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CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) COPD is a functional diagnosis given to any pathological process that decreases the

ability of the lungs and bronchi to perform their function of ventilation (hence there is airway obstruction). It is an umbrella term that includes pulmonary emphysema and chronic bronchitis. These diseases can exist in their pure form but they most commonly coexist with overlapping clinical manifestations. It is preventable and treatable but not fully reversible. It is characterized by progressive airflow limitation and an abnormal inflammatory lung response to noxious particles and gases. COPD can coexist with other respiratory diseases.

Causes Intrinsic/Extrinsic Smoking Passive smoking Environmental & Occupational allergens dust, chemicals Ambient air pollution Genetic abnormalities alpha 1; antitrypsin, an enzyme inhibitor that normally counteracts the destruction of lung tissue by certain other enzymes. Smoking depresses the activity of scavenger cells and affects the respiratory tracts 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, diminishing lung

capacity. Smoking also irritates the goblet cells and mucous glands, causing an increased accumulation of mucus, which in turn produces more irritation, infection, and damage to the lung. In addition, carbon monoxide (a byproduct of smoking) combines with hemoglobin to form carboxyhemoglobin. Hemoglobin that is bound by carboxyhemoglobin cannot carry oxygen efficiently.

Pathophysiology COPD may occur as a result of increased airway resistance secondary to bronchial muscosal oedema or smooth muscle contraction. It may be the result of decreased elastic recoil, as seen in emphysema, which results in decreased lung deflation. In COPD, the airflow limitation is both progressive and associated with an abnormal inflammatory response of the lungs to noxious particles and gases. The inflammatory response occurs throughout the proximal and peripheral airways, lung parenchyma (bronchioles & alveoli), and pulmonary vasculature. In the proximal airways, changes include increased numbers of goblet cells and enlarged submucosal glands, both of which lead to hypersecretion of mucus. In the peripheral airways, inflammation causes thickening of the airway wall, peribronchial fibrosis, exudate in the airway, and overall airway narrowing (obstructive bronchiolitis). In the lung parenchyma, alveolar wall destruction leads to loss of alveolar attachments and a decrease in elastic recoil.

The chronic inflammatory process affects the pulmonary vasculature and causes thickening of the lining of the vessel and hypertrophy of smooth muscle, which lead to pulmonary hypertension. It is because of the chronic inflammation and the bodys attempt to repair it, changes and narrowing occur in the airways.

Over time, this on-going injury-and-repair process causes scar tissue formation and narrowing of the airway lumen. Processes related to imbalances of substances (proteinases and antiproteinases) in the lung may also contribute to airflow limitation. When activated by chronic inflammation, proteinases and other substances may be released, damaging the parenchyma of the lung. These parenchymal changes may also occur as a consequence of inflammation or environmental or genetic factors (eg, alpha 1-antitrypsin deficiency).

Clinical Manifestations Although the natural history of COPD is variable, it is generally a progressive disease characterized by three primary symptoms: o *Chronic cough precede the development of airway limitation for many years. o *Sputum production - precede the development of airway limitation for many years. o *Dyspnea on exertion and shortness of breathpersistent and may occur at rest. Breathing is energy depleting. o Weight loss dyspnea interferes with eating; Weight gain lack of exercise and oedema.

o Use of accessory muscles - As the work of breathing increases over time, the accessory muscles are recruited in an effort to breathe. o Wheezing o Chest tightness Dyspnea and shortness of breath occurs with daily activities and is caused by blocked or clogged airways and damaged or destroyed alveoli where oxygen is absorbed and carbon dioxide is released. Symptoms of COPD slowly worsen o Muscle loss and declining endurance o Morning headaches o Clubbing of fingers o Bluish or greyish color underneath the fingernails decreased oxygen levels in the blood. o Barrel chest (COPD with a primary emphysematous component) chronic hyperinflation causes a more fixed position (stays partially expanded) of the ribs in the inspiratory position and loss of lung elasticity. o Prolonged expiration o Pulmonary infection o Chronic hypoxemia o Chronic hypercapnia (excessive level of carbondioxide in the blood)

Diagnostic Assessment The nurse should obtain a thorough health history from patients with known or potential COPD. Pulmonary function studies are used to help confirm the diagnosis of COPD, determine disease severity, and monitor disease progression. A physical examination, chest x-ray (congestion, hyperinflation), pulmonary function tests (increased residual volume, increased functional residual capacity, decreased vital capacity), arterial blood gases (ABG) (respiratory acidosis, hypoxemia), sputum analysis (positive identification of organism), and CT scan are the procedures used to diagnose COPD.

Possible Complications Respiratory insufficiency and failure are major life-threatening complications of COPD. Other complications of COPD include pneumonia, chronic atelectasis, spontaneous pneumothorax, pulmonary arterial hypertension (cor pulmonale), right-sided heart failure, and carbon dioxide narcosis.

Medical Management Treatment is aimed at improving ventilation, to facilitate the removal of bronchial secretions, preventing further lung damage, relieving symptoms and slowing the progression of inical manifestations, preventing complications, and to promote health maintenance and client management of the disease.

o Pharmacologic therapy bronchodilators (Isoproterenol/Isuprel); via nebulizer (Albuterol/Proventil) relieve bronchospasm by altering smooth muscle tone and reduce airway obstruction by allowing increased oxygen distribution throughout the lungs and improving alveolar ventilation hence opening the air passages in the lung; corticosteroids treatment with oral corticosteroids is not recommended in COPD and can cause steroid myopathy, leading to muscle weakness, decreased ability to function, and, in advanced disease, respiratory failure (Hydrocortisone/Solu-Cortef) reduce airway inflammation and help make breathing easier; antibiotics (Ampicillin/Omnipen) in the event of respiratory infections; Combination long-term beta2 -agonists plus corticosteroids in one inhaler may be appropriate (Formoterol/Symbicort). o Oxygen therapy 1 -3L by nasal cannula when the client has severe exertional or resting hypoxemia (PaO2 < 40 mmHg) to raise the PaO2 to no less than 60 mmHg. Oxygen is used cautiously in clients with emphysema because of the long-standing hypercapnia. The respiratory drive in emphysematous clients is triggered by low oxygen levels rather than increased carbon dioxide levels. The drive to breath is the opposite of normal in clients with emphysema so if high levels of oxygen are administered to these clients, their respiratory drive can be obliterate and carbon dioxide retention can occur. The aim of controlled oxygen therapy is to raise PaO2 without worsening the acidosis. An exacerbation of COPD is defined as an event in the natural course of the disease characterized by an acute change in the patients baseline dyspnea, cough, or sputum production beyond the normal day-to-day variations. It may warrant a change in regular medications. Indications for hospitalization for acute exacerbation of COPD include severe dyspnea that does not respond adequately to initial therapy, confusion or lethargy, respiratory muscle fatigue,

paradoxical chest wall movement, peripheral oedema, worsening or new onset of central cyanosis, persistent or worsening hypoxemia, and the need for non-invasive or invasive assisted mechanical ventilation. Optimization of bronchodilator medications is first line therapy and involves identifying the best medication or combinations of medications taken on a regular schedule for a specific patient. Depending on the signs and symptoms, corticosteroids, antibiotic agents, oxygen therapy, and intensive respiratory interventions may also be used.

Nursing Interventions Administer medication as prescribed. Medication is very important in decreasing the clinical manifestations of the disease. E.g. Bronchodilators relax bronchial smooth muscle facilitating air flow. Administer low flow oxygen as prescribed. Oxygen corrects existing hypoxemia. Excessive increases in oxygen may diminish respiratory drive and increase carbon dioxide retention further. Provide chest physiotherapy (moves secretions from the small to the large airways from which they may be expelled), intermittent positive pressure breathing, turning, postural drainage, and suction; encourage coughing, deep breathing, and the use of incentive spirometer. Promotes lung expansion and diaphragmatic breathing. It also discourages rapid, shallow panic breathing. It also promotes relaxation, enabling the client to gain control of dyspnea and reduce feelings of panic. It conserves energy, reduces airway collapse, and lessens clients frustration.

Reinforce pursed-lip breathing. Prolongs exhalation and increases airway pressure. Position in the high Fowlers. Lung expansion and enhances air exchange. Monitor and record vital signs, intake and output (I/O), and laboratory studies. Prompt recognition of deteriorating respiratory functioncan reduce potentially lethal outcomes. Awareness of clients condition improvement, stasis, or decline. Hence treatment is catered around these results.

Maintain the clients diet of small, frequent feedings. Clients will have trouble eating because of the dyspnea. Adequate nutrition is essential to maintain respiratory muscle strength.

Encourage fluids. Hydration helps to thinsecretions. Allow activity as tolerated. Enhances cardiovascular fitness and trains respiratory muscles to function more effectively and strengthen. Respiratory muscles can be strengthened even when the lungs are diseased.

Educate the client on the disease, its triggers for exacerbation, and treatment and therapy regime. Advise the client to avoid conditions that increase oxygen demand, such as smoking, temperature extremes, excess weight, and stress. Instruct the client in energy conservation techniques, such as pacing activities throughout the day, interspersed with adequate rest periods. There should also be a gradual increase in daily activities and exercise. Encourages the client to be pro-active in their care and highlights the early signs for assistance. It also promotes relaxation, enabling the client to gain some control of the disease and reduce feelings of panic.

Nursing Diagnosis Impaired gas exchange r/t decreased ventilation and mucous plugs. Ineffective airway clearance r/t excessive secretions and ineffective coughing. Activity intolerance r/t inadequate oxygenation and dyspnea. Anxiety r/t acute breathing difficulties and fear of suffocation.