Elizabeth, age 53, has smoked since she was 16. She worries about heart disease, so she eats right and exercises. Her cholesterol is good, and her blood pressure is normal. However, over the past year Elizabeth gets increasingly short of breath during her Pilates class, and she coughs a lot in the morning. But she believes these symptoms are normal for someone who smokes.

James, 64, has a diagnosis of chronic obstructive pulmonary disease (COPD). He has cut down on his smoking, but it hasn’t helped his breathing much. He uses his quick-acting inhaler four or five times a day just so he can get enough air to do his household chores. James is so worried about having to go on oxygen that he’s afraid to talk to his physician about his symptoms.

James is among the estimated 11.4 million people in the United States known to have COPD, while Elizabeth is among the 24 million who experience symptoms but have not yet been diagnosed.¹ COPD is the fourth leading cause of death in the United States, after heart disease, cancer, and stroke.¹ In the United States, direct and indirect costs of caring for patients with COPD exceed $37 billion annually.¹ The incidence of COPD has increased nearly 42% over the past two decades, and now kills more women than men.^1,2 Nurses can educate patients and families in every healthcare setting about the management and dangers of this treatable and largely preventable disease.

COPD is characterized by airflow limitation that is not fully reversible, is usually progressive, and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases, according to the Global Initiative for Chronic Obstructive Lung Disease, a joint project of the National Heart, Lung, and Blood Institute, the National Institutes of Health, and the World Health Organization.³ The GOLD guidelines provide strategies for healthcare providers around the world to diagnose, manage, and prevent COPD.³  

The life-sustaining work of the lungs occurs within the alveoli. In healthy lungs, capillaries surround alveoli, allowing for the effortless diffusion of oxygen from each alveolus into the bloodstream. At the same time, carbon dioxide moves from the bloodstream into the alveolus and is exhaled. Healthy alveoli are highly elastic, providing a large surface area for gas exchange. If the alveolar surface area from two lungs were spread out, they would be the size of a football field.⁴ The smooth muscles of the bronchi and bronchioles make them somewhat elastic, as well.

Older definitions of COPD emphasize the terms emphysema and chronic bronchitis. However, the newest GOLD guidelines exclude those terms as not fully descriptive of the many pathological changes associated with COPD. In emphysema, alveoli are destroyed; however, the term emphysema fails to describe other structural abnormalities found in COPD. The term chronic bronchitis (presence of cough and sputum for at least three months in two consecutive years) does not reflect the airflow limitation found in COPD.³ This module will not differentiate between the two terms.

The pathological changes of COPD result in mucous hypersecretion, ciliary dysfunction, airflow limitation, air trapping, pulmonary hyperinflation, gas exchange abnormalities, pulmonary hypertension, cor pulmonale (right-sided heart failure), and dysfunction of peripheral and respiratory muscles, usually in this order over the course of the disease.³ Related systemic features can include cachexia, skeletal muscle wasting, osteoporosis, anemia, increased risk of cardiovascular disease, and depression.³

Changes occur in the central and peripheral airways, parenchyma, and pulmonary vasculature:

• Proximal airways (trachea, bronchi, and bronchioles 2 mm and larger): Chronic inflammation of central airways is associated with an increased number of goblet and squamous cells, damaged and destroyed cilia, enlargement of mucus-secreting glands, an increase in the amount of smooth muscle and connective tissue in airway walls, and degeneration of airway cartilage.³
• Peripheral airways (bronchi and bronchioles less than 2 mm): Early changes are similar to those in central airways (chronic inflammation and excess mucous production). The most significant change within the peripheral airways is the repeated cycle of injury and repair of airway walls. This causes structural remodeling of the walls as the result of formation of scar tissue and increased amounts of collagen, causing narrowing of the lumen and partial airway obstruction.³
• Parenchyma destruction (includes alveoli, respiratory bronchioles, and pulmonary capillary system): Dilatation and destruction of respiratory bronchioles occur. Alveoli lose elasticity, and walls between them are destroyed, as is the pulmonary capillary bed, leading to a decrease in functional surface area for gas exchange.^3,4
• Pulmonary vasculature: The intima thickens, smooth muscle increases, and inflammatory cells infiltrate vessel walls. This causes an increase in pulmonary vascular pressure, first occurring with exertion, then later at rest.³ 

Who’s at risk

Risk factors for COPD include environmental and host factors. Cigarette smoking is by far the major environmental risk factor; pipe and cigar smokers have greater COPD morbidity and mortality rates than nonsmokers although their rates are lower than cigarette smokers.³ The risk for COPD in smokers is dose-related, i.e. related to total pack-years smoked (number of packs per day times years of smoking.)³ Between 80% and 90% of COPD deaths are caused by smoking, and it is more deadly for women than men.¹ Among people who die of COPD, 36% are current smokers, 47% are former smokers, and 17% are never-smokers.⁵

Other environmental risk factors include long periods of exposure to second-hand smoke, and indoor and outdoor air pollution. Burning wood, coal, and animal dung in open fires or poorly ventilated stoves lead to very high levels of indoor air pollution in developing countries.³ Occupational contact may be due to people inhaling organic and inorganic dust, vapors, and fumes over a period of time.³ Occupational exposure accounts for over 31% of “never-smokers” who develop COPD and worsens the degree of COPD among smokers by 19.2%.¹

Host factors — those unique to an individual patient — include airway hyper-responsiveness, impaired lung growth, a history of frequent and severe pulmonary infections during childhood, and genetics.^3,4 About 5% of COPD is caused by the inherited deficiency of the protein alpha-1 antitrypsin (AAT), which serves to protect the lungs.¹ Without lifelong AAT replacement therapy, people with this defect are almost certain to develop early (between 32 and 41 years of age) and severe COPD.¹ An estimated 100,000 Americans, largely of Northern European descent, have ATT deficiency.¹

COPD symptoms and diagnosis

Not every patient with COPD will have every symptom, nor will symptoms always develop in the expected order. However, chronic cough is often the initial symptom.^2,3 Patients may discount the cough at first, believing it a normal consequence of smoking, aging, or recovery from a recent bout of the flu or a cold. At first the cough is intermittent. Later it’s present during much of the day and especially on awakening.^2,3 Sputum production may develop although not every COPD patient produces sputum. Sputum is often thick and difficult to raise. Due to cultural and gender variations, many people swallow rather than expectorate it, making its assessment difficult.³ When significant amounts of sputum are present, chronic bronchitis is usually part of the person’s COPD disease process.^2,3

The hallmark symptom of COPD is dyspnea, although it is not usually the first to develop.^2,3 This is the symptom that most often sends patients to their healthcare providers. Dyspnea is usually persistent and progressive, and worsens with activity and during respiratory infections. It’s a major cause of disability and anxiety associated with COPD. At first, dyspnea, or breathlessness, is noted only on unusual effort, such as brisk walking or climbing a flight of stairs. Patients learn to avoid such exertion, often with little conscious awareness. With advanced disease, patients may experience anorexia, weight loss, and coughing spells that can result in syncope, severe depression, cor pulmonale, dyspnea at rest, and frequent exacerbations of COPD, which may require repeated hospitalizations.

Wheezing and chest tightness may be present, as well. These are nonspecific symptoms that may vary between days and over the course of a single day. Wheezing and chest tightness may be a sign of asthma, or a sign of Stage 3 or Stage 4 COPD (described below). Wheezing may be widespread upon auscultation. Chest tightness often follows exertion and may arise from irregular contraction of the intercostal muscles.³ The absence of wheezing and chest tightness does not exclude a diagnosis of COPD, nor does its presence confirm a diagnosis of asthma.³

Healthcare providers may be challenged when faced with a patient complaining of breathing problems. The differential diagnoses for COPD may include the following:²

• COPD: onset in midlife, symptoms progress slowly, long smoking history, dyspnea during exercise, largely irreversible airflow limitation.
• Asthma: onset early in life, symptoms vary from day to day but may be worse at night and in the early morning, history of allergies (for example, rhinitis and eczema), largely reversible airflow limitation.
• Congestive heart failure: fine basilar crackles on auscultation, chest X-ray shows dilated heart and perhaps pulmonary edema, pulmonary function tests indicate volume restriction but no airflow limitation.
• Bronchiectasis: large volume of purulent sputum, often associated with bacterial infection, coarse crackles on auscultation, chest X-ray shows bronchial dilation and bronchial wall thickening.
• Tuberculosis: onset at any age, chest X-ray shows lung infiltrate or nodular lesions, laboratory confirmation, known exposure to tuberculosis.

COPD should be considered in patients presenting with chronic cough and sputum, persistent and progressive dyspnea, and a history of exposure to risk factors, especially cigarette smoking. While obtaining a medical history and performing a physical examination are always an important part of care, their value is limited in establishing a COPD diagnosis.

The gold standard for diagnosis is measurement of airflow limitation through spirometry (one component of pulmonary function testing).³ For best results, patients must be capable of full cooperation. Expected results are calculated based on the patient’s age, height, sex, and race as readings have a direct correlation to lung and chest size, as well as to the stage of lung disease.³ The three readings taken most often during spirometry are:⁶

• Forced vital capacity (FVC) — the volume of air which can be forcibly and maximally exhaled out of the lungs until no more can be expired/exhaled
• Forced expiratory volume in one second (FEV1) — the volume of air that can be forcefully expelled from a maximally inflated lung during the first second
• The ratio of FEV1/FVC

Because people with COPD have airflow limitation, they cannot exhale as forcefully or as quickly as can people with normal lungs. For example, a healthy person may have an FEV1 of 4.15 liters of air while a person with COPD may have an FEV1 of 2.35 liters.³ An outcome of 80% or more of predicted values is considered normal.⁶ For a diagnosis of COPD, the FEV1/FVC must be less than 70% of predicted value and the FEV1 must be impaired. For example, someone with moderate COPD has an FEV1 between 50% and 80% of predicted.³

Additional studies may include bronchodilator reversibility testing. In this procedure, FEV1 is measured before and after administration of a bronchodilator. Partial reversibility is defined as improvement in airflow by 12% of baseline and 200 mL after administration of a bronchodilator.³ If FEV1 returns to the predicted normal range, the patient’s airflow limitation is likely due to asthma.³ If it improves, but not to predicted normal, COPD is probably present.³ Chest X-ray (to exclude alternative diagnoses), arterial blood gas, and screening for AAT (for a symptomatic young person) may be performed, as well.^3,4 After diagnostic testing, the physician must determine the patient’s COPD stage before deciding upon treatment. The stages are:³

• Stage 0 — at risk: Chronic cough and sputum production. Lung function measured by spirometry is normal.
• Stage 1 — mild: Mild airflow limitation, usually with chronic cough and sputum production. Many patients do not yet realize they have COPD. FEV1 is over 80% predicted.
• Stage 2 — moderate: Worsening airflow limitation, progression of symptoms, and noticeable dyspnea on exertion. This is the stage at which most patients first seek care and are diagnosed. FEV1 is between 50% and 80% predicted.
• Stage 3 — severe: Further worsening of airflow limitation, increased shortness of breath, and repeated exacerbations that reduce quality of life. FEV1 is between 30% and 50% predicted.
• Stage 4 — very severe: Severe airflow limitation or the presence of chronic respiratory failure (PaO2 less than 60 mm Hg with or without PaCO2 greater than 50 mmHg on room air. Patients are likely to have cor pulmonale and periodic life-threatening exacerbations.) FEV1 is under 30% or under 50% predicted with chronic respiratory failure.

Treatment, but no cure

While COPD cannot yet be cured, it can be treated and, to some extent, fairly well controlled (especially if the patient has stopped smoking). According to the evidence-based clinical GOLD guidelines, treatment goals for COPD are to:³

• Relieve symptoms
• Prevent disease progression
• Improve exercise tolerance
• Improve health status
• Prevent and treat complications
• Prevent and treat exacerbations
• Reduce mortality

Put another way, the major goals of COPD management are to maximize functional capacity, prevent and treat secondary medical complications, and improve the quality of life by reducing respiratory symptoms.² Treatment for COPD nearly always includes one or more medications. Many patients use medication in inhaled form, through propellant-based or powdered inhalers, or in nebulizers. One study showed that when properly administered, the different delivery systems for inhaled medications are equally efficacious.⁷

Bronchodilators are the first medication introduced to the patient with COPD followed by glucocorticosteroids, based on the severity of the disease and clinical symptoms.3 Medications include —^2,3,8

• Bronchodilators act by relaxing smooth muscle in the airways, thus fostering improved expiration. They may be prescribed prn or for daily maintenance therapy and come in a variety of forms (inhalers, liquid for nebulizer use, pills, and syrups). Bronchodilators include short-acting beta2 agonists such as albuterol and terbutaline, and longer-acting beta2 agonists like salmeterol (Serevent) and formoterol (Foradil). In October 2006, the FDA approved arformoterol (Brovana), the first long-acting beta2 agonist for use in nebulizers, offering a new choice for patients who have trouble managing powdered inhalers. Other bronchodilators include short-acting anticholinergics, such as ipratropium (Atrovent), the longer-acting anticholinergic tiotropium (Spiriva), and, in some cases, methylxanthines (aminophylline and theophylline).
• Glucocorticosteroids are not as useful in the treatment of COPD as they are in asthma, but may be indicated for patients who have asthma with COPD, have frequent exacerbations, or have a documented response to treatment. They come in inhaled and oral form. Inhaled glucocorticosteroids include fluticasone (Flovent), flunisolide (AeroBid), beclomethasone (QVAR), triamcinolone (Azmacort), and budesonide (Pulmicort). Oral glucocorticosteroids include prednisone and methylprednisolone. While nurses may still encounter patients on long-term systemic glucocorticosteroids, current GOLD guidelines limit their recommended use to short periods of time such as during acute exacerbations.
• Combination inhalers containing two medications of differing onset, duration, and action offer convenience and ease of use: Combivent inhalers and Duoneb for nebulizers (albuterol and ipratropium), and Advair (fluticasone and salmeterol).
• Other medications used for COPD include antibiotics for bacterial infection, mucolytics, and antitussives (in some circumstances). COPD patients should be immunized against pneumococcal infections and receive annual influenza vaccinations, which can reduce serious illness and death in COPD patients by about 50%.^1,3,4 Nurses should consult a drug handbook for dosage and adverse effects of all medications.

Nonpharmacologic treatment may include pulmonary rehabilitation, which can reduce symptoms and respiratory hospitalizations, improve quality of life, and increase physical function and participation in daily activities. As COPD progresses, patients experience significant deconditioning. Pulmonary rehabilitation programs are often managed and monitored by nurses and respiratory therapists. Essential components include assessment, patient education (for example, about COPD pathophysiology, nutrition, breathing training, and energy conservation), supervised exercise programs, psychosocial intervention, and follow-up.² Pulmonary rehab has been shown to increase peak workload by 18%, peak oxygen consumption by 11%, and endurance time by 87% of baseline.³ This translates into a significant improvement in quality of life and ability to participate in everyday activities.³ Early referral to such programs can also help to prevent deterioration and progression of the disease process.²

Oxygen therapy is the standard treatment for chronic hypoxia due to COPD.² The American Lung Association estimates that over 800,000 Americans with COPD are maintained on oxygen.² Most patients with Stage 4 COPD and some Stage 3 patients will be on oxygen.³ Oxygen may be used with exercise, at night, during dyspneic episodes, or continually, using various delivery rates and mechanisms. Long-term use of oxygen, greater than 15 hours a day, is the only treatment that has been shown to increase survival for COPD patients.³ The goal of oxygen therapy is to increase PaO2 to 60 mmHg at rest and to maintain an oxygen saturation of 90% or more.³ Patients should be cautioned to never increase oxygen flow without the advice of their healthcare providers because it may lead to excessive retention of CO2.

While surgery is not appropriate for most people with COPD, three procedures may benefit carefully selected patients:

1. Bullectomy, removal of large bulla (areas of ruptured, useless alveoli), decompresses adjacent lung tissue.³ It may be performed via thoracoscopy and can reduce dyspnea and improve lung function.³
2. Lung volume reduction surgery (LVRS) removes diseased parts of the lung to reduce hyperinflation. It improves effectiveness of respiratory muscles and increases elastic recoil pressure of the lung.^2,3 One study of 1,200 patients comparing LVRS with medical treatment showed that after 4.3 years, patients with upper-lobe disease and low exercise capacity who received the procedure had a greater survival rate than those who did not.³
3. Lung transplantation may improve quality of life and functional capacity for people with Stage 4 although it is uncertain if it confers a survival benefit after two years.³ COPD patients account for about 30% of lung transplants; however, the shortage of donors limits the availability of this procedure.²

What nurses can do

Because smoking is the leading cause of COPD, providers should document the smoking status of all patients annually.⁹ It takes less than three minutes to ask about smoking, assess the desire to quit, and advise the patient to quit.⁹ It’s a misconception that smokers don’t want to quit; up to 80% are eager to stop.⁹ Nurses can make referrals to organizations offering smoking cessation programs, such as state and local health departments, the American Lung Association, the American Cancer Association, hospital community service departments, and patients’ insurance companies. Effective programs combine education, counseling, social support, and medication — nicotine replacement products and medications such as bupropion (Wellbutrin, Zyban) and the newest, varenicline (Chantix), which binds to nicotinic brain receptors. No matter how long people have smoked or how advanced their lung disease is, smoking cessation will benefit them.

Nurses can participate in community screening programs to detect COPD in undiagnosed patients in order to intervene early. For example, in one study, clinical nurse specialists screened nearly 250 patients with a simple handheld spirometry device.¹⁰ About 86% were at risk for COPD, and 23% already had mild or moderate COPD.¹⁰

Nurses can ensure that patients are using inhalers correctly and that they understand the difference between prn and daily maintenance medications. Nurses can discuss avoidable risk factors like cigarette smoke, fumes, and indoor and outdoor air pollution. Nurses can teach patients how to pace themselves, how to use breathing techniques, and how to time daily activities in such a way to maximize available energy. COPD cannot yet be cured, but nurses can do much to help improve the quality of life for patients.