COPD Chronic Obstructive Pulmonary Disease DEFINITION Chronic obstructive pulmonary disease (COPD) is comprised primarily of three rel

ated conditions -chronic bronchitis, chronic asthma, and emphysema. In each cond ition there is chronic obstruction of the flow of air through the airways and ou t of the lungs, and the obstruction generally is permanent and may be progressiv e over time. While asthma features obstruction to the flow of air out of the lun gs, usually, the obstruction is reversible. Between "attacks" of asthma the flow of air through the airways typically is normal. These patients do not have COPD . However, if asthma is left untreated, the chronic inflammation associated with this disease can cause the airway obstruction to become fixed. That is, between attacks, the asthmatic patient may then have abnormal air flow. This process is referred to as lung remodeling. These asthma patients with a fixed component of airway obstruction are also considered to have COPD. Often patients with COPD are labeled by the symptoms they are having at the time of an exacerbation of their disease. For instance, if they present with mostly shortness of breath, they may be referred to as emphysema patients. While if the y have mostly cough and mucus production, they are referred to as having chronic bronchitis. In reality, it is better to refer to these patients as having COPD since they can present with a variety of lung symptoms. There is frequent overlap among COPD patients. Thus, patients with emphysema may have some of the characteristics of chronic bronchitis and chronic asthma and v ice a versa. TYPES A. Chronic Bronchitis

Chronic bronchitis involves inflammation and swelling of the lining of the airwa ys that leads to narrowing and obstruction of the airways. The inflammation also stimulates production of mucous (sputum), which can cause further obstruction o f the airways. Obstruction of the airways, especially with mucus, increases the likelihood of bacterial lung infections. Chronic bronchitis usually is defined c linically as a daily cough with production of sputum for three months, two years in a row. This definition was developed primarily for research so that like pat ients could be compared. B. Emphysema There is permanent enlargement of the alveoli due to the destruction of the wall s between alveoli in emphysema. The destruction of the alveolar walls reduces th e elasticity of the lung overall. Loss of elasticity leads to the collapse of th e bronchioles obstructing airflow out of the alveoli. Air becomes "trapped" in t he alveoli and reduces the ability of the lung to shrink during exhalation. This trapped air takes up space and results in a reduced amount of air that can be t aken in during the next breath. As a result, less air gets to the alveoli for th e exchange of gasses. This trapped air also can compress adjacent less damaged l ung tissue, preventing it from functioning to its fullest capacity. The exchange of carbon dioxide and oxygen between air and the blood in the capil laries takes place across the thin walls of the alveoli. Destruction of the alve olar walls decreases the number of capillaries available for gas exchange. This adds to the decrease in the ability to exchange gases. C. Chronic Asthma It is a disease of the airways. Obstruction to the flow of air is due to inflamm ation of the airways as well as spasm of muscles surrounding the airways in asth ma. The narrowing that results from spasm of the muscles is called bronchospasm. Generally, bronchospasm in asthma is reversible and subsides spontaneously or w

ith the use of bronchodilators (medications that relax the muscles surrounding t he airways). We now know that a major component of asthma is inflammation of the airways, and this inflammation causes thickening of the walls of the airways. T his inflammation involves different inflammatory cells and mediators than those seen in chronic bronchitis. CAUSES A. Smoking Exposure to cigarette smoke is measured in pack-years,[23] the average number of packages of cigarettes smoked daily multiplied by the number of years of smokin g. The likelihood of developing COPD increases with age and cumulative smoke exp osure, and almost all lifelong smokers will develop COPD, provided that smokingrelated, extrapulmonary diseases (cardiovascular, diabetes, cancer) do not claim their lives beforehand. B. Occupational exposures Intense and prolonged exposure to workplace dusts found in coal mining, gold min ing, and the cotton textile industry and chemicals such as cadmium, isocyanates, and fumes from welding have been implicated in the development of airflow obstr uction, even in nonsmokers.[25] Workers who smoke and are exposed to these parti cles and gases are even more likely to develop COPD. Intense silica dust exposur e causes silicosis, a restrictive lung disease distinct from COPD; however, less intense silica dust exposures have been linked to a COPD-like condition.[26] Th e effect of occupational pollutants on the lungs appears to be substantially les s important than the effect of cigarette smoking.[27] C. Air Pollution Studies in many countries have found people who live in large cities have a high er rate of COPD compared to people who live in rural areas.[28] Urban air pollut ion may be a contributing factor for COPD, as it is thought to slow the normal g rowth of the lungs, although the long-term research needed to confirm the link h as not been done. D. Genetcs COPD is more common among relatives of COPD patients who smoke than unrelated sm okers.[30] The genetic differences that make some peoples' lungs susceptible to the effects of tobacco smoke are mostly unknown. Alpha 1-antitrypsin deficiency is a genetic condition that is responsible for about 2% of cases of COPD. In thi s condition, the body does not make enough of a protein, alpha 1-antitrypsin. Al pha 1-antitrypsin protects the lungs from damage caused by protease enzymes, suc h as elastase and trypsin, that can be released as a result of an inflammatory r esponse to tobacco smoke.[31] E. Autoimmune Disease T here is mounting evidence that there may be an autoimmune component to COPD, t riggered by lifelong smoking.[32] Many individuals with COPD who have stopped sm oking have active inflammation in the lungs.[33] The disease may continue to get worse for many years after stopping smoking due to this ongoing inflammation.[3 3] This sustained inflammation is thought to be mediated by autoantibodies and a utoreactive T cells. F. Acute Exacerbations An acute exacerbation of COPD is a sudden worsening of COPD symptoms (shortness of breath, quantity and color of phlegm) that typically lasts for several days. It may be triggered by an infection with bacteria or viruses or by environmental pollutants. Typically, infections cause 75% or more of the exacerbations; bacte ria can be found in roughly 25% of cases, viruses in another 25%, and both virus es and bacteria in another 25%. Pulmonary emboli can also cause exacerbations of COPD. Airway inflammation is increased during the exacerbation, resulting in in creased hyperinflation, reduced expiratory air flow and worsening of gas transfe r. This can also lead to hypoventilation and eventually hypoxia, insufficient ti ssue perfusion, and then cell necrosis. NURSING DIAGNOSIS: 1) Impaired gas exchange related to altered oxygen delivery and alveoli des truction -Elevate the head of the bed/ position the client appropriately, provide airway

adjuncts and suction as indicated to maintain airway. - Administer medications as indicated (bronchodilators, antibiotics) - Encourage frequent position changes and deep breathing or coughing exercises 2) Ineffective airway clearance related to increased production of tenacious sec retions -Provide opportunities for rest:limit activities to level of res piratory tolerance. -Give bronchodilators as ordered. -Monitor serial chest x-rays, ABG readings. 3) Activity intolerance related to imbalance between oxygen supply and demand, a nd generalized weakness -Plan care with rest periods between activities to reduce fatigu e. -Provide or monitor response to supplemental oxygen and medicati ons and changes in treatment regimen. -Encourage expression of feelings resulting from the condition. 4) Imbalanced nutrition less tan body requirements related to inability to inges t adequate nutrients -Monitor intake and output regularly. -Auscultate bowel sounds. Note characteristics of stool. -Give small frequent feedings. 5) Risk for infection -Monitor visitors and caregivers to prevent exposure of patient. -Encourage early ambulation, deep breathing, coughing, position change for mobilization of respiratory secretions. -Provide regular catheter/ perineal care. Reduces risk of ascend ing UTI. LABORATORY AND DIAGNOSTIC TESTS > Arterial Blood Gas - This blood test measures how well your lungs are bringing oxygen into your blood and removing carbon dioxide. The blood is usually drawn from an artery in your wrist. Normal PaO2 = 80-100 mm Hg PaCO2 = 35-45 mm Hg pH = 7.35-7.45 HCO3 = 22-26 mEq/l SaO2 = 95-99% Panic Values for ABGs PaO2: < 40 PaCO2: < 20 or > 70 pH: < 7.2 or > 7.6 HCO3: < 10 or > 40 SaO2: < 60% Degrees of Hypoxia: mild: PaO2 of 60-80 mm mod: PaO2 of 40-60 mm severe: PaO2 < 40 mm > Hematocrit Normal Female: 36-46% Male: 42-52% Low values = Anemia: monitor for fatigue, dyspnea, tachycardia, tachypnea > Hemoglobin (Hgb)

Normal Female: 12-15 g/dl Male: 14-17 g/dl Low values = Anemia: monitor for fatigue, dyspnea, tachycardia, tachypnea > RBC Count Normal Female: 4 -5.5 million/mm3 Male: 4.5 - 6.2 million/mm3 Low values = Anemia: monitor for fatigue, dyspnea, tachycardia, tachypnea High values: In COPD, may indicate Polycythemia, a compensation for pulmonary dy sfunction that makes blood thicker, and increases risk of CVA, etc. > Sputum examination. Analysis of the cells in the mucus you cough up, which is known as sputum, can help identify the cause of your lung problems and help rule out some lung cancers. If you have a productive cough, identifying a bacterial pathogen and treating it before it causes pneumonia is good preventive medicine. > CHEST X-RAYS Chest x-rays are used to rule out other causes of airway obstruction, such as me chanical obstruction, tumors, infections, effusions, or interstitial lung diseas es. In acute exacerbations of COPD, chest x-rays are used to look for pneumothor ax, pneumonia, and atelectasis (collapse of part of a lung) (Wise, 2007). In its later phases, COPD produces a number of changes that can be seen in chest x-rays: When COPD includes significant emphysema, the chest is widened, the diaphragm is flattened, and the lung fields have fainter and fewer vascular markings. Emphys ema can make the heart look long, narrow, and vertical, and the airspace behind the heart can be enlarged. When COPD includes significant chronic bronchitis, chest x-rays have a dirty look. The re are more vascular markings and more nonspecific bronchial markings, and the w alls of the bronchi look thicker than normal when viewed end-on. Often, the hear t appears enlarged (Swadron & Mandavia, 2009). > COMPUTED TOMOGRAPHY (CT) SCANS CT scans are now the imaging technique of choice for lung evaluations (Coxson et al., 2009). CT scans, especially high-resolution scans, are better than chest x -rays at resolving the details of the lung abnormalities caused by COPD. Specifi cally, CT scans can help define which areas of a patient s lungs are predominately e mphysematous and which are predominately bronchiolitic. CT scans are also better than chest x-rays at identifying other diseases, such as tumors or infections, that may be complicating a patient s COPD. Late in the disease, CT scans are used to evaluate COPD patients who are to be treated surgically. MEDICAL MANAGEMENT COPD is a life-long disease. It requires special medical treatment durin g acute exacerbations, and after the disease reaches the level called moderate COPD , it requires daily medications and permanent adjustments to a patient s lifestyle. Gro ss (2008) and Gold (2009) are guides to the management of COPD. At each stage of the disease, there are some characteristic medical therapies: Mild COPD is usually treated with short-acting bronchodilators, which are used a s needed for dyspnea. Moderate COPD requires regular treatments with bronchodilators, sometimes with t he addition of inhaled corticosteroids. At this stage, patients are often enroll ed in a pulmonary rehabilitation program. Severe COPD typically requires two or more bronchodilators regularly. Inhaled co rticosteroids are added to the regimen to prevent repeated acute exacerbations. Very severe COPD usually needs the addition of long-term oxygen therapy. Surgica

l treatments can be appropriate at this stage. Oxygen Therapy Supplemental oxygen improves levels of blood oxygenation and reduces the rate at which patients need to breathe. For people with COPD, supplemental oxygen also slows the rate at which muscles fatigue. These effects make it easier for patien ts to breathe more deeply and to exercise for longer periods. For patients with advanced COPD, supplemental oxygen reduces mortality rates. Oxygen therapy is expensive and involves special equipment. Therefore, when peop le with COPD can maintain a blood oxygenation level of PaO2 >55 60 mm Hg (an oxygena tion saturation of more than ~89%), supplemental oxygen therapy is not routinely prescribed (Rich & McLaughlin, 2007; Chesnutt et al., 2010). BULLECTOMY In some cases, individual large empty air spaces (bullae) can be surgically remo ved. Typical bullae in a patient with emphysema are a few centimeters in diamete r. Occasionally, however, bullae can be huge, taking up as much as a third of th e chest space. These giant bullae squeeze the healthier lung tissue and compress the adjacent blood vessels. By removing giant bullae, the remaining lung tissue can reexpand, and some of the circulation will be restored. As with lung volume reduction surgery, a major postsurgical complication of bullectomy is persisten t air leakage. LUNG VOLUME REDUCTION As noted earlier, the lungs of an emphysematous patient become hyperinflated wit h air spaces that contribute little to gas exchange. The widened chest caused by hyperinflated lungs is difficult for the patient to expand farther when attempt ing to inhale. By removing lung tissue that contains dead air space, surgery can sometimes reduce the patient s work of breathing. In lung volume reduction surgery, 20% to 30% of the lung volume is removed from both sides of the chest. As a result, survivors can usually exercise more than t hey could before the surgery. Those patients who have mainly upper-lung emphysem a also have an increased lifespan after this surgery. For other COPD patients, h owever, longevity is not increased and it may even be shortened. The major postoperative complication of lung volume reduction surgery is continu ing air leakage from the lungs into the chest. Operative mortality rates are fro m 4% to 10% in hospitals providing the procedure. ANTIBIOTICS FOR ACUTE EXACERBATIONS OF COPD Respiratory infections are frequent causes of acute exacerbations of COPD. When an acute exacerbation includes signs of infection (e.g., fever, elevated white b lood-cell count, purulent sputum, or a suggestive chest x-ray), the empirical ad ministration of antibiotics is usually recommended. Likely microbes include Stre ptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Pseudom onas aeruginosa, and appropriate antibiotics include: cefuroxime (Zinacef) azithromycin (Zithromax) clarithromycin (Biaxin) PREVENTION 1. Don't smoke: The best way to keep COPD from starting or from getting worse is to not smoke. There are clear benefits to quitting, even after years of smoking. When you stop smoking, you slow down the damage to your lungs. For most people who quit, loss of lung function is slowed to the same rate as a nonsmoker's. Today's medicines offer lots of help for people who want to quit. You will doubl e your chances of quitting even if medicine is the only treatment you use to qui t. And your odds get even better when you combine medicine and other quit strate gies, such as counseling.1 For more information, see the topic Quitting Smoking. Stopping smoking is especially important if you have low levels of the protein a lpha-1 antitrypsin. People who have this may lower their risk for severe COPD if they get timely shots of alpha-1 antitrypsin that has been obtained from human plasma. 2. Avoid bad air: Other airway irritants (such as air pollution, chemical fumes,

and dust) also can make COPD worse, but they are far less important than smokin g in causing the disease. Preventing other problems Flu vaccines: If you have COPD, you need to get a flu vaccine every year. When p eople with COPD get the flu, it often turns into something more serious, like pn eumonia. A flu vaccine can help prevent this from happening. Also, getting regular flu vaccines may lower your chances of having COPD flare-u ps.8 Pneumococcal shot: People with COPD often get pneumonia. Getting a shot can help keep you from getting very ill with pneumonia. Usually, people need only one sh ot, but doctors sometimes recommend a second shot for some people who got their first shot before they turned 65. Talk with your doctor about whether you need a second shot.