Cindy Claire L.

Alcantara N40; Group 4 BEDSIDE CLINIC

Chronic Bronchitis, Hepatomegaly with Cholelithiasis

I. INTRODUCTION A. Chronic Bronchitis Bronchitis is a term that describes inflammation of the bronchial tubes (bronchi and the smaller branches termed bronchioles) that results in excessive secretions of mucus into the tubes, leading to tissue swelling that can narrow or close off bronchial tubes. There are two major types of bronchitis, acute and chronic. Many investigators conclude that recurrent incidences of acute bronchitis are the first steps that can lead to developing chronic bronchitis. Acute bronchitis is bronchitis that is short-lived; the bronchitis lasts about two weeks and usually people recover with no permanent damage to the bronchial tree. Viruses such as influenza, respiratory syncytial virus (RSV), and rhinoviruses cause the majority (about 90%) of cases of acute bronchitis, while the remainder are caused by bacteria (for example, Mycoplasma, Pneumococcus) or short-term exposure to chemical irritants (for example, tobacco smoke, gastric reflux contents, inhaled solvents). Symptoms of acute bronchitis may include:

a cough, mild wheezing, fever, chills and malaise, and shortness of breath especially with exertion.

Some people may cough up phlegm. Chronic bronchitis differs from acute bronchitis in several ways described below (for example, pathology, progression of disease, major causes, treatments, and outcomes). Chronic bronchitis is defined as a cough that occurs every day with sputum production that lasts for at least 3 months, two years in a row. This definition was developed to help select uniform patient populations for research purposes, for example, to study medication therapies for treatment of chronic bronchitis. Many of the bronchi develop chronic inflammation with swelling and excess mucus production. The inflammation causes a change in the lining cells of the airways to

varying degrees. Many cells that line the airway lose the function of their cilia (hair-like appendages that are capable of beating rapidly), and eventually the ciliated cells are lost. Cilia perform the function of moving particles and fluid (usually mucus) over the lining surface in such structures as the trachea, bronchial tubes, and nasal cavities to keep these hollow structures clear of particles and fluids. These ciliated cells that help in clearance of secretions are often replaced by so-called goblet cells. This group of cells secretes mucus into the airway. The warm moist environment of the airway along with the nutrients in the mucus is an excellent medium for growing bacteria. The mucus often becomes infected and discolored from the bacterial overgrowth and the body's inflammatory response to it. The inflammation, swelling, and mucus frequently and significantly inhibit the airflow to and from the lung alveoli by narrowing and partially obstructing the bronchi and bronchioles. The muscles that surround the some of the airways can be stimulated by this airway irritation. This muscular spasm also known as bronchospasm can result in further airway narrowing. With long standing inflammation, as can be seen in chronic bronchitis, this muscular spasm and inflammation results in a fixed, nonreversible narrowing of the airway and the condition is termed chronic obstructive pulmonary disease (COPD). Chronic coughing develops as the body attempts to open and clear the bronchial airways of particles and mucus or as an overreaction to ongoing inflammation. Chronic bronchitis can be a progressive disease; symptoms (listed below) increase over time. Some NIH investigators consider chronic bronchitis a type of COPD. COPD also includes the entities of emphysema, chronic bronchitis, and chronic asthma. These conditions are not always separable and patients often have components of each. In the case of chronic bronchitis, the fixed airway obstruction, airway inflammation and retained secretions can result in a mismatch of blood flow and airflow in the lungs. This can impair oxygenation of the blood as well as removal of the waste product, carbon dioxide. Although people of any age can develop chronic bronchitis, the majority of people diagnosed with the disease are 45 years of age or older. There can be many causes of chronic bronchitis, but the main cause is cigarette smoke. Statistics from the US Centers for Disease Control and Prevention (CDC) suggest that about 49% of smokers develop chronic bronchitis and 24% develop emphysema/COPD. Some researchers suggest that about 90% of cases of chronic bronchitis are directly or indirectly caused by exposure to tobacco smoke. Many other inhaled irritants (for industrial pollutants, and solvents) can chronic bronchitis. example, smog, also result in

Viral and bacterial infections that result in acute bronchitis may lead to chronic bronchitis if people have repeated bouts with infectious agents. Also, underlying disease processes (for example, asthma, cystic fibrosis, immunodeficiency, congestive heart failure, familial genetic predisposition to bronchitis, and congenital or acquired dilation of the bronchioles, known as bronchiectasis) may cause chronic bronchitis to develop, but these are infrequent causes compared to cigarette smoking. The major risk factor for individuals to develop chronic bronchitis is tobacco smoking and second-hand tobacco smoke exposure. However, there are others, such as repeated exposure to pollutants (especially airborne materials such as ammonia, sulfur dioxide, chlorine, bromine, hydrogen sulfide), dust, repeated bouts of acute bronchitis or pneumonia, and gastric reflux (by inhalation of gastric contents). The major symptoms of chronic bronchitis are as follows:

Cough and sputum production are the most common symptoms; they usually last for at least 3 months and occur daily. The intensity of coughing and the amount and frequency of sputum production vary from patient to patient. Sputum may be clear, yellowish, greenish, or occasionally, blood-tinged. Since cigarette smoke is the most common cause for chronic bronchitis, it should not be surprising that the most common presentation is so called smoker's cough. This is characterized by a cough that tends to be worse upon arising and is often productive of discolored mucus in the early part of the day. As the day progresses, less mucus is produced. Dyspnea (shortness of breath) gradually increases with the severity of the disease. Usually, people with chronic bronchitis get short of breath with activity and begin coughing; dyspnea at rest usually signals that COPD or emphysema has developed. Wheezing (a coarse whistling sound produced when airways are partially obstructed) often occurs.

In addition, symptoms of fatigue, sore throat, muscle aches, nasal congestion, and headaches can accompany the major symptoms. Severe coughing may cause chest pain; cyanosis (bluish/grayish skin coloration) may develop in people with advanced COPD. Fever may indicate a secondary viral or bacterial lung infection. When symptoms worsen or become more frequent, this is often referred to as an exacerbation of chronic bronchitis. These exacerbations often require antibiotics, and may need steroid medication and an increase in respiratory inhaled medications. B. Hepatomegaly

Hepatomegaly is enlargement of the liver. The liver edge is normally palpable in children and thin adults and some patients may have a palpable right lobe of the liver. It is smooth, uniform, non-tender and descends to meet the palpating fingers on inspiration. The best way to assess size is by percussion - a normal sized liver can appear enlarged if displaced downwards by lung disorders. An enlarged liver expands down and across towards the left iliac fossa. To avoid missing a really big liver, always begin liver palpation in the LIF and work back towards the right upper quadrant.

Associated symptoms may be few or rather vague, eg loss of appetite, weight loss and lethargy. There may be symptoms relating to liver dysfunction, eg jaundice, bruising, gynaecomastia, spider naevi, ascites; or related to the underlying cause, eg xanthelasma suggests autoimmune liver disease. Measure the hepatomegaly by percussing the upper and lower borders (will rule out causes such as emphysema which can push the liver down giving a false impression of hepatomegaly). On palpation:

Smooth hepatomegaly suggests: hepatitis, chronic heart failure, sarcoid, early alcoholic cirrhosis, tricuspid incompetence with a pulsatile liver. Craggy hepatomegaly suggests: primary hepatoma or secondary tumours. C. Cholelithiasis Cholelithiasis is the medical term for gallstone disease. Gallstones are concretions that form in the biliary tract, usually in the gallbladder. Gallstones develop insidiously, and they may remain asymptomatic for decades. Migration of a a gallstone into the opening of the cystic duct may block the outflow of bile during gallbladder contraction. The resulting increase in gallbladder wall tension produces a characteristic type of pain (biliary colic). Cystic duct obstruction, if it persists for more than a few hours, may lead to acute gallbladder inflammation (acute cholecystitis). Choledocholithiasis refers to the presence of one or more gallstones in the common bile duct. Usually, this occurs when a gallstone passes from the gallbladder into the common bile duct. A gallstone in the common bile duct may impact distally in the ampulla of Vater, the point where the common bile duct and pancreatic duct join before opening into the duodenum. Obstruction of bile flow by a stone at this critical point may lead to abdominal pain and jaundice. Stagnant bile above an obstructing bile duct

stone often becomes infected, and bacteria can spread rapidly back up the ductal system into the liver to produce a life-threatening infection called ascending cholangitis. Obstruction of the pancreatic duct by a gallstone in the ampulla of Vater also can trigger activation of pancreatic digestive enzymes within the pancreas itself, leading to acute pancreatitis. Chronically, gallstones in the gallbladder may cause progressive fibrosis and loss of function of the gallbladder, a condition known as chronic cholecystitis. Chronic cholecystitis predisposes to gallbladder cancer. Ultrasonography is the initial diagnostic procedure of choice in most cases of suspected gallbladder or biliary tract disease. The treatment of gallstones depends upon the stage of disease. Asymptomatic gallstones may be managed expectantly. Once gallstones become symptomatic, definitive surgical intervention with excision of the gallbladder (cholecystectomy) is usually indicated. Cholecystectomy is among the most frequently performed abdominal surgical procedures. Complications of gallstone disease may require specialized management to relieve obstruction and infection. II. ANATOMY AND PHYSIOLOGY A. Respiratory System

The lungs constitute the largest organ in the respiratory system. They play an important role in respiration, or the process of providing the body with oxygen and releasing carbon dioxide. The lungs expand and contract up to 20 times per minute taking in and disposing of those gases. Air that is breathed in is filled with oxygen and goes to

the trachea, which branches off into one of two bronchi. Each bronchus enters a lung. There are two lungs, one on each side of the breastbone and protected by the ribs. Each lung is made up of lobes, or sections. There are three lobes in the right lung and two lobes in the left one. The lungs are cone shaped and made of elastic, spongy tissue. Within the lungs, the bronchi branch out into minute pathways that go through the lung tissue. The pathways are called bronchioles, and they end at microscopic air sacs called alveoli. The alveoli are surrounded by capillaries and provide oxygen for the blood in these vessels. The oxygenated blood is then pumped by the heart throughout the body. The alveoli also take in carbon dioxide, which is then exhaled from the body. Inhaling is due to contractions of the diaphragm and of muscles between the ribs. Exhaling results from relaxation of those muscles. Each lung is surrounded by a two-layered membrane, or the pleura, that under normal circumstances has a very, very small amount of fluid between the layers. The fluid allows the membranes to easily slide over each other during breathing. B. Hepatobiliary System

The liver is the second largest organ of the body, weighing 1200 to 1500 grams, or 4-5% of body weight. It is located in the right upper abdominal quadrant, or the right hypochondriac and epigastric regions, behind the lower ribs. The falciform ligament divides the liver anatomically into two unequal lobes: right and left. Two additional smaller lobes, the quadrate and caudate lobes are more visible in cross section. Physiologically though, the division is equal, following the fossa for gall bladder and inferior vena cava. There is no evidence for difference in functions among the four anatomical lobes. The gall bladder is a saccular organ located posterior to the liver that functions to store b i l e . I t h a s a m e a n c a p a c i t y o f 3 0 - 5 0 m L . Mucosal folds, called the spiral valves of Heister, maintain patency of the cystic duct to allow passage of bile. Presence of fats in the duodenum stimulates the gall bladder to contract.

III.

Pathophysiology A. Chronic Bronchitis

CHRONIC BRONCHITIS

B. Hepatomegaly

IV. NURSING PROFILE A. Patients Profile

Patient X, a 63 year old woman, weighing 84 kilograms, a Roman catholic by birth was admitted by two of her daughters, to Manuel J. Santos Hospital last October 8, 2012, Monday due to difficulty of breathing and jaundice with icteric sclera. As her daughter narrated, Patient X had suffered from on and off fever,and cough for about two weeks prior to admission but was said to have been underestimated by Patient X as common flu. Unexpectedly, on the said day of admission at about 10 oclock in the morning, Patient X had experienced difficulty of breathing and was cyanotic. Patients jaundice and yellowish discoloration of the her eyes had worsened Patient Xs familys worries that had made them decide to submit Patient X to the hospital for appropriate medical management. Thus, her daughters rushed Patient X from their home in Purok 3, Emelia Compound, Barangay Holy Redeemer, Butuan City to Manuel J. Santos Hospital. It was exactly 10:45 am when they arrived in the Emergency Room of the said hospital. Patient X was then seen by her attending physician, Dr. Virginia Lim-Yu. She was then administered with Oxygen and was was subjected to several tests, namely Chest X-ray, Serum Potassium, Calcium, Sodium, Creatinine, Urea Nitrogen, ALT (SGPT), and Complete Blood Count. The tests had revealed that patient had atherosclerotic, clear lung fields but with non-dilated bronchial tree, which is suggestive of bronchitis. Patient Xs past history revealed that she had failed to continue taking her maintenance drug for her bronchitis for about seven years already, of which she had forgot already the drug name. Furthermore, Patient was then submitted for an Ultrasound on the next day which in turn revealed that she had hepatomegaly and cholelithiasis. She also had undergone serologic test for typhoid fever, of which the result was negative. She too was additionally indicated for a CT Scan to rule malignancy and involvement of the mass in her liver, and unfortunately, she and her family refused to submit to such diagnostic test because of financial reasons. Patient X has been admitted to be monitored and treated in the Annex Station at Room 327 Bed C. Her condition had shown persistent problem with oxygenation and breathing. She also experienced constant pain on her abdomen, particularly on her epigastric region which occur more frequently at night. She has been treated with very potent antibiotics IVTT and orally, and it showed that after several days of therapy, onset and severity of pain has reduced and became infrequent and rare. Moreover, her attending Physician had noticed that her abdominal girt had reduced, and bloating was no longer noted. Patient X with her condition was supposedly for surgery, particularly cholecystectomy, however Dr.

Lim-Yu did not consider such as a good option considering patients age and heart condition, and that any surgery performed would bring extreme danger to her. Last October 16, 2012, I had been able to take part of her care. Wherein upon assessment, Patient X was lethargic, with fast shallow breathing, elevated BP of 160/90 mm Hg and was quite cyanotic with hooked IVF, D50.9NaCl 1 liter, regulated at KVO rate at right metacarpal vein. She had an O2 inhalation at 3 liters per minute via nasal cannula. She too had a Foley bag catheter attached to drain to a urobag. In our care, Patient Rob had been given with Domperidone (Dompenyl) orally, GIT protector and a anti-flatulent drug to prevent and lessen risks of duodenal ulcer, which can occur because of inflammatory process of the gall bladder and liver, Tramadol + Paracetamol (Algesia) orally, for pain and inflammation in the GIT, and Ipratropium + Salbutamol (Duavent) via nebulisation for bronchospasm, vital signs monitoring was done every 4 hours. I was able to witness her condition for 7 days, and during the course of our care, and I noticed Patients X gradual improvements. At first, she was lethargic and dependent with her significant others for her needs. She too, could not tolerate breathing without oxygen inhalation. She was very sedentary and was lying down her bed without trying to sit up at times and her temperature fluctuates from time to time. But days after, as her condition improved, she was now able to sit up on bed at times and during times of eating and drinking oral medications and her febrile episodes were no longer present. She was tried to be weaned of her supplemental O2 inhalation on October 17, 18 and 19, 2012 and her O2 saturation was observed. Immediately after removal, her O2 inhalation was within the normal range however, an hour or two after, her O2 saturation had went down to 82% to 91% only even with aid of deep breathing and sitting up, thus, her O2 inhalation was continued. The nurses notes on the weekends, October 20 and 21, 2012 revealed that her O2 inhalation was tried to be weaned on the Sunday and was indicated for a 24-hour observation to decide patients tolerance and ability for discharge. However, her O2 inhalation was again administered back because her O2 saturation had been persistently low. On October, 23, 2012, her O2 inhalation was again removed for observation, and this time, it showed that Patient X could now tolerate independent breathing with good O2 saturation. Fortunately, her attending physician and her family agreed to discharge Patient X for home care. Thus, on October 24, 2012, Patient X was finally discharged at about 4 in the afternoon with prescribed home medications and low salt, low fat diet. She was

advised to come back for a follow up check up with Dr. Lim-Yu on November 11, 2012, at her clinic. A diet list of Low Salt, Low fat diet was explained and provided to her. Each home medications indications and schedules were also explained and that she too understood the side effects of the drugs.

V.

Laboratory Tests and Interpretation 10/8/12 Chest X-ray Interpretation: Atherosclerotic Aorta

- Blood Chemistry Uric Acid = 6.1 mg/dl (2.7-7.3) INCREASED Creatinine = 0.78 mg/dl (0.7-1.3) NORMAL ALT (SGPT) 24.0 u/L (<49) NORMAL

- Complete Blood Count

10/9/12 10/17/12 VI. DRUG STUDY Beta-agonists

White Blood Cell = 27.3 x 109/L INCREASED Segmenters = 0.9 H INCREASED Lymphocyte = 0.04 L DECREASED Band = 0.00 DECREASED Monocyte = 0.05 DECREASED Serologic Test for Typhoid Fever NEGATIVE Ultrasound Hepatomegaly with a large size fairly to well defined complex cystic mass in the Right hepatic lobe as described Slightly distended gallbladder with small calculi as prescribed. Normal size kidneys with bilateral cortical cysts as described Unremarkable sonogram of pancreas, urinary bladder, involuting uterus, and both adnexal areas. Non-dilated biliary tree. Repeat Chest X-ray Interpretation: Suggestive of Pneumonia and Pulmonary Edema

a. 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. b. 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. c. Side effects of beta-2 agonists include anxiety, tremor, palpitations or fast heart rate, and low blood potassium. Anti-cholinergic Agents
a. 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 + Albuterol sulfate (Duavent) dilate airways by blocking the receptors for acetylcholine on the muscles of the airways and preventing them from narrowing. Ipratropium bromide + Albuterol sulfate (Duavent) 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. b. 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
a. 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. b. 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 a. 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. b. 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. Lists of Patients Drugs: DRUG NAME Captopril ( Capomed) 25 mg 1 tab SL every 6 hours for BP 160/100 Telmisartan (Pritor) 40 mg/tab OD Isosorbide Mononitrate (Imdur) 60 mg tab OD ASA (Aspilet) 80 mg 1 tab OD Erdosteine (Zertin) 300 mg 1 cap BID Paracetamol (Tempra Forte) 1 tab every 4 hours for fever Tramadol + Paracetamol (Algesia) 1 tab TID Ipratropium + Salbutamol (Duavent) 1 UDV every 6 hours Domperidone (Dompenyl) 1 tab TID Omeprazole (Omepron) 20 mg 1 cap BID CLASSIFICATION ACE Inhibitor Angiotensin receptor blocker Vasodilator Analgesic, NSAID Mucolytic Antipyretic,

NSAID, Antipyretic Analgesic, Antipyretic Anti-cholinergic Anti-flatulent, GIT Protector Proton Pump Inhibitor

VII. Nursing Management 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 patients 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 patients 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 patients 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.

REFERENCES: Brunner and Suddarths. Medical and Surgical Nursing Udan, Josie Quiambao. Medical Surgical Nursing Lippincott. Manuals of Nursing Practice Mosby. Medical Surgical Nursing Shaker SB, Dirksen A, Bach KS, Mortensen J (June 2007). Bach PB, Brown C, Gelfand SE, McCrory DC (2001). "Management of acute exacerbations of chronic obstructive pulmonary disease: a summary and appraisal of published evidence". Ann. Intern. Med. 134 (7): 60020.