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CASE STUDY PRESENTATION

CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Chronic Bronchitis

Bronchi are red and swollen, and congested with mucous secretions Healthy Bronchy Alveoli are enlarged and destroyed Emphysema Healthy Alveoli

SYMPTOMS

EMPHYSEMA

Dyspnea (shortness of breath)

Most noticeable during physical activity

As emphysema progresses, dyspnea occurs at rest

CHRONIC BRONCHITIS

Chronic cough and sputum production

The sputum is usually clear and thick

As bronchitis progress infections occur more frequently

Periodic infections can cause fever, dyspnea, coughing,

production of purulent sputum and wheezing

OVERVIEW OF THE CASE

Patient history:

• Medical Dx: stage 1 COPD (emphysema) 5 years ago

• Meds: Combivent (ipratropium bromide and albuterol sulfate)

• PMH: Bronchitis and upper respiratory infections during winter

• Smoker: 1 ppd for 46 years – has quit 1 year ago

• Family hx: CA – mother, 2 aunts died from lung cancer

OVERVIEW OF THE CASE

Physical exam:

• General appearance: 62-years-old female in no acute distress

• Vitals: Temp. 98.8ºF HR 92 bpm RR 22bpm BP 130/88

• Heart: Regular rate and rhythm; mild jugular distension noted

• Extremities: 1+ bilateral pitting edema. No cyanosis or clubbing

OVERVIEW OF THE CASE

• Neurologic: Alert, oriented; cranial nerves intact

• Skin: Warm, dry

• Chest/lungs: Decreased breath sounds, percussion hyperresonant; prolonged expiration with wheezing; ronchi throughout; using accessory muscles at rest

• Abdomen: Liver, spleen palpable; nondistended, nontender, normal bowel sounds Hospital course:

• Admitting dx: Acute exacerbation of COPD, increasing dyspnea, hypercapnia, r/o pneumonia

• Tx plan: O2 1L/min via nasal cannula, O2 saturation 90-91% IVF D5 ½ NS with 20mEq KCL @ 75 cc/hr

Corticosteroid -Methylprednisone: Solumedrol

Antibiotic -Chephalosporin: Ancef

Bronchodilator: Ipratropium bromide, Albuterol sulfate

ABGs q 6 hours, CXR, sputum cultures and Gram stain

OVERVIEW OF THE CASE

The Physician ordered a nutrition consult

Nutrition history:

• Appetite is poor, fast satiety

• Meal preparations are difficult

• In the previous 2 days, she has eaten very little

• Coughing has made eating difficult

• Food doesn’t taste good, it has a bitter taste

• 5 years ago she weighted 145-150lb, now she is 119lb, 5’3”

• She didn’t weight herself for a while, but clothes are bigger, dentures fit

loosely her family tells her how thin she has gotten

• Avoids milk: “People say it will increase mucus production”

• No previous MNT

• No vit/min supplementation

ASSESSMENT

Physical Examination Data

Head and neck

Teeth: Poorly fitting dentures

Skin

Skin: dry

Edema, peripheral: 1+ bilateral

Vital Signs

↑ Temperature: 98.8ºF

↑ Respiratory Rate: 22 bpm

Shortness of breath

ASSESSMENT

Client History Data

Social history

Physical activity, easy fatigue with increased activity; unable to

achieve desired levels

Medical/ Health history

Chronic Obstructive Pulmonary Disease

Upper respiratory infections or pneumonia

Signs and symptoms

Shortness of breath or dyspnea on exertion or at rest

Meds and supplements

Medications that cause anorexia: Albuterol sulfate

What Is COPD?

COPD, or chronic obstructive pulmonary (PULL-mun-ary) disease, is a progressive disease that makes it hard to breathe. "Progressive" means the disease gets worse over time.

COPD can cause coughing that produces large amounts of mucus (a slimy substance), wheezing, shortness of breath, chest tightness, and other symptoms.

Cigarette smoking is the leading cause of COPD. Most people who have COPD smoke or used to smoke. Long-term exposure to other lung irritants—such as air pollution, chemical fumes, or dust—also may contribute to COPD.

Overview

To understand COPD, it helps to understand how the lungs work. The air that you breathe goes down your windpipe into tubes in your lungs called bronchial (BRONG-ke-al) tubes or airways.

Within the lungs, your bronchial tubes branch into thousands of smaller, thinner tubes called bronchioles (BRONG-ke-ols). These tubes end in bunches of tiny round air sacs called alveoli (al-VEE-uhl-eye).

Small blood vessels called capillaries (KAP-ih-lare-ees) run through the walls of the air sacs. When air reaches the air sacs, oxygen passes through the air sac walls into the blood in the capillaries. At the same time, carbon dioxide (a waste gas) moves from the capillaries into the air sacs. This process is called gas exchange.

The airways and air sacs are elastic (stretchy). When you breathe in, each air sac fills up with air like a small balloon. When you breathe out, the air sacs deflate and the air goes out.

In COPD, less air flows in and out of the airways because of one or more of the following:

The airways and air sacs lose their elastic quality.

The walls between many of the air sacs are destroyed.

The walls of the airways become thick and inflamed.

The airways make more mucus than usual, which can clog them.

Normal Lungs and Lungs With COPD

Figure A shows the location of the lungs and airways in the body. The inset image shows a detailed cross-section of the bronchioles and alveoli. Figure B shows lungs damaged by COPD. The inset image shows a detailed cross-section of the damaged bronchioles and alveolar walls.

In the United States, the term "COPD" includes two main conditions—emphysema (em-fih-SE-ma) and chronic bronchitis (bron-KI-tis). (Note: The Health Topics article about bronchitis discusses both acute and chronic bronchitis.)

In emphysema, the walls between many of the air sacs are damaged. As a result, the air sacs lose their shape and become floppy. This damage also can destroy the walls of the air sacs,

leading to fewer and larger air sacs instead of many tiny ones. If this happens, the amount of gas exchange in the lungs is reduced.

In chronic bronchitis, the lining of the airways is constantly irritated and inflamed. This causes the lining to thicken. Lots of thick mucus forms in the airways, making it hard to breathe.

Most people who have COPD have both emphysema and chronic bronchitis. Thus, the general term "COPD" is more accurate.

Outlook

COPD is a major cause of disability, and it's the third leading cause of death in the United States. Currently, millions of people are diagnosed with COPD. Many more people may have the disease and not even know it.

COPD develops slowly. Symptoms often worsen over time and can limit your ability to do routine activities. Severe COPD may prevent you from doing even basic activities like walking, cooking, or taking care of yourself.

Most of the time, COPD is diagnosed in middle-aged or older adults. The disease isn't passed from person to person—you can't catch it from someone else.

COPD has no cure yet, and doctors don't know how to reverse the damage to the airways and lungs. However, treatments and lifestyle changes can help you feel better, stay more active, and slow the progress of the disease.

Other Names for COPDChronic bronchitis - Chronic productive cough for 3 months in 2 successive years

• Emphysema – Defined as a pathological term referring to permanent changes in terminal bronchioles & alveoli

• Asthma – Inflammatory disease of airways, with reversible changes

Chronic bronchitis

Chronic obstructive airway disease

Chronic obstructive lung disease

Emphysema

What Causes COPD?• Exposure to pipe, cigar, tobacco smoke

• Exposure to second hand smoke

• Exposure to heavy air pollution

• Exposure to heavy dust

• Exposure to chemical/toxic fumes

• Genetic conditions

Risk Factors

• Major

• • Age

• • Male

• • Occupation

• • Smoking

• • Alpha – one – antitrypsin

• Deficiency

Risk Factors

• Minor

• • Air Pollution

• • Alcohol

• • Race

• • Nutritional Status

• • FH

• • Bronchial Reactivity

What Are the Signs and Symptoms of COPD?• Wheezing

• Coughing

• Sputum production

• Shortness of breath

• Chest tightness

• ANATOMY AND PHYSIOLOGY:

•  The respiratory system consists of all the organs involved in breathing. These include the nose, pharynx, larynx, trachea, bronchi and lungs. The respiratory system does two very important things: it brings oxygen into our bodies, which we need for our cells to live and

function properly; and it helps us get rid of carbon dioxide, which is a waste product of cellular function. The nose, pharynx, larynx, trachea and bronchi all work like a system of pipes through which the air is funneled down into our lungs. There, in very small air sacs called alveoli, oxygen is brought into the bloodstream and carbon dioxide is pushed from the blood out into the air. When something goes wrong with part of the respiratory system, such as an infection like pneumonia, chronic obstructive pulmonary diseases, it makes it harder for us to get the oxygen we need and to get rid of the waste product carbon dioxide. Common respiratory symptoms include breathlessness, cough, and chest pain

• The Upper Airway and Trachea• When you breathe in, air enters your body through your nose or mouth. From there, it

travels down your throat through the larynx (or voice box) 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 µlobes¶, or big sections of tissue separated by µfissures¶ 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 broncho pulmonary segments .These are pyramidal-shaped areas which are also separated from each other by membranes.There are about 10 of them in each lung. Each segment receives its own blood supply and air supply. 

• Blood supply The lungs are very vascular organs, meaning they receive a very large blood supply. This is because the pulmonary arteries, which supply the lungs, come directly from the right side of your heart. They carry blood which is low in oxygen and high in carbon dioxide into your lungs so that the carbon dioxide can be blown off, and more oxygen can be absorbed into the bloodstream. The newly oxygen-rich blood then travels back through the paired pulmonary veins into the left side of your heart. From there, it is pumped all around your body to supply oxygen to cells and organs.

• The Work of Breathing The Pleurae•  The lungs are covered by smooth membranes that we call pleurae. The pleurae have two

layers, a visceral layer which sticks closely to the outside surface of your lungs, and a µparietal 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.

Thediaphragm, a large, sheet-like muscle which stretches across your chest under the ribcage, doesmuch of this work. At rest, it is shaped like a dome curving up into your chest. When you breathein, 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 normallyrequire your muscles to work. This is because your lungs are very elastic, and when your 

• muscles relax at the end of inspiration your lungs simply recoil back into their resting position, pushing the air out as they go.

• The Respiratory System and Ageing•  The normal process of ageing is associated with a number of changes in both the

structure andfunction of the respiratory system. These include:

• Enlargement of the alveoli. The air spaces get bigger and lose their elasticity, meaningthat there is less area for gases to be exchanged across. This change is sometimes referredto 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 increasedstress on their respiratory system, such as with an infection like pneumonia, than a younger  person would.

• DIAGNOSTIC EVALUATION 

• PFTs demonstrative airflow obstruction ± reduced forced vital capacity (FVC), FEV1,FEV1 to FVC ration; increased residual volume to total lung capacity (TLC) ratio, possibly increased TLC.2.

• ABG levels- decreased PaO2, pH, and increased CO2.3.• Chest X-ray ± in late stages, hyperinflation, flattened diaphragm, increased

rettrosternalspace, decreased vascular markings, possible bullae.4.• Alpa1-antitrypsin assay useful in identifying genetically determined deficiency

inemphysema

• ABG’s•Mild decrease pO2 early, gradual decrease•Gradual increase pCO2 •May change during sleepErythrocytosis with Hct > 55 as pO2 levels fall; non specific

CT Scan•High resolution 1-2 mm slices•More sensitive than CXR•Does not alter basic therapyCXR Not useful for diagnosing early COPD

Findings•Over distended lungs•Flattened diaphragms•Long narrow cardiac silhouette•Increased retro sternal airspace•Bullae

PATHOPHYSIOLOGY In COPD, the airflow limitation is both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases. The inflammatory response occurs throughout the airways, parenchyma, and pulmonary vasculature. Because of the chronic inflammation and the body attempts to repair it, narrowing occurs in the small peripheral airways. Over time, this injury-and-repair process causes scar tissue formation and narrowing of the airway lumen. Airflow obstruction may also be caused by parenchymal destruction, as is seen with emphysema, a disease of the alveoli or gas exchange units. In addition to inflammation, processes related to imbalances of proteinases and anti proteinases in the lung may be responsible for airflow limitation. When activated by chronic inflammation, proteiness and other substances may be released, damaging the parenchymal of the lung. The parenchymal changes may occur as a consequence of inflammation or environmental or genetic factors (eg. Alpha1-antitrypsin deficiency)Early in the course of  COPD , the inflammatory response causes pulmonary vasculature changes that are characterized by thickening of the vessel wall. These changes may result from exposure to cigarette smoke, use of tobacco products, and the release of inflammatory medicators.

CHRONIC BRONCHITIS Lung damage and inflammation in the large airways results in chronic bronchitis. Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3months of a year, for 2 consecutive years. In the airways of the lung, the hallmark of chronic bronchitis is an increased number (hyperplasia)and increased size (hypertrophy) of the goblet cells and mucous glands of the airway. As a result, there is more mucus than usual in the airways, contributing to narrowing of the airways and causing a cough with sputum. Microscopically there is infiltration of the airway walls with inflammatory cells. Inflammation is followed by scarring and remodeling that thickens the walls and also results in narrowing of the airways. As chronic bronchitis progresses, there is squamous metaplasia (an abnormal change in the tissue lining the inside of the airway) and fibrosis (further thickening and scarring of the airway wall). The consequence of these changes is a limitation of airflow. Patients with advanced COPD that have primarily chronic bronchitis rather than emphysema were commonly referred to as ³blue 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 ³Blue Bloaters.́

ACUTE BRONCHITIS PHYSICAL MANIFESTATIONS One of the most common symptoms of  COPDis shortness of breath (dyspnea). People with COPDcommonly describe this as: ³My breathing requires effort´, ³I feel out of breath ,́ or ³I can not get enough air in .́ People with COPD typically first notice dyspnea during vigorous exercise

when the demands on the lungs are greatest. Over the years, dyspnea tends to get gradually worse so that it can occur during milder, everyday activities such as housework. In the advanced stages of  COPD , dyspnea can become so bad that it occurs during rest and is constantly present. Other symptoms of  COPD are a persistent cough, sputum or mucus production, wheezing, chest tightness, and tiredness. People with advanced (very severe) COPD sometimes develop respiratory failure. When this happens, cyanosis, a bluish discoloration of the lips caused by a lack of oxygen in the blood, can occur. An excess of carbon dioxide in the blood can cause headaches, drowsiness or twitching (asterixis). A complication of advanced COPD is corpulmonal, 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 antero posterior to lateral ratio of the chest(i.e. barrel chest).

Emphysemais a chronic obstructive pulmonary is ease (COPD, as it is otherwise known, formerly termed a chronic obstructive lung disease). It is often caused by exposure to toxic chemicals ,including long-term exposure to tobacco smoke. Emphysema is characterized by loss of elasticity (increased pulmonary compliance) of the lung tissue caused by destruction of structures feeding the alveoli, owing to the action of alpha 1 antitrypsin deficiency. This causes the small airways to collapse during forced exhalation, as alveolar collapsibility has decreased. As a result, airflow is impeded and air becomes trapped in the lungs, in the same way as other obstructive lung diseases. Symptoms include shortness of breath on exertion, and an expanded chest. However, the constriction of air passages isnt always immediately deadly, and treatment is available.

• 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 preventtoxicity.4. 

• Monitor oxygen saturation at rest and with activity.

•• Supportive Care

  • Eliminate all pulmonary irritants, particularly cigarette smoke. Smoking cessation usually

reduces pulmonary irritation, sputum production, and cough. Keep the patients room asdust-free as possible. 

• 2.

 • Use postural drainage positions to help clear secretions responsible

for airwayobstructions.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.8. • Instruct and supervise patient breathing retraining exercises.9. • Use pursed lip breathing at intervals and during periods of dyspnea to control rate and

depth of respiration and improve respiratory muscle coordination.10. • Discuss and demonstrate relaxation exercises to reduce stress, tension, and anxiety.11. • Maintain the patient nutritional status.12. • Reemphasize the importance of graded exercise and physical conditioning programs.13.• Encourage use of portable oxygen system for ambulation for patients with hypoxemia

and marked disability.14. • Train the patient in energy conservation technique.15. • Assess the patient for reactive-behaviors such as anger, depression and acceptance.

Education and heaLth maintenance•  Review with the patient the objectives of treatment and nursing management.2.

 • Advise the patient to avoid respiratory irritants. Suggest that high efficiency particular the

air filter may have some benefit.3. • Warn patient to stay out of extremely hot or cold weather and to avoid

aggravating bronchial obstruction and sputum obstruction.4. 

• Warn patient to avoid persons with respiratory infections, and to avoid crowds and areas with poor ventilation.5. 

• Teach the patient how to recognize and report evidence of respiratory infection promptly such as chest pain, changes in character of sputum (amount, color and consistency),increasing difficulty in raising sputum, increasing coughing and wheezing, increasing of shortness of breath.

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