Placement: NCM 105 Medicine Rotation (2ndst semester), S.Y.

2009-2010

Time Allotment: 1 hour and 30 minutes

Topic Description: This topic focuses with the care of patients with Chronic Obstructive Pulmonary
Disease (COPD), its etiologic factors, its coexisting disorders which is chronic bronchitis, emphysema, and
asthma and its clinical manifestations. It also deals on the, assessment and diagnosis of the disease and
its medical and nursing management. The knowledge to be imparted in this topic is essential for the
learners to be aware and render patient care effectively.

Central Objective: At the end of one hour and thirty minutes, with the relevant facts and information, the
learners shall be able to widen knowledge, skills, and manifest positive attitudes and values in handling
and caring for patients with COPD. The learners shall develop understanding on COPD, its risk factors,
signs and symptoms, and its management.

I. Prayer
Lord, we acknowledge you presence with us today. We also glorify and praise Your name Lord God. We
confess to you our sins. With all humility Father, please forgive as for the wrong doings that we’ve
committed. Help us Lord that we may be pleasing before your eyes.
We thank you dear Lord for the gift of life, the abundance of you blessings, the love and support of our
dear parents, and the guidance of our clinical instructor. Thank you for giving us beautiful day and the
opportunity for us to learn new things in school. We also thank you for guiding us and for loving us
unconditionally.
Father in Heaven , we pray that you would continually help all of us in facing difficulties in our lives,
especially those who are sick, poor and are facing drastic calamities or dangers at this time. Lord please
continue to guide us and our clinical instructor especially in our ward class today. Bless us in the things we
do and always keep us away from harm and most of all protect us from all evil. May you give us strength
to face each day with and courage. This we all ask and humbly pray in the mighty name of our God Jesus
Christ. Amen.

II. Introduction
Chronic obstructive pulmonary disease (COPD) sometimes also called chronic obstructive lung disease
(COLD), is a disease state characterized by airflow limitation that is not fully reversible. T They are
debilitating conditions that affect the individual’s ability to work and function independently. The airflow
limitation is generally progressive and is normally associated with an inflammatory response of the lungs
due to irritants. COPD is an umbrella term used to encompass chronic bronchitis, emphysema and asthma
(Nettina, 2006, page 307).
COPD is the fifth leading cause of death in the United States for all ages and both genders; fifth for
men and fourth for women (National Center for Health Statistics [NCHS], 2000) (Smeltzer, 2008, page
686).

III. Etiologic factors

Cigarette Smoking
The irritating effect of the smoke causes hyperplasia of cells, which subsequently results in incre4ased
production of mucus. Hyperplasia reduces airway diameter and increases difficulty in clearing secretions
(Lewis, 2004, page 659). 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, diminishing lung capacity. Smoking
also produces abnormal dilation of the distal air space with destruction of alveolar walls. In addition,
carbon monoxide (a byproduct of smoking) combines with hemoglobin to form carboxyhemoglobin.
Hemoglobin that is bound by carboxyhemoglobin cannot carry oxygen efficiently (Smeltzer, 2008, page
688).

a. Environmental factors
Some investigators have reported increased respiratory symptoms in those living in urban compared to
rural areas, which may relate to increased pollution in the urban settings. However, the relationship of air
pollution to chronic airflow obstruction remains unproven. Also, genetically susceptible people are
sensitive to environmental factors such as air pollutions, infectious agents, and allergens, and eventually
develop chronic obstructive symptoms (Smeltzer, 2008, page 688).
 b. Occupational factors
Many dusty occupations are more hazardous than exposure to gas or fumes and are associated with
the development of chronic bronchitis and various forms of airway obstructive disease (Bourke, 2003).
Shipyard welders and caulkers are also known to have an increased risk of developing COPD (Hendrick,
1996), as well as those working in the construction industries who are exposed to cement dust (Barnett,
2006, page 8).

c. Alpha1-antitrypsin Deficiency
Patients with alpha-1 antitrypsin defiiciency are at risk of developing emphysema at an early age –
between the ages of 20 and 40 years – and often have a strong family history of the disease. Alpha1
antitrypsin is an an enzyme inhibitor that protects the lung parenchyma from injury. Alpha 1-antitrypsin
serves primarily as an inhibitor of neutrophil elastase, an elastin-degrading protease released by
neutrophils. When alveolar structures are left unprotected from exposure to elastase, progressive
destruction of elastin tissues results in the development of emphysema.

d. Infection
Recurring infections impair normal defense mechanisms, making the bronchioles and alveoli more
susceptible to injury. In addition, the person with COPD is more prone to respiratory infections, which
subsequently intensify the pathologic destruction of lung tissue and the progression of COPD. The most
common causative organisms are Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella
catarrhalis (Lewis, 2004, page 660).

e. Aging
As people age there is gradual loss of the elastic recoil of the lung. The lungs become more rounded and
smaller. The number of functional alveoli decreases as a result of the loss of the alveolar supporting
structures. These changes are similar to those seen in the patient with emphysema (Lewis, 2004, page
660).

IV. Chronic Bronchitis

a. Pathophysiology
Chronic bronchitis is excessive production of mucus in the bronchi accompanied by a recurrent cough
that persists for at least 3 months of the year during at least 2 successive years. Pathologic changes in the
lung consist of (1) hyperplasia of mucous-secreting glands in the trachea and bronchi, (2) increase in
goblet cells, (3) disappearance of cilia, (4) chronic inflammatory changes and narrowing of small airways,
and (5) altered function of alveolar macrophages (Lewis, 2004, page 661). The bronchial tree becomes
inflamed from inhaled irritants, and impaired ciliary function reduces the ability to remove the irritants.
The mucous-producing glands in the airways become hypertrophied, producing excessive thick, tenacious
mucus, which obstructs airways and traps air (Gould, 2007, page 401). In addition to these changes
( hyperplasia, inflammatory swelling, and excess, thick mucus) causes narrowing of the air lumen and
result to diminished airflow. Greater resistance to airflow increases the work of breathing. Because the
constricted bronchioles are clogged with mucus, there is physical barrier to ventilation. As a result, many
areas of the lungs are not ventilated, and O2 diffusion cannot occur. Frequently the patient with chronic
bronchitis requires O2 both at rest and during exercise as the disease progresses. (Lewis, 2004, page 662).

b. Clinical Manifestations
The patient with chronic bronchitis has a chronic productive cough, shortness of breath, and activity
intolerance. Constant productive cough is the significant indicator of chronic bronchitis ,as is tachypnea
and shortness of breath. Frequently secretions are thick and purulent (Williams and Hopper, 2003, page
449). Cough and rhonchi (harsh rattling or whistling sound heard through a stethoscope on examination of
the chest, caused by partial obstruction of the airways) are usually more severe in the morning because
the secretions have pooled during sleep (Gould, 2007, page 401).. Patients with a clinical syndrome of
chronic bronchitis are classically labeled “blue bloaters,” a reference to fluid retention and more marked
cyanosis. A blue bloater has a history of cough with sputum for 3 months to one year or more and
experiences cyanosis due to a decrease in sufficient amounts of oxygen reaching blood (Kasper, Fauci,
Longo, Braunwald, Hauser, & Jameson, 2005, page 1551).

V. Emphysema

a. Pathophysiology
In emphysema, impaired gas exchange (oxygen, carbon dioxide) results from destruction of the walls of
overdistended alveoli. “Emphysema” is a pathological term that describes an abnormal distention of the
air spaces beyond the terminal bronchioles, with destruction of the walls of the alveoli (Smeltzer, 2008,
page 687). Structural changes in emphysema include (1) hyperinflation of alveoli; (2) destruction of
alveolar walls; (3) destruction of alveolar capillary walls; (4) narrowed,tortuous, small air ways ; and (5)
loss of lung elasticity(Lewis, 2004, page 660).
There are to major types of emphysema: centrilobular and panlobular. In centrilobular emphysema
the primary area of involvement is the central part of the lobule. Respiratory bronchioles enlarge, the walls
are destroyed, and the bronchioles become confluent. In contrast panlobular emphysema involves
distention and destruction of the whole lobule. Respiratory bronchioles, alveolar ducts and sacs, and
alveoli are all affected. There is progressive loss of lung tissue and a decreased alveolar-capillary surface
area. Severe panlobular emphysema is usually found in person with AAT deficiency (Lewis, 2004, page
660). Normally, AAT inhibits the action of enzymes that break down proteins. Clients without AAT are at
increased risk for COPD because the walls of the lung are at higher risk for destruction (Black & Hawks,
2005, page 1818)
Cigarette smoking s strongly implicated as a causative factor in most cases of emphysema. It is known
that cigarettes contain over 4000 toxic chemicals (Stratton et al., 2001), which affect the balance between
the antiprotease and proteases within the lungs, causing permanent damage (Crockett, 2000). Connective
tissue in lungs is primarily composed of elastin, collagen, and proteoglycan, which can be damaged and
destroyed by enzymes such as proteases and elastase. The inflammatory cells (macrophages and
neutrophils) produce a proteolytic enzyme known as elastases, which destroys elastin, an important
component of lung tissue. Protease-antiprotease imbalances and cigarette smoke destroy connective
tissue. Because of the loss of elastic recoil, passive expiration is impaired and air is trapped in the alveoli.
Reduction in pulmonary capillaries reduces gas exchange (Barnett, 2006, page 6).
As a result of the destroyed supporting structure of the lungs, there is no pull or traction on the walls of
the bronchioles. Like are being blown into a paper bag, air goes into the lungs easily but unable to come
out on its own and remain in the lung. Thus the bronchioles tend to collapse (especially on expiration) and
air is trapped distal alveoli, resulting in hyperinflation and over distention of the alveoli. This trapped air in
the lungs gives the patient the typical barrel- chested appearance. In emphysema the lungs can be
inflated easily but can deflate only partially (Lewis, 2004, page 661).
b. Clinical Manifestations
The most characteristic symptom of emphysema is progressive shortness of breath, accompanied by
activity intolerance. Patients with predominant emphysema are classically referred to as “pink puffers,” a
reference to acyanotic with compensatory pursed-lip breathing (Kasper, Fauci, Longo, Braunwald, Hauser,
& Jameson, 2005, page 1551). Also, chronic hyperinflation leads to the “barrel chest” thorax
configuration. An early symptom of emphysema is dyspnea, which becomes progressively more severe.
The patient will first complain of dyspnea on exertion that progresses to interfering with ADLs to dyspnea
at rest. Minimal coughing is present, with no sputum or small amounts of mucoid sputum. As more alveoli
become overdistended, increasing amount of air are trapped. This causes a flattened diaphragm and an
increased anteroposterior diameter of the chest, forming the typical barrel chest. Effective abdominal
breathing is decreased because of the flattened diaphragm from the overdistended lungs. The person
becomes more of chest breather, relying on the intercostal and accessory muscles. This type of breathing,
however, is not that effective because the ribs become fixed in an inspiratory position (Lewis, 2004, page
662).
Hypoxemia (especially during exercise) may be present, but hypercapnia does not develop until
late in the disease. The person is characteristicscally underweight, but the exact cause for this is not well
understood. One possibly is that the patient a in a hypermetabolic state with increased energy
requirements that are partly due to the increased work of breathing. However, even when the patient has
adequate calorie intake. Weight loss is still experienced (Lewis, 2004, pages 662-663).

VI. Asthma

a. Pathophysiology
Asthma is characterized by inflammation of the mucosal lining of the bronchial tree and spasm of the
bronchial smooth muscles (bronchospasm). This causes narrowed airways and air trapping. Precipitating
factors include allergens, emotional upheaval, cold weather, exercise, chemicals, medications, and viral
infections (Williams and Hopper, 2003, page 449). Allergy is the strongest predisposing factor for asthma.
The hallmarks of asthma are airway inflammation and non-specific hyperirritability or hyperresonsiveness
of the tracheobronchial tree (Lewis, 2004, page 639).
Asthma is also characterized by inflammation of the mucosal lining of the bronchial tree and spasm of
the bronchial smooth muscles (bronchospasm). This causes narrowed airways and air trapping
Symptoms are intermittent and reversible, with periods of normal airway function. Cells that play a key
role in the inflammation of asthma are mast cells, neutrophils, eosinophils, and lymphocytes. Mast cells,
when activated, release several chemicals called mediators. These chemicals, which include histamine,
bradykinin, prostaglandins,
and leukotrienes, perpetuate the inflammatory response and produce an intense, immediate
inflammatory reaction involving bronchoconstriction, vascular congestion, attraction of white blood cells
to the area, edema formation, and increased mucus production (Smeltzer, 2008, page 710).

b. Clinical Manifestations

The characteristics clinical manifestations of asthma are wheezing, cough, dyspnea, and chest
tightness after exposure to a precipitating factor or trigger (Lewis, 2004, page 640). In some instances,
cough may be the only symptom. Asthma attacks often occur at night or early in the morning, possibly due
to circadian variations that influence airway receptor thresholds. Normally the bronchioles constrict during
expiration. However, as a result of bronchospasm, edema , and mucus in the bronchioles, the airways
becomes narrower than usual. Thus it takes longer for the air to air to move out the bronchioles. This
produces the characteristic wheezing, air trapping and hyperinflation. In addition, bronchospasm may lead
to almost continuous coughing in an attempt ot clear the airway and exhale (Smeltzer, 2008, page 711).

VII. Assessment and Diagnostic Evaluation

a. Physical Examination
The nurse should obtain a thorough health history for a patient with known or potential COPD.
Complete a physical examination with an emphasis on the respiratory and cardiac system. Note the
degree of dyspnea, the presence of orthopnea, decreased breath sounds, and clinical manifest ions of
heart failure. Evaluate mental status because confusion and restlessness may be early indicators of
increasing hypoxia and hypercapnia (Lemone , 2004, page 1118).

b. Spirometry
Spirometry is used to evaluate airflow obstruction, which is determined by the ratio of FEV1 (volume of
air that the patient can forcibly exhale in 1 second) to forced vital capacity (FVC). With obstruction, the
patient either has difficulty exhaling or cannot forcibly exhale air from the lungs, reducing the FEV1.
Obstructive lung disease is defined as a FEV1/FVC ratio of less than 70% (Smeltzer, 2008, page 689).

c. Arterial Blood Gases (ABGs)

ABGs are drawn to evaluate gas exchange, particularly during acute exacerbations of COPD. Clients
with predominant emphysema often have mild hypoxemia and normal or low carbon dioxide tension.
Respiratory alkalosis may be present due to an increased respiratory rate (Lemone, 2004, page 1116).

d. Chest X-ray
Chest x-ray may show flattening of the diaphragm due to hyperinflation and evidence of pulmonary
infection is present (Lemone, 2004, page 1116).

e. Sputum Culture
Sputum is frequently colonized in this group of patients with bacteria such as Haemophilus influenzae,
whose identification without other symptoms is not an indication for antibiotic therapy. However, sputum
culture may be useful in confirming what organisms are present and in detecting resistance to antibiotics
(Barnett, 2006, page 63).

f. Pulse Oximetry
Pulse oximetry is used to monitor oxygen saturation of the blood. Marked airway obstruction and
hypoxemia causes oxygen saturation levels less than 95%. Pulse oximetry maybe continuously monitored
to assess the need for supplemental oxygen (Barnett, 2006, page 63).

VIII. Complications

a. Cor pulmonale
Cor pulmonale is hypertrophy of the right side of the heart, with or without heart failure, resulting from
pulmonary hypertension. In COPD, pulmonary hypertension is caused primarily by constriction of the
pulmonary vessels in response to alveolar hypoxia, with acidosis further potentiating the vasoconstriction.
Normally the right ventricle and pulmonary circulatory system are low-pressure systems compared with
the left ventricle and systemic circulation. When pulmonary hypertension develops, the pressures on the
right side of the heart must increase to push blood into the lungs. Eventually right sided heart failure
develops (Lewis, 2004, page 663).

b. Acute Respiratory Failure

The most common event leading to acute respiratory failure in COPD is acute respiratory tract
infection (usually viral) or acute br0nchitis."‘ Frequently COPD patients wait too long to contact their health
care provider when they develop lever. Increased cough and dyspnea or other symptoms suggestive of
exacerbations of COPD. An exacerbation of cor pulmonale may also lead to acute respiratory failure.
Discontinuing bronchodilator or corticosteroid medication may also precipitate respiratory failure. The use
of B-adrenergic blockers may also exacerbate acute respiratory failure in the patient with an asthmatic
component to the COPD (Lewis, 2004, page 664).

c. Acute exacerbations of Chronic Bronchitis

The airways of patients with stable chronic COPD are colonized with Streptococcus pneumoniae
and Haemophilus influencae, which are relatively nonpathogenic in these patients. Factors that impair
normal function of the mucociliary system and thus slow or prevent the removal of particulate matter may
result in the potential for acute infection. The most common organisms causing acute bronchitis arc H.
influenzae, M. catarrhalis, and S. pnuemonia. As COPD becomes more severe, Pseudomonas, Klebsiella
pneumonia, and E. coli are frequent causes of infection (Lewis, 2004, page 664).
Clinical manifestations of an acute exaccrhation include worsened cough, hemoptysis, wheezing,
increased shortness of breath, and changes in the amount, color, consistency, or viscosity of the sputum.
Patients are treated with antibiotics, increases in bronchodilator usage, possibly corticosteroids,
humidilication, and postural drainage. Teaching the patients and families regarding these treatments is
done to promote self-care management (Lewis, 2004, page 664).

d. Pneumonia
Pneuomomia is a frequent complication of COPD. The most common causative agents are S.
pneumoniae, H. influenzae, and viruses. The most common manifestation is purulent sputum, Systemic
manifestations such as fever, chills and leukocytosis may not be present (Lewis, 2004, page 664).

IX. Medical Management

a. Smoking Cessation
Cessation of cigarette smoking in the early stages is probably the most significant factor in slowing
the progression of the disease. After discontinuation of smoking, the accelerated decline in pulmonary
function slows and pulmonary function usually improves. Thus the smoker stops, the less pulmonary
function is lost and the sooner the symptoms decrease, particularly cough and sputum production (Lewis,
2004, page 665).

b. Pharmacologic Therapy

b.1 Bronchodilators
Bronchodilators relieve bronchospasm and reduce airway obstruction by allowing increased oxygen
distribution throughout the lungs and improving alveolar ventilation. with asthma to bronchodilator
therapy, a reduction in dyspnea and an increase in FEV, are usually achieved. Bronchodilator therapy is
best given as maintenance therapy rather than as a treatment for acute symptoms. Several classes of
bronchodilators are used: beta-adrenergic agonists, anticholinergic agents, and methylxanthines. These
medications may be used in combination to optimize the bronchodilation effect.B2- Adrenergic agonists are
routinely used as bronchodilators in the treatment of COPD." Anticholinergic agents, especially ipratropium
(Atrovent) by inhaler, are even more effective bronchodilators than B2- adrenergic agonists in the patient
with emphysematous COPD. Inhaled anticholinergics are the preferred route of delivery, and they have
minimal side effects (Smeltzer, 2008, page 692-693).

b.2 Corticosteroids
Inhaled and systemic corticosteroids (oral or intravenous) may also be used in COPD but are used more
frequently in asthma. Although it has been shown that corticosteroids do not slow the decline in lung
function, these medications may improve symptoms. Examples of corticosteroids in the inhaled form are
beclomethasone (Beclovent, Vanceril), budesonide (Pulmicort), flunisolide (AeroBid), fluticasone (Flovent),
and triamcinolone (Azmacort) (Smeltzer, 2008, page 692-693).
 b.3 Alpha1- Antitrypsin
Regular replacement of AAT in patients with deficiency may prevent the protease-antiprotease
imbalance that damages the lungs. Although definitive proof of long-term benefits of AAT replacement
therapy is still lacking, a growing body of evidence suggests that patients who are AAT deficient and
receive replacement therapy have a slower rate of lung destruction as measured by spirometry and a
chest computed tomographic scan. It may also reduce mortality. IV infusion of AAT can be given on a
weekly or biweekly basis but most commonly administered monthly (Monahan, Sands, Neighbors, Marek &
Green, 2007, page 677).

c. Oxygen Therapy
Administration of supplemental oxygen is the only therapy proven to alter the course of advanced
stages of COPD. Hypoxemia in patients with COPD adversely affects function and leads to death. Oxygen
therapy is required for patients with COPD who are unable to maintain a PaO2 greater than 55 mmHg or
oxygen saturation greater than 85% or more at rest and for those who cannot carry out ADLs without
becoming short of breath ( Monahan, Sands, Neighbors, Marek & Green, 2007, page 677). Supplemental
O2 is commonly prescribed for patients with severe and progressive hypoxemia. Oxygen therapy improves
exercise tolerance, mental functioning, and quality of life in advanced COPD. Oxygen may be used
intermittently, at night, or continuously.

d. Surgical Management

Two different surgical procedures have been used in severe COPD. One type of surgery is lung
volume reduction surgery (LVRS).” The rationale for this type of surgery is that by reducing the size of the
hyper inflated emphysematous lungs, there is decreased airway obstruction and increased room for the
remaining normal alveoli to function. The procedure reduces lung volume and improves lung and chest
wall mechanics. There are different types of LVRS. In one approach a median sternotomy is performed and
parts of each lung are removed and tissue reattached using a stapling device. Another approach is a
video-assisted thoracoscopy that can be performed unilaterally or bilaterally. In this approach either a
stapling or laser procedure can be done, or they can be done together. The most common postoperative
complication is pneumonia (Lewis, 2004, page 671).
The second surgical procedure is lung transplantation. COPD patients are the largest group of
patients on waiting lists for lung transplantation. Although single-lung transplant is the most commonly
used technique, bilateral transplantation can be performed. In appropriately selected patients ·with COPD,
lung transplantation prolongs life, improves functional capacity, and enhances quality of life. However,
rejection and effects of immunosuppressive therapy remains an obstacle (Lewis, 2004, page 671).

X. Nursing Interventions

a. Promoting Smoking Cessation

Expected Outcomes: verbalizes willingness/interest to quit smoking , verbalizes
information about smoking, risks of continuing, benefits of quitting, and techniques to optimize
cessation efforts (Smeltzer, 2008, page 700)
Because smoking has such a detrimental effect on the lungs, the nurse must discuss smoking cessation
strategies with patients. Although patients may believe that it is too late to reverse the damage from years
of smoking and that smoking cessation is futile, they should be informed that continuing to smoke impairs
the mechanisms that clear the airways and keep them free of irritants. The nurse should educate the
patient regarding the hazards of smoking and cessation strategies and provide resources regarding
smoking cessation, counseling, and formalized programs available in the community (Smeltzer, 2008,
page 697).

b. Improving Gas Exchange

Expected Outcomes : PaCO2 of 35-45 mmHg, return to normal PaO2 to normal range, and improve
mental status (
Bronchospasm, which occurs in many pulmonary diseases, reduces the caliber of the small bronchi and
may cause dyspnea, static secretions, and infection. Bronchospasm can sometimes be detected when
wheezing or diminished breath sounds are heard on auscultation with a stethoscope. Increased mucus
production, along with decreased mucociliary action, contributes to further reduction in the caliber of the
bronchi and results in decreased airflow and decreased gas exchange. This is further aggravated by the
loss of lung elasticity that occurs with COPD (NIH, 2001). These changes in the airway require that the
nurse monitor the patient for dyspnea and hypoxemia. If bronchodilators or corticosteroids are prescribed,
the nurse must administer the medications properly and be alert for potential side effects (Smeltzer, 2008,
page 697).

c. Achieving Airway Clearance

Expected Outcomes: Normal breath sounds , patent airway, and effective coughing technique (Lewis,
2004, page 677)
Diminishing the quantity and viscosity of sputum can clear the airway and improve pulmonary
ventilation and gas exchange. The nurse should teach the patient effective coughing techniques to
minimize airway collapse and aid in proper coughing. Also, position patient in semi-Fowler position to
facilitate cough and prevent aspiration. To thin secretions, 3 to 4 L has traditionally been encouraged
unless contraindicated. The Global Initiative for Chronic Obstructive Lung Disease recommends manual or
mechanical chest percussion and postural drainage in patient producing more than 25 ml of sputum each
day (Smeltzer, 2008, page 697).

d. Improving Breathing Pattern

Expected Outcomes: demonstrate effective breathing pattern, use of controlled breathing techniques
(pursed-lip breathing) and diaphragmatic breathing (abdominal muscle breathing), demonstrate
respiratory rate within near-normal limits ( Monahan, Sands, Neighbors, Marek & Green, 2007, page
681)
The nurse encourages the patient to use controlled breathing techniques, including pursed-lip
breathing, and abdominal breathing, to control dyspnea and anxiety. Pursed-lip breathing decreases
dyspnea when it is used with activities that produce tachypnea, which leads to progressive air trapping. To
teach it, the nurse asks the patient to (1) inhale through the nose for several seconds with mouth closed
and (2) exhale slowly (taking twice as long the inhalation) through pursed lips held in narrow slit. Training
in diaphragmatic breathing reduces the respiratory rate, increases alveolar ventilation, and sometimes
helps expel as much air as possible during expiration (Lemone, 2004, page 1122).

e. Improving Activity Intolerance

Expected Outcomes: Improved activity tolerance by maintaining a realistic activity level and
demonstrating energy conservation techniques (Black and Hawks, 2005, page 1825)
Patients with COPD experience progressive activity and exercise intolerance. Education is focused on
rehabilitative therapies to promote independence in executing activities of daily living. These may include
pacing activities throughout the day or using supportive devices to decrease energy expenditure. The
nurse evaluates the patient’s activity tolerance and limitations and teaching strategies to promote
independent activities of daily living. Also, the patient may be a candidate for exercise training to
strengthen the muscles of the upper and lower extremities and improve exercise tolerance and endurance.
Other health care professionals (rehabilitation therapy, occupational therapy, physical therapy) may be
consulted as additional resources (Smeltzer, 2008, page 697).

XI. Open Forum

XII. Evaluation

Mechanics: The presenter will choose a classmate A to select anyone of his/her classmate to give an
animal sound. If his/her classmate cannot give the animal sound , he/she will be ask a question and
have to answer. If he/she will be able to give the sound of an animal that was ask by his/her classmate
A, classmate A will answer the question.

Questions:

1. What are the distinctive clinical manifestation of emphysema, chronic bronchitis and asthma?
2. Differentiate pathologic factors of emphysema, chronic bronchitis and asthma.
3. Give 1 complication of COPD and define it.
4. What are the pharmacologic therapies for COPD?
5. Give one nursing diagnosis and an applicable nursing intervention.