This action might not be possible to undo. Are you sure you want to continue?
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 emphysema and 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, and asthma that were previously classified as types of chronic obstructive lung disease are now classified 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 COPD commonly become symptomatic during the middle adult years, and the incidence of the disease increases with age. ANATOMY AND PHYSIOLOGY:
There. Common respiratory symptoms include breathlessness. From there. and chest pain. trachea. which is a waste product of cellular function. larynx. oxygen is brought into the bloodstream and carbon dioxide is pushed from the blood out into the air. The Upper Airway and Trachea When you breathe in. air enters your body through your nose or mouth. which we need for our cells to live and function properly. pharynx. The respiratory system does two very important things: it brings oxygen into our bodies. in very small air sacs called alveoli. The Lungs Structure . it makes it harder for us to get the oxygen we need and to get rid of the waste product carbon dioxide. bronchi and lungs. When something goes wrong with part of the respiratory system. larynx. chronic obstructive pulmonary diseases. and it helps us get rid of carbon dioxide. The upper airway is important because it must always stay open for you to be able to breathe. cough. it travels down your throat through the larynx (or voicebox) and into the trachea (or windpipe) before entering your lungs. The nose. All these structures act to funnel fresh air down from the outside world into your body. It also helps to moisten and warm the air before it reaches your lungs. such as an infection like pneumonia. pharynx.The respiratory system consists of all the organs involved in breathing. These include the nose. trachea and bronchi all work like a system of pipes through which the air is funneled down into our lungs.
The right lung has three lobes but the left lung has only two. called µbronchopulmonary segments¶. Traveling in the opposite direction is carbon dioxide. This fresh air has lots of oxygen in it.The lungs are paired. because the heart takes up some of the space in the left side of our chest. which are very small branches of the pulmonary arteries. along with the heart. and get rid of the waste product carbon dioxide. you bring in to your body the oxygen that you need to live. Each segment receives its own blood supply and air supply. In this way. These are pyramidal-shaped areas which are also separated from each other by membranes. Their role is to take oxygen into the body. COPD VERSUS HEALTHY LUNG How they work Air enters your lungs through a system of pipes called the bronchi. There are about 10 of them in each lung. These pipes start from the bottom of the trachea as the left and right bronchi and branch many times throughout the lungs. until they eventually form little thin-walled air sacs or bubbles. or big sections of tissue separated by µfissures¶ or dividers. and some of this oxygen will travel across the walls of the alveoli into your bloodstream. . We each have two lungs. These are divided up into µlobes¶. which crosses from the blood in the capillaries into the air in the alveoli and is then breathed out. and to help us get rid of carbon dioxide. which we need for our cells to live and function properly. Covering each alveolus is a whole network of little blood vessel called capillaries. when you breathe in. a left lung and a right lung. cone-shaped organs which take up most of the space in our chests. which is a waste product. air comes down the trachea and through the bronchi into the alveoli. The lungs can also be divided up into even smaller portions. The alveoli are where the important work of gas exchange takes place between the air and your blood. known as the alveoli. so that oxygen and carbon dioxide can move (or diffuse) between them. So. It is important that the air in the alveoli and the blood in the capillaries are very close together.
a large. the diaphragm contracts and flattens out. 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. This is because your lungs are very elastic. and when your . The pleurae are important because they help you breathe in and out smoothly. They also make sure that when your ribcage expands on breathing in. your lungs expand as well to fill the extra space. without any friction. The pleurae have two layers. including the muscles between your ribs (the intercostal muscles) also help by moving your ribcage in and out.Blood Supply The lungs are very vascular organs. meaning they receive a very large blood supply. This is because the pulmonary arteries. and more oxygen can be absorbed into the bloodstream. does much of this work. The Work of Breathing The Pleurae The lungs are covered by smooth membranes that we call pleurae. The diaphragm. expanding the space in your chest and drawing air into your lungs. The newly oxygen-rich blood then travels back through the paired pulmonary veins into the left side of your heart. Breathing out (expiration) does not normally require your muscles to work. it is shaped like a dome curving up into your chest. your muscles need to work to fill your lungs with air. From there. come directly from the right side of your heart. it is pumped all around your body to supply oxygen to cells and organs. which supply the lungs. a µvisceral¶ layer which sticks closely to the outside surface of your lungs. and a µparietal¶ layer which lines the inside of your chest wall (ribcage). sheet-like muscle which stretches across your chest under the ribcage. Other muscles. When you breathe in. The Diaphragm and Intercostal Muscles When you breathe in (inspiration). At rest.
The strength of the respiratory muscles (the diaphragm and intercostal muscles) decreases. diminished lung . The alveoli greatly distend. The air spaces get bigger and lose their elasticity. and other types of tobacco smoking. The most important risk factor for COPD is cigarette smoking. than a younger person would. passive smoking contributes to respiratory symptoms and COPD. and other foreign matter. such as with an infection like pneumonia. In addition. so that it takes more effort to breathe in and out. 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. Other risk factors are pipe. which keeps breathing passages free of inhaled irritants. When smoking damages this cleansing mechanism. This change is closely connected to the general health of the person. meaning that there is less area for gases to be exchanged across. airflow is obstructed and air becomes trapped behind the obstruction. Smoking depresses the activity of scavenger cells and affects the respiratory tract¶s ciliary cleansing mechanism. pushing the air out as they go. This change is sometimes referred to as ¶senile emphysema¶. The compliance (or springiness) of the chest wall decreases. PREDISPOSING FACTORS Risk factors for COPD include environmental exposures and host factors.muscles relax at the end of inspiration your lungs simply recoil back into their resting position. bacteria. cigar. These include: y y y Enlargement of the alveoli. All of these changes mean that an older person might have more difficulty coping with increased stress on their respiratory system.
the hallmark of chronic bronchitris is an increased number (hyperplasia) and increased size (hypertrophy) of the goblet cells and mucous glands of the airway. CHRONIC BRONCHITIS Lung damage and inflammation in the large airways results in chronic bronchitis. The parenchymal changes may occur as a consequence of inflammation or environmental or genetic factors (eg. These changes may result from exposure to cigarette smoke. Hemoglobin that is bound by carboxyhemoglobin cannot carry oxygen efficiently. When activated by chronic inflammation. the inflammatory response causes pulmonary vasculature changes that are characterized by thickening of the vessel wall. infectious agents. In addition. a disease of the alveoli or gas exchange units. proteiness and other substances may be released. infection.capacity. carbon monoxide (a by product of smoking) combines with hemoglobin to form carboxyhemoglobin. for 2 consecutive years. Genetically susceptible people are sensitive to environmental factors (eg. Airflow obstruction may also be caused by parenchymal destruction. and the release of inflammatory medicators. As a result. and pulmonary vasculature. this injury-and-repair process causes scar tissue formation and narrowing of the airway lumen. damaging the parenchyma of the lung. In addition to inflammation. there is more mucus than usual in the airways. This deficiency predisposes young people to rapid development of lobular emphysema. which in turn produces more irritation. Chronic bronchitis is defined in clinical terms as a cough with sputum production on most days for 3 months of a year. In the airways of the lung. air pollution. Over time. contributing to narrowing of the . Carriers of this genetic defect must be identified so that they can modify environmental risk factors to delay or prevent overt symptoms of disease. causing an increased accumulation of mucus. Early in the course of COPD. Smoking also irritates the goblet cells and mucus glands. The inflammatory response occurs throughout the airways. use of tobacco products. and damage to the lung. as is seen with emphysema. an enzyme inhibitor that protects the lung parenchyma from injury. processes related to imbalances of proteinases and antiproteinases in the lung may be responsible for airflow limitation. Smoking. A host risk factor for COPD is a deficiency of alpha antitrypsin. even if they do not smoke. the airflow limitation is both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases. allergens) and eventually developed chronic obstructive symptoms. Alpha1-antitrypsin deficiency). PATHOPHYSIOLOGY In COPD. Because of the chronic inflammation and the body¶s attempts to repair it. parenchyma. narrowing occurs in the small peripheral airways.
e. An excess of carbon dioxide in the blood can cause headaches. cyanosis. and dyspnea. There are a few signs of COPD that a healthcare worker may detect although they can be seen in other diseases. or ³I can not get enough air in´.´ ACUTE BRONCHITIS PHYSICAL MANIFESTATIONS One of the most common symptoms of COPD is shortness of breath (dyspnea).airways and causing a cough with sputum. particularly the front-to-back distance (hyperinflation) active use of muscles in the neck to help with breathing breathing through pursed lips increased anteroposterior to lateral ratio of the chest (i. 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. and tiredness. Common signs are: y y y y y y tachypnea. a strain on the heart due to the extra work required by the heart to pump blood through the affected lungs. ³I feel out of breath´. seen as swelling of the ankles. Microscopically there is infiltration of the airway walls with inflammatory cells. a bluish discoloration of the lips caused by a lack of oxygen in the blood. chest tightness. People with COPD typically first notice dyspnea during vigorous exercise when the demands on the lungs are greatest. wheezing. The hypoxia and fluid retention leads to them being called ³Blue Bloaters. EMPHYSEMA . Some people have COPD and have none of these signs. dyspnea can become so bad that it occurs during rest and is constantly present. everyday activities such as housework. can occur. The consequence of these changes is a limitation of airflow. Inflammation is followed by scarring and remodeling that thickens the walls and also results in narrowing of the airways. Other symptoms of COPD are a persistent cough. 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. When this happens. dyspnea tends to get gradually worse so that it can occur during milder. In the advanced stages of COPD. People with advanced (very severe) COPD sometimes develop respiratory failure. drowsiness or twitching (asterixis). A complication of advanced COPD is corpulmonale. barrel chest). sputum or mucus production. People with COPD commonly describe this as: ³My breathing requires effort´. 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). Over the years.Symptoms of corpulmonale are peripheral edema.
2. It is often caused by exposure to toxic chemicals. In susceptible individuals. FEV1 to FVC ration. increased rettrosternal space. The chest has hyper resonant percussion notes. airflow is impeded and air becomes trapped in the lungs. decreased vascular markings. owing to the action of alpha 1 antitrypsin deficiency. possible bullae. and treatment is available. hyperinflation. Alpa1-antitrypsin assay useful in identifying genetically determined deficiency in emphysema. pH. The treatment strategies include 1) quitting cigarette smoking. Quitting cigarette smoking The most important treatment for COPD is quitting cigarette smoking. in the same way as other obstructive lung diseases. including long-term exposure to tobacco smoke. formerly termed a chronic obstructive lung disease). As a result. particularly just above the liver. Symptoms include shortness of breath on exertion. and increased CO2. 3) to improve performance of daily activities and quality of life. flattened diaphragm.decreased PaO2. cigarette smoking can result in a much more dramatic loss of lung function. 3) vaccinating against flu influenza and pneumonia and 4) regular oxygen supplementation and 5) pulmonary rehabilitation. FEV1. Emphysema is characterized by loss of elasticity (increased pulmonary compliance) of the lung tissue caused by destruction of structures feeding the alveoli. However. ABG levels. 4. increased residual volume to total lung capacity (TLC) ratio. Chest X-ray ± in late stages.Emphysema is a chronic obstructive pulmonary disease (COPD. In advanced disease. 2) to alleviate symptoms. PHYSICAL MANIFESTATIONS Signs of emphysema include pursed-lipped breathing. . 3. central cyanosis and finger clubbing. There may be decreased breath sounds and audible expiratory wheeze. The face has a ruddy complexion if there is a secondary polycythemia. DIAGNOSTIC EVALUATION 1. This causes the small airways to collapse during forced exhalation. the constriction of air passages isn¶t always immediately deadly. Aging itself can cause a very slow decline in lung function. and an expanded chest. both due to hyperinflation. It is important to note that when one stops smoking the decline in lung function eventually reverts to that of a non-smoker. Patients who continue to smoke have a more rapid deterioration in lung function when compared to others who quit. Sufferers who retain carbon dioxide have asterixis (metabolic flap) at the wrist. and a difficult to palpate apex beat. PFTs demonstrative airflow obstruction ± reduced forced vital capacity (FVC). TREATMENT The goals of COPD treatment are 1) to prevent further deterioration in lung function. as alveolar collapsibility has decreased. possibly increased TLC. 2) taking medications to dilate airways (bronchodilators) and decrease airway inflammation. as it is otherwise known. there are signs of fluid overload such as pitting peripheral edema.
anger. To decrease the deposition of medications on the throat and increase the amount reaching the airways. Proper use of spacer devices can greatly increase the proportion of medication reaching the airways. To maximize the delivery of the medications to the airways. Spacers are tube-like chambers attached to the outlet of the MDI canister. and intense craving for cigarettes. the patient has to learn to coordinate inhalation with each compression. fatigue. if the overinflated portions of lung are removed surgically. LVRS is a surgical procedure used to treat some patients with COPD. therefore.Nicotine in cigarettes is addictive. difficulty concentrating or sleeping. poorly-functioning upper parts of the lung compress and impair function of the better-functioning lung elsewhere. the compressed lung may expand and . Thus. 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. Patients likely to develop withdrawal symptoms typically smoke more than 20 cigarettes a day. therefore. In addition. cessation of smoking can cause symptoms of nicotine withdrawal including anxiety. As compared with bronchodilators given orally. Metered dose inhalers (MDIs) are used to deliver bronchodilators. Even in those smokers who develop symptoms of withdrawal. The premise behind this surgery is that the over-inflated. A standard amount of medication is released with each compression of the MDI. and have difficulty refraining from smoking in non-smoking areas. Pulmonary rehabilitation is a program of education regarding lung function and dysfunction. occupational and physical therapy are used to teach optimal and efficient body mechanics. the symptoms will decrease after several weeks of abstinence. However. depression. Oxygen Therapy Other treatments y y Pulmonary rehabilitation has become a cornerstone in the management of moderate to severe COPD. Bronchodilators can be inhaled. Spacer devices can hold the released medications long enough for patients to inhale them slowly and deeply into the lungs. and proper use of respiratory equipment and medications. Bronchodilators Treating airway obstruction in COPD with bronchodilators is similar but not identical to treating bronchospasm in asthma. proper breathing techniques (diaphragmatic breathing. An MDI is a pressurized canister containing a medication that is released when the canister is compressed. Inhaled bronchodilators are popular because they go directly to the airways where they work. Lung volume reduction surgery (LVRS) has received much fanfare in the lay press. and. taken orally or administered intravenously. less medication reaches the rest of the body. Incorrect use of the MDI can lead to deposition of much of the medication on the tongue and the back of the throat instead of on the airways. spacers can be helpful. some 25% of smokers can stop smoking without developing these symptoms. Bronchodilators are medications that relax the muscles surrounding the small airways thereby opening the airways. pursed lip breathing). there are fewer side effects. need to smoke shortly after waking up in the morning. and. irritability.
In patients with COPD. these medications should be used for symptoms as they develop rather than as maintenance. Dilating airways helps to relieve the symptoms of dyspnea (shortness of breath). Patients primarily with emphysema at the top of their lungs. A national study was completed in 2003. Beta-2 agonists have been shown to relieve dyspnea in many COPD patients. whose exercise tolerance was low even after pulmonary rehabilitation. 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. 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. PHARMACOLOGIC INTERVENTIONS y y Beta-agonists o Beta-2 agonists have the bronchodilating effects of adrenaline without many of its unwanted side effects. The role of LVRS is at present is very limited. pirbuterol (Maxair). but after two years returned to about the same levels as before the procedure. o Side effects of beta-2 agonists include anxiety. Activation of beta-2 receptors relaxes the muscles surrounding the airways and opens the airways. terbutaline (Brethaire). Along with some of these inhalers to be mentioned. their effectiveness is diminished. Ipratropium bromide (Atrovent) usually is administered via a MDI. These are referred to as rescue inhalers. tremor. Levalbuterol (Xopenex) is a recently approved Beta-2 agonist. palpitations or fast heart rate. The action of beta-2 agonists starts within minutes after inhalation and lasts for about 4 hours. On average. Because of their short duration of action. In addition. these are often referred to as maintenance inhalers. such as salmeterolxinafoate (Serevent) and formoterolfumarate (Foradil) may be used routinely as maintenance medications. beta-2 agonists are especially helpful for patients who are acutely short of breath. and low blood potassium. Examples of beta-2 agonists include albuterol (Ventolin. seemed to do the best with this procedure. These drugs last twelve hours and should be taken twice daily and no more. Evidence suggests that when these drugs are used routinely. metaproterenol (Alupent). The best criteria for choosing patients for LVRS are still uncertain. o In contrast. Because of their quick onset of action.function better. Proventil). the diaphragm and the chest cavity achieve more optimal positioning following the surgery. lung function and exercise capacity among surviving surgical patients improved significantly following LVRS. even among those without demonstrable reversibility in airway obstruction. and this improves breathing further. Beta-2 agonists with a slower onset of action but a longer period of activity. and isoetharine (Bronkosol). They are called ³agonists´ because they activate the beta-2 receptor on the muscles surrounding the airways. ipratropium has been shown to . Anti-cholinergic Agents o 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. Beta-2 agonists can be administered by MDI inhalers or orally.
studies suggest that ipratropium may be more effective in dilating airways and improving symptoms with fewer side effects. Ipratropium is especially suitable for use by elderly patients who may have difficulty with fast heart rate and tremor from the beta-2 agonists. o In comparing ipratropium with beta-2 agonists in the treatment of patients with COPD. Dosage and blood levels of theophylline or aminophylline have to be closely monitored. improve exercise tolerance and improve FEV1. Thus. like a beta agonist. corticosteroids) may be beneficial. thinning of the skin and easy bruising. Therefore. a combination of the two drugs sometimes results in a better response than to either drug alone without additional side effects. heart rhythm problems. In patients with heart failure or cirrhosis. Tiotropium (SPIRIVA) is a long acting and more powerful version of Ipratropium and has been shown to be more effective. Theophylline also may increase the force of contraction of the heart and lower pressure in the pulmonary arteries. Theophylline. relaxes the muscles surrounding the airways but also prevents mast cells around the airways from releasing bronchoconstricting chemicals such as histamine. theophylline can help patients with COPD who have heart failure and pulmonary hypertension. vomiting. Corticosteroids o When airway inflammation (which causes swelling) contributes to airflow obstruction. and allopurinol (Zyloprim) also can alter blood levels of methylxanthines. such as cimetidine (Tagamet). emotional changes. Interactions with other medications.y y alleviate dyspnea. Long acting theophylline preparations can be given orally once or twice a day. diabetes mellitus. o The disadvantage of methylxanthines is their side effects. and weight gain. calcium channel blockers (Procardia). dosages of methylxanthines are lowered to avoid high blood levels. and even seizures. many doctors use oral corticosteroids as the treatment of last resort. Slo-Bid. When oral corticosteroids are used. they are prescribed at the lowest possible doses for the shortest period of time to minimize side effects. Ipratropium usually is well tolerated with minimal side effects even when used in higher doses. Patients who have difficulty using inhaled bronchodilators but no difficulty taking oral medications find theophylline particularly useful. Excessively high levels in the blood can lead to nausea. high doses of oral corticosteroids over prolonged periods can have serious side effects. Theolair. Methylxanthines o Theophylline (Theo-Dur. When it is . Unfortunately. insomnia. In patients who respond poorly to either beta-2 agonists or ipratropium alone. bone fractures. including osteoporosis. high blood pressure. Uniphyl. Theo-24) and aminophylline are examples of methylxanthines. anti-inflammatory medications (more specifically. Examples of corticosteroids include Prednisone and Prednisolone. Ipratropium has a slower onset of action but longer duration of action than the shorter-acting beta2 agonists. Twenty to thirty percent of patients with COPD show improvement in lung function when given corticosteroids by mouth. Theophylline also can act as a mild diuretic and increase urination. Methylxanthines are administered orally or intravenously. quinolones (Cipro).
loss of voice. central nervous system stimulation. sputum production. Keep the patient¶s room as dust-free as possible. COMPLICATIONS 1. Replacement of the missing or inactive AAT by injection can help prevent progression of the associated emphysema. 2. Vancenase. reduced dyspnea. budesonide (Pulmicort). This therapy is of no benefit in other types of COPD. overwhelming respiratory infection Right-sided heart failure. 5. to ensure therapeutic level and prevent toxicity. dysrhythmias Depression Skeletal muscle dysfunction NURSING INTERVENTIONS Monitoring 1. reduced adventitious sounds.y necessary to use long term oral steroids. The side effects of inhaled corticosteroids include hoarseness. medications are often prescribed to help reduce the development of the above side effects. 4. A spacing device placed between the mouth and the MDI can improve medication delivery and reduce the side effects on the mouth and throat. and Vanceril). cardiac arrhythmias. Inhaled corticosteroids have been useful in treating patients with asthma. Inhaled corticosteroids have many fewer side effects than long term oral corticosteroids. Monitor condition after administration of aerosol bronchodilators to assess for improved aeration. doctors are less concerned about using inhaled corticosteroids because of their safety. Smoking cessation usually reduces pulmonary irritation. Respiratory failure Pneumonia. Eliminate all pulmonary irritants. Treatment of Alpha-1 antitrypsin deficiency o Emphysema can develop at a very young age in some patients with severe alpha-1 antitrypsin deficiency (AAT). Rinsing out the mouth after use of a steroid inhaler also can decrease these side effects. Monitor for adverse effects of bronchodilators ± tremulousness. hypertension. and cough. as ordered. Monitor serum theophylline level. o Corticosteroids also can be inhaled. Monitor oxygen saturation at rest and with activity. Examples of inhaled corticosteroids include beclomethasonedipropionate (Beclovent. Nevertheless. Supportive Care 1. . 3. but in patients with COPD. fluticasone (Flovent). and oral yeast infections. triamcinolone acetonide (Azmacort). it is not clear whether inhaled corticosteroid have the same benefit as oral corticosteroids. mometasonefuroate (Asmanex) and flunisolide (Aerobid). particularly cigarette smoke. 2. Beconase. 3. 4. tachycardia.
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. 2 to 2. and to avoid crowds and areas with poor ventilation.5 liters daily) within level of cardiac reserve. 13. 3. Train the patient in energy conservation technique. Assess the patient for reactive-behaviors such as anger. Teach the patient how to recognize and report evidence of respiratory infection promptly such as chest pain. color and consistency). 10. Suggest that high efficiency particulate air filter may have some benefit. Warn patient to avoid persons with respiratory infections. Teach controlled coughing. increasing coughing and wheezing. Avoid dairy products if these increases sputum production. Encourage the patient to assume comfortable position to decrease dyspnea. 5. increasing difficulty in raising sputum. increasing of shortness of breath. 14. Encourage high level of fluid intake ( 8 to 10 glasses. 15. vaporizer) to indoor air. depression and acceptance. tension. Advise the patient to avoid respiratory irritants. 8.2. 4. 9. 4. changes in character of sputum (amount. 5. Review with the patient the objectives of treatment and nursing management. Maintain the patient¶s nutritional status. Reemphasize the importance of graded exercise and physical conditioning programs. 6. . Use postural drainage positions to help clear secretions responsible for airway obstructions. and anxiety. 12. 11. Discuss and demonstrate relaxation exercises to reduce stress. 2. Give inhalations of nebulized saline to humidify bronchial tree and liquefy sputum. Education and health maintenance 1. Warn patient to stay out of extremely hot or cold weather and to avoid aggravating bronchial obstruction and sputum obstruction. Instruct and supervise patient¶s breathing retraining exercises. 3. Add moisture (humidifier. 7.
This action might not be possible to undo. Are you sure you want to continue?
We've moved you to where you read on your other device.
Get the full title to continue reading from where you left off, or restart the preview.