Oxygenation Study Guide

COPD

Chronic obstructive pulmonary disease (COPD) is a preventable and treatable slowly progressive respiratory disease of airflow obstruction involving the airways, pulmonary parenchyma, or both.The parenchyma includes any form of lung tissue, including bronchioles, bronchi, blood vessels, interstitium, and alveoli. The airflow limitation or obstruction in COPD is not fully reversible. Most patients with COPD present with overlapping signs and symptoms of emphysema and chronic bronchitis, which are two distinct disease processes. COPD may include diseases that cause airflow obstruction (e.g., emphysema, chronic bronchitis) or any combination of these disorders. Other diseases such as cystic fibrosis (CF), bronchiectasis, and asthma are classified as chronic pulmonary disorders. Asthma is considered a distinct, separate disorder and is classified as an abnormal airway condition characterized primarily by reversible inflammation. COPD can coexist with asthma. Both of these diseases have the same major symptoms; however, symptoms are generally more variable in asthma than in COPD. This chapter discusses COPD as a disease and describes chronic bronchitis and emphysema as distinct disease states, providing a foundation for understanding the pathophysiology of COPD. Bronchiectasis, asthma, and CF are discussed separately. In 2011, COPD and associated respiratory diseases were estimated to affect 24 million adults and was the third leading cause of death in the United States. Whereas mortality from other major causes of death has been decreasing, deaths from COPD have continued to rise. COPD affects more than 5% of the adult population in the United States. An estimated 27 million adults have COPD, including 14 million diagnosed and more than 12 million undiagnosed adults (NHLBI, 2010). Mortality from COPD among women has dramatically increased since World War II; since 2005, more women than men died of COPD. From 1999 through 2007, COPD hospitalization rates declined for both men and women, but COPD death rates declined only for men. The annual direct cost of COPD, asthma, and pneumonia was $66 billion in 2010, with indirect costs of $19 billion (NHLBI, 2010). Pathophysiology 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 normally decrease with age—for example, vital capacity and forced expiratory volume in 1 second (FEV1)—COPD accentuates and accelerates these physiologic changes as described later. In COPD, the airflow limitation is both progressive and associated with the lungs' abnormal inflammatory response to noxious particles or gases. The inflammatory response occurs throughout the proximal and peripheral airways, lung parenchyma, and pulmonary vasculature (GOLD, 2010). Because of the chronic inflammation and the body's attempts to repair it, changes and narrowing occur in the airways. In the proximal airways (trachea and bronchi greater than 2 mm in diameter), changes include increased numbers of goblet cells and enlarged submucosal glands, both of which lead to hypersecretion of mucus. In the peripheral airways (bronchioles less than 2 mm diameter), inflammation causes thickening of the airway wall, peribronchial fibrosis, exudate in the airway, and overall airway narrowing (obstructive bronchiolitis). Over time, this ongoing injury-and-repair process causes scar tissue formation and narrowing of the airway lumen (GOLD, 2010). Inflammatory and structural changes also occur in the lung parenchyma (respiratory bronchioles and alveoli). Alveolar wall destruction leads to loss of alveolar attachments and a decrease in elastic recoil. Finally, the chronic inflammatory process affects the pulmonary vasculature and causes thickening of the lining of the vessel and hypertrophy of smooth muscle, which may lead to pulmonary hypertension (GOLD, 2010). Processes related to imbalances of substances (proteinases and antiproteinases) in the lung may also contribute to airflow limitation. When activated by chronic inflammation, proteinases and other substances may be released, damaging the parenchyma of the lung. These parenchymal changes may also occur as a consequence of inflammation or environmental or genetic factors (e.g., alpha1-antitrypsin deficiency).

Clinical Manifestations of COPD

Clinical Manifestations 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 (GOLD, 2010). These symptoms often worsen over time. Chronic cough and sputum production often precede the development of airflow limitation by many years. However, not all people with cough and sputum production develop COPD. The cough may be intermittent and may be unproductive in some patients (GOLD, 2010). Dyspnea may be severe and interfere with the patient's 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. Patients with COPD are at risk for respiratory insufficiency and respiratory infections, which in turn increase the risk of acute and chronic respiratory failure. In patients with COPD who have a primary emphysematous component, chronic hyperinflation leads to the "barrel chest" thorax configuration. This configuration results from a more fixed position of the ribs in the inspiratory position (due to hyperinflation) and from loss of lung elasticity (Fig. 24-3). Retraction of the supraclavicular fossae occurs on inspiration, causing the shoulders to heave upward (Fig. 24-4). In advanced emphysema, the abdominal muscles may also contract on inspiration. There are systemic or extrapulmonary manifestations of COPD. These include musculoskeletal wasting (see Chapter 5 for discussion of nutrition assessment and Chapter 45 for discussion of nutrition therapy), metabolic syndrome (see Chapter 27), and depression (a frequent comorbidity that accompanies chronic debilitating illnesses). These clinical manifestations beyond the lungs must also be assessed and treated

Risk factors for COPD

Risk factors for COPD include environmental exposures and host factors (Chart 24-1). The most important environmental risk factor for COPD worldwide is cigarette smoking. A dose-response relationship exists between the intensity of smoking (pack-year history) and the decline in pulmonary function. Other environmental risk factors include smoking pipes, cigars, and other types of tobacco. Passive smoking (i.e., secondhand smoke) also contributes to respiratory symptoms and COPD (GOLD, 2010). Smoking depresses the activity of scavenger cells and affects the respiratory tract's 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, which diminishes lung capacity. 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. In addition, carbon monoxide (a by-product of smoking) combines with hemoglobin to form carboxyhemoglobin. Hemoglobin that is bound by carboxyhemoglobin cannot carry oxygen efficiently. Other environmental risk factors for COPD include prolonged and intense exposure to occupational dusts and chemicals, indoor air pollution (e.g., using biomass stoves for cooking, heating in poorly ventilated dwellings), and outdoor air pollution (GOLD, 2010). Host risk factors include a person's genetic makeup. One well-documented genetic risk factor is a deficiency of alpha1- antitrypsin, an enzyme inhibitor that protects the lung parenchyma from injury. Of patients with COPD, 1% to 2% are found to have severe alpha1-antitrypsin deficiency (Loscalzo, 2010). This deficiency predisposes young people to rapid development of lobular emphysema, even in the absence of smoking. Among Caucasians, alpha1-antitrypsin deficiency is one of the most common genetically linked lethal diseases. COPD may also result from gene-environment interactions (GOLD, 2010). Genetically susceptible people are sensitive to environmental factors (e.g., smoking, air pollution, infectious agents, and allergens) and eventually develop chronic obstructive symptoms. Carriers must be identified so that they can modify environmental risk factors to delay or prevent overt symptoms of disease. Genetic counseling should be offered. Alpha-protease inhibitor replacement therapy, which slows the progression of the disease, is available for patients with this genetic defect and for those with severe disease. However, this infusion therapy is costly and is required on an ongoing basis. Other genetic risk factors may predispose a patient to COPD. Work is ongoing to identify specific variants of genes hypothesized to be involved in the development of COPD. These may include specific phenotypes to several chromosomal regions in families with multiple members developing early-onset COPD.

CHART 24-1 Risk Factors Chronic Obstructive Pulmonary Disease

• Exposure to tobacco smoke accounts for an estimated 80%-90% of cases of chronic obstructive pulmonary disease • Passive smoking (i.e., secondhand smoke) • Increased age • Occupational exposure—dust, chemicals • Indoor and outdoor air pollution • Genetic abnormalities, including a deficiency of alpha1- antitrypsin, an enzyme inhibitor that normally counteracts the destruction of lung tissue by certain other enzymes