Chronic obstructive pulmonary disease (COPD) refers to a condition of chronic airflow limitation. Actually, COPD is an umbrella term for two separate diseases—chronic bronchitis (airway disease) and emphysema (parenchymal disease). Worldwide, COPD is a leading cause of death and disability. Experts predict that by 2020, it will be the third most common cause of death—up from sixth place in 1990.
COPD has an insidious onset, with symptoms arising only after 50% to 70% of lung function is lost. Lung changes cause increased work of breathing. Persons with COPD lose lung function at two to three times the normal rate. COPD also increases the risk of lung cancer.
COPD has both pulmonary and comorbid components that contribute to disease severity and related disability. Comorbid components may include cardiovascular disease, malnutrition with skeletal-muscle wasting, osteoporosis, anemia, increased gastroesophageal reflux
disease, and such psychological processes as depression and anxiety.
COPD is initiated by exposure to cigarette smoke and other noxious particles, which results in lung inflammation. Lung tissue is destroyed in response to increased presence of macrophages and CD-8 T lymphocytes. As part of the pathophysiologic cascade, protective antiproteinases are inactivated, which reduces lung-tissue repair and promotes alveolar-wall destruction.
- In chronic bronchitis, the airways thicken and the mucociliary elevator is inactivated while mucus production increases. As airway diameter narrows, airflow decreases.
- In emphysema, destruction of the alveolar septa reduces the surface area available for gas exchange. Elastic recoil (in which the lungs return to their original size after expanding during inspiration) decreases with loss of lung-tissue structure, resulting in air trapping and hyperinflation.
Cigarette smoking is the most significant risk factor for COPD development and progression. Smoking plays a central role in disease pathogenesis and promotes lung-function loss over the life span. (See Smoking cessation and COPD risk by clicking on the PDF icon above.)
Other risk factors include inhaled pollution (occupational, indoor, and outdoor), reduced lung development or severe lung infection during childhood, coexistence of asthma, and female sex. Some experts include lower socioeconomic status and nutrition as risk factors.
Genetic factors also are thought to influence COPD severity. Alpha1-antitrypsin (AAT) deficiency, for example, is a recessive trait resulting in early COPD.
Dyspnea is the primary disabling symptom of COPD—and the most common. A complex phenomenon that varies from person to person, this unpleasant, persistent labored breathing is triggered by increased ventilation secondary to increased work of breathing.
But dyspnea is more than just a physiologic phenomenon. It also has psychophysiologic components, triggered by such factors as anxiety and fear. Persons with COPD fear the sensation of dyspnea that results from inefficient breathing. Therefore, they avoid exercise; as dyspnea progresses, they begin to abandon activities, leading to a downward spiral of disability. Ultimately, they suffer increasing dyspnea even at rest.
Many COPD patients also experience cough, which may be productive or nonproductive. Chronic sputum production indicates chronic bronchitis.
Screening and diagnosis
The U.S. Preventive Services Task Force doesn’t recommend COPD screening for the general population. However, it urges healthcare providers to consider screening in patients with a family history of AAT deficiency to evaluate for clinical features of COPD or other pulmonary diseases, such as asthma.
Spirometry, the diagnostic tool of choice, measures airflow obstruction. Specific spirometry tests include forced expiratory volume in the first second (FEV1) and forced vital capacity (FVC), which reflects the change in lung volume from total lung capacity through sustained expiration to residual volume. The ratio of expired volume to vital capacity (FEV1/FVC) is calculated. Normal FEV1/FVC is 70% or greater; a lower ratio indicates airflow obstruction and is a sensitive indicator of COPD. Generally, in the setting of a reduced FEV1/FVC ratio, the absolute FEV1, expressed as a percentage of the predicted value, is used to assess disease severity. (See Staging COPD by clicking on the PDF icon above.)
The goals of COPD management are to improve functional capacity, treat or prevent secondary complications, and improve quality of life by managing symptoms. With smoking the primary COPD risk factor, smoking cessation is essential.
Bronchodilators, corticosteroids, and pneumonia and influenza vaccinations are important in managing symptoms and reducing complications.
Bronchodilators include beta2-agonists, anticholinergics, and methylxanthines. These drugs usually are introduced in a stepwise approach.
- Beta2-agonists relax smooth airway muscle. They may be short-acting (for instance, albuterol) or long-acting (for instance, formoterol).
- Anticholinergics promote bronchodilation by blocking acetylcholine on postganglionic cholinergic nerves. Tiotropium (Spiriva), a long-acting anticholinergic, has a duration exceeding 24 hours and is the first COPD drug that requires only once-daily dosing.
- Methylxanthines inhibit phosphodiesterase, leading to increased levels of cyclic adenosine monophosphate, which in turn causes bronchodilation. But methylxanthines are metabolized in the liver to caffeine and can reach toxic levels; therefore, inhaled bronchodilators are more commonly used instead.
Although corticosteroids are used to reduce inflammation, they have limited value in COPD. Inhaled corticosteroids haven’t been shown to slow declines in lung function, although they may be indicated to reduce airway inflammation in COPD patients with chronic bronchitis. Similarly, oral corticosteroids haven’t been proven effective in COPD but may be indicated for disease exacerbations.
COPD patients should receive pneumonia and influenza vaccinations. Yearly influenza vaccinations reduce serious complications by 50% in these patients. Patients older than age 65 should get pneumococcal vaccine (Pneumovax) as well. Antibiotics are recommended only for acute exacerbations when a bacterial infection is present.
For patients with stable COPD, other drugs, such as mucolytics, antitussives, antioxidant agents, immunomodulators, and opioids, aren’t recommended.
Oxygen therapy is reserved for patients with hypoxemia. While it doesn’t improve lung function, it can improve survival in hypoxemic patients. The goal is to achieve an oxygen saturation value of 90% or higher. Oxygen should be prescribed in liters/minute for rest, sleep, and activity, with the prescription determined by arterial blood gas values and desaturation and nocturnal desaturation studies.
Oxygen delivery systems include liquid oxygen, compressed gas, and concentrators. Each system carries risks and benefits. Selection hinges on patient mobility and functional goals.
Portable oxygen concentrators are the newest innovation in oxygen delivery, eliminating the need for patients to carry oxygen with them. These devices have been shown to be safe and effective. In 2005, the Federal Aviation Administration adopted new rules that allow patients to fly with portable concentrators. However, the rule doesn’t require airlines to allow these systems on board; therefore, instruct patients to check with the airline regarding oxygen use when planning travel. The National Home Oxygen Patients Association (http://www.oxygenconcentratorstore.com/breathe-easy/resources/nhopa/) also provides information for patients.
While optimal medical management reduces symptoms, it can’t reverse the pathologic changes secondary to COPD. For patients with chronic respiratory impairment, healthcare providers may prescribe pulmonary rehabilitation (PR). This multidisciplinary program is individually tailored to optimize the patient’s physical and social functioning and increase autonomy. It teaches patients how to manage symptoms and reach their maximum functioning level. The scientific basis for PR has been well-established through multiple randomized, controlled clinical trials. Improved activity tolerance reduces disabling symptoms and improves quality of life.
Patients exercise three to five times weekly, with each session lasting 30 to 90 minutes. When the patient completes PR, a home exercise prescription (maintenance exercise) is the usual care. Although patients who complete PR don’t routinely experience changes in lung function, many have better exercise capacity, decreased dyspnea, and improved quality of life.
For selected patients, lung-volume reduction surgery (LVRS) is an option. As COPD progresses, the lungs overdistend inside the chest cavity. LVRS removes part of the lungs, reducing overcrowding of the chest cavity.
The procedure involves removal of lung tissue at the apices, where smoking-induced COPD commonly is most severe. Subsequently, remaining lung tissue can reexpand and function more efficiently. A large, multicenter National Emphysema Treatment Trial that tested LVRS efficacy found that patients with upper-lobe-predominant emphysema and low initial exercise capacity got the most benefit. On the other hand, patients with emphysema distributed in the lower lobes failed to benefit from the surgery.
Lung transplantation is another option for selected patients. (COPD is the most common diagnosis in lung-transplant candidates.) Although limited by scarcity of organ donors, transplantation has a favorable risk-benefit ratio, with good 1- and 2-year survival rates. Lung transplantation isn’t a cure for COPD. Instead, the patient trades end-stage COPD for lifelong immunosuppression therapy to prevent organ rejection. Candidate selection is based on disease severity, comorbid conditions, and probability of surviving to receive a transplant and surviving after transplantation. (For more information, visit www.unos.org.)
Nursing care for COPD patients focuses on managing symptoms, maximizing function, and teaching skills to enhance self-care. Appropriate referral of patients to community resources helps ensure continuity of high-quality care.
Be sure to include the patient’s family in your teaching, as they play a crucial role in care. Educate them about COPD pathophysiology, including how lung changes relate to symptoms. Teach patients to observe their usual symptoms and to contact their healthcare provider when symptoms worsen. Reinforce the importance of good infection control, such as frequent hand washing and avoiding crowds when upper respiratory infections are prevalent.
Provide education on prescribed medications, covering proper use of inhaled drugs (including spacers if indicated), proper sequence for taking medications to maximize their effects, and adverse effects. Make sure patients know how to determine the amount of inhaled medications left so they can avoid running out. Stress the importance of getting pneumococcal and influenza vaccines. Finally, urge any patient who smokes to stop smoking. (See Smoking cessation recommendations by click on the pdf icon above.)
To help patients manage dyspnea, teach them about activities that reduce or control it, as described below.
- Breathing techniques. Techniques such as pursed-lip breathing help reduce respirations while improving the expiratory phase (by increasing laminar flow of expired air). Tell the patient that slow, controlled expiration postpones small-airway
collapse, thereby reducing air trapping that occurs with forced expiration.
- Proper positioning. Explain that the tripod position, in which the patient sits or stands leaning forward with the arms supported, forces the diaphragm down and forward and stabilizes the chest while reducing the work of breathing. If the patient reports increased dyspnea when performing activities of daily living (ADLs), especially when raising the arms above the head, recommend supporting the arms during ADLs, as by resting the elbows on a surface. Point out that this reduces competing demands of the arm, chest, and neck muscles needed for breathing.
- Energy-conservation techniques. Advise patients to pace activities, take frequent rests, use assistive devices, and break activities into smaller tasks to help reduce dyspnea development.
Also help identify the patient’s best “breathing time” of the day, and recommend reserving strenuous activities for this period. Finally, stress the need to avoid environmental triggers of dyspnea, including temperature extremes and exposure to air pollution, pollen, cigarette smoke, chemical fragrances, and dust.
COPD patients commonly have problems maintaining adequate nutritional intake. As the disease progresses, many experience cachexia. Inform patients with reduced nutritional status that the primary-care provider is likely to monitor their hemoglobin and serum albumin levels.
To improve their nutritional status, advise them to eat small, frequent meals high in protein and avoid gas-producing foods. Instruct them to monitor their weight and food intake. If recommended, advise them to use high-calorie nutritional supplements.
Teach patients who need oxygen therapy about the following:
- proper oxygen use, including the importance of avoiding nearby open flames
- oxygen prescription instructions
- correct equipment care
- back-up oxygen system in case of a power outage.
Psychosocial concerns for COPD patients include increasing dependence on others, lack of control over symptoms, and decreased energy. Also, they’re at high risk for depression and anxiety because of symptom burden and functional limitations. These problems can affect their social interactions, role perception, and physical abilities.
Help them verbalize their feelings and develop healthy coping behaviors. However, know that as increasing dyspnea makes talking more difficult, conversation may grow burdensome.
Include family caregivers in your discussions when appropriate. If the patient has significant psychosocial issues, consider a referral to a social worker, psychologist, or psychiatrist.
Sexual intimacy is an area commonly overlooked by healthcare providers. COPD can decrease certain aspects of sexual functioning. Males may develop erectile dysfunction as lung function declines. What’s more, the physical exertion of sexual activity leads to dyspnea in most COPD patients. The effort required for intercourse resembles that needed to climb one flight of stairs at a normal pace. However, point out that sex doesn’t increase blood pressure, heart rate, or respiratory rate to dangerous levels. (For patient teaching related to sexual activity, see Teaching patients about sexual intimacy by clicking on the PDF icon above).
COPD is increasing in prevalence and burden worldwide. By understanding its pathophysiology and learning as much as you can about treatment options, you can help your patients stay independent as long as possible.
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Gerene S. Bauldoff is an associate professor of Clinical Nursing and Specialty Program Director in the Adult Health and Illness Programs in the College of Nursing at The Ohio State University in Columbus. The planners and authors of this CNE activity have disclosed no relevant financial relationships with any commercial companies pertaining to this activity.