COPD: Help your patients breathe easier
Chronic obstructive pulmonary disease is progressive, but it can be managed. Here's how.
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After reading the article you should be able to:
1. Identify symptoms of chronic obstructive pulmonary disease (COPD).
2. Discuss nursing and medical management for a patient with COPD.
3. Develop a teaching plan for a patient with COPD.
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By ANN CRAWFORD, RN, PhD, and HELENE HARRIS, RN, MSN
ANN CRAWFORD is an associate professor of nursing at the University of Mary Hardin-Baylor in Belton, TX. HELENE HARRIS is a nursing instructor at Temple College in Temple, TX. The authors have no financial relationships to disclose. STAFF EDITOR: Linda M. Roman
Chronic obstructive pulmonary disease is progressive, but it can be managed. Here's how.
Chronic obstructive pulmonary disease (COPD), now the fourth leading cause of death in the United States, is projected to move up a notch by 2020.1,2
COPD is a progressive airway disorder associated with an abnormal inflammatory response of the lungs to noxious particles or gases. It's comprised primarily of two related diseases: chronic bronchitis, defined as the presence of cough and sputum production for at least three months in each of two consecutive years, and emphysema, the destruction of the gas-exchanging surfaces of the lung—the alveoli.
The National Heart Lung and Blood Institute estimates that 12 million Americans have diagnosed COPD, and many of them don't get optimal treatment.3 Another 12 million may have COPD but it remains undiagnosed.3 So it's essential for you to know who's at risk and how to assess for this condition, what the current treatment is, and how to manage exacerbations of the disease.
Smoking poses the greatest risk
Suspect COPD in patients who are over 40 and have persistent or progressive dyspnea, chronic cough or sputum production, and a decline in their activity level.3 While 90% of COPD cases are caused by smoking, as few as 25% of smokers develop the disorder.4 This suggests that genetic susceptibility plays a role in the risk for COPD.5
The only genetic risk factor is the condition known as alpha-1 antitrypsin (AAT) deficiency. (AAT is a protease inhibitor, produced by the liver, which acts predominantly by inhibiting neutrophil elastase in the lungs.)6 AAT deficiency accounts for less than 1% of COPD cases in the United States.6
COPD also can be caused by long-term exposure to lung irritants, such as secondhand smoke, dust, chemicals, vapors, exhaust, or other environmental pollutants.3 Frequent, severe lung infections, especially during childhood, may play a role as well, by increasing the risk of lung damage and progression to COPD. However, the use of antibiotics has made this risk factor less prevalent.
Poor diet, low birth weight, and low socioeconomic status, which affect lung growth during gestation and childhood,2,7 also may influence incidence. For a discussion of the pathophysiology of COPD, see "COPD's Pathophysiology" at the end of this article.
What to look for as COPD progresses
Because of the long-term, progressive nature of COPD, patients may not exhibit any significant physical symptoms early in its course. However, a range of signs and symptoms emerges as the disease progresses and may vary based on the presence of other conditions.
Dyspnea is the primary COPD symptom—the one that usually prompts patients to seek medical help. It's typically more pronounced in patients over 50. Individuals may complain of difficulty breathing, initially only with exertion, but later, at rest as well.4 They might also report chest tightness, with increased sputum production.
Coughing is a common manifestation of COPD. It is generally worse in the morning, may or may not be productive, and often accompanies an acute chest illness. The patient may report wheezing that gets worse with activity.
Additionally, patients with COPD may become tachypneic, orthopneic, tachycardic, hypertensive, and anxious.4,8 To facilitate breathing, a patient may assume a "tripod" position: He'll lean forward with his head tilted and his arms resting on his legs or a table. You'll note visible use of accessory muscles in his neck, abdomen, and chest.
In COPD, expiration is prolonged as the patient forces his breath out through obstructed airways. On auscultation, you may hear not only wheezes but crackles, and you may note diminished lung sounds. Chest percussion often reveals hyperresonance. Over time, COPD patients can develop a "barrel chest," in which the anterior-posterior (A-P) diameter increases, and the A-P and lateral diameters of the chest become nearly equal. Normally, the lateral diameter is at least twice the A-P diameter.
More signs of worsening disease
Signs that COPD has progressed include jugular vein distension, peripheral cyanosis, peripheral edema, frequent respiratory infections, and pulse oximetry falling below 90%.
Late signs seen in acute exacerbations include mentation changes, such as anxiousness and restlessness, memory impairment, or confusion, depending on the degree of hypoxia.8 Clubbing of the fingers from long-term hypoxemia is characteristic of advanced COPD.8
As hypoxemia worsens, the slightest increase in activity can produce dyspnea. In turn, severe dyspnea may interfere with the ability to perform even the most basic tasks. For example, patients often find that the effort needed to breathe interferes with the process of eating, since the act of swallowing forces a momentary cessation of respiration.8 This can lead to weight loss when maintaining nutritional balance is essential, as well as potentially exacerbate depression.
Breathing easier with COPD
Treatment for patients with COPD aims at improving the quality of life by preserving optimal lung function and preventing exacerbations.2,6 Generally, treatment consists of therapeutic oxygenation and medication, the mainstays being bronchodilators and inhaled corticosteroids, as well as pulmonary rehabilitation.
Specialists with the Global Initiative for Chronic Obstructive Lung Disease recommends long-term oxygen therapy for patients with a PaO2 of less than 55 mm Hg; a PaO2 of less than 59 mm Hg if there's evidence of polycythemia; or hypertrophy of the right ventricle—cor pulmonale.2 Patients using oxygen will need re-evaluation at one to three months after the start of therapy, because some of them may not require long-term use.4
Continuous-flow nasal cannula is the standard means of oxygen delivery for the stable hypoxemic patient. It's simple and generally well tolerated. Each liter of oxygen flow adds 3% – 4% to the fraction of inspired oxygen (FiO2).4
The other component of treatment, medication, has two goals: to alleviate current symptoms and to prevent complications that might arise during an exacerbation. Drug therapy may include one of more of the following:
Bronchodilators. Medications in this class relieve bronchospasm and reduce airway obstruction, thereby increasing oxygen distribution throughout the lungs and improving alveolar ventilation. Bronchodilators may be delivered via a metered-dose or other type of inhaler, by nebulizer, or by mouth as a pill or liquid. Patients take medication on a regular basis for maintenance, or as needed during episodes of respiratory difficulty; many do both.
Several classes of bronchodilators are available, alone or in combination, including beta2-adrenergic agonists, anticholinergic agents, methylxanthines. The choice of drug depends on each patient's response, in terms of both symptom relief and side effects. Bronchodilators and other drugs for treating COPD are discussed in more detail in the table "Treating COPD" below.
Corticosteroids. Inhaled corticosteroids decrease airway inflammation and are recommended for patients with advanced COPD and repeated exacerbations. When a steroid is combined with a long-acting beta2-agonist, the combination is more effective than either drug given alone.2
Long-term treatment with oral corticosteroids isn't recommended for stable COPD, because it contributes to muscle weakness, respiratory failure, and reduced bone density.2 Inhaled corticosteroids have fewer adverse effects than oral agents.6
In severe cases of COPD, surgery may be considered. Patients with bullous emphysema may be candidates for thoracoscopic bullectomy. Some end-stage COPD patients with localized disease may choose to undergo lung volume reduction surgery. Lung transplantation may be an option, although transplants are associated with multiple other issues and may not significantly improve survival.9
How to manage an exacerbation
Patients with COPD are prone to flare-ups, making acute exacerbation of this condition one of the major reasons for hospital admission in the United States.6 During such an episode, patients experience severe dyspnea with acute hypoxia, putting them at risk for respiratory failure. The increased breathlessness is often accompanied by wheezing and chest tightness, increased cough and sputum production with a change in the color and thickness of the sputum.
In most cases, you'll administer oxygen and increase the dose or frequency of bronchodilators.2 Exacerbations of COPD may respond to inhaled beta2-agonists and anticholinergic aerosols. Oral or IV corticosteroids are recommended as an addition to other therapies.2
During an exacerbation, the patient needs close monitoring. Using a calm, reassuring approach, coach him to breathe using the pursed-lip technique. Improve oxygenation by having him hold his inhaled breath—even for a second—to encourage diffusion of oxygen across alveolar capillary membranes.
The patient will require ICU monitoring if he's confused, lethargic, or has respiratory muscle fatigue, worsening hypoxemia and signs of respiratory failure.6
Outpatient care is a must
Even with the best care, lung function in COPD tends to worsen over time. Still, there are things individuals can do to preserve and maximize remaining functionality. With that in mind, be sure to cover the following points with your patient before discharge:
Smoking cessation. Encourage patients and family members who smoke to quit. This is the single most effective intervention to reduce the risk of developing COPD and slow its progression, according to the Global Initiative for Chronic Obstructive Lung Disease.2 Pharmacotherapy using nicotine replacement, bupropion (Zyban), nortriptyline (Aventyl, Pamelor), or varenicline (Chantix) is recommended when counseling isn't sufficient.
Oxygen therapy. Make sure the patient and his family understand the importance of oxygen use for COPD. Be certain they know how to deliver the appropriate flow rates, and for how long. Also educate them about the safety issues surrounding oxygen use.
Medication. Teach patients, along with their caregivers, about their medications' indications, actions, side effects, contraindications, and storage requirements. Some drugs have specific procedures that should be followed for optimal effectiveness. For example, many COPD medications are administered by metered-dose inhaler (MDI) or dry powder inhaler (DPI) so that the drug goes directly to the lungs. Spacers or tubes may be provided and must be attached to the inhaler to hold the medication until the patient inhales it.
Show the patient how to use his inhaler correctly. If it's an MDI, tell him to shake the inhaler. For both, he should exhale completely, take a slow, deep breath when inhaling the medication, and hold the breath for five to 10 seconds. He should wait at least one minute between breaths if more than one puff is indicated.
Observe the patient as he demonstrates how to use the inhaler. Be sure to document your teaching and the patient's response to it. (Instructions for specific inhalers can be found at chestnet.org/patients/guides/inhaledDevices.php.)
Also, educate patients on the importance of notifying physicians and caregivers about any over-the-counter medications in use. When being treated for COPD, these drugs should be prohibited unless approved by their healthcare providers.
Breathing exercises and conditioning. It's possible the physician will refer your COPD patient for pulmonary rehabilitation.10 In the meantime, you can teach the patient how to take slow, deep breaths through pursed lips. This will help him relax and inhale oxygen and exhale carbon dioxide at a slower pace, decreasing the respiratory rate and preventing alveolar collapse.
Also show him how to position himself for improved chest wall movement. For example, the semi-Fowler's position, with the head of the bed elevated 45 degrees, allows the diaphragm to expand. Alternative therapies, such as guided imagery, playing soothing music, and massage may also be helpful.
Encourage the patient to walk and to perform conditioning exercises to strengthen the muscles used in breathing. Also advise him to pace self-care and other activities throughout the day to conserve strength and decrease dyspnea and fatigue.9
Nutrition. Patients with COPD may have low levels of serum protein, which could contribute to malnutrition and muscle-wasting.11 Refer your COPD patient to a dietitian or perform a nutritional assessment yourself. Unless contraindicated, instruct him to select high-protein foods and those that don't require a lot of energy to prepare and chew.
Coping with a chronic condition. Activity restriction, along with chronic shortness of breath, leads to anxiety and depression. Provide psychosocial support by listening and allowing him to express the emotions that he's experiencing.9 Arrange for a psychological consult, if warranted. Pulmonary rehab programs offer support among patients and usually have a social worker or psychologist available.
Encourage the patient to join a support group like The American Lung Association's Better Breathers Club. To find a local chapter, go to www.lungusa.org/site/pp.asp?c=dvLUK9O0E&b=23051. Community networks sponsored by local institutions may be other avenues for sharing resources among those with the disease.
To monitor the development of patients' COPD, periodic spirometry, or pulmonary function tests (PFTs) must be ordered. In addition to being essential in the diagnosis of COPD, PFTs are helpful in assessing the disease's severity and tracking its progress.6
Patients will also need to get the pneumococcal and influenza vaccines, to prevent infection and exacerbation of their COPD. If they have reactive airway disease or asthma as well as COPD, tell them to avoid potential irritants, such as perfumes, air deodorizers, household cleaners, dust, wood stoves, and kerosene heaters. Caution them against going outdoors if there's significant air pollution.8
Caring for COPD patients is a challenge for nurses because of the many complications that can arise. It's important for us to remain attuned to all aspects of the condition, and to provide an environment for the patient and family that will promote the highest possible degree of wellness.
1. American Lung Association. "Chronic obstructive pulmonary disease fact sheet." 2006. www.lungusa.org/site/pp.asp?c=dvLUK9O0E&b=35020 (7 Nov. 2007).
2. Global Initiative for Chronic Obstructive Lung Disease. "Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease." 2006. www.goldcopd.com/Guidelineitem.asp?l1=2&l2=1 &intId=989 (8 Nov. 2007).
3. National Heart Lung and Blood Institute. "What is COPD?" 2007. www.nhlbi.nih.gov/health/dci/Diseases/Copd/Copd_Wha tIs.html (7 Nov. 2007).
4. Sharma, S, & Graham, L. "Chronic obstructive pulmonary disease." 2005. www.emedicinehealth.com/chronic_obstructive_pulmonary_disease_copd/article_em.htm (7 Nov. 2007).
5. Ohar, J. "An update on the diagnosis of COPD and asthma." 2006. www.medscape.com/viewprogram/6143 (7 Nov. 2007).
6. Sharma, S. "Chronic obstructive pulmonary disease." 2006. www.emedicine.com/med/topic373.htm (7 Nov. 2007).
7. Scullion, J. E. (2004). Chronic obstructive pulmonary disease and community-based pharmacological care. Br J Community Nurs, 9(3), 97.
8. Daniels, R. Nosek, L, & Nicoll, L. (2007). Contemporary medical-surgical nursing. Clifton Park, NY: Thomson Delmar Lear.
9. Smeltzer, S., Bare, B., et al. (2008). Textbook of medical-surgical nursing (11th ed.). Philadelphia: Lippincott Williams & Wilkins.
10. American Thoracic Society Documents. (2006). American Thoracic Society/European Respiratory Society Statement on pulmonary rehabilitation. Am J Respir Crit Care Med, 173(12), 1390.
11. Gronkiewicz, C., & Borkgren-Okonek, M. (2004). Acute exacerbation of COPD: Nursing application of evidence-based guidelines. Crit Care Nurs Q, 27(4), 336.
Chronic obstructive pulmonary disease (COPD) encompasses two disease processes that affect airway patency: inflammation of the large and small airways in chronic bronchitis, and the destruction of lung parenchyma in emphysema. With bronchitis, the mucous glands in the lungs become enlarged, causing increased mucus production and coughing. The combination of excessive mucus and repeated coughing produces inflammation within the bronchioles, which over time causes thickening of the bronchiole walls. These changes, along with the loss of supporting alveolar attachments to the bronchioles, cause the airway to become narrow and deformed, limiting airflow.
With emphysema, patients have abnormal, permanent enlargement of the alveoli and terminal bronchioles. The main types of emphysema include centrilobar and panlobar. In centrilobar emphysema, lung destruction begins in the central respiratory bronchioles and extends toward the periphery. As the tissue walls disintegrate, the bronchioles enlarge and become confluent. Centrilobar, found in long-term smokers, is the more common form of emphysema. Its effects are more severe in the upper lobes, while panlobar emphysema affects the entire lung equally. The latter destroys the lung tissue at the more distal structures and alveolar sacs. It often leaves enlarged, thin-walled air spaces, which are known as "blebs" when they occur near the visceral pleura and "bullae" when they develop in the lung parenchyma.
In both types of emphysema, altered tissue results in reduced elasticity of the lungs, increased dead space, and a heightened risk of airway collapse during expiration, causing airway obstruction. The destruction of the alveoli reduces the surface area at the alveolar-capillary membrane, which decreases gas exchange and reduces surfactant production. Regardless of how the disease process manifests, the end result of COPD is a chronic ventilation-perfusion mismatch: Blood flows past non-oxygenated alveoli, resulting in hypoxemia and progressive hypercapnia.
Sources: 1. Sharma, S., & Graham, L. "Chronic obstructive pulmonary disease." 2005. www.emedicinehealth.com/chronic_obstructive_pulmonary_disease_copd/article_em.htm (2 Nov. 2007). 2. Daniels, R., Nosek, L., & Nicoll, L. (2007). Contemporary medical-surgical nursing. Clifton Park, NY: Thomson Delmar Lear.
Listed below are some of the bronchodilators and corticosteroids commonly prescribed for COPD; there are also combination formulations. These drugs work to relieve symptoms, but they do not cure the disease.
Sources: 1. Global Initiative for Chronic Obstructive Lung Disease. "Pocket guide to COPD diagnosis, management and prevention." 2006. www.goldcopd.com/Guidelineitem.asp?l1=2&l2=1&intId=1116 (2 Nov. 2007). 2. Karch, A. (2006). 2006 Lippincott's nursing drug guide. Philadelphia: Lippincott Williams & Wilkins. 3. Kee, J. L., Hayes, E. R., & McCuistion, L. E. (2006). Pharmacology: A nursing process approach (5th ed.). St. Louis: Saunders Elsevier.