Chronic Obstructive Pulmonary Disorder (COPD)

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 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 12^th 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:
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 voicebox) 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 ‘lobes’, or big sections of tissue separated by ‘fissures’ 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 ‘bronchopulmonary 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.

COPD VERSUS HEALTHY LUNG

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



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 ‘parietal’ 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. The diaphragm, a large, sheet-like muscle which stretches across your chest under the ribcage, does much of this work. At rest, it is shaped like a dome curving up into your chest. When you breathe in, 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 normally require 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 and function of the respiratory system. These include:

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

Risk factors for COPD include environmental exposures and host factors. The most important risk factor for COPD is cigarette smoking. Other risk factors are pipe, cigar, and other types of tobacco smoking. In addition, passive smoking contributes to respiratory symptoms and COPD. Smoking depresses the activity of scavenger cells and affects the respiratory tract’s ciliary cleansing mechanism, which keeps breathing passages free of inhaled irritants, bacteria, and other foreign matter. When smoking damages this cleansing mechanism, airflow is obstructed and air becomes trapped behind the obstruction. The alveoli greatly distend, diminished lung capacity. Smoking also irritates the goblet cells and mucus glands, causing an increased accumulation of mucus, which in turn produces more irritation, infection, and damage to the lung. In addition, carbon monoxide (a by product of smoking) combines with hemoglobin to form carboxyhemoglobin.

Hemoglobin that is bound by carboxyhemoglobin cannot carry oxygen efficiently.
A host risk factor for COPD is a deficiency of alpha antitrypsin, an enzyme inhibitor that protects the lung parenchyma from injury. This deficiency predisposes young people to rapid development of lobular emphysema, even if they do not smoke. Genetically susceptible people are sensitive to environmental factors (eg. Smoking, air pollution, infectious agents, allergens) and eventually developed chronic obstructive symptoms. Carriers of this genetic defect must be identified so that they can modify environmental risk factors to delay or prevent overt symptoms of disease.

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’s 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 antiproteinases in the lung may be responsible for airflow limitation. When activated by chronic inflammation, proteiness and other substances may be released, damaging the parenchyma 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 3 months of a year, for 2 consecutive years. In the airways of the lung, 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, 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 “blue 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 “Blue Bloaters.”

ACUTE BRONCHITIS
PHYSICAL MANIFESTATIONS
One of the most common symptoms of COPD is shortness of breath (dyspnea). People with COPD commonly describe this as: “My breathing requires effort”, “I feel out of breath”, or “I 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 cor pulmonale, 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 anteroposterior to lateral ratio of the chest (i.e. barrel chest).

EMPHYSEMA


Emphysema is a chronic obstructive pulmonary disease (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 isn’t always immediately deadly, and treatment is available.

PHYSICAL MANIFESTATIONS
Signs of emphysema include pursed-lipped breathing, central cyanosis and finger clubbing. The chest has hyper resonant percussion notes, particularly just above the liver, and a difficult to palpate apex beat, both due to hyperinflation. There may be decreased breath sounds and audible expiratory wheeze. In advanced disease, there are signs of fluid overload such as pitting peripheral edema. The face has a ruddy complexion if there is a secondary polycythemia. Sufferers who retain carbon dioxide have asterixis (metabolic flap) at the wrist.

DIAGNOSTIC EVALUATION

1. 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 rettrosternal space, decreased vascular markings, possible bullae.
4. Alpa1-antitrypsin assay useful in identifying genetically determined deficiency in emphysema.

TREATMENT
The goals of COPD treatment are 1) to prevent further deterioration in lung function, 2) to alleviate symptoms, 3) to improve performance of daily activities and quality of life. The treatment strategies include 1) quitting cigarette smoking, 2) taking medications to dilate airways (bronchodilators) and decrease airway inflammation, 3) vaccinating against flu influenza and pneumonia and 4) regular oxygen supplementation and 5) pulmonary rehabilitation.

Quitting cigarette smoking
The most important treatment for COPD is quitting cigarette smoking. Patients who continue to smoke have a more rapid deterioration in lung function when compared to others who quit. Aging itself can cause a very slow decline in lung function. In susceptible individuals, cigarette smoking can result in a much more dramatic loss of lung function. It is important to note that when one stops smoking the decline in lung function eventually reverts to that of a non-smoker.

Nicotine in cigarettes is addictive, and, therefore, cessation of smoking can cause symptoms of nicotine withdrawal including anxiety, irritability, anger, depression, fatigue, difficulty concentrating or sleeping, and intense craving for cigarettes. Patients likely to develop withdrawal symptoms typically smoke more than 20 cigarettes a day, need to smoke shortly after waking up in the morning, and have difficulty refraining from smoking in non-smoking areas. However, some 25% of smokers can stop smoking without developing these symptoms. Even in those smokers who develop symptoms of withdrawal, the symptoms will decrease after several weeks of abstinence.
Bronchodilators
Treating airway obstruction in COPD with bronchodilators is similar but not identical to treating bronchospasm in asthma. Bronchodilators are medications that relax the muscles surrounding the small airways thereby opening the airways. Bronchodilators can be inhaled, taken orally or administered intravenously. Inhaled bronchodilators are popular because they go directly to the airways where they work. As compared with bronchodilators given orally, less medication reaches the rest of the body, and, therefore, there are fewer side effects.

Metered dose inhalers (MDIs) are used to deliver bronchodilators. An MDI is a pressurized canister containing a medication that is released when the canister is compressed. A standard amount of medication is released with each compression of the MDI. To maximize the delivery of the medications to the airways, the patient has to learn to coordinate inhalation with each compression. 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.
To decrease the deposition of medications on the throat and increase the amount reaching the airways, spacers can be helpful. Spacers are tube-like chambers attached to the outlet of the MDI canister. Spacer devices can hold the released medications long enough for patients to inhale them slowly and deeply into the lungs. Proper use of spacer devices can greatly increase the proportion of medication reaching the airways.

Other treatments

• Pulmonary rehabilitation has become a cornerstone in the management of moderate to severe COPD. Pulmonary rehabilitation is a program of education regarding lung function and dysfunction, proper breathing techniques (diaphragmatic breathing, pursed lip breathing), 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. In addition, occupational and physical therapy are used to teach optimal and efficient body mechanics.
• Lung volume reduction surgery (LVRS) has received much fanfare in the lay press. LVRS is a surgical procedure used to treat some patients with COPD. The premise behind this surgery is that the over-inflated, poorly-functioning upper parts of the lung compress and impair function of the better-functioning lung elsewhere. Thus, if the over-inflated portions of lung are removed surgically, the compressed lung may expand and function better. In addition, the diaphragm and the chest cavity achieve more optimal positioning following the surgery, and this improves breathing further. The best criteria for choosing patients for LVRS are still uncertain. A national study was completed in 2003. Patients primarily with emphysema at the top of their lungs, whose exercise tolerance was low even after pulmonary rehabilitation, seemed to do the best with this procedure. On average, lung function and exercise capacity among surviving surgical patients improved significantly following LVRS, but after two years returned to about the same levels as before the procedure. 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. The role of LVRS is at present is very limited.

PHARMACOLOGIC INTERVENTIONS

• Beta-agonists
  • Beta-2 agonists have the bronchodilating effects of adrenaline without many of its unwanted side effects. Beta-2 agonists can be administered by MDI inhalers or orally. They are called “agonists” because they activate the beta-2 receptor on the muscles surrounding the airways. Activation of beta-2 receptors relaxes the muscles surrounding the airways and opens the airways. Dilating airways helps to relieve the symptoms of dyspnea (shortness of breath). Beta-2 agonists have been shown to relieve dyspnea in many COPD patients, even among those without demonstrable reversibility in airway obstruction. The action of beta-2 agonists starts within minutes after inhalation and lasts for about 4 hours. Because of their quick onset of action, beta-2 agonists are especially helpful for patients who are acutely short of breath. Because of their short duration of action, these medications should be used for symptoms as they develop rather than as maintenance. Evidence suggests that when these drugs are used routinely, their effectiveness is diminished. These are referred to as rescue inhalers. Examples of beta-2 agonists include albuterol (Ventolin, Proventil), metaproterenol (Alupent), pirbuterol (Maxair), terbutaline (Brethaire), and isoetharine (Bronkosol). Levalbuterol (Xopenex) is a recently approved Beta-2 agonist.
  • In contrast, Beta-2 agonists with a slower onset of action but a longer period of activity, such as salmeterol xinafoate (Serevent) and formoterol fumarate (Foradil) may be used routinely as maintenance medications. These drugs last twelve hours and should be taken twice daily and no more. Along with some of these inhalers to be mentioned, these are often referred to as maintenance inhalers.
  • Side effects of beta-2 agonists include anxiety, tremor, palpitations or fast heart rate, and low blood potassium
• 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. 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. Ipratropium bromide (Atrovent) usually is administered via a MDI. In patients with COPD, ipratropium has been shown to alleviate dyspnea, improve exercise tolerance and improve FEV1. Ipratropium has a slower onset of action but longer duration of action than the shorter-acting beta-2 agonists. Ipratropium usually is well tolerated with minimal side effects even when used in higher doses. Tiotropium (SPIRIVA) is a long acting and more powerful version of Ipratropium and has been shown to be more effective.
  • In comparing ipratropium with beta-2 agonists in the treatment of patients with COPD, 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. In patients who respond poorly to either beta-2 agonists or ipratropium alone, a combination of the two drugs sometimes results in a better response than to either drug alone without additional side effects.
• Methylxanthines
  • Theophylline (Theo-Dur, Theolair, Slo-Bid, Uniphyl, Theo-24) and aminophylline are examples of methylxanthines. Methylxanthines are administered orally or intravenously. Long acting theophylline preparations can be given orally once or twice a day. Theophylline, like a beta agonist, relaxes the muscles surrounding the airways but also prevents mast cells around the airways from releasing bronchoconstricting chemicals such as histamine. Theophylline also can act as a mild diuretic and increase urination. Theophylline also may increase the force of contraction of the heart and lower pressure in the pulmonary arteries. Thus, theophylline can help patients with COPD who have heart failure and pulmonary hypertension. Patients who have difficulty using inhaled bronchodilators but no difficulty taking oral medications find theophylline particularly useful.
  • The disadvantage of methylxanthines is their side effects. Dosage and blood levels of theophylline or aminophylline have to be closely monitored. Excessively high levels in the blood can lead to nausea, vomiting, heart rhythm problems, and even seizures. In patients with heart failure or cirrhosis, dosages of methylxanthines are lowered to avoid high blood levels. Interactions with other medications, such as cimetidine (Tagamet), calcium channel blockers (Procardia), quinolones (Cipro), and allopurinol (Zyloprim) also can alter blood levels of methylxanthines.
• Corticosteroids
  • When airway inflammation (which causes swelling) contributes to airflow obstruction, anti-inflammatory medications (more specifically, corticosteroids) may be beneficial. Examples of corticosteroids include Prednisone and Prednisolone. Twenty to thirty percent of patients with COPD show improvement in lung function when given corticosteroids by mouth. Unfortunately, high doses of oral corticosteroids over prolonged periods can have serious side effects, including osteoporosis, bone fractures, diabetes mellitus, high blood pressure, thinning of the skin and easy bruising, insomnia, emotional changes, and weight gain. Therefore, many doctors use oral corticosteroids as the treatment of last resort. When oral corticosteroids are used, they are prescribed at the lowest possible doses for the shortest period of time to minimize side effects. When it is necessary to use long term oral steroids, medications are often prescribed to help reduce the development of the above side effects.
  • Corticosteroids also can be inhaled. Inhaled corticosteroids have many fewer side effects than long term oral corticosteroids. Examples of inhaled corticosteroids include beclomethasone dipropionate (Beclovent, Beconase, Vancenase, and Vanceril), triamcinolone acetonide (Azmacort), fluticasone (Flovent), budesonide (Pulmicort), mometasone furoate (Asmanex) and flunisolide (Aerobid). Inhaled corticosteroids have been useful in treating patients with asthma, but in patients with COPD, it is not clear whether inhaled corticosteroid have the same benefit as oral corticosteroids. Nevertheless, doctors are less concerned about using inhaled corticosteroids because of their safety. The side effects of inhaled corticosteroids include hoarseness, loss of voice, and oral yeast infections. A spacing device placed between the mouth and the MDI can improve medication delivery and reduce the side effects on the mouth and throat. Rinsing out the mouth after use of a steroid inhaler also can decrease these side effects.
• Treatment of Alpha-1 antitrypsin deficiency
  • Emphysema can develop at a very young age in some patients with severe alpha-1 antitrypsin deficiency (AAT). Replacement of the missing or inactive AAT by injection can help prevent progression of the associated emphysema. This therapy is of no benefit in other types of COPD.

COMPLICATIONS

1. Respiratory failure
2. Pneumonia, overwhelming respiratory infection
3. Right-sided heart failure, dysrhythmias
4. Depression
5. Skeletal muscle dysfunction

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 prevent toxicity.
4. Monitor oxygen saturation at rest and with activity.

Supportive Care

1. Eliminate all pulmonary irritants, particularly cigarette smoke. Smoking cessation usually reduces pulmonary irritation, sputum production, and cough. Keep the patient’s room as dust-free as possible.
2. Use postural drainage positions to help clear secretions responsible for airway obstructions.
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’s 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’s 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

1. Review with the patient the objectives of treatment and nursing management.
2. Advise the patient to avoid respiratory irritants. Suggest that high efficiency particulate 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.