Chronic Obstuctive Pulmonary Disease
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Chronic Obstructive Pulmonary Disease
COPD, a progressive and irreversible airway obstruction, is a well recognized problem in the United States representing the fourth leading cause of death. It is directly related to smoking. Other risk factors include: industrial fume and dust, genetic predisposition and recurrent pulmonary infections (McCance, Huether, Brashers & Rote, 2010).
Chronic Bronchitis is characterized as productive cough and increase production of mucus lasting for a period of 3 months for 2 years consecutively (McCance, 2010). Chronically inhaled irritants produce airway epithelial inflammation, characterized by inflammatory cell infiltration and release of cytokines: interleukins, lymphocytes, leukotriens, macrophages and neutrophils. Consequently the development of bronchitis is characterized by bronchial edema an increase in a thicker mucus secretion, and inadequate ciliary function allowing bacteria to colonize and reproduce easily (Haemophilus influenza and Streptococcus pneumoniae). These conditions lead to bronchial obstruction during expiration thereby trapping air. There is ventilation/perfusion mismatch, hypoxemia, decrease tidal volume, hypercapnia and hypoventilation (McCance, 2010). In emphysema there is Primary (Inherited deficiency of enzyme α1 antitrypsin) and Secondary emphysema (loss of inhibition of proteolytic enzymes in the lung from airway irritants inhaled) (McCance, 2010). Initially the pathogenesis of emphysema is similar to chronic bronchitis. The inflammatory cytokines cause inhibition of the lungs endogenous antiproteases and an increase in protease activity resulting in break down of elastin in the aleveolar septa producing a loss of elastic recoil of the airway leading to airway obstruction during expiration, alveoli hyperinflation, and formation of bullae and blebs (McCance, 2010). As a result, there is a reduction in gas exchange in the lungs resulting in a decrease in oxygen uptake and removal of carbon dioxide. The accumulating levels of carbon dioxide increases the respiratory rate, but this is not sufficient to meet oxygen demands and to decrease CO2. Clinical presentation of emphysema includes barrel chest, dyspnea, prolonged expiration, pursed lip breathing, tripoid stance, and minimal wheezing (Higgison, 2010). Diagnosis of COPD is made by pulmonary function test with spyrometry (decrease FEV1). Treatment for COPD includes: oxygen therapy, steroids, bronchodilators and antibiotics (Higgison, 2010). Complications of COPD include: Progressive hypoxemia resulting in pulmonary hypertension that can end as cor pulmonale, polycithemia, and respiratory infections (Higgison, 2010).
Taking in consideration the progressive disabilitating characteristics of this pulmonary disease, the most challenging symptom is difficulty breathing, limiting the patients ability to execute activities of daily living (bathing, getting dressed, grooming) without being extremely exhausted and making these patients realize how much they depend on others for help ( Ek &Ternestedt, 2008). Fatigability derives from difficulty breathing. Fatigue by itself can affect the patients level of functioning and how the patient views his/her own health status (Theander, Jakobsson, Torstensson & Unosson, 2008). Loneliness and social withdrawal present as the disease and symptoms progress, resulting from decreased energy, stamina and physical strength, patients inability to manage their own schedule, and not enjoying previous activities or work. This continues to a point where the patients self image and dignity are compromised (Ek &Ternestedt, 2008). Patients anxiety and depression are not adequately assessed. Questionnaires applied in studies are not fully reliable due to poor specificity and sensitivity of the patients full reports. There is a high prevalence of these psychiatric disorders that are underestimated