CHRONIC OBSTRUCTIVE PULMONARY DISORDER

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 12th leading cause of disability. However, by the year 2020 it is estimated that COPD will be the third leading cause of death and the firth leading cause of disability (Sin, McAlister, Man. Et al., 2003). People with COPDcommonly become symptomatic during the middle adult years, and the incidence of the disease increases with age.

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.

COPD VERSUS HEALTHY LUNG

COPD VERSUS HEALTHY LUNG

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.

PATHOPHYSIOLOGY

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.

PATHOPHYSIOLOGY

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.

SIGN & SYMPTOM COPD

One of the most common symptoms of COPD is shortness of breath (dyspnea) 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.Pulmonary Function Tests 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.

PHARMACOLOGIC INTERVENTIONS
1. 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 inhalers or orally.

2. 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.

3. Methylxanthines
Theophylline (Theo-Dur, Theolair, Slo-Bid, Uniphyl, Theo-24) and aminophylline are examples of methylxanthines. 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. Methylxanthines are administered orally or intravenously.

4. Corticosteroids
When airway inflammation (which causes swelling) contributes to airflow obstruction, antiinflammatory medications (more specifically, corticosteroids) may be beneficial. Examples of corticosteroids include Prednisone and Prednisolone. 20-30% 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.

5. 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

ASTHMA
Bronchial asthma is a chronic inflammatory disease of the airways, associated with recurrent, reversible airway obstruction with intermittent episodes of wheezing and dyspnea. Bronchial hypersensitivity is caused by various stimuli, which innervate the vagus nerve and beta adrenergic receptor cells of the airways, leading to bronchial smooth muscle constriction, hypersecretion of mucus, and mucosal edema.

SYMPTOMS
The symptoms of bronchial asthma includes: A feeling of tightness in the chest; Difficulty in breathing or shortness of breath; Wheezing; and Coughing (particularly at night).

Asthma triggers
may include: Tobacco smoke Infections such as colds, flu, or pneumonia Allergens such as food, pollen, mold, dust mites, and pet dander Exercise Air pollution and toxins Weather, especially extreme changes in temperature

 Drugs (such as aspirin, NSAID, and betablockers) Food additives (such as MSG) Emotional stress and anxiety Singing, laughing, or crying Smoking, perfumes, or sprays Acid reflux

Treatment for Asthma

Treatment of acute asthma aims to decrease bronchoconstriction, reduce bronchial airway edema, and increase pulmonary ventilation. After an acute episode, treatment focuses on avoiding or removing precipitating factors, such as environmental allergens or irritants. Drug therapy is most effective when begun soon after the onset of symptoms.

 A patient who doesn't respond to this treatment, whose airways remain obstructed, and who has increasing respiratory difficulty is at risk for status asthmaticus and may require mechanical ventilation.

Nursing Care Plan Chronic Obstructive Pulmonary Disorder & ASTHMA

Nursing Diagnosis
Impaired gas exchange related to altered oxygen supply obstruction of airways by secretions, bronchospasm, air-trapping alveoli destruction Ineffective airway clearance related to obstruction from narrowed lumen and thick mucus Ineffective breathing pattern Fatigue Anxiety Deficient knowledge (treatment regimen, selfcare, and discharge needs)

Nursing Outcomes
Patient will:
1. Maintain adequate ventilation and oxygenation. 2. Maintain a patent airway. 3. Maintain a respiratory rate within five breaths of baseline. 4. Identify strategies to reduce anxiety. 5. Verbalize the importance of balancing activity with adequate rest periods. 6. Verbalize an understanding of appropriate treatment regimen, self-care, and discharge needs

Nursing Interventions
1. Maintaining a patent airway is a priority. 2. Use a humidifier to help the patient mobilize secretions. 3. Encourage the patient to use controlled coughing to clear secretions that might have collected in the lungs during sleep. 4. Instruct the patient to sit at the bedside or in a comfortable chair, hug a pillow, bend the head downward a little, take several deep breaths, and cough strongly .

5. Administer low concentrations of oxygen as ordered. 6. Perform blood gas analysis to determine the patient's oxygen needs and to avoid carbon dioxide narcosis. 7. Teach patients and family that excessive oxygen therapy may eliminate the hypoxic respiratory drive, causing confusion and drowsiness, signs of carbon dioxide narcosis.

8. Emphasize the importance of a balanced diet. Because the patient may tire easily consider using oxygen, administered by nasal cannula, during meals. 9. Help the patient and his family adjusts their lifestyles to accommodate the limitations imposed by this debilitating chronic disease. 10. Instruct the patient to allow for daily rest periods and to exercise daily as his physician directs.

11. As the disease progresses, encourage the patient to discuss his fears. 12. To help prevent COPD, advise all patients, especially those with a family history of COPD or those in its early stages, not to smoke. 13. Assist in the early detection of COPD by urging persons to have periodic physical examinations, including spirometry and medical evaluation of a chronic cough, and to seek treatment for recurring respiratory infections promptly.

Patient Teaching Discharge and Home Healthcare Guidelines For COPD & Asthma
1. Teach the patient and his family how to recognize early signs of infection; warn the patient to avoid contact with people with respiratory infections. 2. Encourage good oral hygiene to help prevent infection. Pneumococcal vaccination and annual influenza vaccinations are important preventive measures.

Patient Teaching Discharge . 3. To promote ventilation and reduce air trapping, teach the patient to breathe slowly, prolong expirations to two to three times the duration of inspiration, and to exhale through pursed lips. 4. To help mobilize secretions, teach the patient how to cough effectively. 5. If the patient is to continue oxygen therapy at home, teach him how to use the equipment correctly.

Patient Teaching Discharge . 6. Be sure the patient and family understand any medication prescribed, including dosage, route, action, and side effects. 7. Instruct the patient to report any signs and symptoms of infection to the primary healthcare provider. Explain necessary dietary adjustments to the patient and family. 8. Recommend eating small, frequent meals, including high-protein, high-density foods.

Patient Teaching Discharge . 9. Encourage the patient to plan rest periods around his or her activities, conserving as much energy as possible. Arrange for return demonstrations of equipment used by the patient and family. 10. To prevent asthma attacks, teach patients the triggers that can precipitate an attack. 11. Teach the patient and his family to avoid known allergens and irritants.

Patient Teaching Discharge .

12. Explain that any Dyspnea unrelieved by medications, and accompanied by wheezing and accessory muscle use, needs prompt attention from a healthcare provider. 13. If the patient develops a fever above 100 F (37.8 C), chest pain, shortness of breath without coughing or exercising, or uncontrollable coughing. Tell the patient to notify the physician 14. Teach the patient and his family an uncontrollable asthma attack requires immediate attention.

Patient Teaching Discharge . 15. Teach the patient diaphragmatic and effective coughing techniques. 16. Urge him to Increase fluid intake to help loosen secretions and maintain hydration. 17. Teach the patient and his family important of Regular medical follow-up care, when to notify healthcare professional of changes in condition, and periodic spirometry testing, chest x-rays, and sputum cultures.

Salamat Sa Inyo