Emphysema, Pulmonary In emphysema, impaired oxygen and carbon dioxide exchange results from destruction of the walls of overdistended alveoli. “Emphysema” is a pathologic term that describes an abnormal distention of the air spaces beyond the terminal bronchioles and destruction of the walls of the alveoli. This is the end stage of a process that progresses slowly for many years. As the walls of the alveoli are destroyed (a process accelerated by recurrent infections), the alveolar surface area in direct contact with the pulmonary capillaries continually decreases. This causes an increase in dead space (lung area where no gas exchange can occur) and impaired oxygen diffusion, which leads to hypoxemia. In the later stages of disease, carbon dioxide elimination is impaired, resulting in increased carbon dioxide tension in arterial blood (hypercapnia) leading to respiratory acidosis. As the alveolar walls continue to break down, the pulmonary capillary bed is reduced in size. Consequently, resistance to pulmonary blood flow is increased, forcing the right ventricle to maintain a higher blood pressure in the pulmonary artery. Hypoxemia may further increase pulmonary artery pressures. For this reason, right-sided heart failure (cor pulmonale) is one of the complications of emphysema. Congestion, dependent edema, distended neck veins, or pain in the region of the liver suggests the development of cardiac failure. There are two main types of emphysema, based on the changes taking place in the lung. Both types may occur in the same patient. In the panlobular (panacinar) type of emphysema, there is destruction of the respiratory bronchiole, alveolar duct, and alveolus. All air spaces within the lobule are essentially enlarged, but there is little inflammatory disease. A hyperinflated (hyperexpanded) chest, marked dyspnea on exertion, and weight loss typically occur. To move air into and out of the lungs, negative pressure is required during inspiration, and an adequate level of positive pressure must be attained and maintained during expiration. Instead of being an involuntary passive act, expiration becomes active and requires muscular effort. In the centrilobular (centroacinar) form, pathologic changes take place mainly in the center of the secondary lobule, preserving the peripheral portions of the acinus. Frequently, there is a derangement of ventilation–perfusion ratios, producing chronic hypoxemia, hypercapnia, polycythemia, and episodes of right-sided heart failure. This leads to central cyanosis and respiratory failure. The patient also develops peripheral edema, which is treated with diuretic therapy. Nursing Management See “Nursing Management” under “Chronic Obstructive Pulmonary Disease” for additional information. Empyema is a collection of thick, purulent (infected) fluid within the pleural space. At first the pleural fluid is thin, with a low leukocyte count, but it frequently progresses to a fibropurulent stage and then to a stage at which it encloses the lung with a thick exudative membrane (loculated empyema). Clinical Manifestations • Patient is acutely ill with signs and symptoms similar to those of an acute respiratory infection or pneumonia (fever, night sweats, pleural pain, cough, dyspnea, anorexia, weight loss). • Symptoms may be vague if the patient is immunocompromised; symptoms may be less obvious if patient has received antimicrobial therapy. Assessment and Diagnostic Methods • Chest auscultation, which demonstrates decreased or absent breath sounds over the affected area; dullness on chest percussion; decreased fremitus • Chest computed tomography (CT) and thoracentesis (under ultrasound guidance
Posted on: Sat, 27 Sep 2014 15:11:28 +0000
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