INTRODUCTION Chronic obstructive pulmonary disease (COPD)also known as chronic obstructive lung disease (COLD), chronic obstructive airway disease (COAD), chronic airflow limitation (CAL) and chronic obstructive respiratory disease (CORD), refers to chronic bronchitis and emphysema, a pair of commonly co-existing diseases of the lungs in which the airways become narrowed. This leads to a limitation of the flow of air to and from the lungs causing shortness of breath. In clinical practice, COPD is defined by its characteristically low airflow on lung function tests. In contrast to asthma, this limitation is poorly reversible and usually gets progressively worse over time. In England, an estimated 842,100 of 50 million people have a diagnosis of COPD; translating into approximately one person in 59 receiving a diagnosis of COPD at some point in their lives. COPD is caused by noxious particles or gas, most commonly from tobacco smoking, which triggers an abnormal inflammatory response in the lung. The inflammatory response in the larger airways is known as chronic bronchitis, which is diagnosed clinically when people regularly cough up sputum. In the alveoli, the inflammatory response causes destruction of the tissues of the lung, a process known as emphysema. The natural course of COPD is characterized by occasional sudden worsening·s of symptoms called acute exacerbations, most of which are caused by infections or air pollution. The diagnosis of COPD requires lung function tests. Important management strategies are smoking cessation, vaccinations, rehabilitation, and drug therapy (often using inhalers). Some patients go on to require long-term oxygen therapy or lung transplantation. Worldwide, COPD ranked as the sixth leading cause of death in 1990. It is projected to be the fourth leading cause of death worldwide by 2030 due to an increase in smoking rates and demographic changes in many countries. COPD is the fourth leading cause of

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death in the U.S. and the economic burden of COPD in the U.S. in 2007 was $42.6 billion in health care costs and lost productivity.


In humans, the trachea divides into the two main bronchi that enter the roots of the lungs. The bronchi continue to divide within the lung, and after multiple divisions, give rise to bronchioles. The bronchial tree continues branching until it reaches the level of terminal bronchioles, which lead to alveolar sacs. Alveolar sacs are made up of clusters of alveoli, like individual grapes within a bunch. The individual alveoli are tightly wrapped in blood vessels and it is here that gas exchange actually occurs. Deoxygenated blood from the heart is pumped through the pulmonary artery to the lungs, where oxygen diffuses into blood and is exchanged for carbon dioxide in the hemoglobin of the erythrocytes. The oxygen-rich blood returns to the heart via the pulmonary veins to be pumped back into systemic circulation. Human lungs are located in two cavities on either side of the heart. Though similar in appearance, the two are not identical. Both are separated into lobes by fissures, with three lobes on the right and two on the left. The lobes are further divided into segments and then into lobules, hexagonal divisions of the lungs that are the smallest subdivision visible to the naked eye. The connective tissue that divides lobules is often blackened in smokers. The medial border of the right lung is nearly vertical, while the left lung contains a cardiac notch. The cardiac notch is a concave impression molded to accommodate the shape of the heart. Lungs are to a certain extent 'overbuilt' and have a tremendous reserve volume as compared to the oxygen exchange requirements when at rest. Such excess capacity is one of the reasons that individuals can smoke for years without having a noticeable decrease in lung function while still or moving slowly; in situations like these only a small portion of the lungs are actually perfused with blood for gas exchange. As oxygen requirements increase due to exercise, a greater volume of the lungs is perfused, allowing the body to match its CO2/O2 exchange requirements.

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Additionally, due to the excess capacity, it is possible for humans to live with only one lung, with the other compensating for its loss.




Chronic Bronchitis, a disease of the airways, is defined as the presence of cough and sputum production for at least 3 months in each of two consecutive years. PATHOPHYSIOLOGY

SMOKING .Irritation in the respiratory tract Increase in mucus secreting glands and goblet cells Increase mucus secretion Thickening of bronchial wall Bronchial lumen narrows Mucus plugged the airway
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Alveoli damaged and fibrosed Altered function of alveolar

CLINICAL MANIFESTATIONS y y y y y y Excessive chronic sputum production Cough and ronchi Dyspnea Anorexia Weight loss Classic appearance of ´blue bloaterµ

DIAGNOSTIC EXAM y y y CBC ² elevated red blood cell count; hemoglobin and hematocrit elevated in later stages Chest X-ray ² reveals enlarged heart, congested lung fields and normal or flatted diaphragm Pulmonary Function Test (PFT) (Spirometry) ² indicates increased residual volume, decreased vital capacity, FEV1, and FEV1/FVC ratio

MEDICATION THERAPY y y y y Immunization against pneumonia and influenza Adjunct theraphy Antibiotics Bronchodilators o Symphatomimetic o Aminophylline
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y y y

o Xanthine derivatives Chest physiotherapy Corticosteroids Anticholinergics ² ipratropium(atrovent)



Emphysema is a pathologic term that describes an abnormal distention of the air spaces beyond the terminal bronchioles, with destruction of the walls of the alveoli. It is the end stage of a process that has progressed slowly for many years. PATHOPHYSIOLOGY SMOKING FOR MANY YEARS Recurrent in infections Repeated inflammations Disappearance of ciliary function Hypertrophy of goblet cells in abnormal sites of the terminal bronchiole Obstruction of airflow Progressive destruction of alveoli Deacrease in contact of alveolar surface area with capillaries
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CLINICAL MANIFESTATION y ´Pink pufferµ characterized by: o barrel chest o pursed-lip breathing (caused by force exhalation) o obvious use of accessory muscles o weight loss exertional dyspnea progresses with advancing disease persistent tachycardia related to inadequate oxygenation diminished breath sounds wheezes or crackles

y y y y

DIAGNOTIS EXAM y y y y ABG analysis ² reveals slightly decreased PO2; PCO2 is elevated in later stage Chest X-ray ² indicates hyperinflated lungs with a flattened diaphragm; heart size is normal or small Spirometry DLCO

MEDICATION THERAPHY y y y Bronchodilators Beta-adrenergic agonists Anticholinergics
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y y

Long-acting theophylline Corticosteroids

NURSING CARE FOR COPD y Patient education o Breathing exercises o Inspiratory muscle training o Self-care activities o Physical conditioning o Oxygen therapy o Nutritional therapy o Coping measures

NURSING RESPONSIBILITIES FOR COPD y y y y y y y y Promoting smoking cessation Improving gas exchange Improving breathing patterns Improving activity intolerance Enhancing self-care strategies Enhancing individual coping strategies Monitor and managing potential complications Promoting home and community-based care

LATEST TREATMENT FOR COPD Currently, there is no latest treatment for COPD

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