INTRODUCTION:
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 12
th 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
- 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.
- ABG levels- decreased PaO2, pH, and increased CO2.
- Chest X-ray – in late stages, hyperinflation, flattened diaphragm,
increased rettrosternal space, decreased vascular markings, possible
bullae.
- 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.
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
- Respiratory failure
- Pneumonia, overwhelming respiratory infection
- Right-sided heart failure, dysrhythmias
- Depression
- Skeletal muscle dysfunction
NURSING INTERVENTIONS
Monitoring
- Monitor for adverse effects of bronchodilators – tremulousness,
tachycardia, cardiac arrhythmias, central nervous system stimulation,
hypertension.
- Monitor condition after administration of aerosol bronchodilators to
assess for improved aeration, reduced adventitious sounds, reduced
dyspnea.
- Monitor serum theophylline level, as ordered, to ensure therapeutic level and prevent toxicity.
- Monitor oxygen saturation at rest and with activity.
Supportive Care
- 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.
- Use postural drainage positions to help clear secretions responsible for airway obstructions.
- Teach controlled coughing.
- Encourage high level of fluid intake ( 8 to 10 glasses; 2 to 2.5 liters daily) within level of cardiac reserve.
- Give inhalations of nebulized saline to humidify bronchial tree and
liquefy sputum. Add moisture (humidifier, vaporizer) to indoor air.
- Avoid dairy products if these increases sputum production.
- Encourage the patient to assume comfortable position to decrease dyspnea.
- Instruct and supervise patient’s breathing retraining exercises.
- Use pursed lip breathing at intervals and during periods of dyspnea
to control rate and depth of respiration and improve respiratory muscle
coordination.
- Discuss and demonstrate relaxation exercises to reduce stress, tension, and anxiety.
- Maintain the patient’s nutritional status.
- Reemphasize the importance of graded exercise and physical conditioning programs.
- Encourage use of portable oxygen system for ambulation for patients with hypoxemia and marked disability.
- Train the patient in energy conservation technique.
- Assess the patient for reactive-behaviors such as anger, depression and acceptance.
Education and health maintenance
- Review with the patient the objectives of treatment and nursing management.
- Advise the patient to avoid respiratory irritants. Suggest that high efficiency particulate air filter may have some benefit.
- Warn patient to stay out of extremely hot or cold weather and to avoid aggravating bronchial obstruction and sputum obstruction.
- Warn patient to avoid persons with respiratory infections, and to avoid crowds and areas with poor ventilation.
- 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.
