Emphysema-audio - NEWNMCLE

Emphysema, a form of chronic obstructive pulmonary disease, is the abnormal, permanent enlargement of the acini accompanied by destruction of alveolar walls without fibrosis. Obstruction results from tissue changes rather than mucus production, which occurs in asthma and chronic bronchitis. The distinguishing characteristic of emphysema is airflow limitation caused by lack of elastic recoil in the lungs
Causes
Cigarette smoking
Deficiency of alpha1-antitrypsin
Pathophysiology
Primary emphysema has been linked to an inherited deficiency of the enzyme alpha1-antitrypsin, a major component of alpha1-globulin. Alpha1-antitrypsin inhibits the activation of several proteolytic enzymes; its deficiency is an autosomal recessive trait that predisposes a person to emphysema.
In emphysema, recurrent inflammation is associated with the release of proteolytic enzymes from lung cells. This causes irreversible enlargement of the air spaces distal to the terminal bronchioles. Enlargement of air spaces destroys the alveolar walls, which results in a breakdown of elasticity and loss of fibrous and muscle tissue, making the lungs less compliant.
The alveolar septa are initially destroyed, eliminating a portion of the capillary bed and increasing air volume in the acinus. This breakdown leaves the alveoli unable to recoil normally after expanding and results in bronchiolar collapse on expiration. The damaged or destroyed alveolar walls can’t support the airways to keep them open. The amount of air that can be exhaled passively is diminished, trapping air in the lungs and leading to overdistention. Hyperinflation of the alveoli produces bullae and air spaces adjacent to the pleura.
Signs and symptoms
Tachypnea
Dyspnea on exertion
Barrel chest
Prolonged expiration and grunting
Crackles and wheezing on inspiration
Decreased breath sounds
Hyperresonance
Clubbed fingers and toes
Decreased tactile fremitus
Decreased chest expansion
Chronic cough with or without sputum production
Accessory muscle use
Mental status changes, if carbon dioxide retention worsens
Diagnostic test results
Chest X-rays in advanced disease show a flattened diaphragm, reduced vascular markings at the lung periphery, overaeration of the lungs, a vertical heart, enlarged anteroposterior chest diameter, and a large retrosternal air space.
Pulmonary function studies indicate increased residual volume and total lung capacity, reduced diffusing capacity, and increased inspiratory flow.
Arterial blood gas analysis usually reveals reduced partial pressure of arterial oxygen and a normal partial pressure of arterial carbon dioxide until late in the disease process.
Electrocardiography shows tall, symmetrical P waves in leads II, III, and aVF; a vertical QRS axis and signs of right ventricular hypertrophy are seen late in the disease.
Complete blood count usually reveals an increased hemoglobin level late in the disease when the patient has persistent, severe hypoxia.
Treatment
Avoidance of tobacco smoke and air pollution
Bronchodilators, such as beta-adrenergic blockers, albuterol, and ipratropium bromide
Antibiotics
Flu vaccine to prevent influenza
Pneumovax to prevent pneumococcal pneumonia
Adequate hydration
Chest physiotherapy
Oxygen therapy
Mucolytics
Aerosolized or systemic corticosteroids
Lung volume reduction surgery
Lung transplantation

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