COPD | Chronic Obstructive Pulmonary Disease | Bronchitis

Liceo de Cagayan University College of Nursing RNP Boulevard, Carmen, Cagayan de Oro City College of Nursing

NCM501204 Related Learning Experience

A Case Study
Submitted To: Mr. Loue Pacamalan, RN,MN September 15, 2010

As Partial Fulfillment of NCM501204 Related Learning Experience

Submitted By: Redmund M. Cuñada Reschelle Maneje Reshie Mesiona Misty Rose Zafra

INTRODUCTION: Chronic obstructive pulmonary disease (COPD) is a disease state characterized by airflow limitation that is not fully reversible. This newest definition COPD, provided by the Global Initiative for Chrnonic Obstructive Lung Disease (GOLD), is a broad description that better explains this disorder and its signs and symptoms (GOLD, World Health Organization [WHO] & National Heart, Lung and Blood Institute [NHLBI], 2004). Although previous definitions have include emphysemaand chronic bronchitis under the umbrella classification of COPD, this was often confusing because most patient with COPD present with over lapping signs and symptoms of these two distinct disease processes. COPD may include diseases that cause airflow obstruction (e.g., Emphysema, chronic bronchitis) or any combination of these disorders. Other diseases as cystic fibrosis, bronchiectasis, andasthma that were previously classified as types of chronic obstructive lung disease are nowclassified as chronic pulmonary disorders.

However, asthma is now considered as a separate disorder and is classified as an abnormal airway condition characterized primarily by reversible

inflammation. COPD can co-exist with asthma. Both of these diseases have the same major symptoms; however, symptoms are generally more variable in asthma than in COPD. Currently, COPD is the fourth leading cause of mortality and the 12th leading cause of disability. However, by the year 2020 it is estimated that COPD will be the third leading cause of death and the firth leading cause of disability (Sin, McAlister, Man. Et al., 2003). People with COPDcommonly become symptomatic during the middle adult years, and the incidence of the disease increases with age.

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

a left lung and a right lung. along with the heart. it travels down your throat through the larynx (or voicebox) and into the trachea (or windpipe) before entering your lungs. From there. The right lung has three lobes but the left lung has only two. These are pyramidal-shaped areas which are also separated from each other by membranes. The upper airway is important because it must always stay open for you to be able to breathe. There are about 10 of them in each lung. The lungs can also be divided up into even smaller portions. air enters your body through your nose or mouth. The Lungs Structure The lungs are paired. 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. because the heart takes up some of the space in the left side of our chest. or big sections of tissue separated by µfissures¶ or dividers. Each segment receives its own blood supply and air supply.The Upper Airway and Trachea When you breathe in. which is a waste product. All these structures act to funnel fresh air down from the outside world into your body. These are divided up into µlobes¶. called µbronchopulmonary segments¶. cone-shaped organs which take up most of the space in our chests. It also helps to moisten and warm the air before it reaches your lungs. We each have two lungs.

This fresh air has lots of oxygen in it.COPD VERSUS HEALTHY LUNG How they work Air enters your lungs through a system of pipes called the bronchi. and get rid of the waste product carbon dioxide. which are very small branches of the pulmonary arteries. In this way. Traveling in the opposite direction is carbon dioxide. when you breathe in. known as the alveoli. until they eventually form little thin-walled air sacs or bubbles. These pipes start from the bottom of the trachea as the left and right bronchi and branch many times throughout the lungs. So. The alveoli are where the important work of gas exchange takes place between the air and your blood. so that oxygen and carbon dioxide can move (or diffuse) between them. Covering each alveolus is a whole network of little blood vessel called capillaries. you bring in to your body the oxygen that you need to live. . which crosses from the blood in the capillaries into the air in the alveoli and is then breathed out. and some of this oxygen will travel across the walls of the alveoli into your bloodstream. air comes down the trachea and through the bronchi into the alveoli. It is important that the air in the alveoli and the blood in the capillaries are very close together.

and more oxygen can be absorbed into the bloodstream. and a µparietal¶ layer which lines the inside of your chest wall (ribcage).Blood Supply The lungs are very vascular organs. This is because the pulmonary arteries. They . The newly oxygen-rich blood then travels back through the paired pulmonary veins into the left side of your heart. From there. which supply the lungs. meaning they receive a very large blood supply. without any friction. it is pumped all around your body to supply oxygen to cells and organs. a µvisceral¶ layer which sticks closely to the outside surface of your lungs. The pleurae have two layers. come directly from the right side of your heart. The Work of Breathing The Pleurae The lungs are covered by smooth membranes that we call pleurae. 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. The pleurae are important because they help you breathe in and out smoothly.

This is because your lungs are very elastic. sheet-like muscle which stretches across your chest under the ribcage. These include:  Enlargement of the alveoli. it is shaped like a dome curving up into your chest. When you breathe in. . Other muscles. your muscles need to work to fill your lungs with air.  The compliance (or springiness) of the chest wall decreases. pushing the air out as they go. This change is closely connected to the general health of the person. including the muscles between your ribs (the intercostal muscles) also help by moving your ribcage in and out. and when your muscles relax at the end of inspiration your lungs simply recoil back into their resting position. expanding the space in your chest and drawing air into your lungs. The air spaces get bigger and lose their elasticity. At rest. The diaphragm.also make sure that when your ribcage expands on breathing in. The Respiratory System and Ageing The normal process of ageing is associated with a number of changes in both the structure and function of the respiratory system. meaning that there is less area for gases to be exchanged across. The Diaphragm and Intercostal Muscles When you breathe in (inspiration). This change is sometimes referred to as µsenile emphysema¶. your lungs expand as well to fill the extra space.  The strength of the respiratory muscles (the diaphragm and intercostal muscles) decreases. so that it takes more effort to breathe in and out. a large. does much of this work. Breathing out (expiration) does not normally require your muscles to work. the diaphragm contracts and flattens out.

which keeps breathing passages free of inhaled irritants. bacteria. diminished lung capacity. Smoking also irritates the goblet cells and mucus glands.All of these changes mean that an older person might have more difficulty coping with increased stress on their respiratory system. In addition. The alveoli greatly distend. causing an increased accumulation of mucus. Other risk factors are pipe. which in turn produces more irritation. Smoking depresses the activity of scavenger cells and affects the respiratory tract¶s ciliary cleansing mechanism. passive smoking contributes to respiratory symptoms and COPD. than a younger person would. When smoking damages this cleansing mechanism. infection. airflow is obstructed and air becomes trapped behind the obstruction. carbon monoxide (a by product of smoking) combines with hemoglobin to form . and other foreign matter. cigar. In addition. and damage to the lung. such as with an infection like pneumonia. PREDISPOSING FACTORS Risk factors for COPD include environmental exposures and host factors. The most important risk factor for COPD is cigarette smoking. and other types of tobacco smoking.

Over time. narrowing occurs in the small peripheral airways. as is seen with emphysema. The inflammatory response occurs throughout the airways. This deficiency predisposes young people to rapid development of lobular emphysema. an enzyme inhibitor that protects the lung parenchyma from injury. PATHOPHYSIOLOGY In COPD. a disease of the alveoli or gas exchange units. this injury-and-repair process causes scar tissue formation and narrowing of the airway lumen. When activated by chronic inflammation. proteiness and other substances may be released. Carriers of this genetic defect must be identified so that they can modify environmental risk factors to delay or prevent overt symptoms of disease. allergens) and eventually developed chronic obstructive symptoms. the airflow limitation is both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases.carboxyhemoglobin. Alpha1-antitrypsin deficiency). parenchyma. In addition to inflammation. Airflow obstruction may also be caused by parenchymal destruction. air pollution. Genetically susceptible people are sensitive to environmental factors (eg. . processes related to imbalances of proteinases and antiproteinases in the lung may be responsible for airflow limitation. and pulmonary vasculature. Hemoglobin that is bound by carboxyhemoglobin cannot carry oxygen efficiently. infectious agents. Because of the chronic inflammation and the body¶s attempts to repair it. The parenchymal changes may occur as a consequence of inflammation or environmental or genetic factors (eg. A host risk factor for COPD is a deficiency of alpha antitrypsin. Smoking. even if they do not smoke. damaging the parenchyma of the lung.

Microscopically there is infiltration of the airway walls with inflammatory cells. As chronic bronchitis progresses. Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3 months of a year. Inflammation is followed by scarring and remodeling that thickens the walls and also results in narrowing of the airways. contributing to narrowing of the airways and causing a cough with sputum.Early in the course of COPD. In the airways of the lung. The hypoxia and fluid retention leads to them being called ³Blue Bloaters. for 2 consecutive years.´ . 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. CHRONIC BRONCHITIS Lung damage and inflammation in the large airways results in chronic bronchitis. there is more mucus than usual in the airways. The consequence of these changes is a limitation of airflow. and the release of inflammatory medicators. 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. 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). use of tobacco products. the hallmark of chronic bronchitris is an increased number (hyperplasia) and increased size (hypertrophy) of the goblet cells and mucous glands of the airway. As a result.

everyday activities such as housework. and tiredness. a strain on the heart due to the extra work required by the heart to pump blood through the affected lungs. There are a few signs of COPD that a healthcare worker may detect although they can be seen in other diseases.ACUTE BRONCHITIS PHYSICAL MANIFESTATIONS One of the most common symptoms of COPD is shortness of breath (dyspnea). dyspnea can become so bad that it occurs during rest and is constantly present. can occur. 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. or ³I can not get enough air in´. Some people have COPD and have none of these signs. People with COPD typically first notice dyspnea during vigorous exercise when the demands on the lungs are greatest. ³I feel out of breath´. An excess of carbon dioxide in the blood can cause headaches. Common signs are:     tachypnea. A complication of advanced COPD is cor pulmonale. Other symptoms of COPD are a persistent cough. Over the years. seen as swelling of the ankles. drowsiness or twitching (asterixis). In the advanced stages ofCOPD. People withCOPD commonly describe this as: ³My breathing requires effort´. cyanosis. People with advanced (very severe) COPD sometimes develop respiratory failure. and dyspnea. dyspnea tends to get gradually worse so that it can occur during milder. sputum or mucus production. wheezing. particularly the front-to-back distance (hyperinflation) . When this happens. chest tightness. Symptoms of cor pulmonale are peripheral edema. a bluish discoloration of the lips caused by a lack of oxygen in the blood.

and a difficult to palpate apex beat. Symptoms include shortness of breath on exertion. EMPHYSEMA Emphysema is a chronic obstructive pulmonary disease (COPD. The face has a ruddy .  active use of muscles in the neck to help with breathing breathing through pursed lips increased anteroposterior to lateral ratio of the chest (i. particularly just above the liver. the constriction of air passages isn¶t always immediately deadly. both due to hyperinflation. Emphysema is characterized by loss of elasticity (increased pulmonary compliance) of the lung tissue caused by destruction of structures feeding the alveoli. However. PHYSICAL MANIFESTATIONS Signs of emphysema include pursed-lipped breathing. there are signs of fluid overload such as pitting peripheral edema.e. The chest has hyper resonant percussion notes. and treatment is available. It is often caused by exposure to toxic chemicals. central cyanosis and finger clubbing. as it is otherwise known. In advanced disease. barrel chest). This causes the small airways to collapse during forced exhalation. owing to the action of alpha 1 antitrypsin deficiency. as alveolar collapsibility has decreased. formerly termed a chronic obstructive lung disease). in the same way as other obstructive lung diseases. There may be decreased breath sounds and audible expiratory wheeze. including long-term exposure to tobacco smoke. airflow is impeded and air becomes trapped in the lungs. As a result. and an expanded chest.

Patients who continue to smoke have a more rapid deterioration in lung function when compared to others who quit. DIAGNOSTIC EVALUATION 1. FEV1 to FVC ration. hyperinflation. 2) taking medications to dilate airways (bronchodilators) and decrease airway inflammation. Chest X-ray ± in late stages. Alpa1-antitrypsin assay useful in identifying genetically determined deficiency in emphysema. Sufferers who retain carbon dioxide have asterixis (metabolic flap) at the wrist. 2.complexion if there is a secondary polycythemia. 3) vaccinating against flu influenza and pneumonia and 4) regular oxygen supplementation and 5) pulmonary rehabilitation. PFTs demonstrative airflow obstruction ± reduced forced vital capacity (FVC). flattened diaphragm. increased rettrosternal space. increased residual volume to total lung capacity (TLC) ratio. ABG levels. 3. 4.decreased PaO2. 3) to improve performance of daily activities and quality of life. Aging itself can cause a very slow decline in lung function. Quitting cigarette smoking The most important treatment for COPD is quitting cigarette smoking. 2) to alleviate symptoms. pH. decreased vascular markings. possibly increased TLC. and increased CO2. possible bullae. FEV1. cigarette smoking can result in a much more dramatic loss of . In susceptible individuals. TREATMENT The goals of COPD treatment are 1) to prevent further deterioration in lung function. The treatment strategies include 1) quitting cigarette smoking.

the patient has to learn to coordinate inhalation with each compression. therefore. Bronchodilators can be inhaled. therefore. irritability. Nicotine in cigarettes is addictive. Metered dose inhalers (MDIs) are used to deliver bronchodilators. Even in those smokers who develop symptoms of withdrawal. cessation of smoking can cause symptoms of nicotine withdrawal including anxiety.lung function. A standard amount of medication is released with each compression of the MDI. and have difficulty refraining from smoking in non-smoking areas. there are fewer side effects. and. Inhaled bronchodilators are popular because they go directly to the airways where they work. Bronchodilators Treating airway obstruction in COPD with bronchodilators is similar but not identical to treating bronchospasm in asthma. As compared with bronchodilators given orally. To maximize the delivery of the medications to the airways. the symptoms will decrease after several weeks of abstinence. need to smoke shortly after waking up in the morning. anger. Incorrect use of the MDI can lead . Patients likely to develop withdrawal symptoms typically smoke more than 20 cigarettes a day. fatigue. It is important to note that when one stops smoking the decline in lung function eventually reverts to that of a non-smoker. and intense craving for cigarettes. difficulty concentrating or sleeping. less medication reaches the rest of the body. some 25% of smokers can stop smoking without developing these symptoms. However. and. depression. Bronchodilators are medications that relax the muscles surrounding the small airways thereby opening the airways. taken orally or administered intravenously. An MDI is a pressurized canister containing a medication that is released when the canister is compressed.

 Lung volume reduction surgery (LVRS) has received much fanfare in the lay press. Pulmonary rehabilitation is a program of education regarding lung function and dysfunction. Spacer devices can hold the released medications long enough for patients to inhale them slowly and deeply into the lungs. In addition. poorly-functioning upper parts of the lung compress and impair function of the better-functioning lung elsewhere. the diaphragm and the chest cavity achieve more optimal positioning following the surgery. the compressed lung may expand and function better. Proper use of spacer devices can greatly increase the proportion of medication reaching the airways. LVRS is a surgical procedure used to treat some patients with COPD. To decrease the deposition of medications on the throat and increase the amount reaching the airways. occupational and physical therapy are used to teach optimal and efficient body mechanics. if the over-inflated portions of lung are removed surgically. Thus. In addition. The premise behind this surgery is that the deposition of much of the medication on the tongue and the back of the throat instead of on the airways. Oxygen Therapy Other treatments  Pulmonary rehabilitation has become a cornerstone in the management of moderate to severe COPD. and proper use of respiratory equipment and medications. An essential ingredient in this program is the use of increasing physical exercise to overcome the reduced physical capacity that usually has developed over time. pursed lip breathing). spacers can be helpful. proper breathing techniques (diaphragmatic breathing. Spacers are tube-like chambers attached to the outlet of the MDI canister. and this improves .

The action of beta-2 agonists starts within minutes after inhalation and lasts for about 4 hours. even among those without demonstrable reversibility in airway obstruction. lung function and exercise capacity among surviving surgical patients improved significantly following LVRS. Patients with forced expiratory volume in FEVI of less than 20% of predicted and either diffuse disease on the CAT scan or lower than 20% diffusing capacity or elevated carbon dioxide levels had higher mortality. Because of their short duration of action. whose exercise tolerance was low even after pulmonary rehabilitation. PHARMACOLOGIC INTERVENTIONS  Beta-agonists  Beta-2 agonists have the bronchodilating effects of adrenaline without many of its unwanted side effects. The best criteria for choosing patients for LVRS are still uncertain. these . They are called ³agonists´ because they activate the beta2 receptor on the muscles surrounding the airways. Dilating airways helps to relieve the symptoms of dyspnea (shortness of breath). but after two years returned to about the same levels as before the procedure. On average. A national study was completed in 2003. Beta-2 agonists can be administered by MDI inhalers or orally.breathing further. Activation of beta-2 receptors relaxes the muscles surrounding the airways and opens the airways. Patients primarily with emphysema at the top of their lungs. Beta-2 agonists have been shown to relieve dyspnea in many COPD patients. Because of their quick onset of action. The role of LVRS is at present is very limited. seemed to do the best with this procedure. beta-2 agonists are especially helpful for patients who are acutely short of breath.

Ipratropium has a slower onset of action but . palpitations or fast heart rate.  Side effects of beta-2 agonists include anxiety.  In contrast. metaproterenol (Alupent). terbutaline (Brethaire). Proventil). and low blood potassium. pirbuterol (Maxair). these are often referred to as maintenance inhalers. such as salmeterol xinafoate (Serevent) and formoterol fumarate (Foradil) may be used routinely as maintenance medications. tremor. improve exercise tolerance and improve FEV1. These are referred to as rescue inhalers. ipratropium has been shown to alleviate dyspnea. Anti-cholinergic drugs such as ipratropium bromide (Atrovent) dilate airways by blocking the receptors for acetylcholine on the muscles of the airways and preventing them from narrowing. Along with some of these inhalers to be mentioned. Ipratropium bromide (Atrovent) usually is administered via a MDI. Levalbuterol (Xopenex) is a recently approved Beta2 agonist. Examples of beta-2 agonists include albuterol (Ventolin. In patients with COPD. Evidence suggests that when these drugs are used routinely. Beta-2 agonists with a slower onset of action but a longer period of activity.medications should be used for symptoms as they develop rather than as maintenance. their effectiveness is diminished.  Anti-cholinergic Agents  Acetylcholine is a chemical released by nerves that attaches to receptors on the muscles surrounding the airway causing the muscles to contract and the airways to narrow. These drugs last twelve hours and should be taken twice daily and no more. and isoetharine (Bronkosol).

a combination of the two drugs sometimes results in a better response than to either drug alone without additional side effects. theophylline can help patients with COPD who have heart failure and pulmonary . relaxes the muscles surrounding the airways but also prevents mast cells around the airways from releasing bronchoconstricting chemicals such as histamine. like a beta agonist. Ipratropium usually is well tolerated with minimal side effects even when used in higher doses. Theophylline also may increase the force of contraction of the heart and lower pressure in the pulmonary arteries. In patients who respond poorly to either beta-2 agonists or ipratropium alone. Long acting theophylline preparations can be given orally once or twice a day. Theolair.  In comparing ipratropium with beta-2 agonists in the treatment of patients with COPD.longer duration of action than the shorter-acting beta-2 agonists. studies suggest that ipratropium may be more effective in dilating airways and improving symptoms with fewer side effects. Thus. Ipratropium is especially suitable for use by elderly patients who may have difficulty with fast heart rate and tremor from the beta-2 agonists. Uniphyl. Theophylline. Theophylline also can act as a mild diuretic and increase urination. Theo-24) and aminophylline are examples of methylxanthines.  Methylxanthines  Theophylline (Theo-Dur. Slo-Bid. Tiotropium (SPIRIVA) is a long acting and more powerful version of Ipratropium and has been shown to be more effective. Methylxanthines are administered orally or intravenously.

Therefore. many doctors use oral corticosteroids as the treatment of last resort. including osteoporosis. thinning of the skin and easy bruising. Unfortunately. high blood pressure. Dosage and blood levels of theophylline or aminophylline have to be closely monitored. heart rhythm problems. Interactions with other medications. In patients with heart failure or cirrhosis. anti-inflammatory medications (more specifically. dosages of methylxanthines are lowered to avoid high blood levels. Excessively high levels in the blood can lead to nausea. they are prescribed at the lowest possible doses for the shortest period of time to minimize side effects. Examples of corticosteroids include Prednisone and Prednisolone. insomnia. high doses of oral corticosteroids over prolonged periods can have serious side effects. Twenty to thirty percent of patients with COPD show improvement in lung function when given corticosteroids by mouth.  The disadvantage of methylxanthines is their side effects. vomiting. corticosteroids) may be beneficial. and even seizures.hypertension. and allopurinol (Zyloprim) also can alter blood levels of methylxanthines. When it is .  Corticosteroids  When airway inflammation (which causes swelling) contributes to airflow obstruction. quinolones (Cipro). bone fractures. emotional changes. and weight gain. Patients who have difficulty using inhaled bronchodilators but no difficulty taking oral medications find theophylline particularly useful. such as cimetidine (Tagamet). calcium channel blockers (Procardia). diabetes mellitus. When oral corticosteroids are used.

A spacing device placed between the mouth and the MDI can improve medication delivery and reduce the side effects on the mouth and throat. triamcinolone acetonide (Azmacort). Vancenase. and Vanceril). Inhaled corticosteroids have been useful in treating patients with asthma. but in patients with COPD. mometasone furoate (Asmanex) and flunisolide (Aerobid). doctors are less concerned about using inhaled corticosteroids because of their safety. Inhaled corticosteroids have many fewer side effects than long term oral corticosteroids. loss of voice.necessary to use long term oral steroids. Rinsing out the mouth after use of a steroid inhaler also can decrease these side effects. Replacement of the missing or inactive AAT by injection can help prevent progression of the associated emphysema. budesonide (Pulmicort). This therapy is of no benefit in other types of COPD. medications are often prescribed to help reduce the development of the above side effects. Examples of inhaled corticosteroids include beclomethasone dipropionate (Beclovent. it is not clear whether inhaled corticosteroid have the same benefit as oral corticosteroids. Nevertheless. fluticasone (Flovent). . and oral yeast infections. Beconase.  Corticosteroids also can be inhaled. The side effects of inhaled corticosteroids include hoarseness.  Treatment of Alpha-1 antitrypsin deficiency  Emphysema can develop at a very young age in some patients with severe alpha-1 antitrypsin deficiency (AAT).

Smoking cessation usually reduces pulmonary irritation. as ordered. cardiac arrhythmias. Monitor condition after administration of aerosol bronchodilators to assess for improved aeration. hypertension. 4. 4. particularly cigarette smoke.5 liters daily) within level of cardiac reserve. reduced adventitious sounds. central nervous system stimulation. Monitor for adverse effects of bronchodilators ± tremulousness. Encourage high level of fluid intake ( 8 to 10 glasses. 2 to 2. Depression 5. dysrhythmias 4. Respiratory failure 2. and cough.COMPLICATIONS 1. Teach controlled coughing. Use postural drainage positions to help clear secretions responsible for airway obstructions. Eliminate all pulmonary irritants. overwhelming respiratory infection 3. tachycardia. to ensure therapeutic level and prevent toxicity. Pneumonia. Skeletal muscle dysfunction NURSING INTERVENTIONS Monitoring 1. 2. 3. Monitor oxygen saturation at rest and with activity. sputum production. Keep the patient¶s room as dust-free as possible. 3. Monitor serum theophylline level. 2. reduced dyspnea. Supportive Care 1. . Right-sided heart failure.

Assess the patient for reactive-behaviors such as anger. Warn patient to stay out of extremely hot or cold weather and to avoid aggravating bronchial obstruction and sputum obstruction. 12. and anxiety. 7. 11. 8. Reemphasize the importance of graded exercise and physical conditioning programs. vaporizer) to indoor air. Encourage the patient to assume comfortable position to decrease dyspnea. 14. tension. Discuss and demonstrate relaxation exercises to reduce stress. 3.5. Suggest that high efficiency particulate air filter may have some benefit. 13. Advise the patient to avoid respiratory irritants. 2. 15. Encourage use of portable oxygen system for ambulation for patients with hypoxemia and marked disability. Use pursed lip breathing at intervals and during periods of dyspnea to control rate and depth of respiration and improve respiratory muscle coordination. 9. Instruct and supervise patient¶s breathing retraining exercises. depression and acceptance. . Add moisture (humidifier. 6. 10. Give inhalations of nebulized saline to humidify bronchial tree and liquefy sputum. Avoid dairy products if these increases sputum production. Train the patient in energy conservation technique. Maintain the patient¶s nutritional status. Review with the patient the objectives of treatment and nursing management. Education and health maintenance 1.

increasing difficulty in raising sputum. . color and consistency). increasing of shortness of breath. Warn patient to avoid persons with respiratory infections. 5. increasing coughing and wheezing. and to avoid crowds and areas with poor ventilation. Teach the patient how to recognize and report evidence of respiratory infection promptly such as chest pain. changes in character of sputum (amount.4.

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