Kingdom of Bahrain Ministry of Health

College of Health Sciences

Nursing Division WHO Collaborating Center for Nursing Development

Generic BSc Nursing Program Nursing 315- Adult Health 2

3rd Year

Case study on (COPD)

Prepared by: Juma Khalid TarrarSt No. 04-083Supervised by: Mrs. Moutza khalifa

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NO Content Page NO

1 Content 2

2 Introduction 3

3 Patient history 4-5

4 Objectives 6

5 Definition of COPD 7-8

6 Incidence of COPD 8

7 Causes of COPD 8-9

8 Risk factor for COPD 9

9 Pathophysiology of COPD 10

10 Clinical manifestation of COPD 11

11 Complication of COPD 12

12 Diagnostic evaluation 13-14-15-

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14 Medical management 17-18-19

15 Surgical management 20

16 Nursing management 21-22-23-

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Summary

References

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Introduction

I am a third year generic BSc.Nursing student, I was having a

clinical training in ward 12 in Al- Salmania medical complex and

I have been assigned to take care of patients with different

clinical presentations, I was interested in patient with COPD, so

I decided with the agreement of my teacher to do a case study

about him.

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Patient Information's

I.A.I is 80 years old, Bahraini male.

He is married, lives in AL-BILAD village and he is the father

of 2 daughters and 4 sons.

Known case of COPD for the last 8 years and not on regular

treatment.

o Chief complain: Come to A/E department with history

of shortness of breath for 1 day duration associated

with dry cough. Shortness of breath aggravated by

sleeping, not relived by medication. Also history of

hyponatremia.

No history of:

Fever

Upper respiratory tract infections

Chest pain

Current health status:

aged male with normal bowel movements, normal urine output

and color, good air entry and bi mild wheezing. Heart sounds

(S1 and S2) is normal with no murrmer. Abdomen is soft and

lax with no organmegally. I.A.I has mild swelling at right leg

(pitting oedema).

Present illness: COPD exacerbation

Family history: Patient family history is not significant and didn't

have any chronic diseases.

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HTN+

Cholester

olSCD

Objectives

Define COPD accurately.

Identify the incidence of COPD around the world and in

Bahrain.

Discuss the causes and predisposing factors of COPD

and relate it to my patient.

Explain the pathophysiology of COPD. Discuss the clinical manifestations of COPD and relate it

to my patient.

Discuss the complication of COPD and relate it to my

patient.

Interpret and discuss the diagnostic tests in COPD and

relate it to my patient.

Discuss the medical management of patient with COPD

and relate it to my patient.

Discuss the surgical management of patient with COPD

and relate it to my patient.

Discuss the nursing management of patient with COPD

and relate it to my patient.

Summary includes the days of care given to my patient.

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Definition of COPD: Chronic obstructive pulmonary disease (COPD) is a term referring to two

lung diseases, chronic bronchitis and emphysema, that are characterized

by obstruction to airflow that interferes with normal breathing.  Both of

these conditions frequently co-exist, hence physicians prefer the term

COPD. It does not include other obstructive diseases such as asthma.

Chronic bronchitis: Chronic bronchitis is the inflammation and eventual

scarring of the lining of the bronchial tubes. When the bronchi are inflamed

and/or infected, less air is able to flow to and from the lungs and a heavy

mucus or phlegm is coughed up.

Emphysema: Is a chronic obstructive lung disease that destroys alveoli

walls.  The alveoli can be compared to a balloon that has been blown up and

the air has been let out.  It no longer snaps back into place when stretched

but lies floppy.  When fresh air enters a lung with emphysema, it enters the

alveoli because of changes in pressure.   The fresh air now in the alveoli

should give off oxygen and take on carbon dioxide to exhale and rid it from

the body.  However, instead of being exhaled, the air becomes trapped and

unable to be pushed out because of the lack of elasticity of the alveoli.

Incidence of COPD around the world:

Worldwide data are sparse, but the rates likely are higher because more than

1.2 billion humans are exposed to the ravages of smoking. A population-

based epidemiologic study from Spain determined the prevalence of COPD in

individuals aged 40-69 years at 9.1% (78% were men).

Incidence of COPD in America:

Mortality/Morbidity: COPD is the fourth leading cause of death in the United States, affecting 32 million adults.

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Sex: Men are more likely to have COPD than women.

Age: COPD occurs predominantly in individuals older than 40 years.

Incidence of COPD in Bahrain:

DISCHLess than 48 hrs More than 48 hrs

Total

Bahraini Non Bahraini Bahraini Non Bahraini

Male - - 5 - 5

Female 1 - 6 - 7

Causes and predisposing factors of COPD:

Causes:

Smoking

Smoking is responsible for 90% of COPD in the United States. Although not all cigarette smokers will develop COPD, it is estimated that 15% will. Smokers with COPD have higher death rates than nonsmokers with COPD. They also have more frequent respiratory symptoms such as coughing and shortness of breath. and more deterioration in lung function than non-smokers.

Cigarette smoking damages the lungs in many ways. For example, the irritating effect of cigarette smoke attracts cells to the lungs that promote inflammation. Cigarette smoke also stimulates these inflammatory cells to release elastase, an enzyme that breaks down the elastic fibers in lung tissue.

Deficiency of alpha-1 antitrypsin (AAT)

Another well-established cause of COPD is a deficiency of alpha-1 antitrypsin (AAT). AAT deficiency is a rare genetic (inherited) disorder that accounts for less than 1% of the COPD in the United States.

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Normal function of the lung is dependent on elastic fibers surrounding the airways and in the alveolar walls. Elastic fibers are composed of a protein called elastin. An enzyme called elastase that is found even in normal lungs can break down the elastin and damage the airways and alveoli. Protein alpha-1 antitrypsin (AAT) which is produced by the liver and released into the blood is present in normal lungs and can block the damaging effects of elastase on elastin.

Individuals who inherit two defective AAT genes (one from each parent) have either low amounts of AAT in the blood or AAT that does not function properly. The reduced action of AAT in these individuals allows the destruction of tissue in the lungs by elastase to continue unopposed.

Individuals with one normal and one defective AAT gene have AAT levels that are lower than normal but higher than individuals with two defective genes. These individuals MAY have an increased risk of developing COPD if they do not smoke cigarettes. however, their risk of COPD probably is higher than normal if they smoke.

Predisposing factors:

Occupational pollutants

Some occupational pollutants such as cadmium and silica do increase the risk of COPD. Persons at risk for this type of occupational pollution include coal miners, construction workers, and metal workers. These occupations are more often associated with interstitial lung diseases, especially the pneumoconiosis. Nevertheless, the adverse effects of smoking cigarettes on lung function are far greater than occupational exposure.

Secondhand smoke

Effects of passive smoking or "second-hand smoke" on the lungs are not well-known; however, evidence suggests that COPD incidents are more common in people who live in households where other smoke.

Air pollution

Air pollution can cause problems for persons with lung disease, but it is unclear whether outdoor air pollution contributes to the development of COPD. However, in the non-industrialized world, the most common incidents of COPD occur where there is indoor air pollution. This is usually due to indoor stoves used for cooking.

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My patient is non smoker, however, he is living in a resident where there are smokers. Also he used to cook food using coal which may contribute to his condition. Also, he was working as cleaner in ministry of education for 20 years.

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Pathophysiology:

COPD is a mixture of 2 separate disease processes that together form the complete clinical and pathophysiological picture. These processes are chronic bronchitis, emphysema.

Chronic bronchitis

In this type, chronic bronchitis plays the major role. Chronic bronchitis is defined by excessive mucus production with airway obstruction and notable hyperplasia of mucus-producing glands.

Damage to the endothelium impairs the mucociliary response that clears bacteria and mucus. Inflammation and secretions provide the obstructive component of chronic bronchitis. In contrast to emphysema, chronic bronchitis is associated with a relatively undamaged pulmonary capillary bed. Emphysema is present to a variable degree but usually is centrilobular rather than panlobular. The body responds by decreasing ventilation and increasing cardiac output. This results in rapid circulation in a poorly ventilated lung, leading to hypoxemia and polycythemia.

Eventually, hypercapnia and respiratory acidosis develop, leading to pulmonary artery vasoconstriction and cor pulmonale. With the ensuing hypoxemia, polycythemia, and increased CO2 retention, COPD patients have signs of right heart failure and are known as "blue bloaters."

Emphysema

The second major type is that in which emphysema is the primary underlying process. Emphysema is defined by destruction of airways distal to the terminal bronchiole.

Physiology of emphysema involves gradual destruction of alveolar septae and of the pulmonary capillary bed, leading to decreased ability to oxygenate blood. The body compensates with lowered cardiac output and hyperventilation. This results in relatively limited blood flow through a fairly well oxygenated lung with normal blood gases and pressures in the lung, in contrast to the situation in blue bloaters. Because of low cardiac output, however, the rest of the body suffers from tissue hypoxia and pulmonary cachexia. Eventually, these patients develop muscle wasting and weight loss and are identified as "pink puffers."

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Clinical manifestations of COPD:

In patients affected predominantly by emphysema, shortness of breath may be the major symptom. Dyspnea usually is most noticeable during increased physical activity, but as emphysema progresses, dyspnea occurs at rest. Patient may be very thin with barrel chest. They typically have little or no cough or expectoration. Breathing may be assisted by using accessory respiratory muscles.

In patients with chronic bronchitis as well as bronchiectasis, chronic cough and sputum production are the major symptoms. The sputum is usually clear and thick. Periodic chest infections can cause fever, dyspnea, coughing, production of purulent sputum and wheezing. Infections occur more frequently as bronchitis and bronchiectasis progress. Use of accessory muscles of respiration is common.

In advanced COPD, patients may develop cyanosis due to a lack of oxygen in blood. They may have Barrarel chest, They also may develop morning headaches due to an inability to remove carbon dioxide from the blood. Weight loss occurs in some patients, primarily (other possibility is reduced intake of food) because of the additional energy that is required just to breathe. In advanced COPD, small blood vessels in the lungs are destroyed, and this blocks the flow of blood through the lungs. As a result, the heart must pump with increased force and pressure to get blood to flow through the lungs. (The elevated pressure in the blood vessels of the lungs is called pulmonary hypertension.) If the heart cannot manage the additional work, right heart failure also known as Cor pulmonale results and leads to swelling of the feet and ankles. Patients with COPD may cough up blood (hemoptysis). Usually hemoptysis is due to damage to the inner lining of the airways and the airways' blood vessels; however, occasionally, hemoptysis may signal the development of lung cancer.

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My patient presents with shortness of breath associated with dry cough. Shortness of breath aggravated by sleeping. Wheezing, weight loss, hyponatremia, mild swelling at right leg (pitting oedema).He was using accessoary muscle for breathing.

Complication of COPD:

Respiratory failure

When respiratory failure occurs, there is a slow decline in lung function and rising levels of carbon dioxide in the blood. The increasing carbon dioxide creates a narcotic effect in the patient, who slowly loses consciousness and stops breathing.

Pneumonia

caused by bacterial infection can lead to respiratory failure in these patients. Streptococcus pneumoniae is the most common cause of bacterial pneumonia in patients with COPD.

Pneumothorax

Occurs when a hole develops in the lung, allowing air to escape into the space between the lung and the chest wall and collapsing the lung. Patients with COPD are at increased risk for spontaneously developing these holes because of weakened lung structure. A pneumothorax can lead to severe respiratory distress and is treated by inserting a tube into the space between the lung and the chest wall to allow the air to escape out of the space and reexpanding the lung. The tube must remain in the space until the hole is repaired.

Polycythemia

in COPD is the body's attempt to adjust to decreased amounts of blood oxygen by increasing the production of oxygen-carrying red blood cells. While this may be helpful in the short term, overproduction eventually clogs small blood vessels.

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My patient presents didn't develope any complication, instead, his condition improved after his admission in ward 12.

Diagnostic evaluation:

Lab Studies:

Arterial blood gas

o Arterial blood gas (ABG) analysis provides the best clues as to acuteness and severity.

o In general, renal compensation occurs even in chronic CO2 retainers thus, pH usually is near normal.

o Generally, consider any pH below 7.3 a sign of acute respiratory compromise.

Serum chemistry

o These patients tend to retain sodium.

o Diuretics, beta-adrenergic agonists, and theophylline act to lower potassium levels; thus, serum potassium should be monitored carefully.

o Beta-adrenergic agonists also increase renal excretion of serum calcium and magnesium, which may be important in the presence of hypokalemia.

CBC to detect Polycythemia

Imaging Studies:

Chest x-ray

o Chronic bronchitis is associated with increased bronchovascular markings and cardiomegaly.

o Emphysema is associated with a small heart, hyperinflation, flat hemidiaphragms, and possible bullous changes.

Other Tests:

Pulse oximetry

o Pulse oximetry does not offer as much information as ABG.

o When combined with clinical observation, this test can be a powerful tool for instant feedback on the patient's status.

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Electrocardiogram

o The presence of underlying cardiac disease is highly likely.

o Establish that hypoxia is not resulting in ischemia.

o Establish that the underlying cause of respiratory difficulty is not cardiac in nature.

Pulmonary function tests (spirometry)

o Decreased forced expiratory volume in 1 second (FEV1) with concomitant reduction in FEV1/forced vital capacity (FVC) ratio

o Poor/absent reversibility with bronchodilators

o FVC normal or reduced

o Normal or increased total lung capacity (TLC)

o Increased residual volume (RV)

o Normal or reduced diffusing capacity

Tests results

Pulmonary function tests (spirometry) FEV1 % predicted : 53%

Chest x ray

-Shows no significant

perfusion defect

-Low probability for

pulmonary embolism

Arterial blood gas

1 st result : 18/7/2007

o PH 7.247 (low)

o PCO2 60.6mmhg

(high)

o PO2 49.3mmhg

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(very low)

o HCO3 27.5 mmol|L

o SaO2 83% (low)

Last result: 22/7/2007

o PH 7.39 (normal)

o PCO2 46mmhg

(within normal)

o PO2 84 mmhg

(normal)

o HCO3 27 mmol|L

o SaO2 98% (normal)

Lab result : (abnormalities)

Blood test 1st result 18/7/2007 Last result 22/7/2007

K+ 3.2 mmol/L low 3.7 mmol/L normal

WBC 26.1 × 9^10 ↑ 16.8 × 9^10 ↑

Hb 8.8 g∕dL ↓ 8.2 g∕dL ↓

Creatnine 60 mmol/L low 64 normal

Urea 2.7 mmol/L low 3.5 mmol/L normal

sodium 129 mmol/L low 124 mmol/L low

chloride 94 mmol/L low 98 mmol/L low

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Medical ManagementSmoking Cessation (if applicable) It is critically important that COPD patients quit smoking. Once a patient has quit, the rate of decline of lung function slows considerably.

There are numerous nicotine replacement systems that help smokers withdraw from nicotine, including nicotine gum, patches, inhalers, and nasal sprays. Nicotine gum was the first nicotine replacement therapy available. Each piece of gum contains 2 mg of nicotine. It is chewed slowly when symptoms of withdrawal are experienced. The gum decreases, but does not eliminate, physical withdrawal symptoms.

Pharmacholigical therapy

Beta2 agonists

It relax the smooth muscle thereby decreasing bronchoconstriction and airflow obstruction. They also improve the ability to clear mucus and the endurance of fatigued respiratory muscles.

Anticholinergic

Anticholinergics such as Ipratropium bromide has a greater bronchodilatory effect than beta2 agonists and has fewer side effects. Ipratropium bromide is generally recommended for COPD patients who experience symptoms daily.

Corticosteroids

Are often used to treat inflamed airways, but their long term benefit is not clear. Steroids have not been shown to slow lung decline in COPD. They may reduce the number of exacerbations and improve symptoms in some patients, but there is no convincing evidence to support this.

It is difficult to wean patients off steroids and many patients are left on inhaled steroids because they do well on them. Corticosteroids are now given, whenever possible, in an inhaled form rather than orally or intravenously. There are many adverse side effects associated with long term use.

Mucolytics

Mucus retention narrows the airways and increases symptoms of COPD. A lot of effort has been put into developing medications that break up and allow mucus to be cleared more effectively from the airways. Unfortunately, this has met with only very modest success.

Antibiotics Antibiotics are generally used only for acute exacerbations. Patients who experience frequent exacerbations with purulent sputum (a sign of infection)

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during the year may be placed on a schedule of prophylactic (preventative) treatment with antibiotics the first 10 days of each month. This is done for special cases only.

Oxygen

Oxygen is the only treatment that has been shown to improve survival. Nasal cannula is the most commonly used oxygen delivery system. Indications for oxygen therapy include: arterial PaO2 < 55 mm Hg, or an O2 saturation of 88% with arterial PaO2 of 55-59 mm Hg, or an O2 saturation of 89% accompanied by cor pulmonale (right-sided heart failure), or polycythemia (proportion of red blood cells above 56% of blood sample).

A patient who does not qualify for oxygen as described may need oxygen while sleeping or exercising. Oxygen may be used at night only if the PaO2 at night is less than 55 mm Hg or the O2 saturation is less than 88%. If the PaO2 is less than 55 mm Hg or the O2 saturation is less than 88% during exercise, oxygen may be prescribed.

Nutritional Support Nutrition is critically important for patients who lose a lot of weight. High fat, low carbohydrate diets are recommended. If a patient is significantly overweight, losing weight may be appropriate.

Patient Drugs:

Drug Purpose

Ventolin 1 ml Q 6 hrs Neb Bronchodilator work by relaxing

the muscles around airways.

This type of medicine helps to

open the airways quickly and

make breathing easier.

Atrovent 1 ml Q 6 hrs Neb To treat the narrowing of lung

airways.

Tazocin 4.5 mg Q 8 hrs IV Bacterial infections are a

common complication of acute

exacerbations

of COPD, and antibiotics are

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used to prevent this infection.

Surgical management

For some people with severe COPD, surgery may be recommended. Surgery

is usually done for people who have:

Severe symptoms

Not had improvement from taking medicines

A very hard time breathing most of the time

surgeries considered in the treatment of severe COPD are:

Bullectomy. In this procedure, doctors remove one or more very large

bullae from the lungs of people who have emphysema. Bullae are air

spaces that are formed when the walls of the air sacs break. The air

spaces can become so large that they interfere with breathing.

Lung volume reduction surgery (LVRS). In this procedure, surgeons

remove sections of damaged tissue from the lungs of patients with

emphysema.

A lung transplant may be done for some people with very severe

COPD. A transplant involves removing the lung of a person with COPD

and replacing it with a healthy lung from a donor.

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My patient condition didn't require any surgical intervention.

Nursing management

Implementation of appropriate nursing interventions, including medications,

controlled oxygen therapy, ventilation modalities, and strategies for secretion

clearance, energy conserving, relaxation, nutrition, and breathing retraining.

Teaching smoking cessation strategies.

Administration of the following pharmacological agents as prescribed:

bronchodilators, oxygen, corticosteroids, antibiotics, psychotropics, opioids

Administration of oxygen therapy as prescribed.

Assessment of inhaler technique and teaching proper technique.

Discuss with client medication's side effects and precautions.

Recommendation of annual influenza vaccination and pneumococcal

vaccine.

Activity pacing is important as client with COPD has decreased exercise

tolerance during specific periods of days especially in the morning.

Promotion of exercise training and pulmonary rehabilitation as appropriate

a) Teaching diaphragmatic breathing which:

• Reduce the respiratory rate

• Increase alveolar ventilation

• Helps expel as much as air as possible during expiration

b )Teaching Pursed lip breathing which:

• Slow expiration

• Prevents collapse of small airways

• Help the client to control the rate & depth of respiration

• Promotes relaxation

• Enabling the pt to gain control of dyspnea & reduce feelings of panic

c) Inspiration muscle training

• This program requires that the client breathe against resistant for 10 to

15 min every day.

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• As the resistant is gradually increases the muscle become better.

Patient education:

o Educate patients to the dangers of smoking and the improvement in quality of life attainable with smoking cessation.

o Instruct patients with COPD to present early during an exacerbation and not wait until they are in distress.

o Teach client about how to use his Medications & home oxygen therapy.

o Teach client the important of following diet regime ordered by dietitian.

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Nursing care plan

Patient problems:

- Deficit in oxygenation at alveoli capillary membrane

- Inspiration and expiration that doesn't provide adequate

ventilation

- Insufficient energey to complete desired daily activities

- Disruption of sleep pattern

- Psychological disturbance related to transfer to new

environment

Nursing diagnosis:

Loss of lung elasticity

- relocation stress syndrome

-Impaired gas exchange R/T

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Subjective data

Objective data Patient problem

Nursing diagnosis

Nursing objectives

Patient c/o shortness of breath

80yrs old--Hypoxia

PO2=49.3 mmhg

-Oxygen saturation

= 83%-Wheezing

breath sound

-deficit in oxygenation

at alveoli capillary

membrane

-Impaired gas exchange R/TLoss of lung

elasticity

-Patient will have adequate oxygenation of

tissues by ABG's results

after my interventions.

interventions rational

-Provide oxygen therapy 2-3 L as doctor order .

-Administer ventolin 1 ml q 8 hrs and atrovent 1 ml q 8 hr as doctor order.

-administer tazocin 4.5mg q 8 hrs as doctor order

-Elevate head of the bed.

-Auscultate breath sounds and assess vital signs.

-To increase oxygen concentration in the body.

-To widened small airways

-To prevent bacterial infection.

-To maintain airway by decreasing pressure on the diaphragm and enhancing drainage to different lung segements.

g- To ascertain respiratory status and note progress.

Evaluation:

- Oxygen saturation has become 98%- Vital sings are stable- wheezing breath sound not heard

Summary includes the days of care given to the patient.

I.A.I is 80 years old, Bahraini male, come to A/E department

with history of shortness of breath for 1 day duration associated

with dry cough. Shortness of breath aggravated by sleeping, not

relived by medication. Also history of hyponatremia. He is

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known case of COPD for the last 8 years and not on regular

treatment.

Dr. Ahmed AL-araidh ordered many tests to be done including:

CBC , Urea, Ca+, Mg+, Na+,urine osmolarity, urine routine

micro ABG, PT,PTT. Also ordered Normal Saline 2L/24 hrs,

maintain I/O chart, restrict oral sweat, Oxygen 2-3L and

medication including: Ventolin, Atrovent, Tazocin.

In the three days that I was taking care of my client and

assessing and evaluating his respiratory status, I also provided

oxygen therapy as doctor ordered and given prescribed

medication, maintaining I/O chart. I also was checking patient

homodynamic status by checking his vital sings. Finally I taught

patient deep breathing exercise and encouraged him to relax to

get better soon.

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References

Brunner & Suddarth's text book of medical surgical nursing,

p:569

http://www.guideline.gov/summary/summary.aspx?

ss=15&doc_id=7008&nbr=4217

http://www.ltcpractice.com/content/node-6/clinicians/cop.htm

http://en.wikipedia.org/wiki/COPD

http://familydoctor.org/online/famdocen/home/articles/

706.html

http://www.medicinenet.com/

chronic_obstructive_pulmonary_disease_copd

http://www.nlm.nih.gov/medlineplus/ency/article/

000091.htm#Definition

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