Time Allotment: 1 hour Topic description: This topic provides an overview of a disease condition of the respiratory system called

Chronic Obstructive Pulmonary Disease. Included herein are its definition, etiology, manifestations, pathophysiology and management. It is also about the complications that might arise in the long run, if COPD is not controlled. Central Objective: At the end of the 1hour ward class, the learners shall have gained knowledge, enhanced skills and develop appropriate values in caring for patients with COPD in the hospital setting as well as in the community setting. Specific Objectives
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Given the necessary information about COPD, the learners shall: 1) Define COPD in their own words accurately.

2) Give three examples of obstructive diseases that can co-exist with COPD.

I. Introduction The Global Initiative for Chronic Obstructive Lung Disease (GOLD) has defined COPD as a preventable and treatable disease with some significant extrapulmonary effects that may contribute to the severity in individual patients. Its pulmonary component is characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious partcles or gases.(GOLD, 2008)

Socialized Discussion

COPD may include diseases that cause airflow obstruction (eg. Emphysema, chronic bronchitis) or any combination of these disorders. While mortality from other major cause of death has been decreasing, deaths from COPD have continued to rise.

People with COPD commonly become symptomatic during the middle adult years, and the incidence of the disease increases with age. Although certain aspects of lung function decrease with age, COPD accentuates and accelerates these physiologic changes. (Smeltzer, et. al., 2010)

3) Explain the risk factors for developing COPD concisely.

II. Risk Factors A. Exposure to tobacco smoke 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, diminishes lung capacity.

4) Determine the role of smoking in the development of COPD.

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.

Carbon monoxide (a byproduct of smoking), combines with hemoglobin to form carboxyhemoglobin. Hemoglobin that is bound by carboxyhemoglobin cannot carry oxygen efficiently. (Smeltzer, et. al., 2010)

B. Occupational exposure--- dust, chemicals Other environmental risk factors for COPD include prolonged and intense exposure to occupational dusts and chemicals, indoor air pollution, and outdoor air pollution. (GOLD, 2008) In the United States, it has been estimated that COPD in 19% of smokers and in as many as 31% of nonsmokers may be attributable to such exposure.

C. Air Pollution Studies in many countries have found people who live in large cities have a higher rate of COPD compared to people who live in rural areas. Urban air pollution may be a contributing factor for COPD, as it is thought to slow the normal growth of the lungs, although the long-term research needed to confirm the link has not been done. Studies of the industrial waste gas and COPD/asthma-aggravating compound, sulfur

dioxide, and the inverse relation to the presence of the blue lichen Xanthoria (usually found abundantly in the countryside, but never in towns or cities) have been seen to suggest combustive industrial processes do not aid COPD sufferers. In many developing countries, indoor air pollution from cooking fire smoke (often using biomass fuels such as wood and animal dung) is a common cause of COPD, especially in women. D. Genetic abnormalities (alpha1- antitrypsin) This deficiency of alpha1- antitrypsin, an enzyme inhibitor that protects the lung parenchyma from injury, predisposes young people to the rapid development of lobular emphysema, even if they dont smoke. Genetically susceptible people are sensitive to environmental factors (eg, smoking, air pollution, infectious agents, allergens) and eventually develop chronic obstructive symptoms. (Smeltzer, et. al., 2010) III. Pathophysiology

5) Trace the pathophysiology of COPD on the concept

Narrowing of the airways reduces the rate at which air can flow to and from the air sacs (alveoli) and limits the effectiveness of the lungs. In COPD, the greatest reduction in airflow occurs when breathing out (during expiration) because the pressure in the chest tends to compress rather than expand the

map provided for.

airways. In theory, airflow could be increased by breathing more forcefully, increasing the pressure in the chest during expiration. In COPD, there is often a limit to how much this can actually increase airflow, a situation known as expiratory flow limitation. If the rate of airflow is too low, a person with COPD may not be able to completely finish breathing out (expiration) before he or she needs to take another breath. This is particularly common during exercise, when breathing has to be faster. A little of the air of the previous breath remains within the lungs when the next breath is started, resulting in an increase in the volume of air in the lungs, a process called dynamic hyperinflation. Dynamic hyperinflation is closely linked to dyspnea in COPD. It is less comfortable to breathe with hyperinflation because it takes more effort to move the lungs and chest wall when they are already stretched by hyperinflation. Another factor contributing to shortness of breath in COPD is the loss of the surface area available for the exchange of oxygen and carbon dioxide with emphysema. This reduces the rate of transfer of these gases between the body and the atmosphere and can lead to low oxygen and high carbon dioxide levels in the body. A person with emphysema may have to breathe faster or more deeply to compensate,

6) Determine the effect of obstruction in patients with COPD.

which can be difficult to do if there is also flow limitation or hyperinflation. Some people with advanced COPD do manage to breathe fast to compensate, but usually have dyspnea as a result. Others, who may be less short of breath, tolerate low oxygen and high carbon dioxide levels in their bodies, but this can eventually lead to headaches, drowsiness and heart failure. Advanced COPD can lead to complications beyond the lungs, such as weight loss (cachexia), pulmonary hypertension and right-sided heart failure (cor pulmonale). Osteoporosis, heart disease, muscle wasting and depression are all more common in people with COPD. Several molecular signatures associated to lung function decline and corollaries of disease severity have been proposed, a majority of which are characterized in easily accessible surrogate tissue, including blood derivatives such as serum and plasma. A recent 2010 clinical study proposes alpha 1Bglycoprotein precursor/A1BG, alpha 2-antiplasmin, apolipoprotein A-IV precursor/APOA4, andcomplement component 3 precursor, among other coagulation and complement system proteins as corollaries of lung function decline, although ambiguity between cause and effect is unresolved.

IV.

Clinical Manifestations

7) Explain correctly the signs and symptoms manifested by a patient with COPD.

Although the natural history of COPD is variable, it is generally a progressive disease characterized by three primary symptoms: chronic cough, sputum production, and dyspnea on exertion. (GOLD, 2008) The cough may be intermittent and may be unproductive in some patients. Dyspnea may be severe and often interferes with patients activities. It is usually progressive, is worse with exercise, and is persistent. As COPD progresses, dyspnea may occur at rest. Weight loss is common, because dyspnea interferes with eating and the work of breathing is energy depleting. As the work of breathing increases over time, the accessory muscles are recruited in an effort to breathe. In patients with COPD that has primary emphysematous component, chronic hyperinflation leads to the barrel chest thorax configuration. Retraction of the supraclavicular fossae occurs on inspiration, causing the shoulders to heave upward. In advanced emphysema, the abdominal muscles may also contract on inspiration. (Smeltzer, et. al., 2010)

V. Diagnostic Tests A. Spirometry 8) Give a brief and accurate description of the diagnostic tests done to a patient with COPD. Spirometry is used to evaluate airflow obstruction, which is determined by the ratio of FEV1 to forced vital capacity (FVC). Spirometric results are expressed as an absolute volume and as a percentage of the predicted value using appropriate normal values for gender, age, and height. With obstruction, the patient either has difficulty exhaling or cannot forcibly exhale air from the lungs, reducing the FEV1. B. Arterial Blood Gas (ABG) analysis Arterial blood gas measurements may also be obtained to assess baseline oxygenation and gas exchange and are especially important in advanced COPD. (Smeltzer, et. al., 2010) 9) Analyze a certain blood gas result correctly. C. Chest X- ray On chest x-ray, the classic signs of COPD are overexpanded lung (hyperinflation), a flattened diaphragm, increased retrosternal airspace, and bullae. It can be useful to help exclude other lung diseases, such as pneumonia, pulmonary edema or apneumothorax. 4 Stages of COPD 1) Mild- defined by an FEV1/ FVC < 70% and FEV1 greater than or equal to 80%

without cough and sputum production

10) Briefly discuss the 4 stages of COPD concisely.

2) Moderate- defined by an FEV1/ FVC < 70%, FEV1 50%- 80% - shortness of breath upon exertion 3) Severe- defined as FEV1/ FVC < 70% and FEV1< 30- 50% - shortness of breath, reduced exercise capacity and repeated exacerbations 4) Very Severe- defined as FEV1/ FVC, 70% and FEV1 < 30-50% - has signs and symptoms of chronic respiratory failure

VI. Medical Management A. Pharmacologic Therapy Bronchodilators -relieves bronchospasm by altering smooth muscle tone and reduce airway obstruction by allowing 11) Give 2 examples of increased oxygen distribution throughout the lungs each of the medications and improving alveolar ventilation. These agents can be delivered through a metered- dose inhaler under the classifications of drugs (MDI) or other type of inhaler, by nebulization, or via the oral route in pill or liquid form. They may that were discussed. also be used prophylactically to prevent breathlessness by having the patient use them before participating in or completing an activity such as eating or walking.

Bronchodilators are key to symptom management in stable COPD. Before these agents are used, the following information should be considered: 1) Inhaled therapy is preferred. 2) Choice of bronchodilator depends on the availability and individual response in terms of symptom relief and side effects. 3) They may be prescribed on an as- needed or regular basis to reduce symptoms. 4) Long- acting bronchodilators are more convenient for patient use. 5) Combining bronchodilators with different durations of action and different mechanisms may optimize symptom management. (GOLD, 2008) Classes of bronchodilators: Beta- adrenergic agonists 2 agonists stimulate 2 receptors on airway smooth muscles, causing them to relax. There are several 2 agonists available. Salbutamol(common brand name: Ventolin) and terbutaline are widely used short acting 2 agonists and provide rapid relief of COPD symptoms. Long acting 2 agonists (LABAs) such assalmeterol and formoterol are used as maintenance therapy and lead to improved airflow, exercise capacity, and quality of life. Anticholinergic agents

Anticholinergic drugs cause airway smooth muscles to relax by blocking stimulation from cholinergic nerves. Ipratropium provides short-acting rapid relief of COPD symptoms. Tiotropium is a long-acting anticholinergic whose regular use is associated with improvements in airflow, exercise capacity, and quality of life. Ipratropium is associated with increased cardiovascular morbidity. While tiotropium in pill form reduces the risk of all cause mortality, cardiovascular mortality and cardiovascular events[53] that in mist form increases mortality Corticosteroids Although inhaled and systemic corticosteroids may improve symptoms of COPD, they do not slow the decline in lung function. Long- term 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. (GOLD, 2008) Other Medications Other medications include alpha1- antitrypsin augmentation therapy, antibiotics, mucolytic agents, antitussive agents, vasodilators, and narcotics. Vaccines may also be effective.

12) Choose one surgical management and explain it in their own words.

B. Surgical Management Bullectomy- a surgical option for patients with bullous emphysema. Bullae are enlarged airspaces that do not contribute to ventilation but occupy space in the thorax; these areas may be surgically excised. These bullae compress areas of the lung and may impair gas exchange. Bullectomy may help reduce dyspnea and improve lung function. It can be performed via a videoassisted thoracoscope or a limited thoracotomy incision. Lung Volume Reduction Surgery- a palliative surgical option in selected subset of patients. Involves the removal of a portion of the diseased lung parenchyma. This reduces hyperinflation and allows the functional tissue to expand, resulting in improved elastic recoil of the lung and improved chest wall and diaphragmatic mechanics.

C. Oxygen Therapy Supplemental oxygen or oxygen therapy does not greatly improve shortness of breath but can allow people with COPD and low oxygen levels to do more exercise and household activity. Long-term oxygen therapy for at least 16 hours a day can improve the quality of life and survival for people with COPD and arterial hypoxemia or with complications of hypoxemia such as pulmonary hypertension, cor pulmonale, or secondary

13) Give the rationale of the management done to a patient with COPD.

erythrocytosis. High concentrations of supplemental oxygen can lead to the accumulation of carbon dioxide and respiratory acidosis for some people with severe COPD; lower oxygen flow rates are generally safer for these individuals. Another safety issue concerning the use of oxygen for patients with COPD is smoking, because the combination of smoking and oxygen can result in fire accidents. Nowadays oxygen is generally only given to patients who have stopped smoking. D. Pulmonary Rehabilitation Pulmonary rehabilitation is a program of exercise, disease management and counseling coordinated to benefit the individual.[58] Pulmonary rehabilitation has been shown to improve shortness of breath and exercise capacity. It has also been shown to improve the sense of control a patient has over their disease as well as their emotions.

14) Give at least 3 nursing diagnosis together with 2 of the interventions appropriate for each of

VII. Nursing Management Nursing Diagnoses: 1) Impaired gas exchange r/t chronic inhalation of toxins 2) Impaired gas exchange r/t ventilationperfusion inequality 3) Ineffective airway clearance r/t bronchoconstriction, increased mucus

those 3 diagnoses.

production, ineffective cough 4) Ineffective breathing pattern r/t shortness of breath, bronchoconstriction 5) Activity intolerance r/t fatigue, hypoxemia, and ineffective breathing patterns Nursing Interventions: Assist patient in positioning---sitting/ tripod positioning Help loosen secretions by doing chest physiotherapy/ postural drainage. Administer oxygen therapy as ordered. (maximum of 3 LPM only) Encourage patient to stop smoking. Promote adequate hydration. Administer medications as ordered. Promote exercise. a. Progressively increase walking distance of patient. b. Teach deep breathing and coughing exercises to train respiratory muscles to function more effectively. Teach patient on proper diet: avoid too much CHO since it increases production of CO2 leading to respiratory distress. Monitor and manage potential complications.

1) 2) 3) 4) 5) 6) 7)

8)

9)

Guidelines for Teaching patients on MDI 1) Inhale through the nose then slowly breathe

out completely 2) Place mouthpiece in mouth. 3) Press down on inhaler while simultaneously inhaling 1 puff deeply; breathe in air from around. VIII. Prognosis COPD usually gradually gets worse over time and can lead to death. The rate at which it gets worse varies among individuals. The factors that predict a poorer prognosis are:

15) Discuss correctly the prognosis of patients with COPD.

Severe airflow obstruction (low FEV1) Poor exercise capacity Shortness of breath Significantly underweight or overweight Complications like respiratory failure or cor pulmonale Continued smoking Frequent acute exacerbations Prognosis in COPD can be estimated using the Bode Index. This scoring system uses FEV1, body-mass index, 6-minute walk distance, and the modified MRC dyspnea scale to estimate outcomes in COPD.

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Referrences: Agarwal R, Aggarwal AN, Gupta D, Jindal SK. Inhaled corticosteroids vs placebo for preventing COPD exacerbations: a systematic review and metaregression of randomized controlled trials. Chest. 2010; 137(2):318-325. Hoogendoorn M, Feenstra TL, Hoogenveen RT, Rutten-van Mlken MP. Long-term effectiveness and cost-effectiveness of smoking cessation interventions in patients with COPD. Thorax. 2010;65(8):711-718. Shapiro SD, Reilly JJ Jr., Rennard SI. Chronic bronchitis and emphysema. In: Mason RJ, Broaddus VC, Martin TR, et al. Murray & Nadel's Textbook of Respiratory Medicine. 5th ed. Philadelphia, Pa: Saunders Elsevier; 2010:chap 39.

COLLEGE OF NURSING Silliman University Dumaguete City

Submitted by: LEA LUZ MARIE D. TAN PASTOR Submitted to: ASST. PROF. DAWN JANICE A. TIEMPO August 7, 2012