8/7/2019 Chronic Obstructive Pulmonary Disorder http://slidepdf.com/reader/full/chronic-obstructive-pulmonary-disorder 1/15 Chronic Obstructive Pulmonary Disorder (COPD) Case Study 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
Chronic Obstructive Pulmonary Disorder (COPD) Case Study
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 andsymptoms (GOLD, World Health Organization [WHO] & National Heart, Lung and Blood Institute
[NHLBI], 2004). Although previous definitions have include emphysema and chronic bronchitis under theumbrella 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 werepreviously 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 abnormalairway 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 leadingcause of disability (Sin, McAlister, Man. Et al., 2003). People with COPD commonly become symptomaticduring 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 andto 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
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 carbondioxide 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
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 carryblood 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 arevery 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
• 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 anincreased 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 environmentalfactors (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.
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 obstructionmay 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 isdefined 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). Theconsequence 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.”
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 canbecome 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 advancedCOPD 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 termeda 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, andtreatment is available.
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, bothdue 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) atthe wrist.
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 lungfunction eventually reverts to that of a non-smoker.
Nicotine in cigarettes is addictive, and, therefore, cessation of smoking can cause symptoms of nicotinewithdrawal 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 treatingbronchospasm 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
(Maxair), terbutaline (Brethaire), and isoetharine (Bronkosol). Levalbuterol (Xopenex) is
a recently approved Beta-2 agonist.
o 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 takentwice daily and no more. Along with some of these inhalers to be mentioned, these are
often referred to as maintenance inhalers.o Side effects of beta-2 agonists include anxiety, tremor, palpitations or fast heart rate, and
low blood potassium.
• Anti-cholinergic Agents
o 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 toleranceand 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.o 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 drugalone without additional side effects.
• Methylxanthines
o 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 chemicalssuch 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 inthe 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.
o 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
o 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
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. Rinsingout the mouth after use of a steroid inhaler also can decrease these side effects.
• Treatment of Alpha-1 antitrypsin deficiency
o 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 aspossible.
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.
