Beclovent, Beconase,
Vancenase, and Vanceril), triamcinolone acetonide (Azmacort), fluticasone
(Flovent), budesonide (Pulmicort), mometasone furoate (Asmanex) and
flunisolide (Aerobid). Inhaled corticosteroids have been useful in treating
patients with asthma, but in patients with COPD, it is not clear whether
inhaled corticosteroid have the same benefit as oral corticosteroids.
Nevertheless, doctors are less concerned about using inhaled corticosteroids
because of their safety. The side effects of inhaled corticosteroids include
hoarseness, loss of voice, and oral yeast infections. A spacing device placed
between the mouth and the MDI can improve medication delivery and reduce
the side effects on the mouth and throat. Rinsing out the mouth after use of a
steroid inhaler also can decrease these side effects.
• Treatment of Alpha-1 antitrypsin deficiency
○ Emphysema can develop at a very young age in some patients with severe
alpha-1 antitrypsin deficiency (AAT). Replacement of the missing or inactive
AAT by injection can help prevent progression of the associated emphysema.
This therapy is of no benefit in other types of COPD.
COMPLICATIONS
1. Respiratory failure
2. Pneumonia, overwhelming respiratory infection
3. Right-sided heart failure, dysrhythmias
4. Depression
5. Skeletal muscle dysfunction

NURSING INTERVENTIONS
Monitoring
1. Monitor for adverse effects of bronchodilators – tremulousness, tachycardia, cardiac
arrhythmias, central nervous system stimulation, hypertension.
2. Monitor condition after administration of aerosol bronchodilators to assess for
improved aeration, reduced adventitious sounds, reduced dyspnea.
3. Monitor serum theophylline level, as ordered, to ensure therapeutic level and prevent
toxicity.
4. Monitor oxygen saturation at rest and with activity.
Supportive Care
1. Eliminate all pulmonary irritants, particularly cigarette smoke. Smoking cessation
usually reduces pulmonary irritation, sputum production, and cough. Keep the
patient’s room as dust-free as possible.
2. Use postural drainage positions to help clear secretions responsible for airway
obstructions.
3. Teach controlled coughing.
4. Encourage high level of fluid intake ( 8 to 10 glasses; 2 to 2.5 liters daily) within level
of cardiac reserve.
5. Give inhalations of nebulized saline to humidify bronchial tree and liquefy sputum.
Add moisture (humidifier, vaporizer) to indoor air.
6. Avoid dairy products if these increases sputum production.
7. Encourage the patient to assume comfortable position to decrease dyspnea.
8. Instruct and supervise patient’s breathing retraining exercises.
9. Use pursed lip breathing at intervals and during periods of dyspnea to control rate and
depth of respiration and improve respiratory muscle coordination.
10. Discuss and demonstrate relaxation exercises to reduce stress, tension, and anxiety.
11. Maintain the patient’s nutritional status.
12. Reemphasize the importance of graded exercise and physical conditioning programs.
13. Encourage use of portable oxygen system for ambulation for patients with hypoxemia
and marked disability.
14. Train the patient in energy conservation technique.
15. Assess the patient for reactive-behaviors such as anger, depression and acceptance.
Education and health maintenance
1. Review with the patient the objectives of treatment and nursing management.
2. Advise the patient to avoid respiratory irritants. Suggest that high efficiency
particulate air filter may have some benefit.
3. Warn patient to stay out of extremely hot or cold weather and to avoid aggravating
bronchial obstruction and sputum obstruction.
4. Warn patient to avoid persons with respiratory infections, and to avoid crowds and
areas with poor ventilation.
5. Teach the patient how to recognize and report evidence of respiratory infection
promptly such as chest pain, changes in character of sputum (amount, color and
consistency), increasing difficulty in raising sputum, increasing coughing and
wheezing, increasing of shortness of breath.