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DAVAO DOCTORS COLLEGE

Gen. Malvar St. Davao City


BACHELOR OF SCIENCE IN NURSING

Nursing Management of a Patient with

Chronic Obstructed Pulmonary Disease

In Partial Fulfillment of the Requirements in

NCM 106

Submitted by:

Alben Kendrick Colegio BSN 14B

Submitted To:

Ms. Gina Salvador RN, MN

August 26,2018

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Table of Contents

I. Definiton 3-5

II. Signs and Symptoms 6-7

III. Laboratory Tests and Diagnostic Tools 8-10

IV. Pathophysiology 11-16

V. Medical Management 17-20

VI. Nursing Management 21-23

VII. References 24

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I. Definition

Chronic Obstructive Pulmonary Disease (COPD) is an umbrella term used to

describe progressive lung diseases including emphysema, chronic bronchitis, and

refractory (non-reversible) asthma. This disease is characterized by increasing

breathlessness. COPD is a progressive and (currently) incurable disease, but with the

right diagnosis and treatment, there are many things you can do to manage

your COPD and breathe better. People can live for many years with COPD and enjoy

life.

In Emphysema the tiny, delicate air sacs (alveoli) in your lungs are damaged.

The walls of the damaged air sacs become stretched out and your lungs actually get

bigger, making it harder to move your air in and out. Old air gets trapped inside the

alveoli so there is little or no room for new air to go. In emphysema it is harder to get

oxygen in and carbon dioxide (the waste product of your breathing) out. Chronic

bronchitis is an inflammation of the breathing tubes (bronchial airways) inside your

lungs. Tiny hair-like structures (cilia) line your airways and sweep mucus up, keeping

your airways clean. When cilia are damaged, they can’t do this, and it becomes harder

for you to cough up mucus. This can make your airways swollen and clogged. These

changes limit airflow in and out of your lungs, making it hard to breathe. Refractory

(non-reversible) asthma is a type of asthma that does not respond to usual asthma

medications. In an asthma attack, bronchial airways tighten up and swell. Medications

can usually reverse this, opening up the airways and returning them to how they were

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before the asthma attack. In refractory asthma, medications cannot reverse the

tightening and swelling of the airways.

Most cases of COPD are caused by inhaling pollutants; that includes tobacco

smoking (cigarettes, pipes, cigars, etc.), and second-hand smoke. Fumes, chemicals

and dust found in many work environments are contributing factors for many individuals

who develop COPD. Genetics can also play a role in an individual’s development

of COPD even if the person has never smoked or has ever been exposed to strong lung

irritants in the workplace. COPD most often occurs in people 40 years of age and older

who have a history of smoking. These may be individuals who are current or former

smokers. While not everybody who smokes gets COPD, most of the individuals who

have COPD (about 90% of them) have smoked. However, only one in five smokers will

get significant COPD. Researchers are trying to find out why some smokers

get COPD and others don’t. (learn more about the COPD PPRN research study.) It is

very important to quit smoking if you haven’t! Quitting smoking helps slow the disease. It

makes treatment more effective. COPD can also occur in those who have had long term

exposure and contact with harmful pollutants in the workplace. Some of these harmful

lung irritants include certain chemicals, dust, or fumes. Heavy or long-term contact with

secondhand smoke or other lung irritants in the home, such as organic cooking fuel,

may also cause COPD. Individuals who have worked for many years around these

irritants are at risk for developing mild COPD.

Even if an individual has never smoked or been exposed to pollutants for an

extended period of time, they can still develop COPD. Alpha-1 Antitrypsin Deficiency

(AATD) is the most commonly known genetic risk factor for emphysema2. Alpha-1

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Antitrypsin related COPD is caused by a deficiency of the Alpha-1 Antitrypsin protein in

the bloodstream. Without the Alpha-1 Antitrypsin protein, white blood cells begin to

harm the lungs and lung deterioration occurs. The World Health Organization and the

American Thoracic Society recommends that every individual diagnosed with COPD be

tested for Alpha-1. For more information about AATD and how to get tested, visit

the ALPHA-1 FOUNDATION WEBSITE or call 1-877-2 CURE-A1.

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II. Signs and Symptoms

At first, COPD may cause no symptoms or only mild symptoms. As the disease gets

worse, symptoms usually become more severe. Common signs and symptoms of

COPD include:

 An ongoing cough or a cough that produces a lot of mucus; this is often called

smoker's cough.

 Shortness of breath, especially with physical activity

 Wheezing or a whistling or squeaky sound when you breathe

 Chest tightness

If you have COPD, you also may often have colds or other respiratory infections such

as the flu, or influenza.

Not everyone who has the symptoms described above has COPD. Likewise, not

everyone who has COPD has these symptoms. Some of the symptoms of COPD are

similar to the symptoms of other diseases and conditions. Your doctor can determine if

you have COPD.

If your symptoms are mild, you may not notice them, or you may adjust your lifestyle to

make breathing easier. For example, you may take the elevator instead of the stairs.

Over time, symptoms may become severe enough to cause you to see a doctor. For

example, you may become short of breath during physical exertion.

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The severity of your symptoms will depend on how much lung damage you have. If you

keep smoking, the damage will occur faster than if you stop smoking.

Severe COPD can cause other symptoms, such as swelling in your ankles, feet, or legs;

weight loss; and lower muscle endurance.

Some severe symptoms may require treatment in a hospital. You—or, if you are unable,

family members or friends—should seek emergency care if you are experiencing the

following:

 You are having a hard time catching your breath or talking.

 Your lips or fingernails turn blue or gray, a sign of a low oxygen level in your

blood.

 People around you notice that you are not mentally alert.

 Your heartbeat is very fast.

 The recommended treatment for symptoms that are getting worse is not working.

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III. Laboratory tests and Diagnostic Tests

A spirometry test measures how well your lungs are working. It’s a simple and

easy test that can help diagnose COPD.

A person may have Chronic Obstructive Pulmonary Disease (COPD) but not notice

symptoms until it is in the moderate stage. This is why it’s important to ask your doctor

about taking a spirometry test if you are a current or former smoker, have been exposed

to harmful lung irritants for a long period of time, or have a history of COPD in your

family, such as ALPHA-1 ANTITRYPSIN DEFICIENCY related COPD.

Spirometry is a simple, non-invasive test that is used to diagnose COPD. When you

take the test, you will be asked to blow all the air out of your lungs into a mouthpiece

connected to a machine known as a spirometer.

The machine will calculate two numbers: the amount of air you blow out in the first

second, and the amount of air you blow out in 6 seconds or more.

These numbers are represented as FEV1 and FVC (sometimes FEV6 is used). FEV1

stands for the Forced Expiratory Volume in the first second—the amount of air you

exhaled in the first second of blowing. FVC stands for Forced Vital Capacity—the

amount of air that you exhaled in one entire breath.

A spirometry test can also show your doctor how severe your COPD may or may not

be. There are several stages of COPD. The extent of your COPD is classified into 4

different stages that are defined by your symptoms and the results of your Spirometry

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Test. The stages do not determine how long you can expect to live, or in many cases

how drastically your symptoms are affecting your quality of life. The stages are

designed to help your physician in prescribing your treatment protocol. In order to

determine what stage you are in, your pulmonologist, based on your symptoms, may

administer one or more pulmonary tests.

People with COPD have an FEV1/FEV6 (FVC) ratio less than 70%. The

FEV1 percentage predicted indicates how severe the airways are obstructed (blocked or

narrowed).

Less than 80% of predicted is considered moderate COPD, and less than 50% of

predicted is severe. People with asthma will have a low FEV1/FEV6 ratio when they are

having an attack, and then will return to normal or almost normal after using fast-acting

medications.

Your doctor may order additional tests to see if your symptoms are caused by lung

disorders other than COPD. One is Bronchodilator Reversibility Testing, which

determines if your lung function improves significantly with medication.Your doctor may

also order a chest x-ray or a chest CT (high resolution computed tomography), which

shows your lungs in much greater detail, to see if your symptoms are brought on by

other problems instead of COPD.

Who should get tested for COPD?

If you have any of these symptoms, you are at risk for developing COPD.

Anyone with the following should get tested:

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 Has a history of smoking

 Has long-term exposure to air pollutants (including pollution and second-hand

smoke)1

 Has chronic coughing with or without sputum

 Has wheezing

 Has shortness of breath that has become worse over time

 Cannot keep up with people of your own age

It is important to get tested because leaving symptoms misdiagnosed, untreated, or

undertreated may cause them to worsen faster than if they were treated with proper

medication and therapy. Many adults are incorrectly diagnosed with asthma. Providing a

proper diagnosis means individuals will receive the right treatments and follow up

monitoring. There’s no cure yet for COPD but treatments are available to help

individuals live better.

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IV. Pathophysiology

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Emphysema Chronic Bronchitis

Pathogenesis The inflammatory response, Mucous gland enlargement,

Am J Respir Cell mediated by neutrophils, goblet cell hyperplasia and

Mol Biol. 2005 macrophages and CD8+ T-cells, mucociliary dysfunction

May;32(5):367-72. release inflammatory mediators and occur in larger airways,

enzymes that damage the lung causing excessive mucus

parenchyma. Proteases like production and build-up

elastase and matrix reducing the airway

metalloproteinases (MMPs) lumen.Although these

released by these inflammatory cells pathological changes in the

break down the connective tissue of large airways, it appears

the alveolar walls and the septae. A that the major site of

loss of elastic recoil leads increased airway resistance

to diminished expiratory flow rates, is the small airways (≤

air trapping and airway collapsing. 2mm). Fibrosis and smooth

muscle hypertrophy may

occur along with excess

mucus

production and cellular

infiltration in the peripheral

airways.

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Pathophysiology Parenchymal destruction: Recurrent Small airway

BMJ. 2006 May damage to the alveoli eventually inflammation: Mechanisms

20; 332(7551): leads to septal destruction along discussed above lead to

1202–1204. with the capillary bed also. inflammation in the smaller

Matched V/Q defect: Since both the bronchioles and mucus

terminal bronchioles and alveoli secretions further narrow

along with the capillary bed have the airway lumen. Despite

been destroyed, a matched defect this, the parenchyma are

exists between the ventilation and relatively less damaged.

perfusion; areas of low ventilation V/Q mismatch: The

also have poor perfusion. physiologic response leads

Mild hypoxia: Despite the “matched” to a drop in ventilation and

V/Q defect, overtime compensation with the rise

hyperventilation develops and in CO. Increased perfusion

cardiac output (CO) drops which in the areas of poor

leads to areas of poor blood flow in ventilation takes place

relatively well oxygenated areas. eventually causing hypoxia

Due to this poor CO, the rest of the and secondary

body suffers from tissue hypoxia. polycythemia.

Cachexia: At the pulmonary level, Severe hypoxia and

the low CO leads to pulmonary hypercarbia: Chronic V/Q

cachexia; which induces weight loss mismatch leads to

and muscle wasting. This gives decreased

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these patients the characteristic oxygenation/deoxygenation

“pink-puffer” appearance. of the blood resulting in

hypoxemia and increased

CO2 retention (respiratory

acidosis ensues).

Pulmonary hypertension

and cor pulmonale: Chronic

hypercapnia and respiratory

acidosis lead to arterial

vasoconstriction in the

lungs. With the retrograde

pressure build-up, the right

ventricular pressures

continue to rise and

eventually causing RV

failure. Otherwise, known

as cor pulmonale.

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Clinical “Pink puffer” – type A “Blue bloater” – type B

signs/symptoms Severe constant dyspnea/tachypnia Copious sputum

(“puffing”): Likely related to production: High amount of

increasing end-expiratory volume sputum produced by the

(decreased recoil), making each goblet cells. See

breath less efficient. Patients use Pathogenesis above.

accessory muscles (tripod position) Cough: Irritation of the

and breath faster (hyperventilation) cough receptors, by the

to compensate for feeling of mucous, in the smaller and

inadequate ventilation. Dyspnea is the large airways.

also related to respiratory muscle Cyanotic (“blue”): The

fatigue from increased use as well mismatched V/Q defect

as the flattening of the diaphragm leads to inadequate

which impairs its function. oxygenation of the blood;

Am J Respir Crit Care Med. 2008 most prominent in the lips

Mar 15;177(6):564-5. and the nail beds.

Mild cough: Irritation of the smaller Volume overload

airway can lead to the production of (“bloater”): Most likely from

cough. from the right ventricular

Non cyanotic (“pink”): Matched V:Q (RV) failure, known as cor

defect; no hypoxemia. pulmonale.

Thin/cachexic: Loss of skeletal Wheezy on

muscle and subcutaneous fat due to auscultation: Due to airway

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inadequate oral intake as well as obstruction. Compared to

high levels of inflammatory asthma, there is less

cytokines (TNF-α) that cause such bronchospasm and more

wasting. mucus/hypertrophy in

Diminished breath sounds on COPD.

auscultation: Hyperinflation of alveoli Rhonchi is a gurgling sound

and destruction of alveolar that may be heard due to

architecture causes decreased mucus hypersecretion in

airway resistance. the airways.

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V. Medical Management

COPD has no cure yet. However, lifestyle changes and treatments can help you feel

better, stay more active, and slow the progress of the disease.

The goals of COPD treatment include:

 Relieving your symptoms

 Slowing the progress of the disease

 Improving your exercise tolerance or your ability to stay active

 Preventing and treating complications

 Improving your overall health

To assist with your treatment, your family doctor may advise you to see a

pulmonologist. This is a doctor who specializes in treating lung disorders.

Medicines

Bronchodilators relax the muscles around your airways. This helps open your

airways and makes breathing easier. Depending on the severity of your COPD, your

doctor may prescribe short-acting or long-acting bronchodilators. Short-acting

bronchodilators last about 4–6 hours and should be used only when needed. Long-

acting bronchodilators last about 12 hours or more and are used every day. Most

bronchodilators are taken using a device called an inhaler. This device allows the

medicine to go straight to your lungs. Not all inhalers are used the same way. Ask your

health care providers to show you the correct way to use your inhaler. If your COPD is

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mild, your doctor may only prescribe a short-acting inhaled bronchodilator. In this case,

you may use the medicine only when symptoms occur. If your COPD is moderate or

severe, your doctor may prescribe regular treatment with short- and long-acting

bronchodilators.

COMBINATION BRONCHODILATORS PLUS INHALED GLUCOCORTICOSTEROIDS

(STEROIDS)

In general, using inhaled steroids alone is not a preferred treatment. If your COPD is

more severe, or if your symptoms flare up often, your doctor may prescribe a

combination of medicines that includes a bronchodilator and an inhaled steroid. Steroids

help reduce airway inflammation. Your doctor may ask you to try inhaled steroids with

the bronchodilator for a trial period of 6 weeks to 3 months to see whether the addition

of the steroid helps relieve your breathing problems.

If you have severe COPD and low levels of oxygen in your blood, oxygen therapy can

help you breathe better. For this treatment, oxygen is delivered through nasal prongs or

a mask.

You may need extra oxygen all the time or only at certain times. For some people who

have severe COPD, using extra oxygen for most of the day can help them: Do tasks or

activities while experiencing fewer symptoms, Protect their hearts and other organs

from damage, Sleep more during the night and improve alertness during the day, and

Live longer.

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DRUG STUDY (EXAMPLE OF A BRONCHODILATOR)

Mechanism Indication Contraindic Side effects Nursing

of Action ations Management

Generic Long-acting Prevention Contraindica CNS: Assess

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of inhaler; use

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mayworsen

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physician.

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experienceexercis

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use it 30–60 min

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VI. Nursing Management

Nursing Care Plan

Subjective:

“Inuubo ako”, as verbalized by the patient

Objective:

 Increased RR – 29

 With crackles

 With chest pain

 With back pain

Nursing Diagnosis

 Ineffective airway clearance related to increase production of mucus in

thetracheo bronchial tree as evidenced by productive cough, crackles, chestpain

& back pain.

Planning

Short Term:

 Within 15 mins of duty, difficulty of breathing will be lessened

Long Term:

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 After 1 day Pt will demonstrate improvement inventilation and adequate

oxygenation within normal limits and having absence symptoms of respiratory

distress.

 After 3 days Pt will be able to verbalize understanding regarding factors that

would contribute to exacerbation of disease and will participate in treatment

regimen.

Nursing Interventions

Independent:

 Elevate the headof the bed 45○ (semi-fowler’s) position. It maximize lung

expansion thus sustain open airway

 Advised the pt tokeep calm during episodes of breathing difficulty to prevent

aggravation of the disease

 Encouraged deep controlled breathing exercise. It promotes optimal chest

expansion

Dependent:

 O2 inhalation via NC as ordered by physician

Evaluation

Short Term:

 Goal partially met

Long Term:

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 Patient was able to verbalize in understanding of the disease and its course of

treatment

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VII. References:

http://www.pathophys.org/copd/#Pathogenesis_pathophysiology_and_clinical_features

https://www.nhlbi.nih.gov/health-topics/copd

http://www.who.int/news-room/fact-sheets/detail/chronic-obstructive-pulmonary-disease-

(copd)

https://www.bmj.com/content/332/7551/1202

https://medlineplus.gov/copd.html

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